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舒张功能障碍在主动脉瓣狭窄中的作用及临床意义。

The role and clinical implications of diastolic dysfunction in aortic stenosis.

机构信息

Department of Medicine, Division of Cardiology, Weill Cornell Medicine - New York Presbyterian Hospital, New York, New York, USA.

Society of Junior Doctors, Athens, Greece.

出版信息

Heart. 2017 Oct;103(19):1481-1487. doi: 10.1136/heartjnl-2017-311506. Epub 2017 Jul 6.

Abstract

Diastolic dysfunction in aortic stenosis results primarily from left ventricular hypertrophy and myocardial fibrosis due to chronically elevated left ventricular systolic pressure. Currently, diastolic dysfunction does not have an explicit clinical role in management of patients with aortic stenosis. Studies have shown that improvement in diastolic dysfunction follows left ventricular remodelling after aortic valve replacement and that it occurs gradually or incompletely. Retrospective studies suggest that advanced grades of diastolic dysfunction at baseline are associated with increased mortality and adverse events even after aortic valve replacement. Recent studies have also associated myocardial fibrosis, a hallmark of diastolic dysfunction, with worse outcomes. In addition, these results were independent of the degree of aortic stenosis or valve replacement. Indirect evidence of the role of diastolic dysfunction in aortic stenosis also comes from paradoxical low-flow, low-gradient aortic stenosis, where disproportionate left ventricular hypertrophy leads to underfilling of the left ventricle, low-flow state and is associated with worse prognosis. Lastly, a limited number of studies suggest that worse diastolic dysfunction at baseline is detrimental in patients who develop aortic regurgitation after transcatheteraortic valve replacement, due to superimposition of volume overload on a stiff left ventricle. Current major limitations in our understanding of the prognostic role of diastolic dysfunction are the lack of universally accepted classification schemes, its dependence on dynamic loading conditions and the lack of larger prospective studies.

摘要

主动脉瓣狭窄患者的舒张功能障碍主要由左心室收缩压长期升高引起的左心室肥厚和心肌纤维化引起。目前,舒张功能障碍在主动脉瓣狭窄患者的管理中没有明确的临床作用。研究表明,主动脉瓣置换术后左心室重构后舒张功能障碍得到改善,且其逐渐发生或不完全改善。回顾性研究表明,基线时舒张功能障碍程度较高与主动脉瓣置换术后死亡率和不良事件增加相关。最近的研究还将舒张功能障碍的标志性特征心肌纤维化与较差的预后相关联。此外,这些结果独立于主动脉瓣狭窄的严重程度或瓣膜置换。舒张功能障碍在主动脉瓣狭窄中的作用的间接证据还来自于矛盾的低流量、低梯度主动脉瓣狭窄,其中不成比例的左心室肥厚导致左心室充盈不足、低流量状态,并与预后较差相关。最后,少数研究表明,经导管主动脉瓣置换术后发生主动脉瓣反流的患者,由于左心室僵硬导致容量超负荷叠加,基线时舒张功能障碍恶化会产生不良影响。目前,我们对舒张功能障碍预后作用的理解主要存在以下局限性:缺乏普遍接受的分类方案、其对动态负荷条件的依赖性以及缺乏更大规模的前瞻性研究。

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