Giorgio Olivetti, M.D., Rakesh Abbi, M.D., Federico Quaini, M.D., Jan Kajstura, Ph.D., Wei Cheng, M.D., James A. Nitahara, M.D., Eugenio Quaini, M.D., Carla Di Loreto, M.D., Carlo A. Beltrami, M.D., Stanislaw Krajewski, M.D., Ph.D., John C. Reed, M.D., Ph.D., and Piero Anversa, M.D.
Background Loss of myocytes is an important mechanism in thedevelopment of cardiac failure of either ischemic or nonischemicorigin. However, whether programmed cell death (apoptosis) isimplicated in the terminal stages of heart failure is not known.We therefore studied the magnitude of myocyte apoptosis in patientswith intractable congestive heart failure.
Methods Myocardial samples were obtained from the hearts of36 patients who underwent cardiac transplantation and from thehearts of 3 patients who died soon after myocardial infarction.Samples from 11 normal hearts were used as controls. Apoptosiswas evaluated histochemically, biochemically, and by a combinationof histochemical analysis and confocal microscopy. The expressionof two proto-oncogenes that influence apoptosis, BCL2 and BAX,was also determined.
Results Heart failure was characterized morphologically by a232-fold increase in myocyte apoptosis and biochemically byDNA laddering (an indicator of apoptosis). The histochemicaldemonstration of DNA-strand breaks in myocyte nuclei was coupledwith the documentation of chromatin condensation and fragmentationby confocal microscopy. All these findings reflect apoptosisof myocytes. The percentage of myocytes labeled with BCL2 (whichprotects cells against apoptosis) was 1.8 times as high in thehearts of patients with cardiac failure as in the normal hearts,whereas labeling with BAX (which promotes apoptosis) remainedconstant. The near doubling of the expression of BCL2 in thecardiac tissue of patients with heart failure was confirmedby Western blotting.
Conclusions Programmed death of myocytes occurs in the decompensatedhuman heart in spite of the enhanced expression of BCL2; thisphenomenon may contribute to the progression of cardiac dysfunction.
Source Information
From the Departments of Medicine (G.O., J.K., W.C., J.A.N., P.A.) and Pathology (R.A.), New York Medical College, Valhalla; the Department of Pathology, University of Parma, Parma, Italy (F.Q.); the Department of Pathology, University of Udine, Udine, Italy (C.D., C.A.B.); the De Gasperis Division of Cardiac Surgery, Milan, Italy (E.Q.); and the Burnham Institute, La Jolla, Calif. (S.K., J.C.R.).
Address reprint requests to Dr. Anversa at the Department of Medicine, Vosburgh Pavilion 302, New York Medical College, Valhalla, NY 10595.
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