Plasticity of the pathologic heart.

This review addresses two relevant issues concerning the adaptation of the failing heart: myocyte growth and myocyte death. Recent results are summarized to support the notion that adult ventricular myocytes are not terminally differentiated cells and myocyte replication occurs in the normal heart and is potentiated by overloads. On this basis, myocyte hypertrophy and proliferation both contribute to the remodeling of the pathologic heart in animals and humans. Additionally, the controversy regarding the activation of apoptosis in the stressed myocardium is emphasized and published results are discussed. Available information demonstrates unequivocally that cell death by this mechanism takes place in the diseased heart and may have significant implications in the progression of ventricular dysfunction to end-stage failure. The importance of recognizing that electron microscopy is inappropriate for the identification and quantification of myocyte apoptosis is strongly indicated. Moreover, myocyte necrosis is presented as a relevant component of the decompensated heart. In summary, the dogma that myocytes cannot reenter the cell cycle and undergo mitotic division is proven to be obsolete and invalid. Similarly, the dogma that myocytes can die only by necrosis is contrary to any objective interpretation of published findings. Myocyte necrosis and apoptosis, and myocyte hypertrophy and proliferation are major elements of the plasticity of the heart.