tag:blogger.com,1999:blog-46145552853461224042024-02-07T06:23:37.917-08:00Journal of Cardiothoracic and Vascular Anesthesia BlogJCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.comBlogger13125tag:blogger.com,1999:blog-4614555285346122404.post-49688745033239705012013-05-10T12:24:00.002-07:002013-05-10T12:24:54.299-07:00E-CHALLENGES & CLINICAL DECISIONS<strong><span style="font-size: large;">E-CHALLENGES & CLINICAL DECISIONS</span></strong><br />
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<em>Feroze Mahmood, MD Madhav Swaminathan, MD</em><br />
<em>Section Editors</em><br />
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<strong><span style="font-size: large;">Major Surgery, Hemodynamic Instability, and a Left Atrial Appendage Clot: What to Do?</span></strong><br />
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<span style="font-size: x-small;"><em>Remco Bergman, MD, Omair Shakil, MD, Bilal Mahmood, BA, and Robina Matyal, MD</em></span><br />
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A 77-YEAR-OLD PATIENT was scheduled for emergency spinal surgery for multiple cervical vertebral fractures. He had sustained bilateral fractures of the C5 and C6 pedicles after falling from his bed. Of note, the injury was associated with neurologic deficits (motor and sensory) in the upper and lower extremities and the patient’s cervical spine was deemed unstable. His medical history was significant for coronary artery disease, congestive heart failure, and transient ischemic attacks and he had an automatic internal cardiac defibrillator placed recently for recurrent ventricular tachycardia.<br />
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After obtaining intravenous access by 2 peripheral catheters and 1 arterial catheter, the patient was brought to the operating room. The induction of general anesthesia was uneventful and the airway was secured with modified rapid-sequence induction using a glidescope while maintaining inline traction. Immediately after the start of the surgery, the patient went into atrial fibrillation (AF), with a heart rate of 120-130 beats/min, accompanied by a decrease in blood pressure from 110/80 to 80/50 mmHg. There were no accompanying ST-segment changes on the electrocardiogram. The position of his endotracheal tube was confirmed, the depth of anesthesia was ensured, and he was administered a rapid fluid bolus of lactated Ringer’s solution, 500 mL. Intermittent boluses of intravenous phenylephrine (500 [H9262]g) and esmolol (total 50 mg) also were administered to support his systolic blood pressure and control his heart rate, respectively. With these measures, the patient’s heart rate decreased to 90 beats/min and his blood pressure improved to 90/50 mmHg. Given his medical history of coronary artery disease and persistent hemodynamic instability, transesophageal echocardiography (TEE) was performed to assess his volume status and cardiac function. The TEE demonstrated mild symmetric left ventricular hypertrophy with cavity dilation, global moderate-to-severe systolic dysfunction, an ejection fraction of 30%, and severe diastolic dysfunction (decreased compliance) with an E/e= of 15. There also was moderate aortic stenosis (AS) with an aortic valve area of 1.0 cm2. Although the degree of myocardial dysfunction was known from the patient’s history, the moderate AS was a new finding. In addition, the left atrium was dilated moderately, with a sluggish flow and significant spontaneous echocardio-graphic contrast in the left atrial appendage (LAA). Interestingly, an echodensity measuring 2 cm [H11003] 1.5 cm also was visualized in the LAA; the appearance of which was consistent with a thrombus (Fig 1).<br />
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Fig 1. Midesophageal 2-chamber view showing the left atrial appendage with an echodensity most consistent with a thrombus.<br />
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<strong>ECHOCARDIOGRAPHIC FINDINGS</strong><br />
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1. The presence of a significant compliance abnormality of the left ventricle, given the patient’s history of congestive heart failure, necessitated a judicious approach to fluid administration.<br />
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2. The occurrence of AF with moderate AS, leading to a loss of an atrial contribution to left ventricular filling, required fluid administration.<br />
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3. The moderate AS and LAA thrombus were unexpected findings.<br />
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From the Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA<br />
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Address reprint requests to Omair Shakil, MD, Research Fellow, Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, One Deaconess Road, CC-470, Boston, MA 02215. E-mail: oshakil@bidmc.harvard.edu<br />
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<span style="font-size: x-small;">© 2013 Elsevier Inc. All rights reserved. 1053-0770/2703-0001$36.00/0 http://dx.doi.org/10.1053/j.jvca.2012.09.007</span><br />
<span style="font-size: x-small;"><br /></span><span style="font-size: x-small;">Journal of Cardiothoracic and Vascular Anesthesia, Vol 27, No 3 (June), 2013: pp 625-626</span><br />
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<span style="font-size: x-small;">625</span><br />
<span style="font-size: x-small;">626 BERGMAN ET AL</span><br />
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<strong>CLINICAL CHALLENGES</strong><br />
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1. To achieve optimal fluid management, despite the contradictory demands of the patient’s clinical situation; ie, AF and AS requiring fluid administration versus the conservative approach demanded by the decreased left ventricular compliance.<br />
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2. Optimal management of the AF and LAA thrombus; ie anticoagulation (risk of persistent hemodynamic instability) versus cardioversion (risk of thrombus dislodgement).<br />
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<strong>CLINICAL DECISIONS</strong><br />
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1. The patient’s blood pressure was supported with pre-load augmentation and [H9251]-adrenergic drugs (phenylephrine).<br />
2. Heart rate control was achieved with [H9252]-adrenergic blocking drugs (esmolol).<br />
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3. A mutual decision was reached with the surgical team to withhold cardioversion to decrease the risk of possible LAA thrombus dislodgement.<br />
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4. A cardiology consultation was scheduled in the immediate postoperative period to manage the anticoagulation and AF.<br />
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<strong>DISPOSITION</strong><br />
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Afterwards, the patient was extubated uneventfully and transferred to the coronary care unit. On the second postoperative day, intravenous heparin infusion was started, which was bridged to oral anticoagulation with coumadin. The patient was discharged a few days later in stable condition.<br />
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<strong><span style="font-size: large;">EDITORIAL</span></strong><br />
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<strong>Anesthesiologists and Transesophageal Echocardiography: Echocardiographers or Echocardiologists?</strong><br />
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DURING HEMODYNAMIC INSTABILITY, clinicians choose to use monitors which they are most accustomed to.1 The time-limited nature of decision-making in the perioperative arena necessitates an approach that quickly can establish a diagnosis and dictate treatment. The use of TEE under such circumstances has been established as an essential monitor.2 The therapeutic impact of intraoperative TEE traditionally has been defined as a change in the surgical/anesthetic management or the addition of postoperative follow-up.3 Life-threatening hypoxia and intractable hypotension are considered category I indications for intraoperative TEE3 and there is unequivocal evidence of the impact of TEE for these indications. However, the use of intraoperative TEE to confirm a clinical suspicion with no change in therapy generally is not considered a major therapeutic intervention. Although arguably equally valuable, such an impact is difficult to quantify and therefore not considered, possibly leading to an underestimation of the true therapeutic effect.<br />
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The case presented in this issue of the Journal highlights many of these very important and debatable issues.4 The presented patient undergoing emergency cervical spine surgery suddenly developed significant hemodynamic instability shortly after the start of surgery. At this point, the anesthesia team did not have adequate access to the patient to place invasive monitoring lines, and the traumatic nature of the case made it a rather urgent situation. The team quickly had to establish or exclude a diagnosis for the sudden hemodynamic instability. Under the circumstances, a rapid TEE examination was the most obvious and logical choice. However, although the TEE examination provided the necessary answers, it raised certain questions. A thrombus was visualized unexpectedly in the left atrial appendage during TEE. Although atrial fibrillation and hemodynamic instability are indications for an emergency cardioversion, the presence of a left atrial appendage<br />
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thrombus was a complicating factor. The risk of possible dislodgment of the thrombus with cardioversion had to be weighed against the risk of further hemodynamic deterioration. Although a discussion of the pros and cons of cardioversion under these circumstances is beyond the scope of this editorial, this intraoperative situation represented a decision-making dilemma. The multiple complicating factors (history of trauma, nature of the injury/surgery, atrial fibrillation, and the unexpected finding of a left atrial appendage thrombus) necessitated a patient-specific approach in a multidisciplinary fashion.<br />
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Although the patient did not have “life-threatening” hemodynamic instability, the circumstances were such that a diagnosis had to be established or excluded rapidly. Although TEE provided the desired information, ironically it created a clinical challenge, with no absolutely correct answers. Not only did TEE assist in resuscitation and the exclusion of diagnoses, it also had an enormous therapeutic impact in the conventional sense, in that it changed the anesthetic management and eventual disposition of the patient.5<br />
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With the increasing use of intraoperative TEE, anesthesiologists are finding themselves in unchartered territories and increasingly are involved in the decision-making that was once considered outside the scope of their traditional practice and expertise. There seems to have been a gradual transformation of anesthesiologists’ role from perioperative “echocardiographer” to “echocardiologist.” This changes the anesthesiologists’ role from a service provider to an active decision-maker with the ability to affect outcome.5<br />
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Remco Bergman, MD Feroze Mahmood, MD<br />
Department of Anesthesia, Critical Care, and Pain Medicine<br />
Beth Israel Deaconess Medical Center <br />
Harvard Medical School<br />
Boston, MA<br />
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<strong>REFERENCES</strong><br />
1. Jacka MJ, Cohen MM, To T, et al: The use of and preferences for the transesophageal echocardiogram and pulmonary artery catheter among cardiovascular anesthesiologists. Anesth Analg 94:1065-1071, 2002<br />
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2. Mahmood F, Christie A, Matyal R: Transesophageal echocardiography and noncardiac surgery. Semin Cardiothorac Vasc Anesth 12:265-289, 2008<br />
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3. American Society of Anesthesiologists and Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography: Practice guidelines for perioperative transesophageal echocardiography. An updated report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Anesthesiology, 112:1084-1096, 2010<br />
4. Bergman R, Shakil O, Mahmood B, et al: Major surgery, hemo-dynamic instability, and left atrial appendage clot: What to do? J Cardiothorac Vasc Anesth 2012 (in press)<br />
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5. Suriani RJ, Neustein S, Shore-Lesserson L, et al: Intraoperative transesophageal echocardiography during noncardiac surgery. J Cardiothorac Vasc Anesth 12:274-280, 1998<br />
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© 2013 Elsevier Inc. All rights reserved. 1053-0770/2703-0001$36.00/0 http://dx.doi.org/10.1053/j.jvca.2012.09.008<br />
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<br />JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-14313466513366143742013-03-22T10:01:00.000-07:002013-03-22T10:01:55.856-07:00<br />
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<span style="font-size: large;"><span style="font-weight: normal;">E-CHALLENGES & CLINICAL DECISIONS</span></span><span style="font-size: 18pt;"><o:p></o:p></span></h2>
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<i>Feroze Mahmood, MD Madhav Swaminathan, MD</i><o:p></o:p></div>
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<i>Section Editors</i></div>
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<b style="text-indent: -71.95pt;"><span style="font-size: large;">Percutaneous Closure of an Atrial Septal Defect and 3-Dimensional Echocardiography</span></b></div>
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Faraz Mahmood, BA,*† Omair Shakil, MD,*† Jeniffer R. Gerstle, MD,*† and Robina Matyal, MD*†<o:p></o:p></div>
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<span style="font-family: Times, Times New Roman, serif; font-size: small;"><b>A</b>N OTHERWISE HEALTHY 50-year-old man was scheduled for percutaneous atrial septal defect (ASD) closure with an Amplatzer Septal Occluder (AGA Medical Corp, Plymouth, MN). The patient initially had presented to an outside hospital 1 year earlier with an episode of chest pain at rest. A chest x-ray performed during that admission showed a widened mediastinum. A subsequent computed tomography scan and transthoracic echocardiogram (TTE) revealed a 2.1-cm wide secundum ASD (<span style="color: #172b82;">Fig 1</span>) with a dilated right ventricle and moderately dilated right and left atria. The patient did not follow through with recommendations for a TEE and possible ASD closure and was lost to follow-up. A year later, he returned to the authors’ institution with a 6-month long history of dyspnea and episodic chest pain with moderate exertion that was relieved by rest. He underwent cardiac catheterization to assess for the presence of coronary artery disease, but which was negative for any flow-limiting lesions. Resting hemodynamics revealed normal right-sided pressures, and oxygen saturation measurements that were consistent with a left-to-right shunt (Qp/Qs [H11005] 2.4). He subsequently was referred for ASD closure under TEE guidance. After an uneventful induction of general anesthesia, a TEE examination was performed using an IE-33 Ultrasound System X7-2E Probe (Philips Medical Systems, Andover, MA) capable of real-time 3-dimensional (3D) imaging.<br /><!--[if !supportLineBreakNewLine]--><br /><!--[endif]--><o:p></o:p></span></h1>
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<b><span style="font-family: Times, Times New Roman, serif;">ECHOCARDIOGRAPHIC FINDINGS<o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;">The preliminary TEE examination revealed a 2.1-cm (edge-to-edge) wide secundum ASD (<span style="color: #172b82;">Fig 1</span>). A left-to-right shunt with a large flow across the interatrial septum was detected, and the right atrium was also dilated; the left atrium was normal in size. Although the right ventricular cavity was dilated, the overall left ventricular systolic function was normal (left ventricular ejection fraction [H11022]55%). Mild mitral regurgitation ([H11001]1) was noted, but the aortic and mitral leaflets appeared structurally normal. No spontaneous echocardiographic<o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;"> contrast or thrombi were seen in the left atrium, the right atrium, or the left and right atrial appendages. There was also a small patent foramen ovale along the inferior edge of the interatrial septum with a left-to-right shunt. The edge of the secundum ASD were seen to consist of a thin mobile filamentous tissue (<span style="color: #172b82;">Video 1 </span>supplementary videos are available online]).</span></b><br />
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<b><span style="font-family: Times, Times New Roman, serif;"><b><span style="font-family: Times, Times New Roman, serif;">Video 1</span></b></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;">CLINICAL CHALLENGES<o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;">Although the procedure itself was relatively uncomplicated, the clinical team faced considerable difficulty in the deployment of the Amplatzer device and its seating. Initially, a size 22 Amplatzer device was percutaneously deployed across the ASD, but TEE imaging showed significant residual left-to-right shunting, and the device was assessed to be mechanically insecure in that it was not well seated on the relatively large ASD. As a result, this device was removed (<span style="color: #172b82;">Video 2</span>). Next, a larger, 24-mm Amplatzer device was deployed with some reduction in residual shunting, but the mechanical seating of the device was again evaluated to be insecure with a likelihood of dislodgement (<span style="color: #172b82;">Video 2</span>).</span></b><br />
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Video 2</div>
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<b><span style="font-family: Times, Times New Roman, serif;">The clinical challenges encountered during the case were as follows: (1) Has the ASD size been measured accurately? (2) Should the thin and mobile portion of the ASD be excluded from ascertaining the ASD diameter? and (3) Would a larger device be suitable for this ASD?<br /><!--[if !supportLineBreakNewLine]--><br /><!--[endif]--><o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;"><i>From the *Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, MA; and †Harvard Medical School, Boston, MA.</i><o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;"><i>Address reprint requests to Omair Shakil, MD, Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, One Deaconess Road, CC-470, Boston, MA 02215. E-mail: <span style="color: #172b82;">oshakil@bidmc.harvard.edu</span></i><o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;"><i>© 2013 Elsevier Inc. All rights reserved. 1053-0770/2702-0001$36.00/0 <span style="color: #172b82;">http://dx.doi.org/10.1053/j.jvca.2012.09.016</span></i><i><span style="color: #172b82;"><br /></span></i><i>Key words: atrial septal defect, 3-dimensional transesophageal echocardiography, Amplatzer device</i></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;">Fig 1. The ASD had a diameter of 2.1 cm on 2-dimensional transesophageal echocardiography. RA, right atrium; LA, left atrium. (Color version of figure is available online.)<br /><br /><br /><!--[endif]--><o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;">400 <i>Journal of Cardiothoracic and Vascular Anesthesia, </i>Vol 27, No 2 (April), 2013: pp 400-401<o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;">PERCUTANEOUS CLOSURE OF AN ASD<br /><!--[if !supportLineBreakNewLine]--><br /><!--[endif]--><o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;"><br /><!--[if !supportLineBreakNewLine]-->Fig 2. MPRF of volumetric data acquired during transesophageal echocardiography confirmed the diameter of the ASD to be 3.4 cm. (Color version of figure is available online.)<br /><br /><br /><!--[endif]--><o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;">ECHOCARDIOGRAPHIC ANALYSIS<br /><!--[if !supportLineBreakNewLine]--><br /><!--[endif]--><o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;">At this point, the size of the ASD was measured again using the multiplanar reformatting (MPRF) of the volumetric 3D data acquired during the TEE examination. Using the 3D quantification function of the Q-Lab software (Philips Medical Systems), the filamentous tissue of the ASD was excluded from the measurement of the diameter (<span style="color: #172b82;">Fig 2</span>). The diameter obtained<o:p></o:p> with the MPRF method was 3.4 cm (<span style="color: #172b82;">Fig 2</span>). Based on this new reading, the team decided to deploy a size 34 Amplatzer occluding device. The device was deployed uneventfully and was seated securely across the rim of the ASD. The absence of any residual shunt on fluoroscopy and 3D transesophageal echocardiography confirmed the optimal positioning of the device. The rest of the case proceeded uneventfully, and the patient was discharged a few days later.<br /><br /><!--[if !supportLineBreakNewLine]--><br /><!--[endif]--><o:p></o:p></span></b></div>
