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量化心脏和动脉重塑对高血压的影响。

Quantification of the contribution of cardiac and arterial remodeling to hypertension.

作者信息

Segers P, Stergiopulos N, Westerhof N

机构信息

Laboratory for Physiology, Institute for Cardiovascular Research, Free University of Amsterdam, the Netherlands.

出版信息

Hypertension. 2000 Nov;36(5):760-5. doi: 10.1161/01.hyp.36.5.760.

Abstract

The study aim was to quantify the individual and combined contributions of both the arterial system and the heart to systolic blood pressure in hypertension. We assessed the parameters of a heart-arterial model for normotensive control subjects and hypertensive patients with left ventricular adaptation patterns classified as normal, concentric remodeling, concentric hypertrophy, or eccentric hypertrophy. The present simulations show that vascular stiffening alone increases the pulse pressure without increasing systolic blood pressure. It is only in combination with an increased peripheral resistance that arterial stiffening leads to systolic hypertension in concentric remodeling and concentric hypertrophy. The contribution of cardiac pump function to the increase in blood pressure depends on cardiac remodeling, hypertrophy, or both. In hypertensive patients with a normal left ventricle, the heart is responsible for 55% of the increase in systolic blood pressure. In concentric remodeling, concentric hypertrophy, and eccentric hypertrophy, the cardiac contribution to the increase in systolic blood pressure is 21%, 65%, and 108%, respectively. We conclude that along with arterial changes, cardiac remodeling and hypertrophy contribute to hypertension.

摘要

该研究的目的是量化动脉系统和心脏对高血压患者收缩压的单独及联合作用。我们评估了血压正常的对照受试者以及左心室适应模式分为正常、向心性重塑、向心性肥厚或离心性肥厚的高血压患者的心脏 - 动脉模型参数。目前的模拟结果表明,单纯血管硬化会增加脉压,但不会增加收缩压。只有在外周阻力增加的情况下,动脉硬化才会导致向心性重塑和向心性肥厚患者出现收缩期高血压。心脏泵功能对血压升高的作用取决于心脏重塑、肥厚或两者兼有。在左心室正常的高血压患者中,心脏对收缩压升高的贡献率为55%。在向心性重塑、向心性肥厚和离心性肥厚患者中,心脏对收缩压升高的贡献率分别为21%、65%和108%。我们得出结论,除了动脉变化外,心脏重塑和肥厚也会导致高血压。

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