Obstructive sleep apnea (OSA)-induced biological changes include intermittent hypoxia, intermittent hypercapnia, intrathoracic pressure changes, sympathetic activation and sleep fragmentation. OSA can cause metabolic dysregulation, endothelial dysfunction, systemic inflammation, oxidative stress and hypercoagulation, and neurohumoral changes. There is evidence suggesting that OSA is independently associated with metabolic syndrome. OSA has been shown to increase the risk for systemic hypertension, pulmonary vascular disease, ischemic heart disease, cerebral vascular disease, congestive heart failure and arrhythmias. Although there are evidences accumulating that there may be a causal relationship between OSA and cardiovascular disorders, there is a need for more data from randomized controlled intervention trials to confirm this relationship. Many risk factors of OSA (age, male gender and obesity) are also known risk factors for cardiovascular disease. Severe OSA-hypopnea significantly increases the risk of fatal and nonfatal cardiovascular events in both men and women, and continuous positive airway pressure treatment reduces this risk in both. Neurocognitive consequences of OSA include daytime sleepiness, loss of alertness, memory deficit, reduced vigilance, impaired executive function, increased risk for automobile and occupational accidents, and decreased quality of life.