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<b><span style="font-family: Times, Times New Roman, serif;">For further information and follow-up discussion of the E-Challenge, please go to:<br />(1) <i>JCVA </i>online web page for the video images at <span style="color: #172b82;">www.JCVAonline.com</span><span style="color: #172b82;"><br /></span>(2) <i>JCVA </i>blog site for adding your comments or for viewing the other responses: <span style="color: #172b82;">http://JCVAblog.blogspot.com</span></span></b><span style="font-size: 9pt;"><br /><!--[if !supportLineBreakNewLine]--><br /><!--[endif]--></span><span style="font-family: "Times-Roman","serif"; mso-bidi-font-family: Times-Roman;"><o:p></o:p></span></div>
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<b><span style="font-family: "Myriad-Bold","sans-serif"; mso-bidi-font-family: Myriad-Bold;">BLOG</span></b><o:p></o:p></div>
JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-39239373813686066252012-07-13T16:13:00.002-07:002012-07-13T16:13:55.074-07:00E-CHALLENGES & CLINICAL DECISIONS<div align="right">
<span style="font-size: x-small;"><em>Feroze Mahmood, MD</em></span></div>
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<span style="font-size: x-small;"><em>Madhav Swaminathan, MD</em></span></div>
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<span style="font-size: x-small;"><em>Section Editors</em></span></div>
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<strong><span style="font-size: x-large;">Dynamic Mitral Regurgitation Without Regional Wall Motion Abnormality</span></strong></div>
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<span style="font-size: xx-small;"> <span style="font-size: x-small;">Greg Balfanz, MD,</span></span><span style="font-size: x-small;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;">* Harendra Srora, MD,<span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;">* Brett C. Sheridan, MD,<span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;">† Jason N. Katz, MD, MHS, <span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;">‡ &</span></span></span></span><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"> Priya A. Kumar, MD<span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;">*</span></span></span></span></span></span></div>
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<span style="font-size: xx-small;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;">*Department of Anesthesiology, University of North Carolina, Chapel Hill, NC </span></span></span></span></span></span><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;">†</span>Department of Surgery, University of North Carolina, Chapel Hill, NC</span></span></span></span></span></span></span><br />
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<span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-size: xx-small;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;">†</span>Department of Medicine, University of North Carolina, Chapel Hill, NC</span></span></span></span></span></span></span></div>
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<span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-size: xx-small;">Address reprint requests to Priya A. Kumar, MD, Department of Anesthesiology, N2201 University of North Carolina Hospitals, Campus Box 7010, Chapel Hill, NC 27599-7010. E-mail: </span><a href="mailto:pkumar@aims.unc.edu"><span style="font-size: xx-small;">pkumar@aims.unc.edu</span></a></span></span></span></span></span></span></div>
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<span style="font-size: xx-small;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;">Key words: dynamic mitral regurgitation</span></span></span></span></span></span></span></div>
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<span style="font-size: xx-small;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-size: small;">A 55-YEAR-OLD white man was transferred from an outside hospital with complaints of chest tightness and pain radiating to his jaw and left arm. These symptoms were associated with shortness of breath and diaphoresis. A cardiac catheterization revealed triple-vessel coronary artery disease (75% stenosis in the left anterior descending artery, 80% stenosis in the left circumflex artery near the takeoff of the obtuse marginal artery, and 80% stenosis in the right coronary artery). A transthoracic echocardiogram showed normal left ventricular (LV) function and mitral valve leaflets that were mildly thickened with normal mobility and trivial-to-mild mitral regurgitation (MR) (Video 1). The patient consented to coronary artery bypass graft (CABG) surgery. </span></span></span></span></span></span></span></span><span style="font-size: xx-small;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: "Times New Roman", "serif"; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"></span></span></span></span></span></span></span></div>
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<span style="font-family: Times, "Times New Roman", serif;">The patient underwent uneventful anesthetic induction. The initial intraoperative transesophageal echocardiogram (TEE) showed normal LV systolic function with impaired relaxation by mitral inflow pulse-wave and tissue Doppler studies. Two-dimensional echocardiographic examination revealed the mitral valve leaflets as mildly thickened, with normal coaptation in the midesophageal 4-chamber, 2-chamber, and long-axis views. Annular dimensions in the midesophageal commissural and long-axis views were measured at 3.6 and 3.3 cm, respectively. Color-flow Doppler interrogation of the mitral valve in the midesophageal views showed a trivial centrally directed MR jet. The right ventricular function was normal with a mild central tricuspid regurgitation jet. </span><br />
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<span style="font-family: Times, "Times New Roman", serif;">Approximately 1 hour after the induction of anesthesia, before the sternotomy incision, an abrupt increase in the mean pulmonary arterial pressures (PAPs) (mmHg) from the mid-20s to the mid-60s occurred. At about the same time, the heart rate (beats/min) changed from the 50s to the 70s, without any associated ST-T wave changes on the electrocardiogram. The mean arterial pressures (mmHg) ranged from the 60s to the 90s. On the TEE, this corresponded with the appearance of a severe centrally directed MR jet along with a systolic reversal of the pulmonary venous flow (Video 2 and Figs 1 and 2).The mechanism of the MR involved symmetric tethering of both the anterior and posterior leaflets, with a complete lack of coaptation and restricted leaflet motion. Although there was no obvious regional wall motion abnormality (RWMA), there were subtle decreases in the global left and right ventricular contractility. The decreased right ventricular contractility was associated with a worsening of the central tricuspid regurgitant jet. </span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiAntWOubTIMP41ox4JSDwzOV-GhybHhfr2KQduM2cbg-L7VSWEZnDr_QVG9ADMl7jS5Ht7B8Fh5KxDYGKx8RDPtq4yEn6KiLr76Y23u-svbqMcPOGNPo3qXo1wGE768Bx6-2VJRx8Ete3s/s1600/gr+1+sm.JPG" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img $ca="true" border="0" height="238" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiAntWOubTIMP41ox4JSDwzOV-GhybHhfr2KQduM2cbg-L7VSWEZnDr_QVG9ADMl7jS5Ht7B8Fh5KxDYGKx8RDPtq4yEn6KiLr76Y23u-svbqMcPOGNPo3qXo1wGE768Bx6-2VJRx8Ete3s/s320/gr+1+sm.JPG" width="320" /></a></div>
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<span style="font-family: Times, "Times New Roman", serif;"><span style="font-size: x-small;">Fig 1. A transesophageal 2-dimensional echocardiographic image showing the midesophageal 4-chamber view along with color-flow Doppler across the mitral valve showing the lack of leaflet coaptation during systole and severe mitral regurgitation.</span></span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgmV3epLthcDB3PuxDk_x1gE8yeupw_qpjCsCBBJmXfkE5herTxSSVwIgRaOzBMOQAFWVrMH1pNwY_YDLI8mvUuX4fnBV8YqXwEsCA60UytegXAqQc_qwifMz4IXgNFyyAmIlBJ2PvCi6Ih/s1600/gr+2+lrg.JPG" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img $ca="true" border="0" height="240" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgmV3epLthcDB3PuxDk_x1gE8yeupw_qpjCsCBBJmXfkE5herTxSSVwIgRaOzBMOQAFWVrMH1pNwY_YDLI8mvUuX4fnBV8YqXwEsCA60UytegXAqQc_qwifMz4IXgNFyyAmIlBJ2PvCi6Ih/s320/gr+2+lrg.JPG" width="320" /></a></div>
<span style="font-size: x-small;">Fig 2. A pulse-wave Doppler signal in the left upper pulmonary vein showing systolic reversal of flow. (Color version of figure is available online.)</span> <br />
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<strong>Challenge 1: What Was the Cause for the Abrupt Pulmonary Hypertension? </strong></div>
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The differential diagnosis for pulmonary hypertension included the following: (1) pulmonary arterial causes (eg, idiopathic vasospasm, hypoxia, hypercarbia, increased cardiac output, pulmonary embolus, and unmasking of congenital left-right shunts), (2) pulmonary parenchymal dysfunction (eg, parenchymal disease, pneumothorax, light anesthesia, and bucking), and (3) pulmonary venous obstruction (thrombus, mitral stenosis, and mitral regurgitation). <br />
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To rule out these causes, the anesthetic depth, bilateral breath sounds, oxygenation, ventilation, and muscle relaxation were reconfirmed. A comprehensive TEE examination was repeated to rule out a pulmonary thromboembolic etiology or any unmasking of congenital shunts. Milrinone and nitric oxide were instituted briefly to rule out a reversible component of pulmonary arterial vasospasm, with no benefit. Small doses of phenylephrine and nitroglycerin were used to maintain the coronary perfusion. <br />
The PAPs remained persistently elevated for a total of 105 minutes, followed by acute normalization. At this time, the heart rate (beats/min) reverted to the 50s, whereas other hemodynamic parameters were remarkably unchanged from baseline. The TEE once again showed trivial-to-mild central MR with normal leaflet coaptation, normal ventricular contractility, and disappearance of the systolic flow reversal pattern on pulse-wave Doppler of the pulmonary venous flow (Video 3 and Figs 3 and 4). <br />
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<span style="font-size: x-small;">Fig 3. A transesophageal 2-dimensional echocardiographic image showing the midesophageal 4-chamber view along with color-flow Doppler across the mitral valve showing trivial MR and normal leaflet coaptation. (Color version of figure is available online.)</span></div>
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<span style="font-size: x-small;">Fig 4. A pulse-wave Doppler signal in the left upper pulmonary vein showing the disappearance of the systolic reversal of flow.</span></div>
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<strong>Challenge 2: What is the Cause for the Wide Range of Variability in the Degree of MR? </strong></div>
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Dynamic MR that is ischemic in origin is the result of incomplete closure of the mitral leaflets from geometric distortion of the mitral apparatus.1 This occurs in the setting of normal mitral leaflets, and the causes may include annular dilatation, LV dilatation, or distortion resulting in papillary muscle displacement and tethered chordae, all leading to restricted leaflet closure. Left ventricular contraction provides the closing force to oppose the tethering force of the subvalvular apparatus. The presence of LV dysfunction results in an imbalance in favor of this tethering force, thereby aggravating ischemic MR. Transient ischemia of the papillary muscle also can lead to papillary muscle dysfunction, thereby resulting in dynamic MR. <br />
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Acute changes in the loading conditions can alter the degree of MR dynamically, which may decrease in severity in a reduced afterload state, such as under general anesthesia. By contrast, acute volume overload and congestive heart failure may worsen MR, whereas a reduced preload of the LV may improve it.2 Lancellotti et al1 and Lebrun et al3 showed that patients with mild MR at rest may have severe MR when provoked by exercise accompanied by an increase in PAPs. The tenting area (the area enclosed between the annular plane and mitral leaflets) and coaptation height (the distance between the annular plane and the mitral leaflet coaptation plane) were the major determinants of exercise-induced increases in MR although their population comprised patients with some degree of LV dysfunction at rest.1 <br />
<br />
Other causes of dynamic MR may include LV dyssynchrony, which is observed in patients with systolic heart failure.4,5 Its magnitude may be altered significantly by various conditions, such as inducible ischemia, tachycardia, exercise, and pharmacologic agents. This dynamic phenomenon can be unmasked with exercise or dobutamine stress echocardiography even in the absence of detectable ischemia. Because dyssynchronous contraction is inefficient at ejecting the ventricular volume, it can result in delayed mitral valve opening and distorted mitral annulus, hence worsening MR.6 Emerging echocardiographic techniques combining speckle-tracking analysis and 3-D echocardiography are useful in screening patients for LV dyssynchrony. Cardiac resynchronization therapy can result in reverse ventricular remodeling and thereby improve MR because of papillary muscle dyssynchrony. Diastolic dysfunction can also cause functional MR because of the variation in loading conditions.7 <br />
<div style="text-align: center;">
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<strong>Challenge 3: Would CABG Surgery Alone Be Sufficient to Correct Dynamic MR? </strong></div>
<br />
Considerable controversy exists regarding the appropriate therapy in patients with MR undergoing CABG surgery.8,9 Surgical correction of ischemic MR is associated with poor long-term survival. It is difficult to decide whether valve replacement or repair would be the most appropriate surgical treatment because of the lack of randomized trials and long-term survival data. Gillinov et al,10 in a retrospective review of 482 patients with ischemic MR, concluded that although late survival in this surgical population is poor, patients may benefit from repair. However, in the more complex high-risk population, there was no survival advantage after repair as compared with replacement. <br />
<br />
After an extensive discussion with the surgical team, the therapeutic options considered were the following:<br />
<br />
1. CABG surgery alone: a reasonable option with the hope that resolution of the subclinical myocardial ischemia would cure the dynamic severe MR. Reverse remodeling of the myocardium with a final resolution of MR could take months to occur. Also, the target vessels for CABG surgery in this case were believed to be acceptable but not ideal, which left a risk for potentially persistent residual MR. The challenges of a redo sternotomy to address persistent MR at a later time, in light of a left internal mammary artery-to-left anterior descendingartery graft, certainly could increase the risk to the patient. <br />
<br />
2. Mitral valve repair: there was no apparent annular dilatation, and the mechanism appeared to be dynamic tethering of mitral leaflets. An undersized annuloplasty ring could result in better coaptation of the leaflets to relieve the dynamic severe MR. However, undersizing could also add the risk of possible iatrogenic mitral stenosis or a dynamic outflow tract obstruction with the occurrence of systolic anterior motion. <br />
3. Mitral valve replacement: with a somewhat nebulous understanding of the true mechanism of the symptomatic dynamic severe MR in this patient, normal annular dimensions, less-than-ideal target vessels, a lack of obvious RWMAs, a relatively young age, and mildly thickened mitral leaflets and chordae, a surgical decision was made to replace the mitral valve with a St Jude's mitral prosthesis. <br />
<br />
A post-cardiopulmonary bypass TEE showed an appropriately seated mechanical valve with no paravalvular leak. The patient had an uncomplicated hospital course and subsequently was discharged home. <br />
<div style="text-align: center;">
<strong>Conclusions </strong></div>
<br />
The acute shortness of breath and symptomatology that this patient experienced likely were caused by the intermittent severe MR that he might have suffered in his daily life. The strikingly dynamic nature of MR in this case, along with the subtle changes in the global right and left ventricular contractility, were suspected to be ischemic in origin (Video 4). However, the impressive change in the grade of MR from trivial to severe likely would have been associated with some RWMA. However, this was conspicuously absent. A 30% increase in heart rate from baseline was possibly a cause for coronary demand-supply mismatch. It probably resulted in ventricular distortion and leaflet tethering, resulting in severe MR and an associated acute increase in PAPs, which resolved when the heart rate returned to baseline. <br />
<br />
Mitral valve dysfunction can be elusive in CABG surgery patients if evaluated exclusively at rest. Successful mitral valve repair must target the mechanism of dysfunction. An intraoperative TEE evaluation of the mitral valve with a hemodynamic challenge, such as varying loading conditions, heart rate, and perfusion pressure, can unmask a dynamic condition for which a repair or replacement may be indicated. In this patient, the preoperative echocardiogram showed trivial MR; hence, the patient was scheduled for CABG surgery alone. The incidentally observed intraoperative dynamic changes in MR, which increased from a trivial to a severe grade, changed the surgical approach. The subtle change in the geometry of the LV possibly resulted in symmetric mitral valve leaflet tethering, a type IIIB mechanism. This, in turn, led to a severe and clinically significant change in the degree of MR, warranting a mitral valve replacement in addition to CABG surgery. <br />
<br />
References <br />
<br />
1. P. Lancellotti, F. Lebrun, L.A. Pierard. Determinants of exercise induced changes in mitral regurgitation in patients with coronary artery disease and left ventricular dysfunction J Am Coll Cardiol 42:1921-1928, 2003 <br />
