Sleep Apnea: The Slept-Upon Cardiovascular Risk Factor

Abstract

Background: Obstructive sleep apnea (OSA) is prevalent and often underdiagnosed in cardiology. Worldwide, approximately 936 million adults aged 30-69 are affected by OSA, with the highest numbers in the USA, China, Brazil, and India. In cardiovascular clinics, OSA is found in about 40-80% of patients with hypertension, heart failure, coronary artery disease, atrial fibrillation, or stroke. Meta-analyses link OSA to nearly twice the risk of cardiovascular disease, stroke, and all-cause mortality. Continuous positive airway pressure (CPAP) therapy addresses the underlying mechanisms of OSA and enhances intermediate cardiovascular indicators. Materials and Methods: We conducted a narrative review using major medical search engines (PubMed, Embase, Cochrane) to examine recent statements, meta-analyses, large cohorts, and key trials. The review focused on the cardiovascular burden of sleep apnea and its pathophysiology-including arrhythmic, hemodynamic, vascular, and coagulation aspects-as well as the effects of CPAP on intermediate cardiovascular outcomes. We aimed to provide a synthesised overview of current cardiovascular evidence related to the burden and mechanisms of OSA, and to summarise the effects of continuous positive airway pressure (CPAP) on intermediate and clinical cardiovascular outcomes. Results: Intermittent hypoxia, sleep fragmentation, and major negative fluctuations in intrathoracic pressure create a clear pathway leading to adverse cardiovascular outcomes. This occurs through mechanisms like sympathetic activation, RAAS activation, endothelial dysfunction, oxidative stress, and inflammation, linking OSA to these health issues. Studies show that greater severity of OSA correlates with higher cardiovascular risk, including increased incidence and recurrence of AF, resistant hypertension, and new cases of heart failure. CPAP effectively lowers AHI and enhances nocturnal oxygen levels, as well as intermediate cardiovascular indicators such as blood pressure, sympathetic activity, and certain aspects of ventricular function, with clinical benefits most evident in adherent patients. Conclusions: OSA is a significant, modifiable risk factor for cardiovascular disease. Routine cardiovascular care should include targeted screening for OSA, especially in cases of resistant hypertension, atrial fibrillation, and heart failure, along with timely sleep testing and adherence-focused CPAP therapy, in addition to traditional risk-reduction methods.

Keywords: CPAP; cardiovascular involvement; sleep apnea.

Figure 1

OSA-related intermittent hypoxia, hypercapnia, large negative intrathoracic pressure swings and sleep fragmentation trigger sympathetic and RAAS activation, leading to endothelial dysfunction, inflammation, oxidative stress, and nocturnal blood-pressure surges. ↓: decrease, ↑: increase.