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遗传性人类高血压中的左心室质量:糖皮质激素可抑制性醛固酮增多症。

Left ventricular mass in hereditary human hypertension: glucocorticoid-suppressible hyperaldosteronism.

作者信息

Jamieson A, Murdoch D, Kennedy J A, Connell J M

机构信息

Department of Medicine and Therapeutics, Western Infirmary, Glasgow, UK.

出版信息

J Hypertens. 1995 May;13(5):551-6. doi: 10.1097/00004872-199505000-00011.

DOI:10.1097/00004872-199505000-00011
PMID:7561013
Abstract

BACKGROUND

The mineralocorticoid hormone aldosterone may be an important mediator of pathological ventricular hypertrophy and heart failure. Much of the evidence for this arises from experimental work in rat models of mineralocorticoid-dependent hypertension, and a pathological role in humans is still uncertain.

SUBJECTS

Eleven subjects with glucocorticoid-suppressible hyperaldosteronism, a hereditary form of hyperaldosteronism and hypertension, and 10 age- and sex-matched control subjects were studied.

RESULTS

The subjects with glucocorticoid-suppressible hyperaldosteronism had a higher mean blood pressure and plasma aldosterone concentration, and lower plasma renin concentration, than the control subjects. Left ventricular mass index was not significantly different in the subjects with glucocorticoid-suppressible hyperaldosteronism than in the control subjects. When the subjects with glucocorticoid-suppressible hyperaldosteronism were subdivided into those with and those without hypertension, no difference in left ventricular mass index could be detected between the subgroups or between either subgroup and the control subjects. However, there was a significant correlation between basal plasma aldosterone and left ventricular mass index in the subjects with glucocorticoid-suppressible hyperaldosteronism (r = 0.66, P < 0.03).

CONCLUSIONS

Despite marked elevations in plasma aldosterone concentrations from birth in subjects with glucocorticoid-suppressible hyperaldosteronism, left ventricular hypertrophy did not occur. The degree of hyperaldosteronism in the subjects was mild compared with other conditions and, although an effect on left ventricular mass index could be detected, the present results indicate that other factors may be necessary for the development of left ventricular hypertrophy.

摘要

背景

盐皮质激素醛固酮可能是病理性心室肥厚和心力衰竭的重要介质。这一观点的许多证据来自于盐皮质激素依赖性高血压大鼠模型的实验研究,其在人类中的病理作用仍不明确。

研究对象

对11例糖皮质激素可抑制性醛固酮增多症患者(一种遗传性醛固酮增多症和高血压形式)以及10例年龄和性别匹配的对照者进行了研究。

结果

与对照者相比,糖皮质激素可抑制性醛固酮增多症患者的平均血压和血浆醛固酮浓度更高,而血浆肾素浓度更低。糖皮质激素可抑制性醛固酮增多症患者的左心室质量指数与对照者相比无显著差异。当将糖皮质激素可抑制性醛固酮增多症患者分为高血压患者和非高血压患者时,各亚组之间或任一亚组与对照者之间的左心室质量指数均无差异。然而,在糖皮质激素可抑制性醛固酮增多症患者中,基础血浆醛固酮与左心室质量指数之间存在显著相关性(r = 0.66,P < 0.03)。

结论

尽管糖皮质激素可抑制性醛固酮增多症患者自出生起血浆醛固酮浓度就显著升高,但并未发生左心室肥厚。与其他情况相比,该组患者的醛固酮增多程度较轻,尽管可检测到其对左心室质量指数有影响,但目前的结果表明,左心室肥厚的发生可能还需要其他因素。

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