Myocyte loss via apoptosis exceeds necrotic cell death in the pathologic heart of ischemic origin, driving wall thinning and chamber dilation in heart failure.
Decompensated eccentric ventricular hypertrophy characterizes the transition from compensated pressure or volume over-load hypertrophy to myocardial dysfunction and failure. Myocyte loss is the major etiologic factor of wall thinning and chamber dilation and may condition the progression of the cardiac myopathy. Myocyte death can occur by apoptosis or necrosis, but the activation of the suicide program of myocytes exceeds necrotic cell death in the pathologic heart of ischemic origin. Whether reactive fibrosis constitutes a primary event in the initiation of ventricular dysfunction or a secondary reaction to myocyte death is an important unanswered question.
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Anversa et al. (Wed,) conducted a review in Heart failure. Myocyte loss via apoptosis exceeds necrotic cell death in the pathologic heart of ischemic origin, driving wall thinning and chamber dilation in heart failure.
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Current Opinion in Cardiology
New York Medical College
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