Epidemiologic studies show that sleep apnea increases risks for cardiovascular disease independently of individuals’ demographic characteristics or risk markers i.e., smoking, alcohol, obesity, diabetes, dyslipidemia, atrial fibrillation, and hypertension. Individuals with severe sleep apnea are at increased risk for pulmonary arterial hypertension. The underlying mechanisms explaining associations between obstructive sleep apnea and pulmonary arterial hypertension are not entirely delineated. Several intermediary mechanisms might be involved including sustained sympathetic activation, intrathoracic pressure changes, and oxidative stress. Other abnormalities such as disorders in coagulation factors, endothelial damage, platelet activation, and increased inflammatory mediators might also play a role in the pathogenesis of pulmonary hypertension and cardiovascular disease. Linkage between obstructive sleep apnea and pulmonary arterial hypertension is corroborated by evidence that treatment of sleep apnea with continuous positive airway pressure reduces systolic blood pressure, improves left ventricular systolic function, and diminishes platelet activation. Several systematic studies are necessary to explicate complex associations between sleep apnea and pulmonary hypertension.