Cardiovascular Consequences of Obstructive Sleep Apnea

Christopher J. Lettieri, MD


May 14, 2010

In This Article

Cardiovascular Effects of OSA


The causal link between OSA and systemic hypertension has been clearly established. Several studies have shown that sleep apnea increases the relative risk for hypertension, independent of other confounding factors.[1,2,3,4] In a cross-sectional analysis of more than 6000 patients, the Sleep Heart Health Study showed a linear relationship between mean systolic and diastolic blood pressures and OSA severity.[1] Likewise, the prevalence of hypertension linearly increased with the presence and severity of OSA.[1,2] A large Canadian population-based study found that each apneic event per hour increased the odds of hypertension by 1%, and each 10% reduction in nocturnal oxygen saturation increased the likelihood of hypertension developing by 13%.[2]

Approximately 50% of patients with OSA have hypertension, compared with only 30% of the general public. Because of the strength of evidence linking OSA with the development of hypertension, the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VII) now lists sleep apnea as a significant cause of secondary hypertension.[3]

Pulmonary Hypertension

OSA results in hemodynamic derangements and dysfunction of the pulmonary vasculature and may contribute to the progression of underlying pulmonary hypertension. The 2004 American College of Chest Physicians (ACCP) consensus panel found that pulmonary hypertension occurred in 17% to 53% of individuals with OSA, and a review from Johns Hopkins found that 82% of patients with pulmonary hypertension had underlying sleep-disordered breathing.[4] The nocturnal desaturation, hypoxic-vasoconstriction, reperfusion injuries, ventilatory instability, impaired nitric oxide synthesis, endothelial dysfunction, and vascular remodeling that result from repetitive obstructive respiratory events can lead to the development of pulmonary vascular disease. However, whether OSA independently causes clinically significant pulmonary hypertension remains controversial. Thus, the current ACCP guidelines do not recommend evaluating patients with OSA for pulmonary hypertension unless it is clinically suspected.

Ischemic Heart Disease

Because of overlapping risk factors, the true association between OSA and coronary artery disease (CAD) remains difficult to prove, especially in the presence of mild disease. However, more substantial evidence links CAD with moderate-to-severe OSA. Several studies have suggested that the prevalence of CAD is 3 to 5 times higher in patients with OSA compared with control populations.[7,18] More importantly, long-term observational studies found that severe OSA significantly increases the risk for both fatal and nonfatal cardiovascular events.[6,19] OSA may be an independent risk factor for CAD. OSA causes or contributes to hypertension, arterial noncompliance, atherosclerosis, and glucose intolerance. Moreover, OSA produces carotid arterial wall thickness in a dose-response manner, which has been shown to be a marker of cardiovascular disease and a predictor of morbidity and mortality[18] Similarly, among patients with known CAD, the respiratory disturbance index was the only independent predictor of mortality in a 5-year study.[20] Ablation of obstructive respiratory events during sleep by continuous positive airway pressure (CPAP) has been shown to decrease the risk for cardiovascular events and prevent the development of new ischemic heart disease.[20] Given the growing body of evidence, it appears that OSA is an independent contributor to ischemic heart disease. The treatment of OSA should mitigate this increased risk; however, the true effects on cardiovascular morbidity and mortality remain controversial.

Heart Failure

Underlying sleep-disordered breathing is highly prevalent among patients with heart failure, and obstructive respiratory events are common in individuals with systolic and diastolic dysfunction.[8,9,10] Numerous risk factors for OSA and heart failure overlap, as they do between OSA and CAD. The role of sleep-disordered breathing in the development of left ventricular dysfunction is not well-defined. However, a prospective study of patients with left ventricular failure found concurrent sleep apnea in 50% of patients.[8] Furthermore, CPAP has been shown to be effective in patients with heart failure, regardless of the presence of underlying OSA. Randomized controlled trials have shown that treatment of OSA with CPAP is associated with significant improvements in cardiac function, sympathetic activity, and quality of life.[9,10] Similarly, patients with severe OSA experience a reduction in left ventricular hypertrophy after 6 months of CPAP therapy.[10] In the Canadian Positive Airway Pressure study, CPAP improved nocturnal oxygenation, increased left ventricular function, lowered norepinephrine levels, and improved functional capacity among patients with central sleep apnea and heart failure.[21] Unfortunately, CPAP therapy did not improve survival. Given the increasing awareness of this association, it is prudent to assess for OSA in individuals diagnosed with heart failure, because treatment of the underlying sleep-disordered breathing may improve cardiac function and quality of life.


Cardiac arrhythmias, especially tachy-brady syndrome, ventricular ectopy, and atrial fibrillation are commonly identified in patients with OSA.[11,12,13] The Sleep Heart Health Study noted that patients with sleep-disordered breathing have a higher likelihood of having complex arrhythmias compared with control patients.[12] Specifically, these patients had a fourfold increase in atrial fibrillation, a threefold increase in nonsustained ventricular tachycardia, and a twofold increase in complex ventricular ectopy.[12] These rhythm disturbances likely correlate with nocturnal hypoxia, sleep fragmentation, and elevated sympathetic tone. Treatment of OSA in patients with known congestive heart failure has been shown to reduce the frequency of premature beats, which in turn may decrease the morbidity of ventricular arrhythmias.[22] In addition, CPAP therapy has been shown to reduce the rate of arrhythmias even after controlling for heart failure and other independent variables.[13]


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