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左心室肥厚的逆转:一个理想的治疗目标?

Reversal of left ventricular hypertrophy: a desirable therapeutic goal?

作者信息

Schmieder R E, Messerli F H

机构信息

Department of Medicine, Universität Erlangen-Nürnberg, F.R.G.

出版信息

J Cardiovasc Pharmacol. 1990;16 Suppl 6:S16-22.

PMID:1707110
Abstract

It is controversial whether myocardial hypertrophy in essential hypertension represents an adaptive physiologic or pathological response to increased pressure load imposed on the heart. Cardiac structural adaptations in endurance athletes fulfill the criteria of physiologic hypertrophy: maintained cardiac performance and full reversibility of cardiac structural changes following cessation of endurance training. In contrast, there is some evidence that cardiac hypertrophy in arterial hypertension is a pathological process. Diastolic function of the left ventricle is impaired; systolic function, although maintained in the early stages of myocardial hypertrophy, becomes reduced beyond a critical mass; and cardiac structural changes are not fully reversible. An increasing number of prospective studies document that left ventricular hypertrophy in essential hypertension represents an independent risk factor for cardiovascular mortality and morbidity, in particular for sudden cardiac death. Ventricular arrhythmias were regarded as the pathophysiologic link between cardiac structural adaptation and the increased risk of sudden death due to left ventricular hypertrophy. Structural changes of the coronary circulation may represent one confounding factor in the relationship between left ventricular hypertrophy and its cardiovascular risk. As a consequence, optimal antihypertensive therapy should aim at reducing both arterial hypertension and left ventricular hypertrophy. Whether regression of myocardial hypertrophy indeed reduces cardiovascular risk cannot be definitively answered from the available data.

摘要

原发性高血压中的心肌肥厚究竟是对心脏所承受的压力负荷增加的适应性生理反应还是病理性反应,这一点存在争议。耐力运动员的心脏结构适应性符合生理性肥厚的标准:心脏功能得以维持,且在耐力训练停止后心脏结构变化可完全逆转。相比之下,有证据表明动脉高血压中的心脏肥厚是一个病理过程。左心室舒张功能受损;收缩功能虽在心肌肥厚早期得以维持,但超过一定程度后会降低;且心脏结构变化并非完全可逆。越来越多的前瞻性研究表明,原发性高血压中的左心室肥厚是心血管疾病死亡率和发病率的独立危险因素,尤其是心源性猝死的危险因素。室性心律失常被视为心脏结构适应性与左心室肥厚导致的猝死风险增加之间的病理生理联系。冠状动脉循环的结构变化可能是左心室肥厚与其心血管风险之间关系中的一个混杂因素。因此,最佳的抗高血压治疗应旨在降低动脉高血压和左心室肥厚。现有数据无法确切回答心肌肥厚的消退是否真的能降低心血管风险。

相似文献

1
Reversal of left ventricular hypertrophy: a desirable therapeutic goal?左心室肥厚的逆转:一个理想的治疗目标?
J Cardiovasc Pharmacol. 1990;16 Suppl 6:S16-22.
2
[Ventricular arrhythmia and sudden cardiac death: the significance of left ventricular hypertrophy as risk factor].[室性心律失常与心源性猝死:左心室肥厚作为危险因素的意义]
Schweiz Med Wochenschr. 1993 Jan 30;123(4):99-107.
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Is reversal of cardiac hypertrophy a desirable goal of antihypertensive therapy?心脏肥大的逆转是抗高血压治疗的一个理想目标吗?
Circulation. 1987 Jan;75(1 Pt 2):I113-7.
4
[Heart effect of arterial hypertension. Heart hypertrophy as a risk factor. Study technics (electrocardiogram, echocardiography, exercise test and Holter].动脉高血压的心脏效应。心脏肥大作为一个危险因素。研究技术(心电图、超声心动图、运动试验和动态心电图)
Rev Esp Cardiol. 1990;43 Suppl 1:54-64.
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J Assoc Acad Minor Phys. 1991;2(4):156-61.
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[Antihypertensive treatment and left ventricular hypertrophy].[抗高血压治疗与左心室肥厚]
Ann Ital Med Int. 1993 Oct;8 Suppl:97S-103S.
8
[Left ventricular hypertrophy: favorable or unfavorable compensatory mechanisms?].
Herz. 1991 Sep;16 Spec No 1:330-3.
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Risk for cardiac involvement in essential hypertension.原发性高血压患者发生心脏受累的风险。
Cardiol Clin. 1986 Feb;4(1):81-93.
10
Structural and functional adaptation in the rat myocardium and coronary vascular bed caused by changes in pressure and volume load.压力和容量负荷变化引起的大鼠心肌和冠状血管床的结构与功能适应性改变。
Acta Physiol Scand Suppl. 1985;540:1-47.

引用本文的文献

1
Does a reduction in left ventricular hypertrophy reduce cardiovascular morbidity and mortality?左心室肥厚的减轻是否能降低心血管疾病的发病率和死亡率?
Drugs. 1992;44 Suppl 1:141-6. doi: 10.2165/00003495-199200441-00027.