Jagat Narula, M.D., Ph.D., Nezam Haider, Ph.D., Renu Virmani, M.D., Thomas G. DiSalvo, M.D., Frank D. Kolodgie, Ph.D., Roger J. Hajjar, M.D., Ulrich Schmidt, M.D., Marc J. Semigran, M.D., G. William Dec, M.D., and Ban-An Khaw, Ph.D.
Background Heart failure can result from a variety of causes,including ischemic, hypertensive, toxic, and inflammatory heartdisease. However, the cellular mechanisms responsible for theprogressive deterioration of myocardial function observed inheart failure remain unclear and may result from apoptosis (programmedcell death).
Methods We examined seven explanted hearts obtained during cardiactransplantation for evidence of apoptosis. All seven patientshad severe chronic heart failure: four had idiopathic dilatedcardiomyopathy, and three had ischemic cardiomyopathy. DNA fragmentation(an indicator of apoptosis) was identified histochemically byin situ end-labeling as well as by agarose-gel electrophoresisof end-labeled DNA. Myocardial tissues obtained from four patientswho had had a myocardial infarction one to two days previouslywere used as positive controls, and heart tissues obtained fromfour persons who died in motor vehicle accidents were used asnegative controls for the end-labeling studies.
Results Hearts from all four patients with idiopathic dilatedcardiomyopathy and from one of the three patients with ischemiccardiomyopathy had histochemical evidence of DNA fragmentation.All four myocardial samples from patients with dilated cardiomyopathyalso demonstrated DNA laddering, a characteristic of apoptosis,whereas this was not seen in any of the samples from patientswith ischemic cardiomyopathy. Histologic evidence of apoptosiswas also observed in the central necrotic zone of acute myocardialinfarcts, but not in myocardium remote from the infarcted zone.Rare isolated apoptotic myocytes were seen in the myocardiumfrom the four persons who died in motor vehicle accidents.
Conclusions Loss of myocytes due to apoptosis occurs in patientswith end-stage cardiomyopathy and may contribute to progressivemyocardial dysfunction.
Source Information
From Massachusetts General Hospital and Harvard Medical School, Boston (J.N., T.G.D., R.J.H., U.S., M.J.S., G.W.D., B.-A.K.); Northeastern University, Boston (J.N., N.H., B.-A.K.); and the Armed Forces Institute of Pathology, Washington, D.C. (R.V., F.D.K.).
Address reprint requests to Dr. Khaw at 205 Mugar, Northeastern University, 360 Huntington Ave., Boston, MA 02115.
Apoptosis in the Heart
Saraste A., Voipio-Pulkki L.-M., Parvinen M., Pulkki K., Narula J., Dec G. W., Virmani R., Khaw B.-A.
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N Engl J Med 1997;
336:1025-1026, Apr 3, 1997.
Correspondence
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