How does Obstructive Sleep Apnea (OSA) contribute to Hypertension (HTN)?

From the Guidelines

Obstructive sleep apnea (OSA) significantly contributes to the development and exacerbation of hypertension (HTN) through various mechanisms, including intermittent hypoxia, sympathetic nervous system activation, and oxidative stress, as supported by the most recent evidence 1. The relationship between OSA and HTN is complex and bidirectional. OSA can lead to HTN due to the repeated episodes of upper airway obstruction during sleep, causing intermittent hypoxia and hypercapnia, which triggers sympathetic nervous system activation 1. This increased sympathetic activity persists even during waking hours, leading to peripheral vasoconstriction and elevated blood pressure. Additionally, OSA disrupts normal sleep architecture, causing sleep fragmentation and preventing the natural nocturnal blood pressure dipping that typically occurs during healthy sleep.

The intermittent hypoxia associated with OSA also generates oxidative stress and systemic inflammation, damaging vascular endothelium and reducing nitric oxide availability, which impairs vasodilation 1. OSA activates the renin-angiotensin-aldosterone system, promoting fluid retention and vasoconstriction. These mechanisms create a vicious cycle where OSA worsens hypertension, and hypertension can exacerbate OSA by contributing to upper airway edema. Effective treatment of OSA with continuous positive airway pressure (CPAP) therapy can significantly reduce blood pressure in many patients, highlighting the causal relationship between these conditions.

Key points to consider:

• OSA is associated with a 70% relative increased risk of cardiovascular morbidity and mortality 1
• Screening for and treating OSA in patients with chronic coronary artery disease and hypertension may result in decreased cardiac events and cardiac death 1
• CPAP therapy can reduce blood pressure in patients with OSA, with benefits seen even with use for less than 4 hours per night 1
• The safety of CPAP therapy has been established, with primarily mild adverse effects 1

From the Research

Mechanisms of Obstructive Sleep Apnea (OSA)-Related Hypertension

• Sympathetic activity due to intermittent hypoxia and/or fragmented sleep is a key mechanism triggering the elevation in blood pressure in OSA 2.
• The pathophysiologic mechanism of the relationship between OSA and hypertension is due to the distinctive pattern of intermittent hypoxia seen in OSA, which increases sympathetic tone, oxidative stress, inflammation, and endothelial dysfunction 3.
• OSA-related hypertension is characterized by resistant hypertension, nocturnal hypertension, abnormal blood pressure variability, and vascular remodeling 2.

Treatment of OSA-Related Hypertension

• Continuous positive airway pressure (CPAP) therapy is effective at lowering blood pressure, but the magnitude of the decrease in blood pressure is relatively modest 2, 4.
• Antihypertensive medications targeting sympathetic pathways or the renin-angiotensin-aldosterone system have theoretical potential in OSA-related hypertension 2, 5.
• Beta-blockers and renin-angiotensin system inhibitors may be effective in the management of OSA-related hypertension, but current evidence is limited 2, 5.
• Other potential treatments for OSA-related hypertension include angiotensin receptor-neprilysin inhibitor (ARNI), sodium-glucose cotransporter 2 inhibitors (SGLT2i), and glucose-dependent insulinotropic polypeptide receptor/glucagon-like peptide-1 receptor agonist (GIP/GLP-1 RA) 2.

Importance of Screening for OSA in Hypertensive Patients

• OSA should be considered as part of the workup of patients with hypertension 3.
• Screening for OSA is particularly important in patients with refractory hypertension, as OSA is a common comorbidity in these patients 6.
• Home sleep studies are noninferior to formal polysomnography for OSA diagnosis, making it easier to screen for OSA in hypertensive patients 6.