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Quantitative analysis of apoptotic markers in human end‐stage heart failure
Author(s) -
BottFlügel Lorenz,
Weig HansJörg,
Ühlein Heiko,
Nabauer Michael,
Laugwitz KarlLudwig,
Seyfarth Melchior
Publication year - 2008
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2007.12.013
Subject(s) - heart failure , medicine , troponin , apoptosis , myocardial infarction , troponin complex , troponin i , cardiology , tropomyosin , dna fragmentation , myosin , programmed cell death , microbiology and biotechnology , biology , biochemistry
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.