Román O
Universidad de Chile, Hospital San Borja-Arriarán, Santiago de Chile.
Rev Med Chil. 1994 Mar;122(3):333-8.
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.
高血压与左心室肥厚发展之间存在直接致病关系的经典概念受到了一些观察结果的挑战，比如血压与左心室肥厚程度之间的适度相关性、某些抗高血压药物可使其频繁逆转，以及低剂量血管紧张素转换酶抑制剂在不改变血压的情况下对其进行实验性预防。这些证据促使人们对参与左心室肥厚发展的机制或因素进行重新审视。本文对交感神经和肾素 - 血管紧张素系统、遗传和内皮因素的作用进行了综述。得出的结论是，血压并非左心室肥厚的唯一成因，而是一种或多种局部或组织机制的附带现象，这些机制可能是原发性的，也可能是由未知遗传因素引发的。
