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实验性心力衰竭中,心脏支持装置带来的逆向重构和增强的心肌收缩储备。

Reverse remodeling and enhanced inotropic reserve from the cardiac support device in experimental cardiac failure.

作者信息

Kass David A, Saavedra W Federico, Sabbah Hani N

机构信息

Division of Cardiology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287, USA.

出版信息

J Card Fail. 2004 Dec;10(6 Suppl):S215-9. doi: 10.1016/j.cardfail.2004.09.003.

Abstract

Progressive chamber remodeling plays a major role in the pathophysiology of chronic cardiac failure. Recent studies have begun exploring the potential for a passive external containment to impede such progressive dilation. In dogs with ischemic dilated cardiomyopathy, surgical placement of a thin external polyester mesh led to reversal of chronic chamber dilation after 3 to 6 months. Systolic function was preserved compared with the earlier time point. Both end-systolic and end-diastolic chamber volumes were reduced by about 20%, whereas end-diastolic pressure and chamber diastolic stiffness were not altered. These findings differ from the natural progression of this model, which involves progressive dilation and systolic dysfunction. In conjunction with reverse remodeling, cardiac inotropic reserve to beta-receptor agonists was markedly enhanced. Furthermore, these changes were induced without adversely affecting Frank-Starling reserve, supporting the lack of constriction.

摘要

进行性心室重构在慢性心力衰竭的病理生理学中起主要作用。最近的研究已开始探索被动外部约束阻止这种进行性扩张的可能性。在患有缺血性扩张型心肌病的犬中,手术放置薄的外部聚酯网在3至6个月后导致慢性心室扩张逆转。与较早时间点相比,收缩功能得以保留。收缩末期和舒张末期心室容积均减少约20%,而舒张末期压力和心室舒张硬度未改变。这些发现不同于该模型的自然进展,后者涉及进行性扩张和收缩功能障碍。与逆向重构相结合,心脏对β受体激动剂的变力储备显著增强。此外,这些变化的诱导并未对Frank-Starling储备产生不利影响,支持无收缩作用。

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