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Ann Thorac Surg 2007;83:570-571
© 2007 The Society of Thoracic Surgeons
Heart, Lung, and Esophageal Surgery Institute, University of Pittsburgh Medical Center, UPMC/Presbyterian University Hospital, Suite C-700, 200 Lothrop St, Pittsburgh, PA 15213
(Email: zehrkj{at}upmc.edu).
Feringa and colleagues [1] present a meta-analysis of 24 studies involving 470 patients undergoing mitral valve repair and 724 patients undergoing mitral valve replacement for endocarditis in the last decade. One of the strengths of the review is the fact that all patients were operated on after 1995, and thus after maturity of most mitral valve repair techniques. Virtually all early and late outcome variables assessed strongly support repairing the valve whenever possible.
Unfortunately, a retrospective review like this has many of the problems of outcome reporting for valvular surgery: (1) focus on the procedure performed regardless of the chronicity and presenting condition of the patient; (2) the bias of selective publication of high risk cohorts, and (3) the study of a large number of small, nonhomogenous cohorts. These problems often cause readers to dismiss a study in favor of their own anecdotally driven biases. I would urge that the article be read for the truth that is in it.
It is well accepted that patients undergoing mitral valve repair have better long-term survival compared with patients undergoing mitral valve replacement in the absence of endocarditis. Conventional wisdom has been that the reoperation rate would be higher in patients undergoing repair in the setting of endocarditis due to loss of tissue available for repair and inadequate debridement of infected tissue. This review refutes this concept. The importance of this study is that it adds additional grade A level 1c evidence that patients undergoing successful valve repair do better compared to those undergoing valve replacement in the setting of a patient preoperatively compromised by endocarditis (ie, sepsis, heart failure, renal insufficiency, embolism, and so forth).
This is likely true for two reasons. Prosthetic valve replacement is an abnormal anatomical construct. As my Harefield professor often said, "You need to recreate the anatomy." Indeed restoration of normal anatomy is the principle behind the success and durability of many cardiac surgical operations (eg, the arterial switch, ventricular remodeling, valve-sparing aortic root reconstruction, valve repair, and stretching the point, cardiac transplantation). The recreation of the anatomy by mitral valve repair allows for nonturbulent inflow into the left ventricle and unimpeded laminar flow through the left ventricular outflow tract. The left ventricular geometrical dimensions are maintained with the chordal preservation associated with repair. This translates to normalizing flow and contractility. In replaced patients, turbulent flow patterns likely place the patient at incremental risk for recurrent endocarditis and result in increased transvalvular gradients both across the mitral valve and the left ventricular outflow tract. The loss of chordae tendinea contributes to decreased contractility, which may translate to long-term heart failure. Even partial or complete chordal sparing valve replacement does not recreate normal hemodynamics due to flow disturbances. The second reason is the often underemphasized long-term morbidity and mortality associated with valve replacement, the requirement for anticoagulation, paravalvular leak, valve thrombosis, embolism, structural deterioration, pannus formation, endocarditis, and biocompatibility issues. This review found that patients undergoing valve replacement had significantly poorer outcomes in regard to early mortality (14.4% vs 2.3%), late mortality (40.5% vs 7.8%), need for reoperation (12.7% vs 2.2%), early cerebrovascular events (11.5% vs 4.7%), late cerebrovascular events (24.4% vs 1.6%), and late recurrent endocarditis (7.3% vs 1.8%).
The argument can be made that the better results in the repair group are related to the fact that the patients undergoing replacement are sicker. In this review, replaced patients did have a higher prevalence of acute endocarditis (77.8% vs 66.3%), congestive heart failure (62.8% vs 55.2%), uncontrolled sepsis (37.4% vs 15.8%), abscess (11% vs 0%), and Staphylococcus infection (31% vs 24%). Although this may account for much of the early excess morbidity and mortality in the valve replacement group, it is doubtful that it accounts for 40.5% versus 7.8% late mortality rate for a similar follow-up period. The argument is often made that only the destroyed valves are replaced in the modern era. In this review only 22.7% of patients undergoing mitral valve replacement had complete leaflet destruction. A large subgroup of the remainder with perforations, vegetations, and chordal rupture likely had repairable valves. In fact, according to The Society of Thoracic Surgeons’ database, approximately 50% of patients undergoing isolated mitral valve surgery still undergo replacement. It is not logical that the surgeons routinely replacing noninfected myxomatous valves would attempt a repair in the setting of infection.
Innovation does not only encompass the creation of new devices and techniques but it also can be manifested by applying known techniques to other diseased states. An example is the use of creative valve repair techniques to repair the mitral valve in the setting of endocarditis. These techniques include patching of perforations, vegetation resection and leaflet patching, near complete anterior leaflet replacement with autologous or bovine pericardium, commissural debridement and reconstruction, left ventricular abscess debridement with patch annular reconstruction, and leaflet re-suspension with artificial chordae tendineae. To offer our patients the best long-term results, mitral valve surgery in the setting of endocarditis should be approached with the full armamentarium of mitral valve repair techniques and often requires the most creativity that we can muster. Infection should not be used as an excuse to perform an easy mitral valve replacement.
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  T. Shimokawa, H. Kasegawa, S. Matsuyama, H. Seki, S. Manabe, T. Fukui, S. Morita, and S. Takanashi Long-term outcome of mitral valve repair for infective endocarditis. Ann. Thorac. Surg., September 1, 2009; 88(3): 733 - 739. [Abstract] [Full Text] [PDF]
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