<br />
2. L.B. Rosario, L.W. Stevenson, S.D. Solomon, et al. The mechanism of decrease in dynamic mitral regurgitation during heart failure treatment: Importance of reduction in the regurgitant orifice size J Am Coll Cardiol 32:1819-1824, 1998 <br />
<br />
3. F. Lebrun, P. Lancellotti, L.A. Pierard. Quantitation of functional mitral regurgitation during bicycle exercise in patients with heart failure J Am Coll Cardiol 38:1685-1692, 2001 <br />
<br />
4. P. Lancleotti, M. Moonen. Left ventricular dyssynchrony: A dynamic condition Heart Fail Rev 2011 Jul 29 [Epub ahead of print] <br />
<br />
5. P. Lancellotti, P.Y. Stainier, F. Lebois, et al. Effect of dynamic left ventricular dyssynchrony on dynamic mitral regurgitation in patients with heart failure due to coronary artery disease Am J Cardiol 96:1304-1307, 2005<br />
<br />
6. J.K. Ho, A. Mahajan. Cardiac resynchronization therapy for treatment of heart failure Anesth Alalg 111:1353-1361, 2010 <br />
<br />
7. T. Karaahmet, K. Tigen, C. Dundar, et al. Papillary muscle dyssynchrony as a cause of functional mitral regurgitation in non-ischemic dilated cardiomyopathy patients with narrow QRS complexes Anadolu Kardiyol Derg 9:196-203, 2009 <br />
<br />
8. L. Aklog, F. Filsoufi, K.Q. Flores, et al. Does coronary artery bypass grafting alone correct moderate ischemic mitral valve regurgitation? Circulation 104:168-175, 2001 <br />
<br />
9. I.G. Duarte, Y. Shen, M.J. MacDonald, et al. Treatment of moderate mitral regurgitation and coronary disease by coronary bypass alone: Late results Ann Thorac Surg 68: 426-430, 1999 <br />
<br />
10. A.M. Gillinov, P.N. Wierup, E.H. Blackstone, et al. Is repair preferable to replacement for ischemic mitral regurgitation? J Thorac Cardiovasc Surg 122: 1125-1114, 2001 <br />
<br />
Fig 1 A transesophageal 2-dimensional echocardiographic image showing the midesophageal 4-chamber view along with color-flow Doppler across the mitral valve showing the lack of leaflet coaptation during systole and severe mitral regurgitation. <br />
<br />
Fig 2 A pulse-wave Doppler signal in the left upper pulmonary vein showing systolic reversal of flow. <br />
<br />
Fig 3 A transesophageal 2-dimensional echocardiographic image showing the midesophageal 4-chamber view along with color-flow Doppler across the mitral valve showing trivial MR and normal leaflet coaptation. <br />
<br />
Fig 4 A pulse-wave Doppler signal in the left upper pulmonary vein showing the disappearance of the systolic reversal of flow. <br />
<br />
<br />
<br /></div>JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-21974974502596764992012-05-17T11:16:00.001-07:002012-05-17T11:16:24.612-07:00E-CHALLENGE & CLINICAL DECISIONS<div style="text-align: right;">
<i>Feroze Mahmood, MD</i></div>
<div style="text-align: right;">
<i>Madhav Swaminathan, MD</i></div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
<i>Section Editors</i></div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: right;">
<br /></div>
<div style="text-align: center;">
<span style="font-size: large;"><span style="font-family: Arial,Helvetica,sans-serif;"><b>Severe Tricuspid Valve Regurgitation: </b></span></span></div>
<div style="text-align: center;">
<span style="font-size: large;"><span style="font-family: Arial,Helvetica,sans-serif;"><b>A Case for Laminar Flow</b></span></span></div>
<div style="text-align: center;">
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<span style="font-size: x-small;">Frederick C Cobey, MD, *
Maria Fritock, MD, </span>
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<span style="font-family: "Times New Roman"; font-size: 12pt;">†</span>
<span style="font-size: x-small;"><span style="font-family: "Wingdings 2";">
</span> Frederick W. Lombard, MD, </span>
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<span style="font-size: x-small;"><span style="font-family: "Wingdings 2";">
</span>
Donald D.Glower, MD, § Madhav
Swaminathan, MD, FAHA, FASE‡</span></div>
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<br /></div>
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<span style="font-size: x-small;"> </span><span style="font-size: xx-small;">* Georgetown University, the Washington Hospital Center, Washington, DC</span></div>
<div class="MsoNormal" style="text-align: left;">
<span style="font-size: xx-small;"><span style="font-family: "Times New Roman";">†Department of Anesthesiology, Mayo Clinic, Rochester, MN</span></span></div>
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<span style="font-size: xx-small;">§Department of Surgery, Division of Thoracic Surgery, Duke University Health System, Durham, NC</span><span style="font-size: xx-small;"><span style="font-family: "Times New Roman";"> </span></span></div>
<div class="MsoNormal" style="text-align: left;">
<span style="font-size: xx-small;"><span style="font-family: "Times New Roman";"> </span></span><span style="font-size: xx-small;">‡Department of Anesthesiology, Division of Cardiothoracic, Anesthesiology and Critical Care Medicine, Duke University Health System, Durham, NC</span></div>
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<br /></div>
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<span style="font-size: x-small;"><span style="font-size: xx-small;">Address reprint requests to Madhav Swaminathan, MD, FAHA, FASE, Department of Anesthesiology, Division of Cardiothoracic, Anesthesiology and Critical Care Medicine, Box 3094/5691F HAFS Building, Duke University Health System, Durham, NC 27710. Email: swami001@mc.duke.edu</span></span></div>
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<span style="font-size: x-small;"><br /></span></div>
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<span style="font-family: "Times New Roman"; font-size: 12pt;"><span style="font-size: x-small;">Key Words: tricuspid regurgitation, Doppler, laminar flow</span></span></div>
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<span style="font-family: "Times New Roman"; font-size: 12pt;"><br /></span><span style="font-size: x-small;"></span></div>
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<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
A 67-YEAR-OLD WOMAN presented with progressive dyspnea
limiting her ability to perform daily activities. Her past medical history was
significant for hyperlipidemia and Hashimoto thyroiditis. Upon further workup,
a transthoracic echocardiogram (TTE) was performed, which revealed severe
mitral regurgitation (MR) with mild tricuspid regurgitation (TR). Subsequently,
she was scheduled for mitral valve repair. After an uneventful induction of
anesthesia, an intraoperative transesophageal echocardiogram (TEE) was
performed using a matrix array transducer and images acquired on an IE33
ultrasound system (Philips Healthcare, Andover, MA). The examination showed
biatrial enlargement and prolapse of both the mitral and tricuspid valves. The
tricuspid annulus in diastole measured 4 cm in the midesophageal 4-chamber
view. The diagnosis of severe MR and mild TR was confirmed. The surgeon
proceeded as planned with a mitral valve repair via a minimally invasive
port-access approach. After cardiopulmonary bypass (CPB), the TEE showed a satisfactory
mitral repair. However, there was hemodynamic evidence of TR with right
ventricular dysfunction and an underfilled left ventricle. The central venous
pressure was elevated; there were large "v" waves on the pressure
waveform. Although the echocardiographic examination clearly showed TR, there
was no clearly defined turbulent jet, and, therefore, the TR could not be
quantified simply using the vena contracta, the proximal isovelocity surface
area, or the jet area. The systolic flow across the tricuspid valve was laminar
(Fig 1)and had a low peak velocity of 0.9 m/s. Both hepatic venous systolic
flow reversal and a dense triangular-shaped spectral Doppler tricuspid
regurgitant flow pattern also were noted. </div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjHSRqMvE2nzvmvaCmh-Ha_JqBS6ngNZeDtRoezDTGSc9pp6KETeWhtO9YFzXG2DzGSMglXlMdTSE57y1gOWxEICNErHy_12TmtMqYjSFtjz0cye_Bj0yHT87fxKfxGlv_3WfhlkPeCwEW5/s1600/1-sml_June.gif" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="281" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjHSRqMvE2nzvmvaCmh-Ha_JqBS6ngNZeDtRoezDTGSc9pp6KETeWhtO9YFzXG2DzGSMglXlMdTSE57y1gOWxEICNErHy_12TmtMqYjSFtjz0cye_Bj0yHT87fxKfxGlv_3WfhlkPeCwEW5/s320/1-sml_June.gif" width="320" /></a></td></tr>
<tr align="left" style="font-family: Arial,Helvetica,sans-serif;"><td class="tr-caption"><span style="font-size: x-small;">Fig 1 The midesophageal right ventricle inflow-outflow
view showing laminar regurgitant flow into the right atrium after the
discontinuation of CPB after mitral valve repair.</span></td></tr>
</tbody></table>
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<br /></div>
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<br /></div>
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<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif; text-align: center;">
<span style="font-size: small;"><b>Challenges </b></span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif; text-align: center;">
<b><br /></b></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif; text-align: left;">
<style>
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<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<i>How Should the Severity of TR Be Evaluated and Graded
When a Regurgitant Jet Is Laminar?</i> </div>
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In typical cases of TR with a turbulent flow
regurgitation jet, the simplest, initial, and most common approach is to use
color-flow Doppler to visualize the jet. The severity of TR may be graded by
mapping the area of the color jet in the right atrium.1-3 Other established
approaches include measurement of the vena contracta and proximal isovelocity
surface area.2,4,5 However, TR jets are often ellipsoid, often eccentrically
directed, and are difficult to accurately capture in a 3-dimensional space with
2-dimensional echocardiographic planes.6 These factors likely contribute to the
significant overlap seen in TR severity grades and the underestimation of TR in
20% to 30% of severe cases evaluated with color-flow Doppler.2,7 When flow is
laminar, the borders of a color jet can be so difficult to appreciate that even
a large jet can be missed entirely.8 Regurgitant laminar flow in contrast to
flow that is turbulent allows a much greater regurgitant volume for a given
transvalvular pressure gradient. The lower energy loss of laminar flow likely
results in a smaller pressure drop and sustained flow. The American Society of
Echocardiography (ASE) guidelines for evaluating regurgitant valve lesions
suggest integrating different parameters when evaluating TR severity to avoid
such errors.7 Right-sided anatomic changes consistent with severe TR include
enlarged cardiac chambers with a dilated tricuspid annulus, a lack of leaflet
coaptation, paradoxic septal motion, and a distended venous system.7 The
morphology of the spectral tracing also may be used, with a dense triangular
pattern suggestive of severe TR. A high-velocity jet does not indicate severe
TR, and, indeed, laminar jets generally are associated with velocities <2
m/s.7,9,10 Antegrade and retrograde spectral patterns may almost mirror each
other relating to the "to-and-fro" flow across the valve.7,10 Hepatic
venous systolic flow reversal is a sensitive indicator of severe TR and also should
be present.7 If most of the ASE parameters suggest moderate-to-severe TR, even
in the absence of a clearly visible turbulent jet, then the presence of a
significantly incompetent valve needs to be considered. </div>
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<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<i>How Should Unexpected Moderate-to-Severe TR in the Operating
Room Be Managed? </i></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
Recently, there has been a paradigm shift in how TR is
viewed and when it should be repaired, especially in the context of left-sided
valve disease. Although there is general agreement that severe TR should be
repaired, guidelines are less clear regarding moderate TR.11,12 The development
of late significant TR after left-sided surgery is associated with a higher
rate of cardiovascular death, repeat cardiac surgery, and congestive heart
failure requiring hospital admission.13 Given such findings, a large
meta-analysis concluded that tricuspid dilation may be the most important risk
factor for late TR and that the valve should be repaired regardless of the
regurgitant severity if significant dilation is present.12 New TR that is present
immediately after CPB presents a different management dilemma because this may
be related to myocardial stunning or coronary air embolization and may be
recoverable. </div>
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<br /></div>
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<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif; text-align: center;">
<span style="font-size: small;"><b>Discussion </b></span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif; text-align: center;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif; text-align: left;">
<style>
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<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
In the case presented, the decision was made not to
repair the tricuspid valve given the lack of a firm preoperative diagnosis and
the absence of a conventional turbulent jet that was difficult to quantify. The
patient required significant inotropic support, and on the 3rd postoperative
day a TTE confirmed the presence of a laminar tricuspid jet and worsening right
ventricular function (Fig 2).The patient was taken back to the operating room
for possible tricuspid valve repair. The intraoperative TEE confirmed the
presence of laminar TR (Fig 3)with hepatic vein systolic flow reversal (Fig
4)that resolved after the tricuspid ring annuloplasty (Fig 5).Subsequently, the
patient had an uneventful postoperative recovery and was discharged in a
routine fashion. A summary of echocardiographic video clips and spectral
Doppler images is provided in Video 1. Upon retrospective review of the
echocardiographic images, certainly repairing both valves initially could have
been considered given the dilated tricuspid annulus with a prolapsing valve.
The TR jet seen on both the initial TTE and prebypass TEE was also laminar and
arguably misinterpreted by 2 different echocardiographers. An early case series
suggested that up to a quarter of severe tricuspid jets are laminar.9 Although
this number seems high, it certainly is possible that laminar TR may be an
under appreciated entity. </div>
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<br /></div>
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<br /></div>
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh2SP-mk72dqYoAdlLywodmiVv6xMdJB6SKGYsZyAMTF-GKKts-cATitoYxPqqe0C6n0nkaKM0_BLTaXNZD4rrDrUGUbqr9pOcxLWy3u-JLx4E_QhUlrxKiviQQyI9D2Yru6mgTUVLEXiFg/s1600/2-sml_June.gif" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="281" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh2SP-mk72dqYoAdlLywodmiVv6xMdJB6SKGYsZyAMTF-GKKts-cATitoYxPqqe0C6n0nkaKM0_BLTaXNZD4rrDrUGUbqr9pOcxLWy3u-JLx4E_QhUlrxKiviQQyI9D2Yru6mgTUVLEXiFg/s320/2-sml_June.gif" width="320" /></a></td></tr>
<tr align="left" style="font-family: Arial,Helvetica,sans-serif;"><td class="tr-caption"><span style="font-size: x-small;">Fig 2 The transthoracic apical 4-chamber view showing
severe TR with a laminar jet in the right atrium on the 2nd postoperative day
after mitral valve repair. </span></td></tr>
</tbody></table>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhi04QrQqjYFPrNhgsGIMh_3hidlKcRuKz6JRe9w09FVn-ybC65B6bXzPGzPwiaUP_XazgbnYCKMhgiZ36dfENy2_ZCL199UichYHAYD13M4z5D0mBfi1SYvnAr_pU3meZ4UguVhK8QIOiQ/s1600/3-sml_June.gif" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="282" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhi04QrQqjYFPrNhgsGIMh_3hidlKcRuKz6JRe9w09FVn-ybC65B6bXzPGzPwiaUP_XazgbnYCKMhgiZ36dfENy2_ZCL199UichYHAYD13M4z5D0mBfi1SYvnAr_pU3meZ4UguVhK8QIOiQ/s320/3-sml_June.gif" width="320" /></a></td></tr>
<tr style="font-family: Arial,Helvetica,sans-serif;"><td class="tr-caption" style="text-align: center;"><span style="font-size: x-small;">Fig 3 The midesophageal 4-chamber view confirming a large
laminar jet of TR before tricuspid valve repair.</span></td></tr>
</tbody></table>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiHqL0cOcq2gfCYUGO_CNrs0gRVgpWaq03P8cq9iowUI3JieNE5GeP-4bLi9Ka9mMc0L_Na5bFKBoVrydOMQbFoR_7DzodoYGbPx3EA9reOKK9vQOPNqyYvdVcYqT3kKwuH0_pZijWxnSmL/s1600/4-sm_June.gif" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="250" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiHqL0cOcq2gfCYUGO_CNrs0gRVgpWaq03P8cq9iowUI3JieNE5GeP-4bLi9Ka9mMc0L_Na5bFKBoVrydOMQbFoR_7DzodoYGbPx3EA9reOKK9vQOPNqyYvdVcYqT3kKwuH0_pZijWxnSmL/s400/4-sm_June.gif" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
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<span style="font-size: x-small;">Fig 4 The pulsed-wave Doppler of hepatic vein flow
showing systolic flow reversal (arrow). </span></div>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhzML-GqtApCSOaQRcsS6mTJO1YgZjCd5LlpkaB8lnMmxjK96PJiNCazqcMDIMKbGitIg2hzN_cAFTfRsUDmD5j90uXrp1LIi0cLNadtwJmAsWsQFkds-lhX6UAUeLtNYnvtFT-nJy9dcXD/s1600/5-sml_June.gif" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="250" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhzML-GqtApCSOaQRcsS6mTJO1YgZjCd5LlpkaB8lnMmxjK96PJiNCazqcMDIMKbGitIg2hzN_cAFTfRsUDmD5j90uXrp1LIi0cLNadtwJmAsWsQFkds-lhX6UAUeLtNYnvtFT-nJy9dcXD/s400/5-sml_June.gif" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif; text-align: left;">
<span style="font-size: x-small;">Fig 5 The midesophageal 4-chamber view showing a
satisfactory repair of the tricuspid valve without evidence of TR on color-flow
Doppler. </span></div>
</td></tr>
</tbody></table>
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<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif; text-align: center;">
<b><span style="font-size: small;">Conclusions </span></b></div>
<br />
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The case presented highlights the difficulty in
quantifying a TR jet that shows laminar flow. When this occurs immediately
after CPB intraoperatively in the setting of mitral valve surgery, the issues
become even more complex. Surgical decision making is also complicated after
decannulation, especially in the minimally invasive approach. Given the growing
body of evidence that early intervention may be indicated in cases of TR,
especially in the setting of left-sided valve surgery and the possibility of
laminar flow, vigilance for identifying such cases of "silent"
regurgitation is warranted.9,12 </div>
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<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif; text-align: center;">
<b><span style="font-size: small;">References </span></b></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;">1. Y. Shapira, A. Porter, M. Wurzel, et al. Evaluation of
tricuspid regurgitation severity: Echocardiographic and clinical correlation J
Am Soc Echocardiogr 11:652-659, 1998</span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;"><span lang="FR">2. G.
Grossmann, M. Stein, M. Kochs, et al. </span>Comparison of the proximal flow
convergence method and the jet area method for the assessment of the severity
of tricuspid regurgitation Eur Heart J 19:652-659, 1998 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;"><span lang="FR">3. F.
Gonzalez-Vilchez, J. Zarauza, J.A. Vazquez de Prada, et al. </span>Assessment
of tricuspid regurgitation by Doppler color flow imaging: Angiographic
correlation Int J Cardiol 44:275-283, 1994</span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;"><span lang="FR">4. S.
