Adrenergic mechanisms in left ventricular hypertrophy: significance and clinical implications.
Emerging consensus indicates that the goal of antihypertensive therapy is not merely a reduction in the level of systemic arterial blood pressure; rather, it is prevention of target organ damage and reversal of complications. Among the clinical consequences of hypertension, left ventricular hypertrophy (LVH) is a prominent manifestation. Initially the left ventricle (LV) hypertrophies as an adaptive physiological response to an increase in afterload. However, persistence of LVH can cause a number of cardiac complications. Reversal of LVH is, therefore, likely to be of immense therapeutic benefit. A number of clinical and experimental observations have shown a close correlation between level of adrenergic activity and the development of LVH; adrenergic blockade has been shown to cause regression of LVH. Recent studies have demonstrated that post-synaptic alpha-blockers cause a reduction of LV mass. Terazosin, by virtue of its long duration of action, may attenuate the pathologic adrenergic pathways in the myocardium. These observations suggest the possible role of adrenergic mechanisms in the complex multifactorial pathogenesis of LVH and suggest the therapeutic impact of alpha-adrenergic blockade in promoting regression of LVH.
Ram
C V
CV
University of Texas South Western Medical Center, Dallas.
D000317:Adrenergic alpha-Antagonists / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000818:Animals; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000209:etiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists