[Regression of left ventricular hypertrophy in essential arterial hypertension].
The classic concept of a direct pathogenic relationship between high blood pressure and development of left ventricular hypertrophy has been challenged by observations such as the modest correlations between blood pressure and magnitude of left ventricular hypertrophy, its frequent reversal with some antihypertensive medications and its experimental prevention with low doses of an angiotensin-converting enzyme inhibitor that do not modify blood pressure. This evidence has prompted the revision of mechanisms or factors involved in the development of left ventricular hypertrophy. The roles of sympathetic nervous and renin-angiotensin systems, genetic and endothelial factors, are reviewed in this article. It is concluded that blood pressure is not the sole responsible for left ventricular hypertrophy, but an epiphenomenon of one or more local or tissular mechanisms, primary or unchained by an unknown genetic factor.
Román
O
O
Universidad de Chile, Hospital San Borja-Arriarán, Santiago de Chile.
D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001158:Arteries / Q000503:physiopathology; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000503:physiopathology; D011519:Proto-Oncogenes / Q000502:physiology; D051381:Rats; D012084:Renin-Angiotensin System / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000187:drug effects
D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers
Reversión de la hipertrofia ventricular izquierda en la hipertensión arterial esencial.