Obstructive sleep apnea (OSA) is a prevalent sleep disorder linked to significant cardiovascular morbidity and mortality. It is characterized by repeated episodes of upper airway obstruction during sleep, leading to intermittent hypoxia, sympathetic activation, and disrupted breathing. OSA is associated with various cardiovascular conditions, including hypertension, heart failure, atrial fibrillation, stroke, and coronary artery disease. The mechanisms underlying these cardiovascular effects include sympathetic activation, intermittent hypoxia, inflammation, and alterations in neural control mechanisms. These factors contribute to arrhythmias, hypertension, and heart failure. OSA also has differential effects based on gender and age, with females showing increased cardiovascular mortality and older individuals being more susceptible to its effects. OSA therapies, such as continuous positive airway pressure (CPAP), have been shown to reduce cardiovascular morbidity and improve outcomes in patients with heart failure and atherosclerosis. CPAP improves oxygenation, reduces sympathetic activation, and enhances rhythm control and blood pressure regulation. Other treatments, including oral appliances, surgical interventions like uvulopalatopharyngoplasty (UPPP), and hypoglossal nerve stimulation, are also used to manage OSA. Lifestyle modifications, such as weight loss, smoking cessation, and alcohol reduction, are effective in reducing OSA severity and its cardiovascular consequences. The Apnea-Hypopnea Index (AHI) is a key parameter for diagnosing and classifying the severity of OSA. Mild OSA is defined as an AHI of 5–14 events per hour, moderate as 15–29, and severe as ≥30. OSA significantly increases the risk of cardiovascular events, including heart failure, stroke, and coronary artery disease. Effective management of OSA through CPAP and other therapies can reduce cardiovascular burden and improve long-term outcomes. The interplay between OSA and cardiovascular disease is complex, and understanding these mechanisms is crucial for developing targeted therapeutic strategies.Obstructive sleep apnea (OSA) is a prevalent sleep disorder linked to significant cardiovascular morbidity and mortality. It is characterized by repeated episodes of upper airway obstruction during sleep, leading to intermittent hypoxia, sympathetic activation, and disrupted breathing. OSA is associated with various cardiovascular conditions, including hypertension, heart failure, atrial fibrillation, stroke, and coronary artery disease. The mechanisms underlying these cardiovascular effects include sympathetic activation, intermittent hypoxia, inflammation, and alterations in neural control mechanisms. These factors contribute to arrhythmias, hypertension, and heart failure. OSA also has differential effects based on gender and age, with females showing increased cardiovascular mortality and older individuals being more susceptible to its effects. OSA therapies, such as continuous positive airway pressure (CPAP), have been shown to reduce cardiovascular morbidity and improve outcomes in patients with heart failure and atherosclerosis. CPAP improves oxygenation, reduces sympathetic activation, and enhances rhythm control and blood pressure regulation. Other treatments, including oral appliances, surgical interventions like uvulopalatopharyngoplasty (UPPP), and hypoglossal nerve stimulation, are also used to manage OSA. Lifestyle modifications, such as weight loss, smoking cessation, and alcohol reduction, are effective in reducing OSA severity and its cardiovascular consequences. The Apnea-Hypopnea Index (AHI) is a key parameter for diagnosing and classifying the severity of OSA. Mild OSA is defined as an AHI of 5–14 events per hour, moderate as 15–29, and severe as ≥30. OSA significantly increases the risk of cardiovascular events, including heart failure, stroke, and coronary artery disease. Effective management of OSA through CPAP and other therapies can reduce cardiovascular burden and improve long-term outcomes. The interplay between OSA and cardiovascular disease is complex, and understanding these mechanisms is crucial for developing targeted therapeutic strategies.