Abstract
Usually, when antihypertensive therapy is considered in the hypertensive patient, structural cardiovascular changes are already well established and the structure of the cardiovascular system is redesigned to maintain higher than normal pressure. Left ventricular hypertrophy has been shown to be an independent risk factor for all manifestations of coronary heart disease. In hypertension, the increased pressure load over a long period of time induces degenerative changes in, for example, cerebral, renal, and coronary vessels, with well-known clinical consequences. Independent of the primary cause of hypertension, full reversal to normotension will probably occur only when the structurally reset cardiovascular system has been returned to normal dimensions by regression of structural vascular changes. In animal models severai forms of antihypertensive treatment have prevented the development of or induced regression of left ventricular hypertrophy as well as medial hypertrophy of the vessels. These effects have been related both to the extent of blood pressure reduction and to the degree of inhibition of neurohormonal trophic influences. In humans the results have been somewhat contradictory. Plethysmography has demonstrated a reduction of resistance at maximal dilatation with either combination therapy or pindolol but not with mefruside or atenolol. There may be several explanations for the difficulties in showing regression of structural vascular changes in humans: (1) inadequate treatment of high blood pressure, (2) reflexogenic activation of neurohormonal trophic factors, (3) investigation of an unsultable vascular bed, or (4) treatment started too late. The ultimate goal in the treatment of hypertension is, of course, reduction of cardiovascular morbidity and mortality, but normalization of structural cardiovascular changes is clearly the second most important therapeutic goal.
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