Yamachika, C.L. Reid, D. Savani, et al. </span>Usefulness of color Doppler
proximal isovelocity surface area method in quantitating valvular regurgitation
J Am Soc Echocardiogr 10:159-168, 1997 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;">5. W.I. Yang, C.Y. Shim, M.K. Kang, et al. Vena contracta
width as a predictor of adverse outcomes in patients with severe isolated
tricuspid regurgitation J Am Soc Echocardiogr 24:1013-1019, 2011 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;"><span lang="FR">6. J.M. Song,
M.K. Jang, Y.S. Choi, et al. </span>The vena contracta in functional tricuspid
regurgitation: A real-time three-dimensional color Doppler echocardiography
study J Am Soc Echocardiogr 24:663-670, 2011 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;"><span lang="FR">7. W.A.
Zoghbi, M. Enriquez-Sarano, E. Foster, et al. </span>Recommendations for
evaluation of the severity of native valvular regurgitation with
two-dimensional and Doppler echocardiography J Am Soc Echocardiogr 16:777-802,
2003 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;"><span lang="FR">8. S.
Akamatsu, N. Ueda, E. Terazawa, et al. </span>Mitral prosthetic dehiscence with
laminar regurgitant flow signals assessed by transesophageal echocardiography
Chest 104: 1911-1913, 1993 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;"><span lang="FR">9. K. Yoshida,
J. Yoshikawa, T. Akasaka, et al. </span>Silent severe tricuspid regurgitation:
A study by Doppler echocardiography J Cardiol 19:187-194, 1989 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;"><span lang="FR">10. S.
Minagoe, S.H. Rahimtoola, P.A. Chandraratna. </span>Significance of laminar
systolic regurgitant flow in patients with tricuspid regurgitation: A combined
pulsed-wave, continuous-wave Doppler and two-dimensional echocardiographic
study Am Heart J 119:627-635, 1990 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;">11. R.O. Bonow, B.A. Carabello, K. Chatterjee, et al.
Focused update incorporated into the ACC/AHA 2006 guidelines for the management
of patients with valvular heart disease: A report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines
(writing committee to revise the 1998 guidelines for the management of patients
with valvular heart disease): Endorsed by the Society of Cardiovascular
Anesthesiologists, Society for Cardiovascular Angiography and Interventions,
and Society of Thoracic Surgeons Circulation 2008:e523-e661, 2008 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;"><span lang="FR">12. G.
Bianchi, M. Solinas, S. Bevilacqua, et al. </span>Which patient undergoing
mitral valve surgery should also have the tricuspid repair? Interact Cardiovasc
Thorac Surg 9:1009-1020, 2009 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;">13. H. Song, M.J. Kim, C.H. Chung, et al. Factors
associated with development of late significant tricuspid regurgitation after
successful left-sided valve surgery Heart 95:931-936, 2009 </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;">Fig 1 The midesophageal right ventricle inflow-outflow
view showing laminar regurgitant flow into the right atrium after the
discontinuation of CPB after mitral valve repair. </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;">Fig 2 The transthoracic apical 4-chamber view showing
severe TR with a laminar jet in the right atrium on the 2nd postoperative day
after mitral valve repair. </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;">Fig 3 The midesophageal 4-chamber view confirming a large
laminar jet of TR before tricuspid valve repair. </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;">Fig 4 The pulsed-wave Doppler of hepatic vein flow
showing systolic flow reversal (arrow). </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<span style="font-size: x-small;">Fig 5 The midesophageal 4-chamber view showing a
satisfactory repair of the tricuspid valve without evidence of TR on color-flow
Doppler. </span></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
<br /></div>
<div class="MsoPlainText" style="font-family: Arial,Helvetica,sans-serif;">
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<br /></div>
<div class="MsoNormal">
<br />
<span style="font-size: x-small;"></span></div>JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-13949921902995850972012-03-20T10:26:00.000-07:002012-03-20T10:26:56.051-07:00E-CHALLENGES & CLINICAL DECISIONS<div align="right">
<span style="font-family: Arial; font-size: x-small;"><em>Feroze Mahmood,MD</em></span></div>
<div align="right">
<span style="font-family: Arial; font-size: x-small;"><em>Madhav Swaminathan, MD</em></span></div>
<div align="right">
<span style="font-family: Arial; font-size: x-small;">Section Editors</span></div>
<div align="right">
<br /></div>
<div style="text-align: center;">
<strong><span style="font-family: Arial; font-size: large;">An Incidental Finding During Emergent Vascular Surgery: How Far to Go?</span></strong></div>
<div style="text-align: center;">
<br /></div>
<div style="text-align: center;">
<strong><em><span style="font-family: Arial; font-size: x-small;">Shanaz Ali, MD, Omair Shakil, MD, Tzong-Huei Chen, MD, Haider Javed Warraich, MD, and Robina Matyal, MD</span></em></strong></div>
<div style="text-align: center;">
<br /></div>
<div style="text-align: left;">
<span style="font-size: xx-small;">Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, MA </span></div>
<span style="font-size: xx-small;">Address reprint requests to Shanaz Ali, MD, Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, One Deaconess Road, CC-470, Boston, MA 02215. E-mail: <a href="mailto:seali@bidmc.harvard.edu">seali@bidmc.harvard.edu</a></span><span style="font-size: xx-small;"><br /></span><br />
<span style="font-size: xx-small;">Key words: Amplatzer device, transesophageal echocardiography, intracardiac thrombus </span><br />
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A 40-YEAR-OLD MAN presented to the authors' tertiary care center with an acute onset of pain in his left foot. He was otherwise hemodynamically stable, alert, and oriented. His past medical history was significant for multiple strokes and pulmonary emboli. On a previous admission for stroke workup 5 years earlier, he had a transthoracic echocardiogram that revealed an atrial septal defect (ASD). The defect was closed percutaneously with an Amplatzer device (AGA Medical Corporation, Plymouth, MN). Since the closure of the ASD, the patient had been free of embolic events. A physical examination in the emergency room revealed no palpable pulses in the <br />
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<strong><span style="font-size: xx-small;">Figue 1. Two-dimensional transesophageal echocardiogram: The midesophageal 4-chamber view showing the Amplatzer device in the interatrial septum with 2 clots in the left atrium.</span></strong></div>
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<strong><span style="font-size: xx-small;">Fig 2. Three-dimensional transesophageal echocardiogram: the view throught the left atrial perspective of the mitral valve showing the Amplatzer device in the interatrial septum, with one clot attached to the inferior portion of the device and the smaller clot attached to the posterior wall of the left atrium. (Color version of figure is available online.)</span></strong></div>
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left lower extremity. A computed tomographic angiogram showed occlusion of the left common iliac artery. A heparin drip was initiated, vascular surgery service was consulted, and the patient was scheduled for an emergent thrombectomy under general anesthesia. <br />
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After an uneventful induction of general anesthesia, based on his history of multiple embolic events, the presence of an intracardiac device, and acute limb ischemia, a transesophageal echocardiographic (TEE) examination was performed using an IE-33 Ultrasound System Omni-III TEE Probe (Philips Medical Systems, Andover, MA).<br />
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<strong>Echocardiographic Findings </strong></div>
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TEE interrogation revealed a well-seated septal occluder device across the interatrial septum. A color-flow Doppler study of the interatrial septum did not show any flow across the septum. The left atrium was mildly dilated. Two large echodensites were visualized in the left atrium, which appeared pedunculated and freely mobile with a homogenous consistency and a smooth surface. The larger density measured 2 x 3 cm, and the smaller density measured approximately 0.5 x 1.5 cm (Fig 1 and Video 1 [supplementary videos are available online]. <br />
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<strong><span style="font-size: xx-small;">Figure 3. (A) The Amplatzer device after removal from the patient. (B) Clots removed from the left atrium. (Color version of figure is available online.)</span></strong><br />
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<strong>Echocardiographic Challenge </strong></div>
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On 2-dimensional TEE examination, the larger echodensity seemed attached to the Amplatzer device, whereas the other one seemed to be located just above the mitral annulus. To better delineate the spatial location, it was decided to do a real-time 3-dimensional transesophageal echocardiogram. The 3-dimensional transesophageal echocardiogram established that the larger density was clearly attached to the inferior edge of the septal device, whereas the smaller density, which on a 2-dimensional esophageal echocardiogram had appeared to be attached to the mitral annulus, was actually attached to the posterior wall of the left atrium (Fig 2 and Video 2). <br />
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<strong>Clinical Challenge </strong></div>
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This case posed the following 2 clinical dilemmas to the team: <br />
1. After establishing the presence of thrombi in the left atrium, the risk of embolization in the patient needed to be determined. Based on the patient's presentation and echocardiographic appearance of the thrombi (pedunculated and freely mobile), it was determined that the risk of embolization was significant. <br />
2. The second challenge was whether to proceed to emergent cardiac surgery during the same anesthestic versus obtaining informed consent and proceeding urgently the following day. Would obtaining informed consent and delaying cardiac surgery place the patient at an increased risk for a catastrophic embolic event? <br />
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<strong>Intraoperative Decision </strong></div>
After discussion with the cardiac and vascular surgery teams, it was decided that the patient would require removal of the thrombi along with the possible removal of the Amplatzer device under cardiopulmonary bypass. The situation was discussed with the patient's next-of-kin, and it was decided to place the patient on a therapeutic heparin drip and proceed with cardiac surgery after obtaining informed consent. The patient was brought back to the operating room the next morning. After the initiation of cardiopulmonary bypass, the left atrium was opened, and two large thrombi were removed, one attached to the inferior aspect of the ASD closure device and the other attached to the posterior aspect of left atrium near the mitral valve annulus (Fig 3). The ASD closure device was removed and the defect closed with a core matrix patch. The patient had an uneventful postoperative recovery. A thorough workup was ordered to investigate the possibility of a hypercoagulable disorder, and the patient was found to have protein S and factor X deficiency. Subsequently, the patient was discharged with a prescription for coumadin in therapeutic doses.<br />
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<br /></div>JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-62405058571331114532011-12-22T10:32:00.000-08:002011-12-22T10:41:26.856-08:00E-Challenges & Clinical Decisions<div style="text-align: right;">
<span style="font-size: x-small;"></span><span style="font-size: x-small;">Feroze Mahmood, MD</span></div>
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<span style="font-size: x-small;"> Madhav Swaminathan, MD</span><span style="font-size: x-small;"><i> </i></span></div>
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<span style="font-size: x-small;"><i>Section Editors</i></span></div>
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<span style="font-size: large;"><b>Coronary Artery Disease, Acute Myocardial Infarction, and a Newly Developing Ventricular Septal Defect: Surgical Repair or Percutaneous Closure?</b></span></div>
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<span style="font-size: x-small;">Mona Kulkarni, MD, Antonio Hernandez Conte, MD, MBA, Aaron Huang DO, Lorraine Lubin MD, Takahiro Shiota MD, FACC, FASE, Saibal Kar, MD</span></div>
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<span style="font-size: x-small;">Division of Cardiothoracic Anesthesiology and Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA</span></div>
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<span style="font-size: x-small;"> </span></div>
<div style="text-align: left;">
<span style="font-size: x-small;">M.K. and A.H. are Cardiothoracic Anesthesiology Fellows.</span></div>
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<span style="font-size: x-small;">Address reprint requests to Antonio Hernandez Conte, MD, MBA, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Suite 8211, Loas Angeles, CA 90048. E-mail: antonio.conte@cshs.org</span></div>
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<span style="font-size: x-small;"><b>KEY WORDS:</b> postmyocardial infarction, ventricular septal defect, percutaneous closure devices, Amplatzer</span></div>
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<span style="font-family: "Times New Roman";">A
52-YEAR-OLD MAN presented to an outside hospital with a chief complaint of
severe shortness of breath with severe coughing; the patient had been experiencing
weakness, dizziness, chest tightness, and mild shortness of breath at home for
a total of four days before his arrival. Upon admission to the outside
hospital, the patient was diagnosed via an electrocardiogram with an acute
inferior wall myocardial infarction, and he immediately underwent cardiac
catheterization, which revealed an occluded right coronary artery. He had a
successful percutaneous intervention with stenting of the right coronary
artery. On the same day postprocedure, the patient was found to be in heart
failure with clinical evidence of cardiogenic shock. A transthoracic
echocardiogram (TTE) revealed a postmyocardial infarction (MI) ventricular
septal defect (VSD). An intra-aortic balloon pump was inserted to optimize
emodynamics, and the patient was placed in the intensive care unit without the
need for intubation. An immediate transfer was
arranged, and the patient arrived at the authors' facility later that
evening. The time from admission to the initial hospital followed by coronary
intervention, the identification of the VSD, and the subsequent transfer to the
authors' facility was less than 24 hours. The patient's past medical history
was significant for morbid obesity, non-insulin-dependent diabetes, and Valley
fever. The patient was a nonsmoker without any pertinent family history and
denied any previous surgical procedures. The patient's medications included
aspirin, eptifibatide, and furosemide. A bedside TTE performed at the authors'
institution revealed a basal VSD measuring approximately 1 cm in diameter by 1
cm in length. Additional findings included preserved left ventricular function
with a left ventricular ejection fraction of 55% and normal right ventricular
function; the left ventricle displayed basal inferior hypokinesis. The gradient
across the VSD was 45 mmHg with left-to-right flow and a right ventricular
systolic pressure of 40 mmHg. There were no other associated valvular
abnormalities. Fifty hours after the admission to the authors' facility and
based on the echocardiographic findings and clinical scenario, the treatment
modality was agreed upon by consensus among the medical intensivist, cardiac
surgeon, and interventional cardiologist. It was decided that the patient would
undergo percutaneous closure of the VSD. The preprocedure laboratory studies
were unremarkable. The patient was taken to the interventional cardiology
suites, and after the placement of standard monitors with the insertion of an
arterial catheter, general anesthesia was induced with etomidate and
rocuronium; the airway was secured without difficulty. Anesthesia was
maintained with sevoflurane and cisatracurium. </span></div>
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<b><span style="font-family: "Times New Roman";">Intraoperative
Transesophageal Echocardiographic Findings </span></b></div>
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<span style="font-family: "Times New Roman";">An
intraoperative transesophageal echocardiogram (TEE) was performed using a
Philips iE33 ultrasound system with a x7-2 t transesophageal echocardiographic
probe (Philips Medical Systems, Andover, MA). The noteworthy findings included
the following: (1) normal ventricular function with a left ventricular ejection
fraction of 55%; (2) no evidence of a VSD was notable in the standard
midesophageal 4-chamber and 2-chamber views; (3) in the transgastric short-axis
view at 0-degrees, a VSD was evident measuring approximately 1.1 cm in diameter
and 1 cm in length with left-to-right flow and the presence of an inferior left
ventricular aneurysm (Fig 1); (4) inserting the TEE probe deeper in the
transgastric short-axis view, displayed a continued VSD 1 cm in length; (5) the
right ventricle was moderately dilated with mildly reduced right ventricular
function; and (6) there was moderate tricuspid regurgitation. </span></div>
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<span style="font-family: "Times New Roman";">Fig
1 Transgastric transesophageal echocardiographic images showing (A) left
ventricular aneurysm (arrow) with (B) the VSD (arrow) after MI. RV, right
ventricle; LV, left ventricle. </span></div>
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<b><span style="font-family: "Times New Roman";">Discussion
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<span style="font-family: "Times New Roman";">The
following challenges were met in this case:</span></div>
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<span style="font-family: "Times New Roman";">1.
Should the VSD closure proceed percutaneously as planned, or should the patient
undergo surgical repair? If yes to percutaneous closure, what are the
limitations? If yes to surgical repair, what are the implications and risks in
the operative and postoperative course? </span></div>
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<span style="font-family: "Times New Roman";">2.
How should the percutaneous closure be performed in the context of the
described anatomy and the selection of occluder device size(s)? </span></div>
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<span style="font-family: "Times New Roman";">3.
What are the risks and complications associated with deployment of multiple
occluder devices? </span></div>
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<b><span style="font-family: "Times New Roman";">Optional</span></b><br />
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<span style="font-family: "Times New Roman";">The
following options were considered: (1) percutaneous closure with the use of one
occluder device with potential residual VSD, (2) percutaneous closure with the
deployment of two occluder devices with possible residual VSD or no residual
VSD, and (3) sternotomy with open surgical repair of the VSD with
cardiopulmonary bypass. </span></div>
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<b><span style="font-family: "Times New Roman";">Strategy
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<span style="font-family: "Times New Roman";">After extensive discussion with the medical
intensivist, interventional cardiologist, cardiac surgeon, echocardiologist, and anesthesiologist, a
decision was made to proceed with deployment of at least one and possibly two
Amplatzer (AGA Medical Corp, Plymouth, MN) occluder devices. The final decision
to initiate percutaneous closure was based primarily on the anatomy of the VSD,
which appeared to have a sigmoidal or serpiginous structure, as well as the
adjacent inferior left ventricular aneurysm. An Amplatzer occluder could be
deployed in either one of two distinct segments of the VSD with anticipated
partial obliteration of the VSD. </span></div>
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<b><span style="font-family: "Times New Roman";">Rationale
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<span style="font-family: "Times New Roman";">The
use of the Society of Thoracic Surgeons risk scoring/calculator system does not
support the calculation of risk mortality or morbidity and mortality in the
setting of complex cardiac procedures. Unless the patient undergoes coronary
artery bypass graft surgery and/or valve surgery, the Society of Thoracic
Surgeons risk scoring estimation cannot be performed.1 Therefore, for this
patient, it was very difficult to estimate the risk of mortality or the overall
morbidity/mortality of a percutaneous procedure for the repair of the VSD
versus open surgical repair of the VSD. However, factors to be considered
included a recent MI (<6 days prior) with a VSD coupled with a left
ventricular aneurysm. In addition, cardiogenic shock with the use of an
intra-aortic balloon pump for hemodynamic stabilization also should be
considered when performing a risk analysis; the overall risk can be estimated
to be very high. Although the use of occluder devices for the closure of VSDs
has been fairly well established as an acceptable method of ameliorating
smaller VSDs, its efficacy in closing larger VSDs still is not established.
