Regression of structural cardiovascular changes by antihypertensive therapy.

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Abstract
Left ventricular (LV) hypertrophy is the structural adaptation of the heart in response to chronic LV pressure load. Studies in spontaneously hypertensive rats (SHR), which represent a model of genetically determined arterial hypertension, reveal that cardiac hypertrophy can be controlled by long-term blood pressure normalization with the use of various antihypertensive agents, such as arterial vasodilatators (hydralazine), converting enzyme inhibitors (captopril), beta-receptor blockers (metoprolol), antiadrenergic substances (alpha-methyldopa, guanethidine), and calcium antagonists (nifedipine, felodipine). Additional drug-specific effects modulate the mechanical effect of LV systolic unloading on cardiac hypertrophy: after a combined treatment with metoprolol and hydralazine, LV hypertrophy was quantitatively lower than after single hydralazine therapy, although blood pressure had been lowered to the same extent. LV collagen concentration remained unchanged when medical treatment prevented the development of myocardial hypertrophy. However, when therapy was begun after hypertrophy had been completely established, reversal of hypertrophy was associated with an increased LV collagen concentration. In concentric LV hypertrophy with normal systolic wall stress, LV function was not impaired. Consequently, antihypertensive therapy could not improve LV function in this condition. However, in the case of LV dilatation with increased systolic wall stress, LV systolic unloading by antihypertensive therapy could considerably improve LV pumping function. Preventive studies reveal that chronic blood pressure control can prevent cardiac dysfunction in SHR, as frequently is seen in the later phase of untreated arterial hypertension in humans.

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