Primary aldosteronism and obstructive sleep apnea in hypertension: interplay, target organ damage, and clinical management

Figures

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  Figure 1. Schematic diagram depicting the pathophysiology and clinical consequences of obstructive sleep apnea. The diagram begins with nocturnal upper-airway collapse, which produces intermittent hypoxia and hypercapnia, intrathoracic pressure changes, and sleep-fragmenting arousals. These events increase sympathetic activity and norepinephrine release, oxidative stress, and inflammatory mediators such as TNF-alpha and IL-6. The resulting endothelial and autonomic dysfunction may contribute to cardiovascular disease, metabolic dysfunction, and impaired attention or memory. OSA, obstructive sleep apnea.

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  Figure 2. Pathophysiological mechanisms and clinical management pathways link primary aldosteronism (PA), and obstructive sleep apnea (OSA) to hypertension-mediated organ damage and cardiovascular-renal outcomes. The upper section shows pathways that may connect PA and OSA with organ damage. PA causes aldosterone excess and sodium retention. OSA causes intermittent hypoxia, arousal, sympathetic activation, and intrathoracic pressure changes. These processes promote inflammation, oxidative stress, endothelial injury, and damage involving the brain, heart, vasculature, and kidneys. The lower section summarizes clinical evaluation and treatment. PA evaluation uses the aldosterone-to-renin ratio, with confirmation and subtype testing when indicated. OSA evaluation uses PSG or HSAT in appropriate patients. Treatment pairs PA-directed adrenalectomy or MRA therapy with OSA-directed positive airway pressure, weight management, and control of cardiovascular risk. Blood pressure and intermediate organ measures may improve, but long-term outcome data for combined treatment remain limited. ARR, aldosterone-to-renin ratio; CPAP, continuous positive airway pressure; MRA, mineralocorticoid receptor…