Severity of Obstructive Sleep Apnea is Related to Aldosterone Status in Subjects with Resistant Hypertension

Obstructive sleep apnea (OSA) and hypertension are both independently associated with increased cardiovascular risk.1–7 Furthermore, approximately 50% of patients with OSA have a diagnosis of hypertension, whereas 30% of hypertensive patients have OSA.8–11 Recently published evidence-based hypertension management guidelines identified OSA as an important identifiable cause of hypertension.12 The association of OSA and hypertension is particularly marked among patients with resistant hypertension, with studies reporting an OSA prevalence of 80% to 85% in these patients.13,14 BRIEF SUMMARY Current Knowledge/Study Rationale: We previously described a significant correlation between plasma aldosterone concentration and severity of obstructive sleep apnea in patients with resistant hypertension. This investigation examines the relationship between aldosterone status and obstructive sleep apnea in patients with resistant hypertensive—with and without hyperaldosteronism. Study Impact: The positive relationship between hyperaldosteronism and severity of obstructive sleep apnea (OSA) observed in the current analysis supports the hypothesis that aldosterone excess contributes to the development of OSA. The results highlight the increased likelihood of hyperaldosteronism and OSA coexisting in patients with resistant hypertension and may explain, at least in part, the high prevalence of OSA in patients with resistant hypertension. Hyperaldosteronism is common in patients with resistant hypertension. Approximately 20% of patients with resistant hypertension have biochemical criteria consistent with primary aldosteronism.15–18 In patients with resistant hypertension in whom we had diagnosed hyperaldosteronism, we observed that many had been previously diagnosed with OSA. We, therefore, hypothesized that the 2 diseases may be mechanistically related, that is one contributing to the other. Our center noted increased aldosterone excretion in patients with resistant hypertension who had symptoms of OSA.19 We then showed that a significant correlation exists between plasma aldosterone concentration (PAC) and OSA severity in patients with resistant hypertension but not in normotensive control subjects.14 Although we cannot directly infer causality from these studies, these results are consistent with the hypothesis that aldosterone excess may contribute to worsening severity of OSA. To gain further insight into the association among resistant hypertension, OSA, and hyperaldosteronism, we evaluated the relationship between aldosterone levels and OSA severity in patients with resistant hypertension with and without hyperaldosteronism.