Abstract-Recent reports suggesting that the prevalence of primary hyperaldosteronism may be higher than historically thought have relied on an elevated plasma aldosterone concentration/plasma renin activity ratio to either diagnose or identify subjects at high risk of having primary hyperaldosteronism and have not included suppression testing of all evaluated subjects. In this prospective study of 88 consecutive patients referred to a university clinic for resistant hypertension, we determined the 24-hour urinary aldosterone excretion during high dietary salt ingestion, baseline plasma renin activity, and plasma aldosterone in all subjects. Primary hyperaldosteronism was confirmed if plasma renin activity was Ͻ1.0 ng/mL per hour and urinary aldosterone was Ͼ12 g/24-hour during high urinary sodium excretion (Ͼ200 mEq/24-hour). Eighteen subjects (20%) were confirmed to have primary hyperaldosteronism. The prevalence of hyperaldosteronism was similar in black and white subjects. Of the 14 subjects with confirmed hyperaldosteronism who have been treated with spironolactone, all have manifested a significant reduction in blood pressure. In this population, an elevated plasma aldosterone/plasma renin activity ratio (Ͼ20) had a sensitivity of 89% and a specificity of 71% with a corresponding positive predictive value of 44% and a negative predictive value of 96%. These data provide strong evidence that hyperaldosteronism is a common cause of resistant hypertension in black and white subjects. Key Words: hyperaldosteronism Ⅲ hypertension, essential Ⅲ blacks Ⅲ diuretics Ⅲ renin P rimary hyperaldosteronism (PA) has historically been thought to be an uncommon cause of hypertension, with an estimated prevalence of Ͻ2% among the general hypertensive population. Recent studies, however, have suggested that the prevalence of PA may be as high as 8% to 30% in selected hypertensive populations. 1-10 These reports have been based on either a high plasma aldosterone/plasma renin activity ratio (ARR) or a lack of suppression of plasma or urinary aldosterone in patients identified by an elevated ARR. As PA is generally remediable by treatment with an aldosterone antagonist or, in the case of adrenal adenoma, by adrenalectomy, knowing the true prevalence of PA in selected hypertension populations is clinically important for maximizing diagnosis and treatment.Prior studies determining the prevalence of PA have been based on an elevated ARR or confirmatory suppression testing in subjects preselected for a high ARR. The former approach would tend to overestimate the prevalence of PA, because patients with a falsely elevated ARR would be included, whereas the latter approach would underestimate the prevalence of PA because of the exclusion of patients with a falsely low ARR. Diagnosis of PA by confirmatory suppression testing of all evaluated patients would be necessary to overcome these limitations.The prevalence of PA has not been systematically determined in a population that has included a large proportion of African American subject...
Effective antihypertensive therapy has made a major contribution to the reductions in the morbidity and mortality of cardiovascular disease that have been achieved since the 1960s. However, blood-pressure control with conventional drugs has not succeeded in reducing cardiovascular disease risks to levels seen in normotensive persons. Drugs that inhibit or antagonize components of the renin-angiotensin-aldosterone system are addressing this deficiency by targeting both blood pressure and related structural and functional abnormalities of the heart and blood vessels, thus preventing target-organ damage and related cardiovascular events.
We conclude that low-dose spironolactone provides significant additive BP reduction in African American and white subjects with resistant hypertension with and without primary aldosteronism.
Background-Recent studies suggest that aldosterone may impair endothelium-dependent vascular function through suppression of nitric oxide formation. Assessments of forearm blood flow or arterial compliance suggest a similar effect in humans. The present study was designed to determine whether chronic aldosterone excess in subjects with resistant hypertension impairs endothelium-dependent vascular reactivity as indexed by direct assessment of brachial artery flow-mediated dilation (FMD). Methods and Results-Consecutive subjects (nϭ80) with resistant hypertension were prospectively evaluated with an early-morning ratio of plasma aldosterone to plasma renin activity and 24-hour urinary aldosterone and sodium. Changes in brachial artery diameter during reactive hyperemia were measured by high-resolution ultrasound. Hyperaldosteronism was diagnosed on the basis of a renin activity Ͻ1.0 ng · mL Ϫ1 · h
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