Arnett D K
Division of Epidemiology, School of Public Health, University of Minnesota, 1300 South Second Street, Suite 300, Minneapolis, MN 55454, USA.
Curr Hypertens Rep. 2000 Feb;2(1):50-5. doi: 10.1007/s11906-000-0058-3.
Left ventricular (LV) hypertrophy is a common condition that profoundly affects morbidity and mortality from cardiovascular diseases, including myocardial infarction, congestive heart failure, and stroke. Noninvasive imaging methods have greatly expanded our ability to evaluate cardiac structural and functional characteristics, and enhanced our understanding of the natural history of LV hypertrophy. The etiology of LV hypertrophy is likely due to the effects of multiple genes interacting with other genes and the environment. Although hypertension is recognized as a strong determinant of LV hypertrophy, blood pressure explains only a limited amount of the interindividual variation in LV mass. Moreover, LV hypertrophy occurs in the absence of hypertension, and in some cases precedes its development. Genes encoding proteins involved in the structure of the LV, as well as genes encoding cell signal transduction, hormones, growth factors, calcium homeostasis, and blood pressure, are likely candidates for the development of common forms of LV hypertrophy. An overview of the epidemiology and pathophysiology of LV hypertrophy and dysfunction is provided, in addition to evidence of the genetic basis for LV hypertrophy.
左心室肥厚是一种常见病症，严重影响包括心肌梗死、充血性心力衰竭和中风在内的心血管疾病的发病率和死亡率。非侵入性成像方法极大地扩展了我们评估心脏结构和功能特征的能力，并加深了我们对左心室肥厚自然病程的理解。左心室肥厚的病因可能是多种基因与其他基因及环境相互作用的结果。尽管高血压被认为是左心室肥厚的一个重要决定因素，但血压仅能解释左心室质量个体间差异的有限部分。此外，左心室肥厚在无高血压的情况下也会发生，且在某些情况下先于高血压出现。编码参与左心室结构的蛋白质的基因，以及编码细胞信号转导、激素、生长因子、钙稳态和血压的基因，可能是常见形式左心室肥厚发生发展的候选基因。除了左心室肥厚遗传基础的证据外，本文还提供了左心室肥厚和功能障碍的流行病学及病理生理学概述。
