Obstructive sleep apnea and cardiovascular disease in adults

Author:: Reena Mehra, MD, MS, FCCP, FAASM, FAHA, ATSF
Section Editor:: Nancy Collop, MD
Deputy Editor:: Geraldine Finlay, MD

Literature review current through: Apr 2025. | This topic last updated: Feb 27, 2025.

INTRODUCTION —

Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder characterized by repetitive episodes of upper airway collapse resulting in reduced inspiratory airflow that is complete (apnea) or partial (hypopnea). Patients with OSA are at risk for several cardiovascular disorders that are independent of the confounding influence of obesity, which is common in this population.

The association between OSA and cardiovascular disease and the potential impact of OSA-specific therapy on cardiovascular outcomes are discussed here. The evaluation and management of sleep-related breathing disorders in patients with heart failure and stroke are discussed separately. (See "Sleep-disordered breathing in heart failure" and "Sleep-related breathing disorders and stroke".)

PATHOPHYSIOLOGY —

Several mechanisms may underlie the pathogenesis of cardiovascular disorders in OSA (figure 1) [1]:

●Recurrent upper airway obstruction during sleep is associated with intermittent hypoxemia, possibly hypercapnia, alterations in intrathoracic pressure, and recurrent microarousals. The resulting hemodynamic, autonomic, and metabolic effects; systemic inflammation; and oxidative stress may contribute to the pathogenesis of cardiovascular diseases in OSA [2].

●OSA is associated with a significant increase in sympathetic activity during sleep, which contributes to the loss of the nocturnal decrease in blood pressure and heart rate, eventually leading to systemic hypertension [3]. Increased sympathetic activity appears to be induced through a variety of different mechanisms, including chemoreflex stimulation by hypoxemia and hypercapnia, baroreflexes, pulmonary afferents, impairment in venous return to the heart, alterations in cardiac output, and possibly the arousal response.

●Endothelial dysfunction due to hypoxemia may also play a role [4]. Females with OSA may have increased proclivity to altered endothelial responses [5].

The pathogenesis of OSA and central sleep apnea are discussed separately. (See "Pathophysiology of upper airway obstruction in obstructive sleep apnea in adults" and "Central sleep apnea: Pathogenesis" and "Sleep-disordered breathing in heart failure", section on 'Pathogenesis'.)

ACUTE CARDIOVASCULAR EVENTS —

Severe and moderate OSA is a significant risk factor for acute cardiovascular morbidity and mortality including myocardial infarction, acute coronary syndrome, and stroke. However, based upon some existing clinical trials, positive airway pressure (PAP) therapy does not appear to impact aggregate cardiovascular events when considered as a composite outcome.

Clinical evidence — Severe and moderate OSA is a well-established risk factor for acute cardiovascular events even after adjusting for confounding variables [6-11]. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Complications'.)

●Increased risk of acute cardiovascular events – Evidence supports that severe and moderate (but probably not mild) OSA is associated with an increased risk for acute cardiovascular events.

This is best supported by a prospective cohort study that followed 1651 male patients for a mean of 10 years [9]. Patients with untreated severe OSA (mean apnea-hypopnea index [AHI] of 43 events per hour of sleep) had a higher incidence of fatal and nonfatal cardiovascular events than untreated patients with mild-moderate OSA, simple snorers, and healthy participants. Cardiovascular events included myocardial infarction, acute coronary syndrome, and stroke.

Subsequent studies (including the Sleep Heart Health Study that included patients free of baseline ischemic heart disease) also reported similar findings among patients with untreated severe OSA, compared with patients without OSA [6,7,12-14].

●OSA exacerbates pre-existing coronary artery disease – In a prospective cohort study, polysomnography was performed on 89 consecutive patients who had undergone a percutaneous coronary intervention for acute coronary syndrome [15]. OSA (defined as AHI ≥10 events per hour of sleep) was detected in over half. During a mean follow up of 227 days, the incidence of major adverse cardiac events (cardiac death, reinfarction, target vessel revascularization) was higher among patients with OSA than those without OSA (adjusted hazard ratio [HR] 11.6, 95% CI 2.2-62.2).

●Coronary artery disease may worsen OSA – The impact of coronary artery disease on OSA was demonstrated by a prospective cohort study of 2721 individuals without known cardiovascular disease who were followed for a mean of five years and had polysomnography performed at baseline and at five years [16]. Among the 57 patients who had a myocardial infarction during the study, the AHI increased a mean of 6.37 events per hour of sleep compared with only 2.71 events per hour of sleep among those who had not had a myocardial infarction.

●Possible sex differences – Sex-specific differences have been observed. In males aged 40 to 70 years, severe OSA (AHI >30) predicted a greater likelihood of coronary artery disease than milder disease (AHI <5) [17]. Subcohort analysis also identified that females with OSA had higher troponin-T levels, greater left ventricular mass index, and higher risk of heart failure and death compared with male patients with OSA.

