Development and growth of cardiac muscle tissue is controlled by a variety of intrinsic and extrinsic factors. Fetal growth is by hyperplasia, is strongly governed by inherent factors and is only slightly modified by external environmental factors. The number of cell divisions is species-dependent and normally stops shortly after birth. Developing blood volume and pressure dictate the hypertrophic stage of normal growth, and this may be further modified by abnormal hemodynamic and humoral factors. Connective tissue, neural and vascular components of the myocardium mature along with the myocyte, and alterations in these structures profoundly affect myocyte function. Hypertrophy beyond normal growth is the response of the myocyte by increased protein synthesis to various stimuli including hemodynamic, humoral and ischemic factors. Injury to normal and hypertrophied myocardium may vary due to structural and metabolic adaptations of hypertrophied tissue, such as connective tissue proliferation, vascular supply alterations and glycolytic metabolic potential. Ischemic effects influence not only cell necrosis, but also hypertrophy and congestive myocardial failure.