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[急性心肌梗死与维拉帕米中的心肌存活性]

[Myocardial viability in acute myocardial infarction and verapamil].

作者信息

Iliceto S, Rizzon P

机构信息

Istituto di Cardiologia, Università degli Studi, Bari.

出版信息

Cardiologia. 1994 Dec;39(12 Suppl 1):187-90.

PMID:7634265
Abstract

Following prolonged ischemia, if not adequately reperfused, myocardium undergoes necrosis, scarring and thinning. The myocardium tends to dilate in the noninfarcted ventricular area, giving rise to ventricular remodelling. If the ischemic myocardium is adequately reperfused it can be saved and its temporarily depressed functions eventually be recuperated (viable myocardium). The extent of recovery of the postinfarction viable myocardium seems to affect ventricular remodelling. The integrity of the microcirculation of the non-contractile myocardium following prolonged ischemia is fundamental in maintaining a contractile reserve adequate enough for a functional recovery (myocardial viability). Protection of the microcirculation during ischemia-reperfusion is therefore of great importance for the role that the microcirculation plays in ensuring myocardial viability. Experimental studies and initial clinical observations showed that calcium-antagonists exert a beneficial effect in this respect. VAMI is a multicentre, randomized double-blind, placebo-controlled study whose aim is to ascertain the potentiality of verapamil in limiting regional functional damage in patients with acute myocardial infarction and undergoing early thrombolysis.

摘要

长时间缺血后,如果没有得到充分的再灌注,心肌会发生坏死、瘢痕形成和变薄。在非梗死的心室区域,心肌往往会扩张,从而导致心室重构。如果缺血心肌得到充分的再灌注,它可以被挽救,其暂时受损的功能最终也能恢复(存活心肌)。梗死后存活心肌的恢复程度似乎会影响心室重构。长时间缺血后,无收缩功能心肌的微循环完整性对于维持足够的收缩储备以实现功能恢复(心肌存活能力)至关重要。因此,在缺血再灌注期间保护微循环对于微循环在确保心肌存活能力中所起的作用非常重要。实验研究和初步临床观察表明,钙拮抗剂在这方面发挥有益作用。VAMI是一项多中心、随机双盲、安慰剂对照研究,其目的是确定维拉帕米在限制急性心肌梗死且接受早期溶栓治疗的患者局部功能损害方面的潜力。

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