High prevalence of obstructive sleep apnea among hypertensive patients with primary hyperaldosteronism

Recent reports indicate that primary hyperaldosteronism (PA) is a much more common cause of hypertension than previously thought. The reason for this increased prevalence of PA is unknown. Even though obstructive sleep apnea and hypertension are highly correlated, the mechanism by which sleep apnea increases blood pressure remains obscure. The current study was undertaken to determine if there is an association between PA and OSA among patients with resistant hypertension consistent with the hypothesis that OSA induces hyperaldosteronism. In consecutive patients referred to a university clinic for resistant hypertension, we determined the 24-hour urinary aldosterone excretion during high dietary salt ingestion and baseline plasma renin activity and plasma aldosterone in all subjects. Primary hyperaldosteronism was defined as a plasma renin activity was <1.0 ng/ml/hr and urinary aldosterone was >12 mcg/24-hr during high urinary sodium excretion (>200 mEq/24-hr). In addition, all patients completed the Berlin Questionnaire, a survey designed to identify patients at risk of having sleep apnea. Of the 117 patients evaluated, sleep apnea has been confirmed by polysomnographic evaluation (respiratory distress index ≥5 apnea/hypoapnea events per hour) in 32 patients. Forty-one patients had a low-probability of having sleep apnea based on their responses to the Berlin Questionnaire. Patients with confirmed sleep apnea were over 3 times more likely to have been diagnosed with hyperaldosteronism compared to patients at low-risk of having sleep apnea (50 vs. 16%), tended to lower plasma renin activity (0.7±0.8 vs. 2.0±4.2 ng/ml/hr) and had significantly greater urinary aldosterone excretion (16.6±12.2 vs. 9.4±7.2 mcg/24-hr, p<0.05). These data indicate a very high degree of association between sleep apnea and primary hyperaldosteronism suggesting that sleep apnea may contribute to the development of resistant hypertension by inducing hyperaldosteronism.