Sleep-disordered breathing is very common and is associated with an increased 
risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two 
types of sleep apnea: obstructive and central. The objective of this review is 
to provide a broad perspective of the pathophysiological and clinical aspects of 
the two types of apnea and to discuss their cardiovascular adverse effects. The 
diagnosis of sleep apnea syndrome is based on polysomnography, and severity is 
measured with an apnea-hypopnea index that counts the total number of apneas per 
hour of sleep. Recent large epidemiologic studies have shown that sleep apnea 
affects about 16% of men and 5% of women between 30 and 65 years of age. 
Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal 
airway during sleep, snoring, vigorous inspiratory efforts causing frequent 
arousal, and excessive daytime drowsiness. Central sleep apnea with 
Cheyne-Stokes respiration is a form of periodic breathing with frequent periods 
of hyperventilation, and carries a poor prognosis in patients with heart 
failure. Obstructive apnea can also have substantial health consequences. 
Although the exact mechanism linking sleep apnea with cardiovascular disease is 
unknown, there is evidence that obstructive apnea is associated with a group of 
proinflammatory and prothrombic factors that are also important in the 
development of atherosclerosis. Nocturnal and daytime sympathetic activity is 
elevated after sleep apnea. Autonomic abnormalities include an increased resting 
heart rate, decreased cardiac rhythm activity, and increased blood pressure 
variability. Obstructive apnea is associated with endothelial dysfunction, 
increased C-reactive protein and cytokine expression, elevated fibrinogen levels 
and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, 
leukocyte adhesion and accumulation of endothelial cells are common in both 
obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood 
pressure, ventricular wall tension and afterload adversely affect ventricular 
function. Many studies have shown that patients with obstructive apnea have an 
increased incidence of daytime hypertension, and this syndrome is recognized as 
an independent risk factor for hypertension. Obstructive apnea is associated 
with myocardial ischemia (silent or symptomatic), acute coronary events, stroke 
and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and 
heart failure. Central sleep apnea is frequent in severe heart failure. Most 
heart failure patients with pulmonary congestion chronically hyperventilate 
because of stimulation of vagal irritant receptors and central and peripheral 
chemosensitivity. When PaCO2 falls below the threshold required to stimulate 
breathing, the central drive to respiratory muscles and air inflow ceases and 
central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke 
elevated sympathetic activity, increased afterload and elevated left ventricular 
transmural pressure, and promote the progression of heart failure. Tentative 
relationships have been identified between central apnea and markers of 
inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms 
trials showed that nocturnal use of positive airway pressure in patients with 
the two types of apnea alleviates symptoms, reduces sympathetic activity, 
improves ventricular function and quality of life, and reduces daytime 
drowsiness. More studies are needed to understand the mechanisms underlying the 
relationship between sleep apnea and cardiovascular disease, but clinicians 
should be aware of this link and should attempt to identify patients with these 
syndromes.