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高血压性心脏病中冠状动脉小血管疾病导致心力衰竭的发展?

Development of cardiac failure by coronary small vessel disease in hypertensive heart disease?

作者信息

Strauer B E

机构信息

Medical Clinic and Policlinic B, University of Düsseldorf, Germany.

出版信息

J Hypertens Suppl. 1991 Dec;9(2):S11-20; discussion S20-1. doi: 10.1097/00004872-199112002-00003.

Abstract

In essential hypertension, ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal, even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). One of the profound mechanisms influencing both myocardial and coronary function in hypertensive heart disease is the pressure-dependent development of smooth vascular hypertrophy (media) or coronary resistance vessels. Consequently, the oxygen supply to the myocardium is impaired and secondary lesions occur such as fibrosis, increased myocardial and perivascular collagen content and scars within the heart muscle. Diastolic dysfunction develops, as well as an increase in myocardial stiffness, thus promoting the transition from the concentric (compensated) to the eccentric or dilated (decompensated) state, with the consequence of the occurrence of cardiac failure. On the basis of both functional and morphological criteria, evidence is presented in this report that coronary small vessel disease is one of the underlying mechanism for the development of cardiac failure in hypertensive heart disease.

摘要

在原发性高血压中,心室功能主要由肥厚程度(心肌因素)和冠状动脉的器质性并发症(冠状动脉因素)决定。心室功能与心室大小和收缩期壁应力呈负相关,因为当这两个变量增加时,心室功能会降低。即使是没有血管造影异常的正常大小的年轻高血压心脏似乎也容易发生缺血,因为即使在没有冠状动脉狭窄的情况下,冠状动脉储备也严重受限。与心室扩张性不同,即使存在明显的心肌肥厚,心肌顺应性也可能正常。随着心肌顺应性降低,收缩期壁应力增加,心室功能降低。高血压性心脏是心室壁不规则肥厚的最常见形式,在14%的此类病例中可见。对肥厚程度的分析表明,肥厚可能过高(质量与体积比高,壁应力降低)、适当或过低(质量与体积比正常,壁应力增加)。影响高血压性心脏病心肌和冠状动脉功能的一个重要机制是血管平滑肌(中膜)或冠状动脉阻力血管的压力依赖性肥厚。因此,心肌的氧供应受损,继而出现纤维化、心肌和血管周围胶原含量增加以及心肌内瘢痕等继发性病变。舒张功能障碍以及心肌僵硬度增加,从而促进从向心性(代偿性)向离心性或扩张性(失代偿性)状态的转变,结果是发生心力衰竭。基于功能和形态学标准,本报告提出证据表明冠状动脉小血管疾病是高血压性心脏病发生心力衰竭的潜在机制之一。

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