This article reviews the relationship between sleep apnea and cardiovascular disease (CVD), emphasizing the mechanisms linking the two conditions and the clinical consequences. Sleep apnea, particularly obstructive sleep apnea (OSA), is highly prevalent in patients with CVD and is associated with intermittent hypoxia, oxidative stress, sympathetic activation, and endothelial dysfunction. These factors contribute to the incidence and morbidity of hypertension, coronary heart disease (CHD), arrhythmia, heart failure (HF), and stroke. The article discusses the pathogenesis of OSA and central sleep apnea (CSA), highlighting the role of anatomic and physiological factors, such as obesity, upper airway dilator muscle dysfunction, and fluid accumulation around the upper airway. It also reviews the molecular signatures of sleep apnea, including oxidative stress and inflammatory cascades, and their impact on CVD. The article further explores the clinical consequences of sleep apnea, including arterial blood gas abnormalities, excessive arousals, altered autonomic activity, and negative intrathoracic pressure swings, which can lead to adverse cardiovascular outcomes. It emphasizes the importance of treating sleep apnea in patients with CVD, particularly those with hypertension, HF, stroke, and CHD. The use of continuous positive airway pressure (CPAP) therapy is highlighted as the most effective treatment for OSA, with evidence showing its benefits in reducing blood pressure, improving pulmonary hypertension, and reducing the risk of stroke and CV events. The article also discusses the role of CPAP in treating CSA, the potential benefits of exercise and weight loss as adjunct therapies, and the importance of personalized treatment approaches based on the underlying mechanisms of sleep apnea. Finally, the article suggests future research directions, including the need for randomized controlled trials to assess the impact of sleep apnea intervention on incident CVD and its associated morbidity and mortality. It also highlights the importance of phenotyping to tailor treatments to specific patient subgroups and the potential benefits of combining different therapeutic options to address multiple aspects of sleep apnea.This article reviews the relationship between sleep apnea and cardiovascular disease (CVD), emphasizing the mechanisms linking the two conditions and the clinical consequences. Sleep apnea, particularly obstructive sleep apnea (OSA), is highly prevalent in patients with CVD and is associated with intermittent hypoxia, oxidative stress, sympathetic activation, and endothelial dysfunction. These factors contribute to the incidence and morbidity of hypertension, coronary heart disease (CHD), arrhythmia, heart failure (HF), and stroke. The article discusses the pathogenesis of OSA and central sleep apnea (CSA), highlighting the role of anatomic and physiological factors, such as obesity, upper airway dilator muscle dysfunction, and fluid accumulation around the upper airway. It also reviews the molecular signatures of sleep apnea, including oxidative stress and inflammatory cascades, and their impact on CVD. The article further explores the clinical consequences of sleep apnea, including arterial blood gas abnormalities, excessive arousals, altered autonomic activity, and negative intrathoracic pressure swings, which can lead to adverse cardiovascular outcomes. It emphasizes the importance of treating sleep apnea in patients with CVD, particularly those with hypertension, HF, stroke, and CHD. The use of continuous positive airway pressure (CPAP) therapy is highlighted as the most effective treatment for OSA, with evidence showing its benefits in reducing blood pressure, improving pulmonary hypertension, and reducing the risk of stroke and CV events. The article also discusses the role of CPAP in treating CSA, the potential benefits of exercise and weight loss as adjunct therapies, and the importance of personalized treatment approaches based on the underlying mechanisms of sleep apnea. Finally, the article suggests future research directions, including the need for randomized controlled trials to assess the impact of sleep apnea intervention on incident CVD and its associated morbidity and mortality. It also highlights the importance of phenotyping to tailor treatments to specific patient subgroups and the potential benefits of combining different therapeutic options to address multiple aspects of sleep apnea.