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孤立性瓣环扩张能否导致显著的缺血性二尖瓣反流?对其发病机制的再探讨。

Can isolated annular dilatation cause significant ischemic mitral regurgitation? Another look at the causative mechanisms.

机构信息

Tissue Mechanics Laboratory, Biomedical Engineering Department, Georgia Institute of Technology, Atlanta, GA 30313, United States.

Cardiology Department, The Hartford Hospital, Hartford, CT 06102, United States.

出版信息

J Biomech. 2014 Jun 3;47(8):1792-9. doi: 10.1016/j.jbiomech.2014.03.033. Epub 2014 Apr 2.

DOI:10.1016/j.jbiomech.2014.03.033
PMID:24767703
Abstract

This study was to investigate the mechanisms of ischemic mitral regurgitation (IMR) by using a finite element (FE) approach. IMR is a common complication of coronary artery disease; and it usually occurs due to myocardial infarction. The pathophysiological mechanisms of IMR have not been fully understood, much debate remains about the exact contribution of each mechanism to IMR. Two patient-specific FE models of normal mitral valves (MV) were reconstructed from multi-slice computed tomography scans. Different grades of IMR during its pathogenesis were created by perturbation of the normal MV geometry. Effects of annular dilatation and papillary muscle (PM) displacement (both isolated and combined) on the severity of IMR were examined. We observed greater increase in IMR (in terms of regurgitant area and coaptation length) in response to isolated annular dilatation than that caused by isolated PM displacement, while a larger PM displacement resulted in higher PM forces. Annular dilation, combined with PM displacement, was able to significantly increase the severity of IMR and PM forces. Our simulations demonstrated that isolated annular dilatation might be a more important determinant of IMR than isolated PM displacement, which could help explain the clinical observation that annular size reduction by restrictive annuloplasty is generally effective in treating IMR.

摘要

本研究采用有限元(FE)方法探讨缺血性二尖瓣反流(IMR)的机制。IMR 是冠状动脉疾病的常见并发症;通常由于心肌梗死而发生。IMR 的病理生理机制尚未完全了解,关于每种机制对 IMR 的确切贡献仍存在很大争议。从多层计算机断层扫描重建了两个正常二尖瓣(MV)的特定于患者的 FE 模型。通过对正常 MV 几何形状的干扰,在发病过程中创建了不同程度的 IMR。研究了瓣环扩张和乳头肌(PM)移位(单独和联合)对 IMR 严重程度的影响。我们观察到,与单独的 PM 移位相比,单独的瓣环扩张导致 IMR(反流面积和对合长度)更大的增加,而更大的 PM 移位导致更高的 PM 力。瓣环扩张与 PM 移位相结合,能够显著增加 IMR 和 PM 力的严重程度。我们的模拟表明,与单独的 PM 移位相比,单独的瓣环扩张可能是 IMR 的更重要决定因素,这可以帮助解释临床观察到的通过限制性瓣环成形术缩小瓣环大小通常对治疗 IMR 有效。

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