高血压患者的冠状动脉微血管疾病。

A R Lucarini, E Picano, A Salvetti
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引用次数: 20

摘要

动脉高压可通过几种不相互排斥的机制严重影响冠状动脉循环,即冠状动脉疾病、左室肥厚和微血管疾病。理论和实验数据提示,高血压患者可能存在冠状动脉微血管病变,可引起冠状动脉血流储备减少和冠状动脉血流自动调节曲线右移。为了解决这个问题,我们使用了双啶达摩超声心动图试验,在不同亚群的微血管疾病(综合征X;肥厚性心肌病;急性心脏排斥反应)。我们发现,在心外膜冠状动脉正常、无左心室肥厚、前臂最小血管阻力增加、冠状动脉储备减少的轻中度原发性高血压患者中,输注双吡达摩可引起类似的反应模式(即超声心动图上无ST段抑制)。这种反应模式可识别室性心律失常风险较高的高血压患者,可因舒张压的急性降低而放大,并可与慢性降压治疗降低前臂血管阻力一起逆转。综上所述,这些研究结果表明,高血压患者可能存在微血管冠状动脉疾病,并伴有与实验背景一致的两种不良后果:冠状动脉血流储备减少以及冠状动脉血流自动调节曲线向右移动。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Coronary microvascular disease in hypertensives.

Arterial hypertension can badly affect coronary circulation through several mechanisms that are not mutually exclusive, namely, coronary artery disease, left ventricular hypertrophy, and microvascular disease. Theoretical and experimental data suggest that coronary microvascular disease may exist in hypertensives, in whom it can cause both a reduction of coronary flow reserve and a shift to the right of the coronary flow autoregulation curve. To address this issue, we used dipyridamole- echocardiography test, which causes ischemic-like ST segment depression with no detectable changes in left ventricular function in different subsets of patients with microvascular disease (Syndrome X; Hypertrophic cardiomyopathy; acute heart rejection). We found that dipyridamole infusion can cause a similar pattern of response (i.e., echocardiographically silent ST segment depression) in mild-moderate essential hypertensives with normal epicardial coronary arteries, without left ventricular hypertrophy, with increased forearm minimal vascular resistances and with a reduced coronary reserve. This pattern of response identifies hypertensives with higher risk of ventricular arrhythmias, is amplified by acute reduction of diastolic blood pressure and can be reversed, together with the reduction of forearm vascular resistances by chronic antihypertensive treatment. Taken together these findings suggest that microvascular coronary disease can exist in hypertensives with two adverse consequences, consistent with the experimental background: the reduction of coronary flow reserve as well as a shift to the right of the coronary flow autoregulation curve.

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