EDITORIAL COMMENT
Restrictive Annuloplasty for Ischemic Mitral RegurgitationToo Little or Too Much?*
Thomas H. Marwick, MBBS, PhD, FACC*
Princess Alexandra Hospital and University of Queensland School of Medicine, Brisbane, Australia.
* Reprint requests and correspondence: Prof. Thomas H. Marwick, University of Queensland Department of Medicine, Princess Alexandra Hospital, Ipswich Road, Brisbane, Queensland 4102, Australia. (Email: t.marwick{at}uq.edu.au).
Ischemic mitral regurgitation (MR) remains one of the major unresolved issues in the management of ischemic heart disease. This entity is both common (occurring in 20% to 25% of patients following myocardial infarction and 50% of post-infarct patients with heart failure) (1) and fatal (increasing mortality even when mild) (2). The mechanisms, which have been well documented, are predominantly ventricular rather than valvular. They include displacement of the posterior papillary muscle, ventricular enlargement with increased ventricular sphericity displacing both papillary muscles, annular enlargement, papillary muscle dyssynchrony, and reduced leaflet closing force from left ventricular (LV) dysfunction. All of these functional phenomena may be counterbalanced by changes in LV function and loading, causing the severity of the lesion to vary over time (1).
Attempts to control ischemic MR surgically have been limited by the available tools. Given the contribution of ventricular function, myocardial revascularization is almost always a component of the intervention. However, there is more evidence of an association of cardiac scarring with the degree of MR than there is of cardiac scarring being associated with the typical valve morphology of ischemic MR (e.g., increased tenting area) (3), and the contributions of ischemia and myocardial viability are not well defined. Mitral valve replacement is associated with high surgical risk and the possibility of deterioration of LV function. Restrictive mitral annuloplasty, used in the management of ischemic MR for more than a decade (4), involves the insertion of an undersized annuloplasty ring. This has the effect of reducing the septal to lateral dimension of the valve, improving the apposition of the leaflets. The technique appears to be effective in the short term; indeed, patients with residual MR show significantly worse outcome than those with successful operations. However, severe MR may recur in up to 30% of patients in the course of the first year (5) because of ongoing LV remodeling, particularly involving the posterior wall (6,7).
To this problem of recurrent MR, Magne et al. (8) have demonstrated in this issue of the Journal that restrictive annuloplasty may also induce functional mitral stenosis. In this study of 24 patients with ischemic MR and 20 control patients with coronary artery disease, matched for age, gender, and LV ejection fraction, patients were studied at rest, after dobutamine stress, and in a subgroup after exercise stress. In contrast with the control group, annuloplasty patients demonstrated an increase of resting mitral gradients and pulmonary artery pressure after surgery and a reduction of valve area. Most of the investigated patients showed these changes, with >50% having a valve area of <1.5 cm2 and >40% having a peak gradient of >15 mm Hg. The increase of gradients following stress was substantially larger in the annuloplasty group, with a much smaller increase of valve area with stress. These differences were magnified in the subgroup also studied with exercise stress. Finally, the resting gradients correlated with the pulmonary artery pressure and inversely correlated with exercise capacity, as measured by the 6-min walk test. The authors conclude that restrictive annuloplasty creates functional mitral stenosis, associated with pulmonary hypertension and reduced exercise capacity.
The investigators have produced a valuable addition to published data regarding a complex problem that is challenging to study because of issues relating to the quantitation of regurgitation, valve geometry, and load dependence (9,10). Nonetheless, there are some problems with the study. Dobutamine stress produces an inotropic and vasodilator response that is nonphysiological and may emphasize LV performance including myocardial viability. Exercise, rather than dobutamine, is a preferable stressor for the assessment of valve lesions; indeed, the use of dobutamine rather than exercise may explain why impairment of 6-min walk distance correlated better with the resting than the stress hemodynamics in this study.
As is often the case in studies of ischemic MR, the group was very selected, with the 24 patients representing about half of the patients undergoing restrictive annuloplasty over the study duration. Moreover, the control group is not perfectly matched with patients with mitral regurgitation. Given the differences in LV loading, the presence of a similar ejection fraction preoperatively suggests that the MR patients actually had a worse ventricle to begin with. This may be very relevant, as the degree of scarring is a determinant of LV compliance, which could be an important contributor to the transmitral gradient. In this context, it is reassuring to find that the correlation of mitral gradient with pulmonary artery pressure was better than the correlation of total compliance, which accounts for the resistance of both the mitral valve and LV to filling. Finally, left atrial characteristics may be an important contributor to the LV filling pattern, and left atrial volume measurements would be preferable to left atrial area, as the left atrium does not uniformly increase in size in all dimensions.
