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The term cardiac hypertrophy is defined as a change in either chamber or wall structure that exceeds normal, adaptive changes in response to increased workload. As the ventricular load is increased, there is hypertrophy of the myocytes, producing an increased volume of the ventricular chamber. In a normal heart the myocytes become shorter and thicker as they increase in size, but in cardiac hypertrophy they become longer and thinner, producing a longer wall-to-wall dimension than normal. In systemic hypertension, the hypertrophy is a consequence of mechanical stretch on the myocardium. The hypertrophy is a compensatory response which increases ventricular muscle mass and restores a normal pressure in the ventricular chamber. Hypertrophy of the vasculature also occurs in hypertension and in various models of organ or tissue hypertrophy. It is characterized by an increased mass of the medial layer, consisting of the tunica media, with formation of intimal lesions. The heart contains three components: the myocardium, the interstitium and the blood. While mechanical hypertrophy of the myocardium is a response to an increased workload, wall thickening of the cardiovascular system is a response to increased pressure in the blood vessel. The wall thickening is dependent on two factors: the increased distensibility of the vessel wall and the increases in blood pressure. The first causes increased strain on the vessel wall, and the second increases the effective wall stress. In hypertension there are differences in the contractile and excitatory properties between cardiac muscle cells from various regions. In systemic hypertension the myocardial cells from the subendocardial layers respond with a shift in the effector system with a reduction in responsiveness to Ca++ and an increase in responsiveness to Na+ and guanidinoacetic acid. The response of the myocardial cells from the subepicardial layers is different; a reduction in responsiveness to Ca++ and an increase in responsiveness to Na+ and guanidinoacetic acid are not seen. Differences in the contractile and excitatory properties of cardiac muscle cells from various regions of the heart may explain the anatomic
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