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Ann Thorac Surg 2007;84:1287
© 2007 The Society of Thoracic Surgeons


Original Articles: Cardiovascular

Invited commentary

Hans Joachim Geissler, MD

Department of Cardiovascular Surgery, University of Freiburg, Hugstetter Str 55, Freiburg, 79106 Germany

(Email: joachim.geissler{at}uniklinik-freiburg.de).

Surgical ventricular restoration (SVR) was introduced in the 1960s and has been part of the cardiac surgeon’s armamentarium ever since [1, 2]. Several reports have demonstrated the beneficial effects of this procedure on outcome and cardiac function, which have usually been attributed to restored ventricular geometry and normalized ventricular volume [3, 4]. However, a controversy remains about patient selection and indication for this operation [5, 6].

The issues previously mentioned are not the topic of the present work by Hsu and coworkers [7]. Instead we find an excellent laboratory investigation on the effect of SVR after myocardial infarction on apoptosis of cardiomyocytes in surviving myocardium. To reiterate, the authors compared cardiac function, myocardial infarction size, and rate of apoptosis between animals with and without of left ventricular aneurysm repair in a rat infarction model. They found improved heart function, reduced rate of apoptosis, and a significant decrease in activated caspase-9 in animals with left ventricular aneurysm repair.

The significance of apoptosis in various diseases of the heart has been widely investigated since the late 1980s [8]. Remarkably this article by Hsu and colleagues [7] is the first to show apoptosis reduction by SVR after myocardial infarction. Some questions remain open, such as why some important measurements of apoptosis, namely caspase-3 and Bax showed no difference between groups despite a significantly different rate of apoptosis. However further research into the possible benefits of SVR on the cellular level may help to elucidate these issues. Greater insight into the cellular effects of SVR may actually widen our perspective on it beyond the focus on ventricular geometry and mechanics. It will be interesting to see whether or not these basic scientific findings will have the potential to inspire the current clinical debate on SVR.


    References
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 References
 

  1. Cooley DA, Henley WS, Ahmad KH, Chapman DW. Ventricular aneurysm following myocardial infarction: results of surgical treatment Ann Surg 1959;150:595-612.[Medline]
  2. Houel J, Serradimigni A, Ruf G, Dor V, Malmejac C, Gosset C. Aneurysm of the left ventricleResection under extracorporeal circulation. Mem Acad Chir 1965;91:1021-1026.[Medline]
  3. Di Donato M, Toso A, Maioli M, et al. Intermediate survival and predictors of death after surgical ventricular restoration Semin Thorac Cardiovasc Surg 2001;13:468-475.[Medline]
  4. Athanasuleas CL, Stanley Jr AWH, Buckberg GD, et al. Surgical anterior ventricular endocardial restoration (SAVER) for dilated ischemic cardiomyopathy Sem Thorac Cardiovasc Surg 2001;13:448-458.[Medline]
  5. Doenst T, Velazquez EJ, Beyersdorf F, et al. To STICH or not to STICH: We know the answer, but do we understand the question? J Thorac Cardiovasc Surg 2005;129:246-249.[Free Full Text]
  6. Buckberg GD. Questions and answers about the STICH trial: A different perspective J Thorac Cardiovasc Surg 2005;130:245-249.[Free Full Text]
  7. Hsu C-P, Huang C-Y, Wang J-S, Chiang H-I, Shih C-C. Down-regulation of apoptosis after left ventricular aneurysm repair Ann Thorac Surg 2007;84:1279-1287.[Abstract/Free Full Text]
  8. James TN. Normal and abnormal consequences of apoptosis in the human heartFrom postnatal morphogenesis to paroxysmal arrhythmias. Circulation 1994;90:556-573.[Abstract/Free Full Text]




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