Evidence indicates that the percutaneous closure of larger VSDs with one
occluder, even with a residual defect, may allow significant hemodynamic
stabilization and myocardial fibrosis to form so that a surgical repair of any
residual VSD may be performed at a later time. After the deployment of an
initial occluder device, a substantial residual shunt remained (Fig 2);
therefore, the decision to deploy a second Amplatzer occluder was entertained.
After deployment of the second occluder device, a small residual VSD shunt
remained (Fig 3). There is a paucity of literature describing the use of two
Amplatzer occluder devices to close a VSD; therefore, the long-term ramifications
of double-device deployment are relatively unknown. Regardless of the
intervention performed, the time from VSD diagnosis to intervention is a
significant predictor of morbidity and mortality, and rapid intervention in
this case was critical. </span></div>
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<span style="font-family: "Times New Roman";"> Fig
2 The transgastric view after the first closure device implantation with
significant residual VSD blood flow (arrow). </span><span style="font-family: "Times New Roman";"><br /></span></div>
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<span style="font-family: "Times New Roman";">Fig
3 Three-dimensional transesophageal echocardiographic images displaying double
Amplatzer occluder devices with a small residual shunt (arrow).</span> </div>
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<b><span style="font-family: "Times New Roman";">Postoperative
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<span style="font-family: "Times New Roman";">The
patient tolerated the procedure well without any evidence of anesthetic or
procedural-related complications. During the procedure and postoperatively, the
patient did not require any inotropic agents or pressors. After the procedure,
the patient was transferred to the intensive care unit in stable condition and
remained intubated. On postoperative day 2, the patient was extubated, and the
intra-aortic balloon pump and the pulmonary artery catheter were removed. A
follow-up TTE on postoperative day 2 revealed evidence of a very small (<0.5
cm) residual VSD with no significant gradient. The dual Amplatzer occluders
were well seated with no evidence of a rocking motion.</span></div>
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<span style="font-family: "Times New Roman";">This
case highlights how an acute MI can lead to the formation of a VSD as well as
an inferior left ventricular aneurysm. Although the VSD was initially estimated
via TTE to be fairly small (1 cm x 1 cm), the intraoperative TEE revealed a
complex VSD with aserpiginous anatomic structure. Although larger VSDs traditionally
are corrected with the deployment of one Amplatzer occluder or corrective
cardiac surgery with anticipated residual VSD, this defect was able to be
corrected with the deployment of two Amplatzer occluder devices. The use of an
Amplatzer occluder device for the closure of post-MI VSDs dates back to 1998,
and several centers have reported results from small series of Amplatzer
interventions.2-4 In addition, the results from a US registry assessing
immediate and midterm outcomes from the use of Amplatzer devices for post-MI
VSDs were released in 2004.5 The use of 2-dimensional TEE coupled with
3-dimensional TEE in assessing VSD occluder placement has been shown
previously, and the authors also determined a 3-dimensional TEE to be very
helpful in delineating the VSD anatomy in addition to guiding occluder site
placement and deployment.6 In light of this patient's recent MI and cardiogenic
shock, the decision to proceed with a percutaneous procedure was deemed to pose
less morbidity and mortality compared with traditional surgical repair, and
this approach led to a successful therapeutic outcome. </span></div>
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<b><span style="font-family: "Times New Roman";">References
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<span style="font-family: "Times New Roman";">1.
Society of Thoracic Surgeons Online Risk Calculator, 2011.
http://www.sts.org/quality-research-patient-safety/quality/risk-calculator-and-models/risk-calculator.
Accessed April 30, 2011 </span></div>
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<span style="font-family: "Times New Roman";">2.
E.M. Lee, D.H. Roberts, Walsh: Transcatheter closure of a residual
postmyocardial infarction ventricular septal defect with the Amplatzer septal
occluder. Heart 80:522-524, 1998 </span></div>
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<span style="font-family: "Times New Roman";">3.
J.A. Goldstein, I.P. Casserly, D.T. Balzer, et al: Transcatheter closure of
recurrent postmyocardial infarction ventricular septal defects utilizing the
Amplatzer postinfarction VSD device: A case series. Catheter Cardiologic Intv
59:238-243, 2003 </span></div>
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<span style="font-family: "Times New Roman";">4.
J. Ahmed, P.N. Ruygrok, N.J. Wilson, et al: Percutaneous closure of
post-myocardial infarction ventricular septal defects: A single centre
experience. Heart Lung Circ 17:119-123, 2008 </span></div>
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<span style="font-family: "Times New Roman";">5.
R. Holzer, D. Balzer, Z. Amin, et al: Transcatheter closure of postinfarction
ventricular septal defects using the new Amplatzer muscular VSD occluder:
Results of a U.S. registry. Catheter Cardiovasc Interventions 61:196-201, 2004 </span></div>
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<span style="font-family: "Times New Roman";">6.
D.G. Halpern, G. Perk, C. Ruiz, et al: Percutaneous closure of a
post-myocardial infarction ventricular septal defect guided by real-time
three-dimensional echocardiography. Eur J Echocardiogr 10:569-571, 2009</span></div>
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<br /></div>JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-63639834593229493502011-10-18T12:41:00.000-07:002011-10-18T14:16:47.967-07:00E-Challenges & Clinical Decisions<div style="text-align: right;"><span style="font-size:78%;">Feroze Mahmood, MD<br /></span><div style="text-align: right;"><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhqhpse6bz9wSB6mPIKbkeyUXWttU06EcVwun8Sre7gvCehrT8YI8nI7Myr2YLLpexLUuaF6apVhXQ2WcexocI1gJHohGQbG0xIiGPbQ2GX9EQVAtU8J4Qoq-rmfE0fYtnb8c7S9oZXmWOU/s1600/Picture+3.png"><img style="float: left; margin: 0pt 10px 10px 0pt; cursor: pointer; width: 62px; height: 53px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhqhpse6bz9wSB6mPIKbkeyUXWttU06EcVwun8Sre7gvCehrT8YI8nI7Myr2YLLpexLUuaF6apVhXQ2WcexocI1gJHohGQbG0xIiGPbQ2GX9EQVAtU8J4Qoq-rmfE0fYtnb8c7S9oZXmWOU/s320/Picture+3.png" alt="" id="BLOGGER_PHOTO_ID_5664923013115797490" border="0" /></a><span style="font-size:78%;">Madhav Swaminathan, MD</span><br /></div><img src="file:///Users/jmusson/Desktop/Picture%202.png" alt="" /><img src="file:///Users/jmusson/Desktop/Picture%203.png" alt="" /><span style="font-size:78%;">Section Editor</span><br /><div style="text-align: left;"><br /><br /><div style="text-align: left;"><span style="font-size:78%;">CARDIAC ANESTHESIA FELLOW'S EDUCATION</span><br /><span style="font-size:78%;">Dalia A. Banks, MD<br />Section Editor</span><br /><br /><div style="text-align: center;"><span style="font-weight: bold;">Fate of Mitral Regurgitation After Aortic Valve Replacement for Aortic Stenosis</span><br /><br /><br /><div style="text-align: center;"><span style="font-size:78%;">Haider Javed Warraich, MD, Geoffery Hayward, MD, Robina Matyal, MD, Salid Shahul, MD, and Balachundar Subramaniam, MD, MPH</span><br /><br /><span style="font-size:78%;">Department of Anesthesia, Critical Care and Pain Medicine Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA</span><br /><br /><span style="font-size:78%;">Address Reprint Requests to Haider Javed Warraich, MD, Cardiovascular Anesthesia Research Fellow, CC 454, 1 Deaconess Road, Beth Israel Deaconess Medical Center, Boston MA 02215. E-mail: hwarraiac@bidmc.harvard.edu</span><br /><span style="font-size:78%;"><br /></span> <style>@font-face { font-family: "Courier New"; }@font-face { font-family: "Courier New"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }p.MsoPlainText, li.MsoPlainText, div.MsoPlainText { margin: 0in 0in 0.0001pt; font-size: 10pt; font-family: "Courier New"; }span.PlainTextChar { font-family: "Courier New"; }.MsoChpDefault { font-size: 10pt; }div.WordSection1 { page: WordSection1; }</style> <p class="MsoPlainText"><span style="font-size:78%;">Key words: aortic valve replacement, mitral regurgitation, aortic stenosis </span></p><br /><div style="text-align: left;"> <style>@font-face { font-family: "Courier New"; }@font-face { font-family: "Cambria Math"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }p.MsoPlainText, li.MsoPlainText, div.MsoPlainText { margin: 0in 0in 0.0001pt; font-size: 10pt; font-family: "Courier New"; }span.PlainTextChar { font-family: "Courier New"; }.MsoChpDefault { font-size: 10pt; }div.WordSection1 { page: WordSection1; }</style> <p class="MsoPlainText"><span style=";font-family:";" >A 75-YEAR-OLD MAN with dizziness and shortness of breath underwent a balloon valvuloplasty performed for critical aortic stenosis. After experiencing minimal symptomatic relief, the patient presented to the authors' tertiary care center with worsening symptoms 2 weeks after the procedure. The patient's history was significant for congestive heart failure, type-2 diabetes mellitus, coronary artery disease, chronic atrial fibrillation, and hypertension, and he had undergone a coronary artery bypass graft procedure in 1992. Because of a lack of symptomatic improvement after balloon valvuloplasty and persistence of decompensated congestive heart failure, despite his high risk, it was decided to perform aortic valve replacement (AVR). </span></p> </div><div style="text-align: left;"><br /></div><div style="text-align: left;"> <style>@font-face { font-family: "Courier New"; }@font-face { font-family: "Cambria Math"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }p.MsoPlainText, li.MsoPlainText, div.MsoPlainText { margin: 0in 0in 0.0001pt; font-size: 10pt; font-family: "Courier New"; }span.PlainTextChar { font-family: "Courier New"; }.MsoChpDefault { font-size: 10pt; }div.WordSection1 { page: WordSection1; }</style> <p class="MsoPlainText"><span style=";font-family:";" >After an uneventful induction of general anesthesia, a pre-cardiopulmonary bypass (CPB) transesophageal echocardiographic (TEE) examination was performed; an AV area of 0.5 cm2(critical <0.8 cm2) was calculated with the continuity equation with a peak transaortic valvular gradient of 54 mmHg (normal <20 mmHg) with a mean gradient of 38 mmHg (moderate 25-40 mmHg) and mild aortic insufficiency. The left ventricular (LV) ejection fraction was 45% to 50%, and the LV end-diastolic diameter was 6.1 cm with normal LV wall thickness. Right ventricular function was normal with no hypertrophy.<br /></span></p><p class="MsoPlainText"><br /></p><p class="MsoPlainText"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjzEJcZy2zybpx36pGa9OeWV8aKoibbgeKWgvURhbaqGaodOVqINLJDo0QeZAGik7ZzJGvFS65Juj76kwvpuwvc3PowXvLIRX_TabcnWxjqfC3YtNQMsRpuLLQQ0lvCr3bRlClsBeyxg6bg/s1600/Fig1small_Oct.jpg"><img style="float: left; margin: 0pt 10px 10px 0pt; cursor: pointer; width: 222px; height: 153px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjzEJcZy2zybpx36pGa9OeWV8aKoibbgeKWgvURhbaqGaodOVqINLJDo0QeZAGik7ZzJGvFS65Juj76kwvpuwvc3PowXvLIRX_TabcnWxjqfC3YtNQMsRpuLLQQ0lvCr3bRlClsBeyxg6bg/s320/Fig1small_Oct.jpg" alt="" id="BLOGGER_PHOTO_ID_5664939195546508722" border="0" /></a></p><p class="MsoPlainText"><br /><span style=";font-family:";" ></span></p><p class="MsoPlainText"> <style>@font-face { font-family: "Courier New"; }@font-face { font-family: "Cambria Math"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }p.MsoPlainText, li.MsoPlainText, div.MsoPlainText { margin: 0in 0in 0.0001pt; font-size: 10pt; font-family: "Courier New"; }span.PlainTextChar { font-family: "Courier New"; }.MsoChpDefault { font-size: 10pt; }div.WordSection1 { page: WordSection1; }</style> </p><p class="MsoPlainText"> <style>@font-face { font-family: "Courier New"; }@font-face { font-family: "Cambria Math"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }p.MsoPlainText, li.MsoPlainText, div.MsoPlainText { margin: 0in 0in 0.0001pt; font-size: 10pt; font-family: "Courier New"; }span.PlainTextChar { font-family: "Courier New"; }.MsoChpDefault { font-size: 10pt; }div.WordSection1 { page: WordSection1; }</style> </p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><br /></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" >Fig 1 The prebypass TEE examination from the midesophageal 4-chamber view shows severe MR. (Inset) Midesophageal long-axis view.<br /></span></p><p class="MsoPlainText"><br /></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" >Echocardiographic Findings</span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p> <p class="MsoPlainText"><span style=";font-family:";" ><span style=""> </span></span></p> <p class="MsoPlainText"><span style=";font-family:";" >TEE interrogation of the mitral valve (MV) revealed moderate-to-severe (3+) mitral regurgitation (MR) (Fig 1andVideo 1[supplementary videos are available online]), with vena contracta of 6 mm (severe >=5.5mm) and mildly thickened leaflets; there was no structural abnormality of the MV. The echocardiographic challenge was to rule in or out the presence of any organic/structural cause of MR. A 3-dimensional en face view of the MV from the left atrial perspective revealed failure of coaptation between the A3 and P3 segments of the mitral leaflets (Video 2). There was no evidence of any structural abnormality. The left atrium was dilated with a long-axis dimension of 6.4 cm (normal <4.0 cm). A discussion was initiated with the surgeons regarding different therapeutic options, which included double valve replacement, AVR with MV repair, and AVR alone. </span></p> <p class="MsoPlainText"><span style=";font-family:";" > </span></p> <p></p> <p></p> </div><div style="text-align: left;"> <style>@font-face { font-family: "Courier New"; }@font-face { font-family: "Cambria Math"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }p.MsoPlainText, li.MsoPlainText, div.MsoPlainText { margin: 0in 0in 0.0001pt; font-size: 10pt; font-family: "Courier New"; }span.PlainTextChar { font-family: "Courier New"; }.MsoChpDefault { font-size: 10pt; }div.WordSection1 { page: WordSection1; }</style><p class="MsoPlainText"> <style>@font-face { font-family: "Courier New"; }@font-face { font-family: "Cambria Math"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }p.MsoPlainText, li.MsoPlainText, div.MsoPlainText { margin: 0in 0in 0.0001pt; font-size: 10pt; font-family: "Courier New"; }span.PlainTextChar { font-family: "Courier New"; }.MsoChpDefault { font-size: 10pt; }div.WordSection1 { page: WordSection1; }</style> </p><p class="MsoPlainText"><span style=";font-family:";" >Clinical Challenge<br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p> <p class="MsoPlainText"><span style=";font-family:";" > </span></p> <p class="MsoPlainText"><span style=";font-family:";" >The clinical challenge was to weigh the increased risk of concomitant MV surgery during AVR and to accurately predict the effect of AVR on the severity of MR.<br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p> <p class="MsoPlainText"><span style=";font-family:";" > </span></p> <p class="MsoPlainText"><span style=";font-family:";" >Surgical Decision<br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p> <p class="MsoPlainText"><span style=";font-family:";" > </span></p> <p class="MsoPlainText"><span style=";font-family:";" >After weighing the pros and cons, it was decided to perform AVR alone. A 21-mm Edwards pericardial tissue valve was used. After successful valve replacement and separation from CPB, post-CPB transesophageal echocardiography showed a well-seated bioprosthetic AV. The AV area was noted to be 1.5 cm2with trace central regurgitation and no paravalvular leak. The LV ejection fraction improved to 50-55%, and MR improved to moderate (2+) (Fig 2 and Video 3). A follow-up transthoracic echocardiogram 2 months after surgery revealed MR to still be moderate (2+).