Feroze Mahmood, MD
Madhav Swaminathan, MD
Section Editors
Dynamic Mitral Regurgitation Without Regional Wall Motion Abnormality
Greg Balfanz, MD,* Harendra Srora, MD,* Brett C. Sheridan, MD,† Jason N. Katz, MD, MHS, ‡ & Priya A. Kumar, MD*
*Department of Anesthesiology, University of North Carolina, Chapel Hill, NC †Department of Surgery, University of North Carolina, Chapel Hill, NC
†Department of Medicine, University of North Carolina, Chapel Hill, NC
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: pkumar@aims.unc.edu
Key words: dynamic mitral regurgitation
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.
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.
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.
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.
Challenge 1: What Was the Cause for the Abrupt Pulmonary Hypertension?
Management
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.
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).
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.)
Fig 4. A pulse-wave Doppler signal in the left upper pulmonary vein showing the disappearance of the systolic reversal of flow.
Challenge 2: What is the Cause for the Wide Range of Variability in the Degree of MR?
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.
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
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
Challenge 3: Would CABG Surgery Alone Be Sufficient to Correct Dynamic MR?
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.
After an extensive discussion with the surgical team, the therapeutic options considered were the following:
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.
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.
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.
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.
Conclusions
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.
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.
References
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
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
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
4. P. Lancleotti, M. Moonen. Left ventricular dyssynchrony: A dynamic condition Heart Fail Rev 2011 Jul 29 [Epub ahead of print]
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
6. J.K. Ho, A. Mahajan. Cardiac resynchronization therapy for treatment of heart failure Anesth Alalg 111:1353-1361, 2010
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
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
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
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
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.
Fig 2 A pulse-wave Doppler signal in the left upper pulmonary vein showing systolic reversal of flow.
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.
Fig 4 A pulse-wave Doppler signal in the left upper pulmonary vein showing the disappearance of the systolic reversal of flow.
