Circadian blood pressure variation in hypertensive patients with primary hyperaldosteronism.
Circadian blood pressure variation in hypertensive patients with primary hyperaldosteronism.
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DOI：
10.1161/01.hyp.31.3.843
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发表时间：
1998-03
期刊：
影响因子：
8.3
通讯作者：
G. Mansoor;W. White
中科院分区：
文献类型：
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作者：
G. Mansoor;W. White
夜间血压（BP）低于正常水平的下降与过度的高血压并发症有关。这是令人担忧的，因为继发性高血压通常与所谓的非杓型血压曲线相关。非浸渍型更常见于嗜铬细胞瘤、库欣综合征和睡眠呼吸暂停综合征，但在原发性醛固酮增多症患者中的患病率尚不清楚。因此，我们研究了16例原发性醛固酮增多症高血压患者和同等数量的原发性高血压患者的动态血压曲线。高醛固酮血症患者的醒-睡血压差与原发性高血压患者相似（15/14 ± 3/2 mmHg对14/9 ± 3/2 mmHg，P=NS）。两组中杓型和非杓型的患病率（根据两个不同的标准）相似。对12例原发性醛固酮增多症患者进行特定干预后（3例在手术切除肾上腺腺瘤后，9例在开始并滴定螺内酯治疗后）的重复动态血压监测显示，办公室血压（22/10 +/- 6/4 mm Hg，P<0.05）以及清醒和睡眠血压显著降低。然而，两项研究之间夜间血压下降的程度没有变化（17/16 +/- 3/3 vs 16/12 +/- 2/2 mm Hg，P=NS）。醒-睡差异与血清或尿醛固酮水平或醛固酮-肾素比值之间无相关性。在这项研究中，我们没有发现一组原发性醛固酮增多症高血压患者和对照组原发性高血压患者之间的觉醒-睡眠差异有任何差异。
A less-than-normal decline in nocturnal blood pressure (BP) has been associated with excessive hypertensive complications. This is concerning because secondary hypertension is often associated with this so-called nondipper BP profile. A nondipping pattern is more frequently found in the presence of pheochromocytoma, Cushing's syndrome, and sleep apnea syndrome, but the prevalence is unclear in patients with primary hyperaldosteronism. We therefore studied ambulatory BP profiles in 16 hypertensive patients with primary hyperaldosteronism and an equal number of essential hypertensive subjects. The awake-sleep BP difference of the hyperaldosteronism patients was similar to that of essential hypertensives (15/14 +/- 3/2 versus 14/9 +/- 3/2 mm Hg, P=NS). The prevalence of dippers and nondippers (according to two distinct criteria) in the two groups was similar. Repeat ambulatory BP monitoring in 12 subjects with primary hyperaldosteronism after specific intervention (3 after surgical removal of an adrenal adenoma and 9 after commencement and titration of spironolactone therapy) showed highly significant reductions in office BP (22/10 +/- 6/4 mm Hg, P<.05) and awake and sleep BP. However, the extent of nocturnal BP decline was unchanged between the two studies (17/16 +/- 3/3 versus 16/12 +/- 2/2 mm Hg, P=NS). There was no correlation between the awake-sleep difference and serum or urinary aldosterone levels or the aldosterone-to-renin ratio. In this study, we did not detect any differences in the awake-sleep differences between a group of hypertensives with primary hyperaldosteronism and a control group of essential hypertensives.