The cardiomyopathy of overload: an unnatural growth response

Abstract

The poor prognosis in heart failure, which can be reproduced by overloading the normal heart, may reflect molecular abnormalities associated with cardiac hypertrophy. Because terminally differentiated adult cardiac myocytes have little or no capacity to divide, overload-induced hypertrophy represents an unnatural growth response. The mechanism by which this unnatural growth response shortens survival remains speculative, but may involve apoptosis caused when overload reactivates growth factors to which the adult heart cannot respond with normal cell division. The ability of converting enzyme inhibitors and nitrates, which have growth inhibitory as well as vasodilator effects, to improve prognosis in heart failure may reflect the ability of these drugs to modify this unnatural growth response.