Downstream Influence of Coronary Stenoses 
on Microcirculatory Remodeling: A Histopathology Study.

Guus A de Waard, M. Hollander, Danique Ruiter, Thomas ten Bokkel Huinink, Romain Meer, N. W. van der Hoeven, E. Meinster, J. Beliën, H. Niessen, N. van Royen
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引用次数: 5

Abstract

OBJECTIVE Inducible myocardial ischemia is influenced by contributions of both the epicardial artery and the coronary microcirculation. Experimental studies have found adverse microcirculatory remodeling to occur downstream of severe coronary stenoses. Coronary physiology studies in patients contradict the experimental findings, as the minimal microvascular resistance is not modified by stenoses. The objective was to determine whether microcirculatory remodeling occurs downstream of coronary stenoses in the human coronary circulation. Approach and Results: Myocardium corresponding to 115 coronary arteries of 55 deceased patients was investigated. Histopathologic staining of the microcirculation was performed using antibodies against SMA-α (smooth muscle actin-α) and CD31, to stain arterioles and capillaries, respectively. The following parameters were analyzed: ratio between lumen and vesel area, ratio between lumen and vessel diameter (both ratios for arterioles of <40, 40-100, and 100-200 µm diameter), arteriolar density, and capillary density. From the 55 patients, 32 pairs of an unobstructed coronary artery and a coronary artery with a stenosis were formed. No statistically significant differences between any of the microcirculatory parameters were found. A confirmatory unpaired analysis compared 3 groups: (1) coronary arteries in patients without coronary artery disease (n=53), (2) unobstructed coronary arteries in patients with a stenosis in one of the other coronary arteries (n=23), and (3) coronary stenoses (n=39). No statistically significant differences were observed between the groups. CONCLUSIONS The microcirculation distal to noncritical stenoses does not undergo structural remodeling in the human coronary circulation.
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冠状动脉狭窄
对微循环重构的下游影响:一项组织病理学研究。
目的诱发性心肌缺血受心外膜动脉和冠状动脉微循环共同作用的影响。实验研究发现,不良微循环重构发生在严重冠状动脉狭窄的下游。患者的冠状动脉生理学研究与实验结果相矛盾,因为最小微血管阻力不会因狭窄而改变。目的是确定微循环重构是否发生在冠状动脉狭窄的下游。方法与结果:对55例死亡患者115条冠状动脉对应的心肌组织进行了研究。用SMA-α(平滑肌肌动蛋白-α)抗体和CD31抗体分别对小动脉和毛细血管进行组织病理学染色。分析以下参数:管腔与血管面积之比、管腔与血管直径之比(小动脉直径<40、40-100、100-200µm均为此比值)、小动脉密度、毛细血管密度。从55例患者中,形成32对通畅冠状动脉和狭窄冠状动脉。微循环参数间无统计学差异。一项验证性非配对分析比较了三组:(1)无冠状动脉疾病患者的冠状动脉(n=53),(2)另一条冠状动脉狭窄患者的冠状动脉通畅(n=23),(3)冠状动脉狭窄(n=39)。两组间无统计学差异。结论人类冠状动脉非临界狭窄远端微循环不发生结构重构。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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Editors and Editorial Board. Correction to: Role of LpL (Lipoprotein Lipase) in Macrophage Polarization In Vitro and In Vivo. Tribute to Paul M. Vanhoutte, MD, PhD (1940-2019). Correction to: 18F-Sodium Fluoride Imaging of Coronary Atherosclerosis in Ambulatory Patients With Diabetes Mellitus. Extracellular MicroRNA-92a Mediates Endothelial Cell-Macrophage Communication.
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