The heart in hypertension.
Knowledge concerning the functional and structural changes of the heart in hypertension has increased remarkably over the past three decades. These changes may not at all be the same as with other diseases associated with increased afterload since the etiology, pathophysiological mechanisms, and other associated diseases are very different. Hemodynamic alterations associated with hypertension have a major role in the adaptive cardiac changes; but recent knowledge indicates that they are not exclusive. Nonhemodynamic factors are also very important; they not only include the now-accepted demographic considerations of age, race, gender and associated diseases but also consider newly discovered growth factors as well as prior and present therapy. The heart that provides a physiological adaptation to the increasing overload produced by disease in order to stem the tide from eventual cardiac failure also confers an independent risk of premature cardiovascular morbidity and mortality. It is too early to infer that reversal of the LVH reverses this risk. But, even if this does occur, mechanisms other than only LVH reversal must be considered. Therefore, at this time, the implications and consequences of reversed LVH has yet to be demonstrated.
Frohlich
E D
ED
Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.
D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D006332:Cardiomegaly / Q000453:epidemiology / Q000209:etiology*; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000150:complications*; D012307:Risk Factors
D000959:Antihypertensive Agents