<br /></span></p><p class="MsoPlainText"> <style>@font-face { font-family: "Courier New"; }@font-face { font-family: "Cambria Math"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }p.MsoPlainText, li.MsoPlainText, div.MsoPlainText { margin: 0in 0in 0.0001pt; font-size: 10pt; font-family: "Courier New"; }span.PlainTextChar { font-family: "Courier New"; }.MsoChpDefault { font-size: 10pt; }div.WordSection1 { page: WordSection1; }</style> </p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><br /></p><p class="MsoPlainText"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi1a7kB1_RNl_Deizs7_WeaNqQCgw-fq3V2rgSJARh797p4u3OsXklXn7nsOz1QNvJ3Xf6gxycksX4uYzIlRFtclv3chP_v9rh8jl9VrnUTOoVQx8g9k0mRP0bEihcu6mFYXk6mWdPFNJ2T/s1600/gr2_sm.jpg"><img style="float: left; margin: 0pt 10px 10px 0pt; cursor: pointer; width: 219px; height: 153px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi1a7kB1_RNl_Deizs7_WeaNqQCgw-fq3V2rgSJARh797p4u3OsXklXn7nsOz1QNvJ3Xf6gxycksX4uYzIlRFtclv3chP_v9rh8jl9VrnUTOoVQx8g9k0mRP0bEihcu6mFYXk6mWdPFNJ2T/s320/gr2_sm.jpg" alt="" id="BLOGGER_PHOTO_ID_5664940634189213730" border="0" /></a></p><p class="MsoPlainText"><br /></p><p class="MsoPlainText"><br /></p><p class="MsoPlainText"> <style>@font-face { font-family: "Courier New"; }@font-face { font-family: "Cambria Math"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0in 0in 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }p.MsoPlainText, li.MsoPlainText, div.MsoPlainText { margin: 0in 0in 0.0001pt; font-size: 10pt; font-family: "Courier New"; }span.PlainTextChar { font-family: "Courier New"; }.MsoChpDefault { font-size: 10pt; }div.WordSection1 { page: WordSection1; }</style> </p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" ><br /></span></p><p class="MsoPlainText"><span style=";font-family:";" >Fig 2 The postbypass TEE examination shows improvement of the MR grade to moderate severity. </span></p> <p></p> <p></p> <p></p> <p class="MsoPlainText"><span style=";font-family:";" > </span></p> </div></div></div></div></div><span style="font-weight: bold;"><span style="font-size:85%;"></span></span></div>JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com3tag:blogger.com,1999:blog-4614555285346122404.post-2779199511559930832011-04-12T12:37:00.000-07:002011-04-12T12:55:03.198-07:00E-CHALLENGES & CLINICAL DECISIONS<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiw9tR0mUzuiRZwuwvStRREyW5S8dMk0pI9xUqcqq2LMaEyfb2UGMNRsSxSmnKiG3bx2XoLroreii20XjjkBQCE3bYH5cx_gs-4m5c31MM2-EO2hq3omvnQMorvk7Q8FInsvIOhNG-_N76s/s1600/Fig2_large.jpg" onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}"></a><div><div style="text-align: right;"><div style="text-align: left;"><br /></div></div><div style="text-align: right;"><span class="Apple-style-span" style="font-size:small;">Feroze Mahmood, MD </span></div><div style="text-align: right;"><span class="Apple-style-span" style="font-size:small;">Madhav Swaminathan, MD </span></div><div style="text-align: right;"><span class="Apple-style-span" style="font-size:small;">Section Editors</span><span class="Apple-style-span" style="font-size:x-small;"> </span></div><div style="text-align: left;"><img src="webkit-fake-url://69115153-E1AE-4E37-BCE6-EB8D18617C7B/application.pdf" /></div><div><span class="Apple-style-span" style="font-size: x-small;">CARDIAC ANESTHESIA FELLOWS EDUCATION </span></div><div><i><span class="Apple-style-span" style="font-size: x-small;">Dalia A. Banks, MD, FASE</span></i></div><div><i><span class="Apple-style-span" style="font-size:x-small;"><br /></span></i></div><div><i><span class="Apple-style-span" style="font-size:medium;"><br /></span></i></div><div style="text-align: center;"><b><span class="Apple-style-span" style="font-size:medium;">Aortic Stenosis and Coronary Artery Disease ... and a Challenging Aorta</span></b></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: x-small;"><br /></span></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: x-small;">Brandi A. Bottiger, MD, Robert D. Davis, MD, Robert C. Swift MD, Madhav Swaminathan MD, FASE, FAHA</span></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: x-small;"><br /></span></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: x-small;">Departments of Anesthesiology and Surgery, Duke University Health System, Durham, NC </span></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: x-small;"><br /></span></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: x-small;">Address reprint requests to Madhav Swaminathan, MD, FASE, FAHA, Department of Anesthesiology, Division of Cardiothoracic Anesthesiology and Critical Care Medicine, Box 3094/5691F HAFS Building, Duke University Health System, Durham, NC 27710. E-mail: swami001@mc.duke.edu </span></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: x-small;"><br /></span></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: x-small;">Key words: aortic stenosis, coronary artery disease</span></div><div><br /></div><div><span class="Apple-style-span" style="font-size:small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"> A 77-YEAR-OLD man presented to an outside hospital with the chief complaint of chest pain that radiated to his jaw. He had a known history of coronary artery disease for which he had coronary stents placed 6 years previously. He was diagnosed with a non-ST elevation myocardial infarction and after stabilization was transferred to the authors' facility for further evaluation and management. Transthoracic echocardiography showed preserved left ventricular systolic function with an estimated ejection fraction of >55%, a grade I diastolic relaxation abnormality, normal wall motion, mild left ventricular hypertrophy, and a moderately stenosed aortic valve (45 mmHg peak and 24-mmHg mean transvalvular gradient) with thickened, calcified leaflets. Coronary angiography at the transferring hospital showed severe 3-vessel disease.</span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"> His past medical history was significant for hypertension, hyperlipidemia, tobacco abuse (65-pack-year history), and carotid artery disease with previous left carotid endarterectomy. He denied complications with anesthesia for his past surgeries. Based on his presentation and imaging studies, the patient was scheduled for coronary artery bypass graft (CABG) surgery and aortic valve replacement (AVR) on cardiopulmonary bypass (CPB). </span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"> Preoperative laboratory studies were unremarkable except for anemia (hemoglobin, 10.0 g/dL) and an elevation in creatinine (1.6 mg/dL). He was on a heparin infusion. He was taken to the operating room, and after placement of appropriate monitors, general anesthesia was induced uneventfully and the airway was secured in typical fashion. </span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div style="text-align: center;"><i><span class="Apple-style-span" style="font-size: small;">Intraoperative Transesophageal Echocardiographic Findings </span></i></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"> An intraoperative transesophageal echocardiographic (TEE) examination was performed on an ie-33 ultrasound system with an X7-2t TEE probe (Philips Medical Systems, Andover, MA). The principal findings were the following: (1) preserved left ventricular systolic function, (2) estimated ejection fraction of >55%, (3) a thickened and mildly calcified aortic valve with turbulent flow by color-flow Doppler (Fig 1,left panel), (4) a peak transvalvular gradient of 37 mmHg with a mean gradient of 22 mmHg (Fig 1, right panel), and (5) severe atherosclerotic disease of the descending aorta and aortic arch with multiple atheromatous plaques (Fig 2). Calcified plaques in the ascending aorta also were noted. The surgeon determined by manual palpation that there was dense calcification of the ascending aorta in the region where manipulation (ie, cannulation, cross-clamping, proximal anastomosis, and aortotomy) was planned, the so-called "porcelain aorta" (see supplementary video available online).</span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div style="text-align: center;"><i><span class="Apple-style-span" style="font-size: small;">Discussion </span></i></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;">The following challenges were met in this case.</span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;">1. Should the aortic valve be replaced? If yes, how should the surgery be conducted? If no, what are the </span></div><div><span class="Apple-style-span" style="font-size: small;"> implications of residual aortic stenosis on postoperative outcome?</span></div><div><span class="Apple-style-span" style="font-size: small;">2. How should the CABG surgery be conducted? Should it be on-pump CABG surgery? What are the possible</span></div><div><span class="Apple-style-span" style="font-size: small;">cannulation sites? Where are the possible proximal anastomotic sites? Should it be off-pump CABG surgery? </span></div><div><span class="Apple-style-span" style="font-size: small;"> Where are the possible proximal anastomotic sites? What are the advantages versus the disadvantages of off-</span></div><div><span class="Apple-style-span" style="font-size: small;"> pump CABG surgery?</span></div><div><span class="Apple-style-span" style="font-size: small;"></span><span class="Apple-style-span" style="font-size: small; ">3. What are the risks of perioperative stroke with a calcified aorta?</span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div style="text-align: center;"><i><span class="Apple-style-span" style="font-size: small;">Options </span></i></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"> The following options were considered: (1) CABG surgery and AVR with right axillary cannulation for arterial access instead of direct aortic cannulation; (2) CABG surgery, AVR, and ascending aorta with root replacement under deep hypothermic circulatory arrest; (3) CABG surgery only on CPB with right axillary cannulation for arterial access instead of direct aortic cannulation; and (4) off-pump CABG surgery only with minimal aortic manipulation.</span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div style="text-align: center;"><i><span class="Apple-style-span" style="font-size: small;">Strategy </span></i></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"> After extensive discussions among the referring cardiologist, surgeon, and Anesthesiologist, a decision was made not to replace the aortic valve and proceed with off-pump CABG surgery. The patient had 3 coronary bypass grafts performed, including a left internal mammary artery to the left anterior descending, and saphenous vein grafts to the first marginal and right posterior lateral first branch. One saphenous vein graft was anastomosed to the proximal ascending aorta using a minimally invasive technique (Heartstrings II; Maquet Cardiovascular LLC, Wayne, NJ) without the need for a partial aortic cross-clamp. The proximal anastomosis of the second vein graft was performed on the first vein graft, thereby allowing for only a single aortic proximal anastomotic site. </span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="color:#0000EE;"><span class="Apple-style-span" style="font-size: small;"><br /></span></span></div><div><span class="Apple-style-span" style="color: rgb(0, 0, 238); -webkit-text-decorations-in-effect: underline; "><img src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhw6khWTTHdl_R2VE4tQJB-xmP0SGqP4uobtgIL7DYiXuREXKlmDKb2d0IOJ_nwjciqtHKmpTJqgmTAWQUnzXgoPtQw469NloaQVXkiTsWpatplzPYtG9C4cTYw4xpdzumRJeFEeILsXTAw/s320/Fig1_large.jpg" border="0" alt="" id="BLOGGER_PHOTO_ID_5594779854205620770" style="float: left; margin-top: 0px; margin-right: 10px; margin-bottom: 10px; margin-left: 0px; cursor: pointer; width: 320px; height: 121px; " /></span></div><div><span class="Apple-style-span" style="color:#0000EE;"><span class="Apple-style-span" style="font-size: small;"><br /></span></span></div><div><span class="Apple-style-span" style="color:#0000EE;"><span class="Apple-style-span" style="font-size: small;"><br /></span></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: x-small;">Fig 1 The image on the left shows the midesophageal aortic valve long-axis view with color-flow Doppler across the aortic valve indicating turbulent transvalvular flow. The image on the right represents continuous wave spectral Doppler across the aortic valve in the deep transgastric long-axis view. The measurements are described in the text.</span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div style="text-align: center;"><i><span class="Apple-style-span" style="font-size: small;">Rationale </span></i></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"> According to the Society of Thoracic Surgeons (STS) risk score, his calculated overall mortality risk was 5.1%, morbidity or mortality risk was 34.2%, and stroke risk was 3.9% for CABG surgery and AVR. Without the AVR procedure, his risks for the same outcomes were 3.5%, 26.1%, and 2.4%, respectively. However, the STS risk calculator does not account for the severity of aortic stenosis or a porcelain aorta. This was also balanced with the risk of progression of aortic stenosis without surgical intervention. Given the patient's age and comorbidities, combined with the high risk of morbidity and mortality accompanying the AVR, it was believed that the aortic valve should not be replaced. First, there likely would be limited reduction in the transvalvular gradient from a prosthetic valve and therefore limited benefit in this patient with a mean gradient of 22 mmHg. Second, with close postoperative follow-up, the aortic stenosis could be monitored, and, if required, a percutaneous replacement could be feasible in the future. The off-pump approach was chosen to eliminate cannulation and limit aortic manipulation to reduce the stroke risk. Although the STS risk calculator does not account for the off-pump technique to reduce risk, aortic manipulation in this case was believed to be the most significant factor rather than CPB itself. The potential risk was that the patient may not tolerate surgical handling of the heart or beating-heart surgery and CPB may need to be initiated emergently. A "no-touch" technique of vein graft anastomosis was used to minimize aortic manipulation while retaining the quality of revascularization. </span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="color:#0000EE;"><span class="Apple-style-span" style="color:#000000;"><span class="Apple-style-span" style="font-size: small;"><br /></span></span></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="color: rgb(0, 0, 238); -webkit-text-decorations-in-effect: underline; "><img src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiw9tR0mUzuiRZwuwvStRREyW5S8dMk0pI9xUqcqq2LMaEyfb2UGMNRsSxSmnKiG3bx2XoLroreii20XjjkBQCE3bYH5cx_gs-4m5c31MM2-EO2hq3omvnQMorvk7Q8FInsvIOhNG-_N76s/s320/Fig2_large.jpg" border="0" alt="" id="BLOGGER_PHOTO_ID_5594780152206310402" style="float: left; margin-top: 0px; margin-right: 10px; margin-bottom: 10px; margin-left: 0px; cursor: pointer; width: 320px; height: 216px; " /></span></div><div><span class="Apple-style-span" style="color: rgb(0, 0, 238); -webkit-text-decorations-in-effect: underline; "><span class="Apple-style-span" style="font-size: small;"><br /></span></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span"><span class="Apple-style-span" style="font-size: small;"><br /></span></span></div><div><span class="Apple-style-span"><span class="Apple-style-span" style="font-size: small;"><br /></span></span></div><div><span class="Apple-style-span"><span class="Apple-style-span" style="font-size: small;"><br /></span></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: x-small;">Fig 2 The descending aorta is shown simultaneously in the short-axis (SAX) and long-axis (LAX) views. Significant atheromatous disease is indicated by the arrows in the image.</span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div style="text-align: center;"><i><span class="Apple-style-span" style="font-size: small;"><br /></span></i></div><div style="text-align: center;"><i><span class="Apple-style-span" style="font-size: small;"><br /></span></i></div><div style="text-align: center;"><i><span class="Apple-style-span" style="font-size: small;">Postoperative Course </span></i></div><div style="text-align: center;"><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"> The patient tolerated the procedure well without any complications or the need for inotropic support. After the procedure, he was transferred to the postoperative cardiac surgical intensive care unit in stable condition. In the immediate postoperative period, he continued to do quite well and had a routine discharge 5 days after surgery.</span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div style="text-align: center;"><i><span class="Apple-style-span" style="font-size: small;">Summary </span></i></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"> In summary, this case highlights how a heavily calcified aorta, which was initially detected with transesophageal echocardiography, limited the management of a patient with combined aortic valve stenosis and coronary artery disease. These findings led to a complete change in surgical plan guided by a multidisciplinary discussion of all possible approaches and their implications. Fortunately, the patient had an uneventful in-hospital course as planned. A video summarizing the case including TEE video clips is also presented. </span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div><div><span class="Apple-style-span" style="font-size: small;"><br /></span></div></div><div><br /></div>JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-38555204979784917602010-10-15T14:04:00.000-07:002010-10-15T14:11:44.959-07:00E-Challenges & Clinical Decisions<div style="text-align: right;"><span class="Apple-style-span" style=" ;font-family:Arial;"><span class="Apple-style-span" style="font-size:small;">Feroze Mahmood, MD</span></span></div> <p class="MsoPlainText" style="text-align: right;"><span style="font-family:Arial;mso-bidi-Courier New"font-family:";"><span class="Apple-style-span" style="font-size:small;">Madhav Swaminathan, MD</span><span><span class="Apple-style-span" style="font-size:small;"> </span></span><span class="Apple-style-span" style="font-size:small;"><o:p></o:p></span></span></p> <p class="MsoPlainText" style="text-align: right;"><span style="font-family:Arial;mso-bidi-Courier New"font-family:";"><span class="Apple-style-span" style="font-size:small;">Section Editors</span><o:p></o:p></span></p> <p class="MsoPlainText"><span style="font-family:Arial;mso-bidi-Courier New"font-family:";"><o:p> </o:p></span></p> <p class="MsoPlainText"><span style="font-family:"Courier New";mso-bidi-Courier New"font-family:";"><o:p> </o:p></span></p> <p class="MsoPlainText"><span style="font-family:"Courier New";mso-bidi-Courier New"font-family:";"><o:p> </o:p></span></p> <p class="MsoPlainText"><b><span style="font-family:Arial;mso-bidi-Courier New"font-family:";"><span class="Apple-style-span" style="font-size:large;"><br /></span></span></b></p><p class="MsoPlainText"><b><span style="font-family:Arial;mso-bidi-Courier New"font-family:";"><span class="Apple-style-span" style="font-size:large;">Systolic Anterior Motion After Mitral Valve Repair and a Systolic Anterior Motion Tolerance Test</span></span></b></p><p class="MsoPlainText"><b><span style="font-family:Arial;mso-bidi-Courier New"font-family:";"><span class="Apple-style-span" style="font-size:large;"></span></span></b><span style="font-family:";"><span class="Apple-style-span" style="font-size:small;">Ger</span></span><span style="font-family:";"><span class="Apple-style-span" style="font-size:small;">a</span></span><span style="font-family:";"><span class="Apple-style-span" style="font-size:small;">rd R. Manecke, MD, Liem C. Nguyen, MD, Adam D. Tibble, MD, Eugene Golts, MD, and Dalia Banks, MD</span></span></p> <p class="MsoPlainText"><span style="mso-bidi- mso-bidi-Courier New"font-family:";font-size:10.5pt;"><o:p> </o:p></span></p> <p class="MsoPlainText"><span style="font-size:10.0pt;mso-bidi- font-family:Arial;mso-bidi-Courier New"font-family:";font-size:10.5pt;"><o:p> </o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:small;">From the Department of Anesthesiology and Division of Cardiothoracic Surgery, University of California <o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:small;">San Diego Medical Center, San Diego, CA<o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:small;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:small;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:small;">Address reprint requests to Gerard R. Manecke, MD, Department of Anest</span></span><span class="Apple-style-span" style=" ;font-size:small;">hesiology, University of California San Diego, 200 West Arbor Drive, San Diego, CA 92103.