Obstructive Sleep Apnea–Induced Neurogenic Nocturnal Hypertension

Mar 1, 2021Hypertension (Dallas, Tex. : 1979)

Nighttime Nerve-Driven High Blood Pressure Caused by Obstructive Sleep Apnea: Could Kidney Nerve Treatment Help?

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Abstract

Obstructive sleep apnea (OSA) is associated with hypertension, characterized by high rates of masked hypertension and abnormal blood pressure patterns.

There is a bidirectional, causal relationship between OSA and hypertension.
OSA-related hypertension often features elevated nighttime blood pressure and a nondipper pattern.
Sympathetic activation due to hypoxia and hypercapnia is a key mechanism linking OSA and hypertension.
Continuous positive airway pressure is the standard treatment for OSA, yet its impact on blood pressure is modest.
Current evidence for antihypertensive treatments targeting sympathetic pathways in patients with both conditions is limited.
Renal sympathetic denervation may lead to meaningful reductions in blood pressure in patients with comorbid hypertension and OSA.

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There is a bidirectional, causal relationship between obstructive sleep apnea (OSA) and hypertension. OSA-related hypertension is characterized by high rates of masked hypertension, elevated nighttime blood pressure, a nondipper pattern of nocturnal hypertension, and abnormal blood pressure variability. Hypoxia/hypercapnia-related sympathetic activation is a key pathophysiological mechanism linking the 2 conditions. Intermittent hypoxia also stimulates the renin-angiotensin-aldosterone system to promote hypertension development. The negative and additive cardiovascular effects of OSA and hypertension highlight the importance of effectively managing these conditions, especially when they coexist in the same patient. Continuous positive airway pressure is the gold standard therapy for OSA but its effects on blood pressure are relatively modest. Furthermore, this treatment did not reduce the cardiovascular event rate in nonsleepy patients with OSA in randomized controlled trials. Antihypertensive agents targeting sympathetic pathways or the renin-angiotensin-aldosterone system have theoretical potential in comorbid hypertension and OSA, but current evidence is limited and combination strategies are often required in drug resistant or refractory patients. The key role of sympathetic nervous system activation in the development of hypertension in OSA suggests potential for catheter-based renal sympathetic denervation. Although long-term, randomized controlled trials are needed, available data indicate sustained and relevant reductions in blood pressure in patients with hypertension and OSA after renal denervation, with the potential to also improve respiratory parameters. The combination of lifestyle interventions, optimal pharmacological therapy, continuous positive airway pressure therapy, and perhaps also renal denervation might improve cardiovascular risk in patients with OSA.

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Obstructive Sleep Apnea–Induced Neurogenic Nocturnal Hypertension

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