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高血压性心脏病的病理生理及临床特征

[Physiopathologic and clinical features of hypertensive cardiopathy].

作者信息

Mancia G, Grassi G

机构信息

Cattedra di Medicina Interna, Università degli Studi, Milano.

出版信息

Cardiologia. 1994 Dec;39(12 Suppl 1):291-4.

PMID:7634285
Abstract

Several studies, performed during the past 20 years in different experimental animal models of hypertension and in men, have allowed to clarify important pathophysiological and clinical aspects of the hypertensive cardiovascular disease, i.e. the pathological condition characterized by marked structural and functional alterations of the heart induced by arterial hypertension. Epidemiological studies have indeed clearly shown that the prevalence of left ventricular hypertrophy in large hypertensive population samples is markedly high (40-50%) and that the electrocardiographic evidence of cardiac hypertrophy adversely affects patient's prognosis, by significantly increasing cardiovascular morbidity (myocardial infarction, congestive heart failure and cardiac arrhythmias) and mortality (sudden death). It has also been shown that cardiac hypertrophy is characterized by profound functional alterations in myocardial contractility and impairs neural reflex responses to beta-adrenergic stimulation and to deactivation of cardiopulmonary volume receptors, which are involved in physiological conditions in blood volume homeostasis control. Finally, several interventional studies have unequivocally shown that antihypertensive drugs may allow to obtain, even following 3-6 months of treatment, along with a blood pressure reduction, a clearcut regression of cardiac hypertrophy. By improving cardiovascular hemodynamics and neural control of circulation, regression of cardiac structural alterations is associated with a significant reduction in the patient's cardiovascular risk profile.

摘要

在过去20年中,针对不同高血压实验动物模型和人类开展的多项研究,已使人们得以阐明高血压性心血管疾病的重要病理生理和临床特征,即由动脉高血压导致心脏出现明显结构和功能改变的病理状态。流行病学研究确实清楚地表明,在大量高血压人群样本中,左心室肥厚的患病率显著较高(40%-50%),而且心脏肥厚的心电图证据会通过显著增加心血管疾病发病率(心肌梗死、充血性心力衰竭和心律失常)和死亡率(猝死),对患者预后产生不利影响。研究还表明,心脏肥厚的特征是心肌收缩力发生深刻的功能改变,并损害对β-肾上腺素能刺激以及对心肺容量感受器失活的神经反射反应,而这些感受器参与了血容量稳态控制的生理过程。最后,多项干预性研究明确表明,即使经过3至6个月的治疗,降压药物在降低血压的同时,也可使心脏肥厚明显消退。通过改善心血管血流动力学和循环的神经控制,心脏结构改变的消退与患者心血管风险状况的显著降低相关。

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