Key result
Primary hyperaldosteronism in hypertensive patients was not associated with a difference in awake-sleep blood pressure decline compared to essential hypertension.
Why the study?
Does primary hyperaldosteronism alter circadian blood pressure variation compared to essential hypertension, and does specific intervention change this pattern?
Observational (n=32)
Does primary hyperaldosteronism alter circadian blood pressure variation compared to essential hypertension, and does specific intervention change this pattern?
Primary hyperaldosteronism does not appear to alter the circadian blood pressure dipping pattern compared to essential hypertension, and targeted treatment does not change the extent of nocturnal BP decline.
Answers are grounded in this paper and cite their sources.
No difference in nocturnal BP dipping observed; leaves open whether primary aldosteronism or its treatment alters circadian patterns.
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.
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Mansoor et al. (1998) conducted an observational in Hypertension with primary hyperaldosteronism (n=32). Primary hyperaldosteronism vs. Essential hypertension was evaluated on Awake-sleep blood pressure difference (p=NS). Primary hyperaldosteronism in hypertensive patients was not associated with a difference in awake-sleep blood pressure decline compared to essential hypertension.
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