合并收缩功能不全及心肌炎症的缺血性慢性心力衰竭患者左心室失代偿的临床电流及结构功能状态特征

E. Kruchinkina, T. Ryabova, Y. Rogovskaya, R. Batalov, V. Ryabov
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引用次数: 0

摘要

目的探讨伴有收缩功能障碍和心肌炎症的缺血性CHF患者的CHF失代偿的临床过程及左心室结构和功能状态。材料和方法。本研究是开放的、非随机的、前瞻性的,已在ClinicalTrials.gov网站注册,识别号:NCT02649517。本研究纳入25例缺血性ADHF患者(男性84%,LVEF 29.17±9.4%)。患者平均年龄60.12±9.3岁。所有患者均行超声心动图,包括2d斑点跟踪技术来评估左室变形。所有患者均行有创冠状动脉造影,以排除导致CHC失代偿的冠状动脉粥样硬化进展。行心肌膜活检诊断心肌炎症的存在。结果缺血性CHF合并收缩期左室功能障碍失代偿的临床过程与心肌组织炎症没有明显的关系。然而,在有炎症的患者中,冠状动脉搭桥手术更为常见(p=0.00650)。此外,炎症患者心尖旋转减少(p=0.0313),心尖收缩速度减少(p=0.0157),伴有CHF失代偿。一年后,左室生物力学有所改善,但抗炎治疗后左室整体纵向变形绝对模量继续下降(p=0.0431)。1年后,两组左室舒张末期容积指数分别升高(p=0.0180和p=0.0280),炎症组左室室间隔缩小(p=0.0491),炎症组左室心肌质量指数升高(p=0.04995)。结论:缺血性CHF合并左室收缩功能障碍患者左室尖顶旋转及收缩速度减慢;鉴于最佳心肌血运重建后缺乏临床改善,可能是心肌并发炎症的另一个标准。在缺血性CHF合并左室收缩功能障碍的患者中,炎症组心脏重构更为明显,表现为左室扩张和左室壁变薄。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CHARACTERISTICS OF CLINICAL CURRENT AND STRUCTURAL-FUNCTIONAL STATE OF LEFT VENTRICULAR IN DECOMPENSATION OF CHRONIC HEART FAILURE IN PATIENTS WITH ISCHEMIC CHRONIC HEART FAILURE WITH SYSTOLIC DYSFUNCTION AND INFLAMMATION OF THE MYOCARDIUM
The aimwas to study the clinical course of CHF decompensation and the structural and functional state of the left ventricle in patients with ischemic CHF with systolic dysfunction and myocardial inflammation.Material and Methods.This study is open, non-randomized, prospective, registered on the ClinicalTrials.gov website, identification number: NCT02649517. The analysis included 25 patients (84% men, LVEF 29.17±9.4%) with ADHF of ischemic etiology. The average age of the patients was 60.12±9.3 years. All the patients underwent an echocardiography including 2D-speckle tracking technique to assess LV deformation. All patients underwent invasive coronary angiography to exclude the progression of coronary atherosclerosis, as a cause of CHC decompensation. An endomyocardial biopsy was performed to diagnose the presence of myocardial inflammation. We performed a comparative analysis of clinical, laboratory, instrumental indicators depending on the fact of diagnosis of inflammation in the myocardium.Results.There were no specific features of the clinical course of decompensation of ischemic CHF with systolic LV dysfunction depending on the inflammation in the myocardial tissue. However, in patients with inflammation, aortocoronary bypass surgery was more often performed (p=0.00650). In addition, in patients with inflammation, there was a decrease in apical rotation (p=0.0313), its systolic velocity (p=0.0157 with decompensation of CHF. A year later, improvement in LV biomechanics, but a continuing decrease in the absolute modulus of global longitudinal LV deformation (p=0.0431) after the anti-inflammatory treatment. Also a year later, in both groups there was an increase in the LV end-diastolic volume index (p=0.0180 and p=0.0280, respectively), a decrease in the interventricular septum of the LV (p=0.0491) in the group with inflammation, and an increase in the myocardial mass index of the LV (p=0.04995) in patients with inflammation.Conclusion.Decreased apical LV rotation and its systolic velocity in patients with ischemic CHF and LV systolic dysfunction, in view of the lack of clinical improvement after optimal myocardial revascularization, may be an additional criterion of concomitant inflammation in the myocardium. Among patients with ischemic CHF and LV systolic dysfunction, more pronounced cardiac remodeling, manifested by LV dilatation and thinning of LV wall, was observed in the group with inflammation.
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