• E D Frohlich.
• Am. J. Med. 1983 Sep 26; 75 (3A): 121812-8.

AbstractLeft ventricular hypertrophy is both a target organ response to hypertensive vascular disease as well as a factor that might be responsible for other cardiovascular events. Recent work confirms that the increased cardiac mass associated with hypertension results as a structural adaptation to the increased afterload imposed on the heart. Initially there is a transient period of hyperfunction that is followed by the sustained structural adaptative period of stable hyperfunction. Even before left ventricular failure supervenes, the ventricular mass demonstrates impaired contraction. This article reviews the hemodynamic evidence in favor of this sequence of events but, in addition, points to the pathophysiological and clinical factors that may be responsible for the increased cardiac mass in addition to the pressure overload. These include: the pressor mechanisms per se; the age, sex, and race of the patient; and coexisting diseases. Some of these factors may account in part for the regression of cardiac mass with antihypertensive therapy. However, until we understand more clearly those factors that transduce the physical stimulus for hypertrophy into biochemical events, we shall neither understand completely the development of this structural adaptation of the heart nor its regression with treatment.

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