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      Pathophysiology and clinical aspects of hypertensive hypertrophy.

      European Heart Journal
      Adrenergic beta-Antagonists, therapeutic use, Antihypertensive Agents, Calcium Channel Blockers, Coronary Circulation, drug effects, physiology, Endomyocardial Fibrosis, drug therapy, physiopathology, Hemodynamics, Humans, Hypertension, Hypertrophy, Left Ventricular, Renin-Angiotensin System, Ventricular Function, Left

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          Abstract

          Individuals with hypertension and electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH) have a 10-fold greater risk of developing cardiac failure than hypertensives without ECG evidence of LVH. LVH in hypertension is characterized by myocardial fibrosis and structural changes to the small intramural arteries. Hypertensives with or without LVH have reduced coronary vasodilator reserve due to hypertensive disease of small coronary arteries. Prognosis of arterial hypertension is largely determined by cardiac complications. The aim of treatment of hypertensive heart disease is to reverse myocardial hypertrophy in order to prevent progression to hypertensive heart failure, as well as reversal of the hypertensive disease of small coronary arteries in order to improve coronary reserve. On the development of hypertensive heart failure, administration of digitalis, diuretics and angiotensin converting enzyme (ACE) inhibitors should be initiated. Although regression of LVH can be induced by dihydropyridine calcium channel blockers, ACE inhibitors and sympatholytic substances, clinical evidence of the reversal of hypertensive disease of small coronary arteries has still to be established.

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