Detection of apoptosis using in situ markers for DNA strand breaks in the failing human heart. Fact or epiphenomenon?

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Abstract
The role of apoptosis and the methods used for its detection in failing human hearts are controversial. Recent data have challenged the hypothesis that in situ markers for DNA strand breaks mirror apoptotic (TUNEL and Taq in situ ligation assay) and/or necrotic (Pfu in situ ligation assay) cell death, and thus provide evidence that apoptotic cell loss contributes to the progression of heart failure. Experimental data cast doubt not only upon the specificity of the TUNEL technique but also the Taq in situ ligation assay as a reliable method for the detection of apoptotic cell death and provide compelling new evidence that the occurrence of cardiomyocyte cell death as defined by the detection of DNA strand breaks using either TUNEL or Taq and Pfu in situ ligation assays is an epiphenomena that is not related to the evolution of heart failure. Cardiomyocyte positivity for in situ markers of DNA strand breaks is a feature of hypertrophic cardiomyopathic hearts, irrespective of the underlying pathology or the presence or absence of heart failure. These data raise concerns regarding the extent of apoptosis in cardiomyopathy and the contribution of this process to the progression of heart failure. Copyright © 2003 John Wiley & Sons, Ltd.

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