What should we conclude from this study? First, the results should highlight the fact that there is no place for complacency in the search for a surgical solution to ischemic MR and that the matter is far from solved. Second, the findings argue against calls for even more restrictive mitral annuloplasty, as post-stress mitral gradients in patients with restrictive annuloplasty in this study are already similar to those in mitral stenosis (11). This suggests that whatever gains are obtained in the reduction of recurrent MR by even more restrictive annuloplasties, they are likely to be lost by the introduction of mitral stenosis. Third, and controversially, the results warrant further consideration of the use of mitral valve replacement, because the peak stress gradients are similar or even less following mitral valve replacement than with restrictive annuloplasty (12). Nonetheless, it is important to acknowledge that a direct comparison against mitral valve replacement has not been performed in this study, and that there are risks of valve replacement, including anticoagulation, reoperation, patient-prosthesis mismatch, and adverse effects on LV function, that still make this an undesirable intervention. Finally, these results should encourage us to further consider the contributions of newer approaches such as cardiac resynchronization therapy (13) and new techniques for overcoming the alterations of LV shape that drive this process (1).
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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References
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1. Levine RA, Schwammenthal E. Ischemic mitral regurgitation on the threshold of a solution: from paradoxes to unifying concepts Circulation 2005;112:745-758.[Free Full Text]2. Grigioni F, Enriquez-Sarano M, Zehr KJ, Bailey KR, Tajik AJ. Ischemic mitral regurgitation: long-term outcome and prognostic implications with quantitative Doppler assessment Circulation 2001;103:1759-1764.[Abstract/Free Full Text] 3. Srichai MB, Grimm RA, Stillman AE, et al. Ischemic mitral regurgitation: impact of the left ventricle and mitral valve in patients with left ventricular systolic dysfunction Ann Thorac Surg 2005;80:170-178.[Abstract/Free Full Text] 4. Bolling SF, Deeb GM, Bach DS. Mitral valve reconstruction in elderly, ischemic patients Chest 1996;109:35-40.[CrossRef][Web of Science][Medline] 5. McGee EC, Gillinov AM, Blackstone EH, et al. Recurrent mitral regurgitation after annuloplasty for functional ischemic mitral regurgitation J Thorac Cardiovasc Surg 2004;128:916-924.[Abstract/Free Full Text] 6. Hung J, Papakostas L, Tahta SA, et al. Mechanism of recurrent ischemic mitral regurgitation after annuloplasty: continued LV remodeling as a moving target Circulation 2004;110:II85-II90.[Web of Science][Medline] 7. Zhu F, Otsuji Y, Yotsumoto G, et al. Mechanism of persistent ischemic mitral regurgitation after annuloplasty: importance of augmented posterior mitral leaflet tethering Circulation 2005;112:I396-I401.[CrossRef][Web of Science][Medline] 8. Magne J, Sénéchal M, Mathieu P, Dumesnil JG, Dagenais F, Pibarot P. Restrictive annuloplasty for ischemic mitral regurgitation may induce functional mitral stenosis J Am Coll Cardiol 2008;511692–701. 9. Schwammenthal E, Chen C, Benning F, Block M, Breithardt G, Levine RA. Dynamics of mitral regurgitant flow and orifice area. Physiologic application of the proximal flow convergence method: clinical data and experimental testing. Circulation 1994;90:307-322.[Abstract/Free Full Text] 10. Song JM, Kim MJ, Kim YJ, et al. Three-dimensional characteristics of functional mitral regurgitation in patients with severe left ventricular dysfunction: a real-time 3-dimensional color Doppler echocardiography study Heart 2007Jul 23;[Epub ahead of print]. 11. Reis G, Motta MS, Barbosa MM, Esteves WA, Souza SF, Bocchi EA. Dobutamine stress echocardiography for noninvasive assessment and risk stratification of patients with rheumatic mitral stenosis J Am Coll Cardiol 2004;43:393-401.[Abstract/Free Full Text] 12. Hobson NA, Wilkinson GA, Cooper GJ, Wheeldon NM, Lynch J. Hemodynamic assessment of mitral mechanical prostheses under high flow conditions: comparison between dynamic exercise and dobutamine stress J Heart Valve Dis 2006;15:87-91.[Web of Science][Medline] 13. Kanzaki H, Bazaz R, Schwartzman D, Dohi K, Sade LE, Gorcsan III J. A mechanism for immediate reduction in mitral regurgitation after cardiac resynchronization therapy: insights from mechanical activation strain mapping J Am Coll Cardiol 2004;44:1619-1625.[Abstract/Free Full Text]
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