Apoptosis--programmed cell death--has been implicated in a variety of cardiac diseases, including myocardial infarction and chronic heart failure. This study was conducted to quantify the amount of apoptotic markers in human end-stage heart failure and to correlate the results to clinical parameters of heart failure. Myocardial samples from 44 patients with end-stage heart failure and 5 controls were collected at the time of heart transplantation. Lysates of tissue samples were analysed for cleavage of alpha actin, alpha actinin, troponin T, tropomyosin, essential myosin light chain-1 (MLC-1v), and gelsolin. We observed cleavage of alpha actin, and alpha actinin. Troponin I, tropomyosin, and MLC-1v were not detectably cleaved. The amount of active caspase-3 was low in all samples (1.10+/-0.1 ng/ml). The same applied for DNA histone fragments (0.61+/-0.04). In patients with acutely decompensated heart failure we observed a striking increase in caspase-3 activity, but not DNA fragmentation. When calculated for the entire group there was no correlation between caspase-3 activity, DNA fragmentation and haemodynamic or echocardiographic variables. Relevant increases in apoptosis were only observed in patients with acute decompensated heart failure.
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Bott‐Flügel et al. (2008) studied this question.
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