</span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:small;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:small;">E-mail: gmanecke@ucsd.edu </span></span><span class="Apple-style-span" style=" ;font-size:small;">© 2010 Elsevier Inc. All rights reserved. </span><span class="Apple-style-span" style=" ;font-size:small;">1053-0770/2405-0026$36.00/0 </span><span class="Apple-style-span" style=" ;font-size:small;">doi :10.1053/j.jvca.2010.07.021.</span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:small;">Key words:</span><span><span class="Apple-style-span" style="font-size:small;"> </span></span><span class="Apple-style-span" style="font-size:small;">mitral valve repair, systolic anterior m</span></span><span style="font-size:10.0pt;mso-bidi- font-family:Arial;mso-bidi-Courier New"font-family:";font-size:10.5pt;">otion <o:p></o:p></span></p> <p class="MsoPlainText"><span style="font-size:10.0pt;mso-bidi- font-family:Arial;mso-bidi-Courier New"font-family:";font-size:10.5pt;"><o:p> </o:p></span></p> <p class="MsoPlainText"><span style="font-size:10.0pt;mso-bidi- font-family:Arial;mso-bidi-Courier New"font-family:";font-size:10.5pt;"><o:p> </o:p></span></p> <p class="MsoPlainText" style="mso-outline-level:1"><span style="font-size:10.0pt; mso-bidi-font-family:Arial;mso-bidi-Courier New"font-family:";font-size:10.5pt;"><br /></span></p><p class="MsoPlainText" style="mso-outline-level:1"><span style="font-family:";"><span class="Apple-style-span" style="font-size: medium;">A 62-YEAR-OLD MA</span></span><span class="Apple-style-span"><span class="Apple-style-span" style="font-size: medium;">N with an unremarkable medical history presented for mitral valve repair and single-vessel coronary art</span></span><span class="Apple-style-span"><span class="Apple-style-span" style="font-size: medium;">er</span></span><span class="Apple-style-span" style="font-size:medium;">y bypass. He had experienced a 2-month period of increasing dyspnea on exertion, and his cardiologist noted a IV/VI systolic murmur. His lifestyle was sedentary; he performed basic chores and occasional climbing</span><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;">of a flight of stairs. He did not partake in regular exercise. A preoperative transthoracic echocardiogram showed moderate/severe mitral regurgitation (MR), thickened mitral leaflets, prolapse of the posterior mitral leaflet, a mildly dilated left atrium, and normal left ventricular function. Cardiac catheterization revealed an 85% lesion in the distal left anterior descending artery.</span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">Intraoperative monitoring included a radial arterial catheter, pulmonary artery catheter, and transesophageal echocardiography (TEE). Anesthetic induction (midazolam/fentanyl/relaxant) and maintenance (isoflurane in oxygen) were uneventful. The pre-cardiopulmonary bypass (CPB) transesophageal echocardiographic findings were in agreement with those of the preoperative transthoracic echocardiogram (Fig 1 and Video 1</span><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;">^[supplementary videos are available online^]). Representative pre-CPB hemodynamics were as follows: heart rate, 72 beats/min; blood press</span></span><span class="Apple-style-span" style=" ;font-size:medium;">ure (BP), 110/70 mmHg; cardiac output (CO), 4.5 L/min; pulmonary artery pressure (PAP), 28/14 mmHg; and central venous pressure (CVP), 6 mmHg.</span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">The surgical procedure, via a midline sternotomy, consisted of a coronary bypass graft to the left anterior descending artery using the left internal mammary artery and mitral valve repair. The repair involved resection of a large, redundant P2 segment and placement of an annuloplasty ring (28-mm Carpentier-Edwards Physio Ring; Edwards Lifesciences, Irvine, CA). The anterior leaflet did not appear particularly redundant upon surgical inspection, so it was not resected. <o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">Separation from CPB was accomplished easily, without the use of vasoactive medications. TEE before decannulation revealed only trace MR, and hemodynamics were favorable (heart rate, 80 beats/min; BP, 110/70 mmHg; PAP, 28/14 mmHg; CO, 5.5 L/min; CVP, 6 mmHg). However, systolic anterior motion (SAM) of the mitral leaflets was noted, with dynamic obstruction of the left ventricular outflow tract (LVOT) and turbulent aortic flow (Fig 2 and Video 2). After discussion with the surgeon,</span></span><span class="Apple-style-span" style=" ;font-size:medium;">a provocative test was performed. This was performed while the great vessels were still cannulated, with the goal of determining if his SAM would be tolerated should he become hypovolemic, tachycardic, and vasodilated postoperatively. For 15 minutes, ventricular pacing at 120 beats/min was instituted, and nitroglycerin, 200 µg/min, and dopamine, 7 µg/kg/min, were administered.The BP dropped to 80/50 mmHg but was then maintained, CO was maintained at >5 L/min, PAP rose to 42/24 mm Hg, and the CVP remained at 6 mmHg. TEE revealed some worsening of the MR (moderate), and the LVOT obstruction appeared to worsen slightly, with the appearance of a "double envelope" on continuous-wave Doppler of the LVOT (Video 2). The decision then was made to discontinue the dopamine, nitroglycerin, and pacing. No further surgery was performed on the mitral valve, and the remainder of the operation was uneventful. His postoperative period was likewise uneventful, and he was discharged on the 9th postoperative day with a prescription for daily β-blockade therapy.</span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText" style="text-align: center;"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">Discussion <o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">SAM is not uncommon after mitral valve repair, having been reported to occur in 8.4% of cases.1 Anatomic risk factors for its development include a short coaptation-septal distance (C-sept)2; low anterior leaflet:posterior leaflet length ratio2; large, redundant leaflets3; and septal hypertrophy.3 Hemodynamic risks include highly contractile state, hypovolemia, tachycardia, and low afterload. This patient presented with all the anatomic risks, including short C-sept (2.24 cm) and low anterior:posterior ratio (0.75) before repair.2</span><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;"><o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">SAM after mitral valve repair often is well tolerated, and, when initially present, may resolve after mitral valve repair.1</span><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;">Indeed, patients with SAM from other causes are often asymptomatic (and undiagnosed) until an inciting injury results in hypovolemia and a high catecholamine state.4</span><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;"><o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">The question was not if SAM was present but rather how well the patient would tolerate it under "SAM-aggravating" conditions. In the authors' experience, when severe SAM occurs after mitral repair, it can result in "wide-open" MR, LVOT obstruction, very high PAP, and hypotension, necessitating a return to CPB. In such cases, it is obvious that the valve must either be rerepaired or replaced. This patient presented a "gray-zone" situation in which hemodynamics were favorable after CPB, but the presence of SAM was clear. <o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">A potentially useful test that may help in determining if a patient is at postoperative risk for SAM has been described by Crescenzi et al.5 This group treats intraoperative SAM with conservative measures (intravascular volume expansion and discontinuation of inotropes) as well as more aggressive ones (β-blockade, increasing afterload by manual compression of the ascending aorta). These authors suggest surgical revision of the repair if conservative measures fail to result in the resolution of SAM. <o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">In contrast, the test the present authors propose, the "SAM tolerance test," is designed to determine, given that SAM is present, how well it will be tolerated postoperatively if SAM-aggravating conditions (hypovolemia, vasodilatation, and high contractile state) develop. The patient's condition deteriorated somewhat with this test, but he did not suffer hemodynamic collapse, severe hypotension, or require reinstitution of CPB. The test was performed with the great vessels still cannulated and before heparin reversal in case a return to CPB became necessary. Considering his sedentary lifestyle and his ability to tolerate (with some struggle) the "SAM tolerance test," the authors believe this patient very likely will tolerate SAM should it persist postoperatively. The authors strongly recommend that such patients receive chronic β-blocker therapy and be advised to remain well-hydrated and to report deteriorating exercise tolerance to their cardiologist immediately.<o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;"><b><i>Readers are encouraged to view the online videos (Videos 1 and 2) and share their thoughts on the potential utility of this test at the JCVA online blog site. <o:p></o:p></i></b></span></span></p><p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;"><br /></span></span></p><p class="MsoPlainText" style="text-align: center;"><span style="font-family:";"><span class="Apple-style-span" style="color: rgb(0, 0, 238); "><img src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi8Y6Bw6Dtb20WXLJxP_Pu2vkQlDPOarxrs851OsJ4292-oDb3IAdIEv5AxmUTYCK0tinfSJJT81vatYcFQVEwBm8zOXp3xb9T1UXCW0gmToSmym4Vm8GJdMUMSuhKp7oNv91q7myLB-QkK/s320/Fig1small.jpg" border="0" alt="" id="BLOGGER_PHOTO_ID_5528381872030626722" style="display: block; margin-top: 0px; margin-right: auto; margin-bottom: 10px; margin-left: auto; text-align: center; cursor: pointer; width: 320px; height: 220px; " /></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"></span></p><span style="font-family:";"><div><span class="Apple-style-span" style="font-size:medium;">Fig 1. Transesophageal echocardiographic midesophageal 4-chamber view with color-flow Doppler showing moderate/severe mitral regurgitation before mitral valve repair.</span></div><p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;"><o:p></o:p></span></span></p><p class="MsoPlainText" style="text-align: center; "><span style="font-family:";"><span class="Apple-style-span" style="color: rgb(0, 0, 238); -webkit-text-decorations-in-effect: underline; "><img src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgu_tQsN9Os7hnPYuhKhwKY1DA5JtBgUM_BqLz3dtf_icQ0RW2yFu0L7onqizCSAa1dgXBNrGbQkz_PBsUU284I2wUDlF-vV5WXbg-eCvYHgBxdvoITCC6epywgedjU6Q1vpYVNekj1RJnu/s320/Fig2small.jpg" border="0" alt="" id="BLOGGER_PHOTO_ID_5528382050740232818" style="display: block; margin-top: 0px; margin-right: auto; margin-bottom: 10px; margin-left: auto; text-align: center; cursor: pointer; width: 320px; height: 232px; " /></span></span></p><div style="text-align: left; "><span class="Apple-style-span" style="font-size:medium;">Fig 2. Transesophageal echocardiographic midesophageal long-axis view </span><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">after mitral valve repair showing mitral leaflets entering the left ventricular outflow tract during systole. In Video 2, the aortic valve is noted to "flutter" during systole</span></span><span style="font-family: 'Courier New'; font-family:";"><span class="Apple-style-span" style="font-size:medium;">,</span></span><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">suggesting turbulent flow.</span></span></div><p></p></span><p></p><p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;"><br /></span></span></p><p class="MsoPlainText" style="text-align: center;"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">Appendix <o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">Supplementary data <o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">Supplementary data associated with this article can be found, in the online version, at doi :10.1053/j.jvca.2010.07.021.</span><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;"><o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;"><o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><span><span class="Apple-style-span" style="font-size:medium;"> </span></span></span><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">References <o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">1. Brown ML, Abel MD, Click RL, et al: Systolic anterior motion after mitral valve repair: Is surgical intervention necessary? J Thorac Cardiovasc Surg 133:136-143, 2007<o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">2. Maslow AD, Regan MM, Haering JM, et al:</span><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;">Echocardiographic predictors of left ventricular outflow tract obstruction and </span><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;">systolic anterior motion of the mitral valve after mitral valve reconstruction for myxomatous valve disease. J Am Coll Cardiol 34:2096-2104, 1999</span><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;"><o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">3. Tewari P, Basu R: Left ventricular outflow tract obstruction after mitral valve replacement.</span></span><span class="Apple-style-span" style=" ;font-size:medium;">Anesth Analg 106:65-66, 2008</span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">4. Luckner G, Margreiter J, Jochberger S, et al: Systolic anterior motion of the mitral valve with left ventricular outflow tract obstruction: Three cases of acute perioperative hypotension in noncardiac surgery. </span></span><span class="Apple-style-span" style=" ;font-size:medium;">Anesth Analg 100:1594-1598, 2005</span></p> <p class="MsoPlainText"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p> <p class="MsoPlainText"><span style="font-family:";"><span><span class="Apple-style-span" style="font-size:medium;"> </span></span><span class="Apple-style-span" style="font-size:medium;"><o:p></o:p></span></span></p> <p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;">5. Crescenzi G, Landoni G, Zangrillo A, et al: Management and decision-making strategy for systolic anterior motion after mitral valve repair. J Thorac Cardiovasc Surg 137:320-325, 2009<o:p></o:p></span></span></p><p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;"><br /></span></span></p><p class="MsoPlainText"><span style="font-family:";"><span class="Apple-style-span" style="font-size:medium;"><br /></span></span></p> <p class="MsoPlainText" style="text-align: center;"><span style="font-family:";"><o:p><span class="Apple-style-span" style="font-size:medium;"> </span></o:p></span></p><p class="MsoPlainText" style="text-align: center;"><span style="font-family:";"><o:p><span class="Apple-style-span" style=" color: rgb(0, 0, 238); -webkit-text-decorations-in-effect: underline; "><span class="Apple-style-span" style="font-size:medium;"><br /></span></span></o:p></span></p><div><span class="Apple-style-span" style="font-size:100%;"><span class="Apple-style-span" style="font-size:13px;"><br /></span></span></div> <!--EndFragment-->JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-68030855812830876482010-09-22T15:21:00.000-07:002010-09-22T22:09:45.433-07:00E-CHALLENGES & CLINICAL DECISIONS<div align="right">Feroze Mahmood, MD<br />Madhav Swaminathan, MD<br />Section Editors<br /></div><br /><div align="center"><br /><span style="font-size:130%;"><strong>Coronary Artery Bypass Graft Surgery and Moderate Aortic Stenosis: When To Leave Well Enough Alone</strong><br /></span>Andrea Xavier, MD, Jason Erlich, MD, and Adam B. Lerner, MD</div><br /><br /><br /><div align="justify">AN 84-YEAR-OLD man with a history of coronary artery disease (CAD) presented with unstable angina. The patient had a history of percutaneous transluminal coronary angioplasty of the circumflex artery 12 years prior but now had increasing angina, increasing dyspnea on exertion, and fatigue. The patient underwent cardiac catheterization that showed severe 3-vessel CAD, normal biventricular systolic function with an ejection fraction of 61%, mild aortic stenosis with an aortic valve area (AVA) of 1.6 cm2 with a maximum transvalvular gradient of 32 mmHg, and trace aortic regurgitation. </div><div align="justify"><br /> </div><div align="justify">The patient’s past medical history was notable for hypertension, non–insulin-dependent diabetes mellitus, chronic renal insufficiency (creatinine of 1.6 mg/dL), hypercholesterolemia, and a Schatzki ring for which he had undergone esophageal dilation several years earlier. His medications included simvastatin, lisinopril, atenolol, hydrochlorothiazide, terazosin, glipizide, and aspirin. The patient was scheduled for coronary artery bypass graft surgery.</div><div align="justify"><br />On arrival to the preoperative unit, the patient was in no distress with a blood pressure of 160/70 mmHg and a heart rate of 68 beats/min. He was 72 inches tall with a weight of 90 kg. His preoperative laboratory workup was unremarkable. His electrocardiogram showed a sinus rhythm with occasional premature atrial beats and a first-degree atrioventricular conduction<br />delay. He was taken to the operating room and underwent an uneventful placement of appropriate monitoring.</div><div align="center"><br />INTRAOPERATIVE TRANSESOPHAGEAL ECHOCARDIOGRAPHIC EXAMINATION<br /></div><br /><div align="justify">After the induction of anesthesia, a transesophageal echocardiographic probe was passed without difficulty. The transesophageal echocardiographic examination was performed with an IE-33 ultrasound system with an OMNI-III TEE probe(Philips Medical Systems, Andover, MA).