Remodeling of left circumflex coronary arterial tree in pacing-induced heart failure.

Remodeling of left circumflex coronary arterial tree in pacing-induced heart failure.
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起搏引起的心力衰竭中左回旋冠状动脉树的重塑。

DOI:
10.1152/japplphysiol.00262.2015
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发表时间:
2015-08
影响因子:
3.3
通讯作者:
Kassab Ghassan S
Kassab Ghassan S
中科院分区:
医学2区
文献类型:
--
作者:
Huo Yunlong;Kassab Ghassan S

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充血性心力衰竭(CHF)是一种非常严重的心脏病,表现为左心室供需失衡。尽管衰竭心脏的机械需求已经得到很好的表征,但缺乏构成心肌供应的整个冠状动脉树的系统性重塑。我们假设,众所周知的CHF期间心室壁应力的增加导致冠状动脉血管稀疏,增加血管流动阻力,这反过来又损害了心脏的灌注。在CHF组(n = 6)和对照组(n = 6)中测量猪左回旋支(LCx)动脉树的形态测量(直径、长度和数量)数据,从该数据中对整个LCx树进行计算机重建,直至毛细血管水平,以实现冠状动脉循环的血流动力学分析。起搏3-4 wk后,左回旋支动脉树第一毛细血管段的血管数和直径明显减少(分别减少约45%和约10%),血流阻力增加约75%。结构重塑显著改变了CHF动物整个LCx动脉树血管段的壁切应力。本研究加深了我们对心力衰竭时冠状动脉树重构的认识,对左心室供求关系恶化有了更深的理解。
Congestive heart failure (CHF) is a very serious heart disease that manifests an imbalance between left ventricle supply and demand. Although the mechanical demand of the failing heart has been well characterized, the systematic remodeling of the entire coronary arterial tree that constitutes the supply of the myocardium is lacking. We hypothesize that the well-known increase in ventricle wall stress during CHF causes coronary vascular rarefaction to increase the vascular flow resistance, which in turn compromises the perfusion of the heart. Morphometric (diameters, length, and numbers) data of the swine left circumflex (LCx) arterial tree were measured in both CHF (n = 6) and control (n = 6) groups, from which a computer reconstruction of the entire LCx tree was implemented down to the capillary level to enable a hemodynamic analysis of coronary circulation. The vascular flow resistance was increased by ∼75% due to a significant decrease of vessel numbers (∼45%) and diameters in the first capillary segments (∼10%) of the LCx arterial tree after 3-4 wk of pacing. The structural remodeling significantly changed the wall shear stress in vessel segments of the entire LCx arterial tree of CHF animals. This study enhances our knowledge of coronary arterial tree remodeling in heart failure, which provides a deeper understanding of the deterioration of supply-demand relation in left ventricle.
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