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急性心肌梗死后心室扩大与重构:机制与处理

Ventricular enlargement and remodeling following acute myocardial infarction: mechanisms and management.

作者信息

Braunwald E, Pfeffer M A

机构信息

Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts 02115.

出版信息

Am J Cardiol. 1991 Nov 18;68(14):1D-6D. doi: 10.1016/0002-9149(91)90255-j.

Abstract

Severe myocardial ischemia, when sustained, leads to a predictable sequence of events, including myocardial necrosis, expansion of the infarct, and later its replacement by scar tissue. The nonischemic tissue sustains ventricular function, but it frequently adapts to the extra load placed on it by dilating. The enlargement and remodeling of the left ventricle may lead to ventricular failure and arrhythmias. Rational management to prevent these complications includes restoration of the patency of the occluded vessel and ventricular unloading. These two interventions may be useful both early and late in the course of infarction.

摘要

严重的心肌缺血若持续存在,会引发一系列可预测的事件,包括心肌坏死、梗死灶扩大,随后被瘢痕组织替代。非缺血组织维持心室功能,但它常常通过扩张来适应额外的负荷。左心室的扩大和重塑可能导致心室衰竭和心律失常。预防这些并发症的合理处理措施包括恢复闭塞血管的通畅和减轻心室负荷。这两种干预措施在梗死过程的早期和晚期可能都有用。

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