[The heart in hypertension. Cardiac protection and cardiac repair].
Studies performed in the last five years have led to the knowledge of new mechanisms by which the hypertensive process produces hypertrophy and cardiac fibrosis, at the same time, favoring development of the atheroesclerotic plaque. The Renin-Angiotensin-Aldosterone axis is relevant by involved in the physiopathology of these alterations, not only by producing hyperplasia and hypertrophy of vascular smooth muscle cells or by increasing protein and DNA syntheses, mediated by Angiotensin II (by itself a potent Growth factor) but also through inflammatory processes exerted upon the vascular smooth muscle cells. These alterations (hypertrophy, fibrosis, inflammation, and destabilization of the atherosclerotic plaque) can now be counteracted by blocking the Angiotensin-Converting enzyme or its AT1 receptors with the consequent improvement in ventricular diastolic functions.
Trevethan Cravioto
Sergio
S
Instituto Nacional de Cardiología Ignacio Chávez, INCICH, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, 14080 México, D. F. trevethan@cardiologia.org.mx
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D006331:Heart Diseases / Q000209:etiology* / Q000517:prevention & control*; D006801:Humans; D006973:Hypertension / Q000150:complications*
D000806:Angiotensin-Converting Enzyme Inhibitors