Obstructive Sleep Apnea and Cardiovascular Disease: Mechanisms, Diagnostics, and Emerging Therapeutic Approaches

Figure 1. Comparison of central sleep apnea (CSA) and obstructive sleep apnea (OSA) patterns. The diagram illustrates idealized differences in airflow and respiratory effort during apneic events. In CSA, there is no airway obstruction, and both chest and abdominal movements cease, indicating a lack of respiratory effort. OSA is characterized by airway obstruction with continued respiratory effort observed in the chest and abdomen without airflow. The highlighted section (red box) shows the absence of airflow in both conditions, with different respiratory efforts.

Figure 2. Mechanistic framework for obstructive sleep apnea and therapeutic targets. OSA arises from four overlapping endotypes: elevated upper airway collapsibility, impaired pharyngeal muscle responsiveness, low arousal threshold, and high loop gain. The effectiveness of targeted interventions including CPAP, hypoglossal nerve stimulation, and pharmacologic modulation may depend on the underlying endotype. Endotype-based phenotyping may help guide personalized OSA treatment strategies and improve therapeutic effectiveness. Created in BioRender. Kay, M. (2026) https://BioRender.com/rjvaf2n, accessed on 19 February 2026.

Figure 3. Pathophysiological mechanisms linking obstructive sleep apnea (OSA) to cardiovascular disease. The diagram illustrates how upper airway collapse in OSA leads to intermittent hypoxia, triggering a cascade of physiological responses including increased sympathetic activation, oxidative stress (ROS), and inflammation, contributing to endothelial dysfunction, platelet coagulation, and atherosclerosis. These responses increase the risk of cardiovascular comorbidities such as heart failure and atrial fibrillation.

Figure 4. Effects of continuous positive airway pressure (CPAP) therapy on sleep apnea parameters. The figure compares representative idealized physiological recordings before and after CPAP treatment. Pre-CPAP shows irregular airflow, ribcage/abdominal movements, fluctuating blood pressure (BP), and decreased oxygen saturation (SpO2). Post-CPAP demonstrates stabilized airflow, consistent ribcage/abdominal movements, normalized BP, and improved SpO2 levels, indicating effective management of sleep apnea symptoms.

Figure 5. Diagram of a typical continuous positive airway pressure (CPAP) system. The illustration depicts the components of a CPAP device, including the air filter, blower motor assembly, motor driver, microprocessor, and pressure sensor. Air is filtered and pressurized before being delivered through a nasal mask to the patient, maintaining an open airway during sleep.

Figure 6. Comparison of hypoglossal and phrenic nerve stimulation therapies for sleep apnea. The diagrams illustrate the anatomical placement of stimulation leads for each therapy, and the physiological changes in the illustrated idealized polysomnography signals. The therapy “on” sections highlight improved respiratory parameters, including airflow, nasal pressure, and oxygen saturation (SpO2), compared to the therapy “off” conditions.