Obstructive Sleep Apnea and Cardiovascular Disease: Where Do We Stand?

Abstract

Obstructive sleep apnea is common in adults with cardiovascular disease. Accumulating evidence suggests an association between obstructive sleep apnea and cardiovascular disease independent of the traditionally recognized cardiovascular disease risk factors. Observational studies indicate that obstructive sleep apnea is a risk factor for development of cardiovascular disease and that alleviation of obstructive events with positive airway pressure may improve cardiovascular disease outcomes. However, recent randomized controlled trials have not supported the beneficial effect of positive airway pressure in cardiac populations with concomitant obstructive sleep apnea. Some evidence suggests that the relationship between obstructive sleep apnea and traditionally recognized cardiovascular disease risk factors is bidirectional, suggesting that patients with cardiovascular disease may also develop obstructive sleep apnea and that efficient treatment of cardiovascular disease may improve obstructive sleep apnea. Recent data also indicate that the apnea-hypopnea index, which is commonly used as a diagnostic measure of obstructive sleep apnea severity, has limited value as a prognostic measure for cardiovascular disease outcomes. Novel markers of obstructive sleep apnea-associated hypoxic burden and cardiac autonomic response seem to be strong predictors of adverse cardiovascular disease outcomes and response to treatment of obstructive sleep apnea. This narrative review and position paper from the Turkish Collaboration of Sleep Apnea Cardiovascular Trialists aims to update the current evidence about the relationship between obstructive sleep apnea and cardiovascular disease and, consequently, raise awareness for health professionals who deal with cardiovascular and respiratory diseases to improve the ability to direct resources at patients most likely to benefit from treatment of obstructive sleep apnea and optimize treatment of the coexisting cardiovascular diseases. Moreover, the Turkish Collaboration of Sleep Apnea Cardiovascular Trialists aims to contribute to strengthening the efforts of the International Collaboration of Sleep Apnea Cardiovascular Trialists in this context.

Figure 1.

A 10-minute long home sleep apnea test recording illustrating intermittent pauses in airflow (OA) in S position with concomitant drops in oxyhemoglobin saturation (SpO₂ levels (Desat) and fluctuations in the pulse rate. Of note, the snoring intensity (audio volume) reaches 100 dB, and breathing efforts during apneas are registered by the thoracic and abdominal belts indicating that the apneic events are obstructive. OA, obstructive apneas; S, supine.

Figure 2.

Relationships between obstructive sleep apnea and cardiovascular events.

Figure 3.

During systole, LV transmural pressure rises to 160 mmHg from 120 mmHg due to an increase of intrapleural negative pressure like −40 mmHg in OSA. This condition is equal to a high (e.g., 160 mmHg) blood pressure, aortic, and LV pressure such as in hypertension. The CPAP therapy decreases LV transmural pressure by increasing intrapleural pressure, like +10 mmHg, in patients with OSA. CPAP, continuous positive airway pressure; LV, left ventricle; OSA, obstructive sleep apnea.