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应激性心肌病:对潜在病理生理学机制的新见解

Tako-Tsubo cardiomyopathy: new insights into the possible underlying pathophysiology.

作者信息

Merli Elisa, Sutcliffe Stephen, Gori Mauro, Sutherland George G R

机构信息

St George's Hospital, Department of Cardiology, Blackshaw Road, London SW 17-0Q8, UK.

出版信息

Eur J Echocardiogr. 2006 Jan;7(1):53-61. doi: 10.1016/j.euje.2005.08.003. Epub 2005 Sep 22.

Abstract

UNLABELLED

Tako-Tsubo cardiomyopathy is characterised by an atypical distribution of left ventricular (LV) dysynergy with apical ballooning and compensatory basal hyperkinesis. Coronary angiography is normal. Several substrates have been put forward to explain the underlying pathophysiology such as raised catecholamine levels (due to physical or emotional stress), multivessel epicardial coronary spasm or diffuse microvascular spasm. However, the pathophysiology has not yet been fully clarified. We present a series of cases whose findings could explain the mechanism underlying this syndrome. Four consecutives patients, all female, were admitted with the clinical features typical of Tako-Tsubo syndrome. In all, severe widespread transient LV mid-apical a/dyskinesia was associated with a mid-cavity dynamic obstruction which resolved prior to the resolution of the LV wall motion abnormalities. In all cases the dynamic LV obstruction was related to localised mid-ventricular septal thickening. After improvement in wall motion, a low-dose strain/strain rate dobutamine stress-echocardiography (DSE) was performed to determine the underlying ischaemic substrate. This provoked an LV mid-cavity gradient at peak dose in all. Regional deformation changes during DSE showed the affected myocardium to have the typical response diagnostic of regional stunning.

CONCLUSION

We postulate that an important unrecognised factor in the development of Tako-Tsubo cardiomyopathy is the presence of abnormal myocardial functional architecture (such as localised mid-ventricular septal thickening), which in the presence of dehydration and/or raised catecholamine levels due to physical or emotional stress, leads the development of a severe transient LV mid-cavity obstruction. This effectively sub-divides the LV into two functionally different chambers with a marked increase in wall stress in the high pressure distal apical chamber. This, in combination with the abnormal high circulating catecholamine levels, induces widespread sub-endocardial ischaemia which is unrelated to a specific coronary artery territory. With rehydration/fall in catecholamine levels the interventricular gradient resolves and distal function recovers. Low dose SR/S DSE confirms that the distal ischaemic substrate is myocardial stunning.

摘要

未标注

应激性心肌病的特征是左心室(LV)运动失调呈非典型分布,表现为心尖部气球样变和代偿性基底段运动增强。冠状动脉造影正常。已提出多种机制来解释其潜在的病理生理学,如儿茶酚胺水平升高(由于身体或情绪应激)、多支心外膜冠状动脉痉挛或弥漫性微血管痉挛。然而,其病理生理学尚未完全阐明。我们报告一系列病例,其发现可解释该综合征的潜在机制。连续4例患者均为女性,因应激性心肌病的典型临床特征入院。总体而言,严重广泛的短暂性左心室心尖中部运动减弱/运动障碍与心腔中部动态梗阻相关,该梗阻在左心室壁运动异常缓解之前消失。所有病例中,左心室动态梗阻均与局部室间隔中部增厚有关。在壁运动改善后,进行低剂量应变/应变率多巴酚丁胺负荷超声心动图(DSE)以确定潜在的缺血机制。这在所有病例中均在峰值剂量时诱发了左心室心腔中部梯度。DSE期间的区域变形变化显示受影响的心肌具有典型的心肌顿抑诊断反应。

结论

我们推测,应激性心肌病发生过程中一个重要的未被认识的因素是存在异常的心肌功能结构(如局部室间隔中部增厚),在因身体或情绪应激导致脱水和/或儿茶酚胺水平升高的情况下,会导致严重的短暂性左心室心腔中部梗阻的发生。这有效地将左心室分为两个功能不同的腔室,高压远端心尖腔室的壁应力显著增加。这与异常高的循环儿茶酚胺水平相结合,导致广泛的心内膜下缺血,这与特定冠状动脉区域无关。随着补液/儿茶酚胺水平下降,心室间梯度消失,远端功能恢复。低剂量SR/S DSE证实远端缺血机制是心肌顿抑。

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