</div><br /><div align="center">FINDINGS<br /></div><div align="justify">Findings included the following: (1) a hyperdynamic leftventricle with an ejection fraction estimated at 75%, (2) mildto-moderate thickening and calcification of the 3 aortic valve leaflets (Fig 1), (3) a mild-to-moderate decrease in aortic valve leaflet mobility, (4) an instantaneous peak gradient of 28<br /></div><div align="justify"></div><br /><br /><p align="center"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjlM5gwVxjLodTuhr6mycVxiSRMr1VoW1xEQOdpHgBi6nia4YPquKWrJrd3F2EPPq-Ks5BpVkStZUWWTgJvchCKFUDO6FIXdxaBZ6dJwcvCFoWVQXwxR3UhMSZRJq_xsotNQVKo7m9giT8H/s1600/E_C_Aug.jpg"><img style="WIDTH: 243px; HEIGHT: 320px; CURSOR: hand" id="BLOGGER_PHOTO_ID_5519871778971394946" border="0" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjlM5gwVxjLodTuhr6mycVxiSRMr1VoW1xEQOdpHgBi6nia4YPquKWrJrd3F2EPPq-Ks5BpVkStZUWWTgJvchCKFUDO6FIXdxaBZ6dJwcvCFoWVQXwxR3UhMSZRJq_xsotNQVKo7m9giT8H/s320/E_C_Aug.jpg" /></a></p><br /><br /><div align="justify"><em><span style="font-size:85%;">Fig 1. (A) A midesophageal short-axis view of the aortic valve from the pre–cardiopulmonary bypass transesophageal echocardiographic examination. The 3 aortic valve leaflets show mild-to-moderate thickening and calcification as well as a mild-to-moderate decrease in leaflet excursion. (B) A midesophageal long-axis view of the aortic valve withcolor Doppler interrogation reveals color aliasing consistent with turbulent flow through a narrowed aortic valve orifice.</span></em></div><br /><em><span style="font-size:85%;"></span></em><br /><br /><em><span style="font-size:85%;"></span></em><br /><br /><p align="center"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhSaB4D4bJ3ijzF0ek6xznalFa_lEt5TQSwAE0ydVHtO4qXtZ2rduEHQLS-d16dYo63XgJZYiRAbOw9fGUyVt3aH61RvmCqXakyq6pRHYH8tlV4Ts_otYKdC7YPP1JhqTIeNkSMnjOZxwpN/s1600/E_C_AugFig2.jpg"><img style="WIDTH: 320px; HEIGHT: 219px; CURSOR: hand" id="BLOGGER_PHOTO_ID_5519871090068175842" border="0" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhSaB4D4bJ3ijzF0ek6xznalFa_lEt5TQSwAE0ydVHtO4qXtZ2rduEHQLS-d16dYo63XgJZYiRAbOw9fGUyVt3aH61RvmCqXakyq6pRHYH8tlV4Ts_otYKdC7YPP1JhqTIeNkSMnjOZxwpN/s320/E_C_AugFig2.jpg" /></a></p><br /><br /><div align="justify"><em><span style="font-size:85%;">Fig 2. The velocity time profile of blood flow through the aortic valve generated with continuous-wave Doppler interrogation from the deep transgastric window. Peak and mean pressure gradients across the aortic valve are shown.</span></em><br /></div><br />mmHg and a mean gradient of 18 mmHg across the aortic valve at a cardiac output of 4.5 L/min (Fig 2), (5) AVA calculated by the use of the continuity equation of 1.2 cm2, (6) trace aortic<br />insufficiency, and (7) trace mitral regurgitation (Figs 1 and 2 and Video).<br /><br /><div align="center">ECHOCARDIOGRAPHIC CHALLENGES </div><div align="center"><br /> </div><div align="justify">The AVA calculated intraoperatively corresponds to moderate aortic stenosis that had been diagnosed as mild stenosis preoperatively. This potential increase in the grade of severity suggests the consideration of adding an aortic valve replacement to the scheduled coronary artery bypass graft procedure. Why is there a discrepancy in the measurements of AVA? Is the measurement of AVA using continuity correct? What can the authors do to confirm the measurement? Are there other echocardiographic findings that the authors can use to help make a decision on what to do for this patient?</div><div align="justify"></div><br /><div align="center">CONFOUNDING VARIABLES</div><br /><div align="justify"></div><div align="justify">Symptoms are an important trigger in the decision tree for the management of aortic stenosis and valve replacement. Are the patient’s symptoms from CAD or aortic stenosis? Adding an aortic valve replacement adds risk to this procedure. Do the risks outweigh the benefits in this patient? The rate of progression of aortic stenosis varies from patient to patient and can impact the decision-making process. Can the authors get some estimate of this rate in the present patient?</div><br /><div align="center">THE AUTHORS’ DECISION </div><div align="center"><br /> </div><div align="justify">After careful consideration, the authors decided not to perform an aortic valve replacement because they felt that the risk of adding in aortic valve replacement was too high given the patient’s age and comorbidities. They felt that mild-to-moderate thickening and calcification of leaflets portended a slower progression of stenosis, and they felt that the patient’s life expectancy was such that he would likely never become symptomatic from aortic stenosis.</div>JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-68709427403544266732010-08-13T14:51:00.000-07:002010-08-13T14:54:18.349-07:00E-CHALLENGES & CLINICAL DECISIONSJCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-92079686246485837782010-04-13T07:23:00.000-07:002010-04-14T16:15:20.588-07:00<div align="center"><br /><br /><strong>Rheumatic Mitral and Aortic Stenosis: To Replace or Not To Replace—That Is the Question—Part 2<br /><br /></strong>Melanie Darke, MD, John Pawloski, MD, Kamal R. Khabbaz, MD, and Feroze Mahmood, MD<br /><br /></div><br /><br /><div align="justify">This is the second part of the E-challenge case presented in the last issue of the Journal. This section includes a narrative of the clinical decisions made in the operating room and the evidence to support them. The readers are re­ferred to the Journal web site for viewing the video presenta­tion of the echo loops and their explanation. In an effort to make the experience/discussion interactive, a web-based dis­cussion forum (blog site) also has been set up on the web site for the readers to comment and share their opinions. To en­hance the educational experience and to keep the discussion focused, the online discussion will be moderated/edited by the section editors.<br /><br />INTRAOPERATIVE CHALLENGE (VIDEOS 1 AND 2)</div><div align="justify"><br />1. Assessment of the severity of aortic stenosis (AS).<br />2. The impact of concomitant mitral stenosis (MS) on the echocardiographic assessment of AS is debat­able.1-3</div><div align="justify">3. The AVA was not calculated in the aforementioned studies, and stenosis severity was estimated with gra­dients during cardiac catheterization. </div><div align="justify">4. Because of slow progression, it is recommended that “prophylactic aortic valve replacement (AVR)” may not be indicated.</div><div align="justify">5. However, it is also recommended that rheumatic AS progresses more rapidly than rheumatic aortic regurgi­tation.5 This is because aortic regurgitation can be caused by only a mild valvular abnormality, whereas AS develops after significant valvular abnormality;5 hence, patients with mild AS in rheumatic heart valve disease.</div><div align="justify">6. The question was as follows: does the increased stroke volume after mitral valve replacement serve to increase the aortic valve area (AVA) or the gradient (ie, im­prove the stenosis or worsen it)?<br />7. Furthermore, there is not a cutoff value of the absolute AVA that is an indication for AVR.6 The need for AVR is determined by the presence of symptoms of ventric­ular decompensation rather than the AVA.6<br />8. The patient’s body surface area was 1.6 m2, with an aortic annular size of 1.8 cm, raising the possibility of a patient prosthesis mismatch after a size 19 prosthetic valve.7<br />9. The increased likelihood of a patient prosthesis mis­match in concomitant AVR during surgery for rheu­matic stenosis of the mitral valve has been reported. This may be because of the greater preponderance of rheumatic heart disease in females who have a smaller body surface area, ascending aorta, and aor­tic annulus.8,9<br /><br /><br />INTRAOPERATIVE COURSE<br /><br />1. Mitral valve replacement only.<br />2. Aortic valve was considered mildly stenotic and not calcified with the hope of eventual improvement of AVA with improved stroke volume.<br />3. Immediate post–cardiopulmonary bypass AVA was measured to be 1.27 cm2 (continuity equation) and a peak gradient of 27 mmHg.<br />4. The pre–cardiopulmonary bypass AVA was 1.07 cm2 via the continuity equation with a peak gradient of 16 mmHg. There was a marginal improvement in the AVA but a simultaneous increase in the peak gradient with similar hemodynamics.<br />5. Improvement in the final AVA and gradient did not specifically meet the criteria for the diagnosis of AS or “pseudo-AS.” 10<br /><br /><br />UNANSWERED QUESTIONS </div><br /><br /><p align="justify">1. Was it really “pseudo-AS” (ie, did the AVA actually significantly improve after the mitral valve replace­ment)?<br />2. Was it more significant AS than anticipated (ie, the AS in AVA, but a simultaneous improvement in peak was more severe than measured because of low flow, gradient)? and this is manifested as an insignificant improvement.<br />3. Should the aortic valve have been replaced? </p><br /><br /><p align="justify">REFERENCES</p><p align="justify">1. Honey M: Clinical and haemodynamic observations on combined mitral and aortic stenosis. Br Heart J 23:545-555, 1961<br /><br />2. Katznelson G, Jreissaty RM, Levinson GE, et al: Combined aortic and mitral stenosis. A clinical and physiological study. Am J Med<br />29:242-256, 1960<br /><br />3. Zitnik RS, Piemme TE, Messer RJ, et al: The masking of aortic stenosis by mitral stenosis. Am Heart J 69:22-30, 1965<br /><br />4. Vaturi M, Porter A, Adler Y, et al: The natural history of aortic valve disease after mitral valve surgery. J Am Coll Cardiol 33:2003-2008, 1999<br /><br />5. Choudhary SK, Talwar S, Juneja R, et al: Fate of mild aortic valve disease after mitral valve intervention. J Thorac Cardiovasc Surg 122:583-586, 2001<br /><br />6. ACC/AHA guidelines for the management of patients with valvularheart disease. A report of the American College of Cardiology/American Heart Association. Task Force on Practice Guidelines (Committee on Management of Patients with Valvular Heart Disease). J Am Coll Cardiol 32:1486-1588, 1998<br /><br />7. Pibarot P, Dumesnil JG: Prosthesis-patient mismatch: Definition,clinical impact, and prevention. Heart 92:1022-1029, 2006<br /><br />8. Roberts WC, Ko JM: Some observations on mitral and aortic valve disease. Proc (Bayl Univ Med Cent) 21:282-299, 2008<br /><br />9. Roberts WC, Ko JM, Schumacher JR, et al: Combined mitral and aortic stenosis of rheumatic origin with double-valve replacement in an octogenarian. Int J Cardiol 2008 [Epub ahead of print]<br /><br />10.Maslow AD, Mahmood F, Poppas A, et al: Intraoperative dobutamine stress echocardiography to assess aortic valve stenosis. J Cardiothorac Vasc Anesth 20:862-866, 2006<br /><br /></p><br /><br /><br /><p align="justify"><br /></p><br /><br /><br /><div align="justify"><br /></div><br /><br /><br /><br /><p align="justify"><br /><br /></p><br /><br /><br /><br /><div align="left"></div>JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com0tag:blogger.com,1999:blog-4614555285346122404.post-43308642207578204932010-02-04T15:50:00.000-08:002010-02-05T13:25:53.534-08:00<span style="font-size:100%;"><br /><br /></span><div style="TEXT-ALIGN: center;font-family:georgia;" ><div style="TEXT-ALIGN: center"><span style="font-size:100%;"><span style="FONT-WEIGHT: bold">Rheumatic Mitral and Aortic Stenosis: </span></span><span style="font-size:100%;"><span style="FONT-WEIGHT: bold">To Replace or Not To Replace</span></span></div><div style="TEXT-ALIGN: center"><span style="font-size:100%;"><span style="FONT-WEIGHT: bold">That Is</span></span><span style="font-size:100%;"><span style="FONT-WEIGHT: bold"></span> </span><span style="font-size:100%;"><span style="FONT-WEIGHT: bold">the Question—Part 1</span></span><br /><br /></div><span style="font-size:85%;"><span style="FONT-WEIGHT: bold">Melanie Darke, MD, John Pawloski, MD, Kamal R. Khabbaz, MD, and Feroze Mahmood, MD</span></span><br /></div><br /><div align="justify"><br />The Patient was a 64-year-old woman who presented to her cardiologist with an episode of shortness of breath. She also gave a history of progressive decline in her functional capacity over the last few months. Her chest radiograph showed bilateral pulmonary congestion. Based on her presentation, she was diagnosed as having congestive heart failure and was admitted to the hospital for diuresis and a workup. A transthoracic echocardiogram was done, which showed normal systolic function, moderate mitral stenosis (MS) with a mitral valve area of 1.41 cm2 with a peak gradient of 22 mmHg, and a mean gradient of 9 mmHg. She also had moderate mitral regurgitation and a question of a bicuspid aortic valve and mild aortic stenosis (AS) with peak and mean gradients of 19 and 13 mmHg, respectively. Her cardiac catheterization did not show any coronary artery disease.<br />Her past medical history was significant for hiatus hernia, hypertension, asthma, and type-2 diabetes mellitus. She had undergone multiple surgeries under general anesthesia in the past without any problems. She was born and grew up in South America, but she did not have a specific history of rheumatic fever. Based on the clinical examination and results of investigations, a diagnosis of rheumatic MS was made, and she was scheduled to undergo an elective mitral valve replacement. She was taking aspirin, enalapril, furosemide, metformin, metoprolol, and sertraline.<br />On the day of the surgery, she was found to be in sinus rhythm, conscious and alert, and in no apparent respiratory distress. She was 5 feet 1 inch tall and weighed 144 lb. Her hematology and blood chemistry results were with in normal limits. She was taken to the operating room, and, after placement of appropriate monitors, general anesthesia was induced uneventfully and the airway was secured.<br /><br /></div><p align="left"><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" style="FONT-FAMILY: georgia" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgqJFGQ6EcwXwFhJrnz5TUOG7_ImSd1Apdhjlmo6tsmvHOE2CRZxLLpkFbCNsuRhqx3l6TTXq9HFvA50MD7ehflHeUxUipZSCvrlFoMJAldXdnPUZaH4ct-hjrDruTBUe8NSs2NgmoGis7D/s1600-h/jcva2.gif"><img id="BLOGGER_PHOTO_ID_5434543633935046098" style="WIDTH: 281px; CURSOR: pointer; HEIGHT: 205px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgqJFGQ6EcwXwFhJrnz5TUOG7_ImSd1Apdhjlmo6tsmvHOE2CRZxLLpkFbCNsuRhqx3l6TTXq9HFvA50MD7ehflHeUxUipZSCvrlFoMJAldXdnPUZaH4ct-hjrDruTBUe8NSs2NgmoGis7D/s320/jcva2.gif" border="0" /></a><span style="font-size:78%;"><br />Fig 1. A midesophageal 4-chamber view showing<br /></span><span style="font-size:78%;">classic diastolic doming of the mitral valve</span> </p><p align="justify">An intraoperative transesophageal echocardiographic (TEE) examination was performed with an IE-33 ultrasound system with an OMNI-III TEE probe (Philips Medical Systems, Andover, MA).<br /><br />Presentation 1 (Video A and B): Mitral Valve (Fig 1)<br /><br />1. Severely thickened and deformed (typical hockey stick deformity)<br />2. Diastolic bowing of mitral valve and moderate mitral regurgitation.<br />3. Subvalvular fibrosis and chordal shortening<br />4. Moderate MS, peak gradient 16 mmHg, and mean gradient 8 mmHg<br />5. Mitral valve area � 1.32 cm2<br /></p><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" style="FONT-FAMILY: georgia" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi07ZchyphenhyphenkgdbmYDwk-GqBFlSHyhR1N9B14J4ZM9bW-b9EDHuSMcMFQsW4gAmg6xFt7sWxwFMtOnf5cok8tU-m7LqQyuiLLYgDh2HhyhNrSD27X0gquVwOiwNzT_Uu1J2-s5cU5oPDWwOAQV/s1600-h/jcva1.gif"><img id="BLOGGER_PHOTO_ID_5434544040572968562" style="WIDTH: 278px; CURSOR: pointer; HEIGHT: 219px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi07ZchyphenhyphenkgdbmYDwk-GqBFlSHyhR1N9B14J4ZM9bW-b9EDHuSMcMFQsW4gAmg6xFt7sWxwFMtOnf5cok8tU-m7LqQyuiLLYgDh2HhyhNrSD27X0gquVwOiwNzT_Uu1J2-s5cU5oPDWwOAQV/s320/jcva1.gif" border="0" /></a><br /><span style="font-size:78%;">Fig 2. A midesophageal short-axis view of the aortic valve during<br />systolic opening and a planimetered aortic valve area of 1.2 cm2.</span><br /><br />Aortic Valve (Fig 2)<br />1. Trileaflet valve<br />2. Mildly thickened and retracted<br />3. Trace aortic regurgitation<br />4. Left ventricular outflow tract and aortic annulus diameter � 1.8 cm<br />5. Aortic valve area (AVA) by planimetry 1.32 cm2,by continuity equation 0.97-1.07 cm2; a peak gradient of 16 mmHg was measured with continuous wave Doppler<br /><br />ECHO CHALLENGES<br />The aortic valve is considered protected when there is MS because of reduced stroke volume and flow. Hence, it is possible to have a "low" gradient despite significant aortic valvular stenosis because concomitant MS leads to a low stroke volume.<br />Is this the case in this patient?<br />If so, then what is the true AVA?<br />Are clinicians "UNDERESTIMATING" the AS due to mitral stenosis?1<br />Low gradient is due to low flow (ie, reduced stroke volume and the actual AS is more than moderate; ie, improved stroke volume may worsen the gradient and the severity of AS).<br />Are clinicians "OVERESTIMATING" the AS due to MS?<br />AVA is flow dependent, and the small AVA is because of low flow; hence, improvement in stroke volume after mitral valve replacement (MVR) will improve the AVA.<br /><br /><div align="justify">CONFOUNDING VARIABLES<br />1. Concomitant aortic valve replacement during MVR for rheumatic disease for mild AS is debatable.<br />2. Is the rheumatic AS severe enough to warrant surgery?<br />3. Does the progression of rheumatic AS differ from the calcific AS?2<br />4. If the aortic valve will eventually require surgery, are the risks of a redo aortic valve replacement more or less than mitral and aortic valves being replaced simultaneously?</div><div align="justify"></div><div align="justify"><br />REFERENCES<br />1. Zitnik RS, Piemme TE, Messer RJ, et al: The masking<br />of aortic stenosis by mitral stenosis. Am Heart J 69:22-30,<br />1965<br />2. Choudhary SK, Talwar S, Juneja R, et al: Fate of mild aortic<br />valve disease after mitral valve intervention. J Thorac Cardiovasc<br />Surg 122:583-586, 2001 </div>JCVAhttp://www.blogger.com/profile/08797976723375556733noreply@blogger.com4