Abstract
Cardiac hypertrophy usually follows an increase in work load that is imposed on the heart. Usually, greater work is due to increased afterload in patients with hypertension or after myocardial infarction in whicfh the remaining muscle must assume the work of the segment that was lost as a result of myocardial cell death and scar formation. In some instances, increased pressure or volume work of the left ventricle is associated with increased release of neurotransmitters or plasma concentrations of hormones that may also have direct effects on cardiac myocyte growth, including activation of the sympathetic nervous system, pheochromocytoma, hyperthyroidism, and high renin hypertension
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