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从左心室肥厚到功能障碍及衰竭。

From Left Ventricular Hypertrophy to Dysfunction and Failure.

作者信息

Lazzeroni Davide, Rimoldi Ornella, Camici Paolo G

机构信息

Prevention and Rehabilitation Unit, Don Gnocchi Foundation & University of Parma.

出版信息

Circ J. 2016;80(3):555-64. doi: 10.1253/circj.CJ-16-0062. Epub 2016 Feb 5.

Abstract

Left ventricular hypertrophy (LVH) is growth in left ventricular mass caused by increased cardiomyocyte size. LVH can be a physiological adaptation to strenuous physical exercise, as in athletes, or it can be a pathological condition, which is either genetic or secondary to LV overload. Physiological LVH is usually benign and regresses upon reduction/cessation of physical activity. Pathological LVH is a compensatory phenomenon, which eventually may become maladaptive and evolve towards progressive LV dysfunction and heart failure (HF). Both interstitial and replacement fibrosis play a major role in the progressive decompensation of the hypertrophied LV. Coronary microvascular dysfunction (CMD) and myocardial ischemia, which have been demonstrated in most forms of pathological LVH, have an important pathogenetic role in the formation of replacement fibrosis and both contribute to the evolution towards LV dysfunction and HF. Noninvasive imaging allows detection of myocardial fibrosis and CMD, thus providing unique information for the stratification of patients with LVH. (Circ J 2016; 80: 555-564).

摘要

左心室肥厚(LVH)是由心肌细胞大小增加导致的左心室质量增长。LVH 可以是对剧烈体育锻炼的生理适应,如运动员的情况,也可以是一种病理状态,其可以是遗传性的或继发于左心室负荷过重。生理性 LVH 通常是良性的,在减少/停止体力活动后会消退。病理性 LVH 是一种代偿现象,最终可能会变得适应不良并发展为进行性左心室功能障碍和心力衰竭(HF)。间质纤维化和替代性纤维化在肥厚性左心室的进行性失代偿中都起主要作用。在大多数病理性 LVH 形式中已得到证实的冠状动脉微血管功能障碍(CMD)和心肌缺血,在替代性纤维化的形成中具有重要的致病作用,并且都有助于向左心室功能障碍和 HF 的发展。非侵入性成像可以检测心肌纤维化和 CMD,从而为 LVH 患者的分层提供独特信息。(《循环杂志》2016 年;80:555 - 564)

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