Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga.
Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga; Division of Cardiothoracic Surgery, Joseph P. Whitehead Department of Surgery, Emory University School of Medicine, Atlanta, Ga.
J Thorac Cardiovasc Surg. 2020 Sep;160(3):e107-e125. doi: 10.1016/j.jtcvs.2019.06.109. Epub 2019 Aug 25.
Mitral regurgitation (MR) developing concomitant with ischemic cardiomyopathy is a frequently diagnosed valvular lesion, for which an optimal therapeutic strategy is unknown. The contribution of MR to the ongoing cardiac remodeling from myocardial infarction (MI) remains controversial. We have developed a novel experimental model in which MI and severe MR can be independently introduced, to study the role of MR in chronic remodeling of the ischemic heart.
A total of 98 rats were induced with MI+MR (group 1), MI (group 2), MR (group 3), or sham surgery (group 4). MR was induced by inserting a needle into the anterior mitral leaflet via the ventricular apex in a beating heart. MI was induced by ligating the left coronary artery. Biweekly ultrasound examinations were performed after surgery, and invasive hemodynamic assessments were performed in some rats at 2, 10, and 20 weeks.
At 2 weeks postsurgery, the mean end-diastolic volume was 432 ± 103 μL in ischemic hearts with MR, compared with 390 ± 76.3 μL in ischemic hearts without MR (a 10.76% difference). By 20 weeks, the mean volume was significantly greater in the former group (767 ± 246 μL vs 580 ± 85 μL; a 32.24% difference). At 2 weeks, mean end-systolic volume was 147 ± 46.8 μL in the ischemic hearts with MR and 147 ± 45.7 μL in those without MR. By 20 weeks, the mean volumes had increased to 357 ± 136.4 μL and 271 ± 82.3 μL, respectively (a 31.73% difference).
MR in ischemic hearts significantly increased end-diastolic and end-systolic volumes of the left ventricle, indicating adverse cardiac remodeling and worse systolic function.
与缺血性心肌病同时发生的二尖瓣反流(MR)是一种经常诊断出的瓣膜病变,对于这种病变,尚不清楚最佳的治疗策略。MR 对心肌梗死(MI)后持续的心脏重构的作用仍存在争议。我们开发了一种新的实验模型,其中可以独立引入 MI 和严重的 MR,以研究 MR 在缺血性心脏的慢性重构中的作用。
共有 98 只大鼠被诱导产生 MI+MR(第 1 组)、MI(第 2 组)、MR(第 3 组)或假手术(第 4 组)。通过在跳动的心脏中从前二尖瓣叶的心室尖部插入一根针来诱导 MR。通过结扎左冠状动脉来诱导 MI。手术后每两周进行超声检查,并在一些大鼠中于 2、10 和 20 周进行侵入性血流动力学评估。
手术后 2 周,有 MR 的缺血性心脏的平均舒张末期容积为 432±103μL,而无 MR 的缺血性心脏为 390±76.3μL(相差 10.76%)。到 20 周时,前者的平均容积明显更大(767±246μL 比 580±85μL;相差 32.24%)。在 2 周时,有 MR 的缺血性心脏的平均收缩末期容积为 147±46.8μL,无 MR 的为 147±45.7μL。到 20 周时,平均容积分别增加到 357±136.4μL 和 271±82.3μL(相差 31.73%)。
缺血性心脏中的 MR 显著增加了左心室的舒张末期和收缩末期容积,表明心脏重构不良和收缩功能更差。