Impact of treatment — Several randomized trials and meta-analyses have examined the effect of PAP therapy on major adverse cardiovascular events (eg, cardiovascular mortality, acute myocardial infarction, stroke). While earlier retrospective analyses suggested possible benefit [18], most randomized trials and meta-analyses since then have not shown a convincing benefit in the reduction of cardiovascular events when considered as a composite outcome [19-27].

This lack of benefit is observed despite improvement in sleep-related respiratory events, such as the AHI, daytime sleepiness, blood pressure control, and biomarkers of cardiovascular stress. However, these studies had small sample sizes, included heterogeneous populations (eg, sleepy or nonsleepy, varying levels of OSA severity and adherence), and had limited observation periods of up to four years. Thus, it remains unclear whether considering larger sample sizes of specific populations (eg, severe OSA) with longer duration of follow-up and adequate PAP adherence may enhance the ability to detect significant cardiovascular benefit.

Specific clinical and physiologic subphenotypes may better identify those with OSA who would most benefit from PAP therapy (eg, sleepiness, sleep apnea-specific hypoxic burden, heart rate arousal response) [28-30].

Data include the following:

●Two meta-analyses of 9 to 10 randomized trials reported PAP treatment in patients with OSA did not result in a reduction in the risk of major cardiovascular events (acute coronary events, myocardial infarction, stroke, heart failure), cardiovascular deaths, or all-cause death when compared with no treatment or sham [23,24]. The lack of benefit was reported despite OSA severity as well as duration of therapy. Several randomized trials support this lack of benefit in both sleepy [22] and nonsleepy [19-21,25] patients with OSA.

●A 2023 meta-analysis that used individual-level participant data from three randomized trials considered at low risk of bias (4186 patients) also reported that the rate of major cardiovascular and cerebrovascular events were similar when patients with OSA on PAP therapy were compared with patients not on PAP therapy [26]. However, a reduced risk of events was associated with good adherence to continuous PAP (≥4 hours per night; HR 0.69, 95%CI 0.52-0.92). Whether the latter finding is due to the "healthy adherer effect" is unknown.

●The effect of PAP alternatives such as oral appliances and hypoglossal nerve stimulation therapy on cardiovascular outcomes is unclear.

HYPERTENSION —

Hypertension and OSA frequently coexist. While positive airway pressure (PAP) therapy consistently reduces blood pressure, this benefit has not been shown to lower the rate of associated acute cardiovascular events. (See 'Impact of treatment' below and 'Acute cardiovascular events' above.)

Clinical evidence — An abundance of evidence supports a relationship between OSA and hypertension.

●Increased prevalence of hypertension in OSA – Approximately 50 percent of patients with OSA have coexisting hypertension. Observational data suggest that the severity of OSA during rapid eye movement (REM) sleep is more strongly associated with hypertension than OSA severity during non-REM sleep [31].

Population-based studies consistently find an increased prevalence of hypertension in patients with OSA compared with patients who do not have OSA, even after controlling for potential confounding factors such as age and obesity [32-37]. The association between hypertension and OSA has been noted across a variety of patient groups, including the general adult population, older adult patients [38], those with spinal cord injury [39], and stroke survivors [40].

The risk of incident hypertension also appears to be increased in OSA. Prospective longitudinal studies have demonstrated an increased risk of incident hypertension in patients with OSA who are normotensive at baseline [32,41], although this finding has not been consistent [42,43].

OSA may impact systolic and diastolic values differently. One study found that OSA is more strongly associated with isolated diastolic or combined systolic/diastolic hypertension compared with systolic hypertension [44]. However, this finding is not consistent.

Patients with resistant hypertension have a very high prevalence of OSA. These data are discussed separately (see "Definition, risk factors, and evaluation of resistant hypertension", section on 'Obstructive sleep apnea').

●Dose-dependent relationship – Most studies support a dose-dependent association between the severity of OSA and the likelihood of hypertension [32-38,43,45]. As an example, a prospective cohort study of 709 patients estimated that patients with mild OSA (apnea-hypopnea index [AHI] of 5 to 15 events per hour of sleep) had twice the risk of newly identified incident systemic hypertension compared with those with an AHI of 0 (adjusted odds ratio [OR] 2.03, 95% CI 1.29-3.17) while participants with an AHI of ≥15 events per hour of sleep had nearly three times the risk (adjusted OR 2.89, 95% CI 1.46-5.64) [32].

●Loss of diurnal pattern – In patients with OSA, blood pressure is often most elevated in the morning. This phenomenon is likely due to the loss of the normal pattern of blood pressure reduction during sleep (ie, a nondipping blood pressure) [46], even in those with established cardiovascular disease or on antihypertensive therapy [47].

Impact of treatment — Randomized trials and meta-analyses have found that PAP reduces systemic blood pressure, regardless of whether the patients are hypertensive at baseline or have resistant hypertension [41,48-63]. However, while consistent, the impact is relatively small and does not render a patient normotensive. In addition, PAP therapy, does not obviate the need for antihypertensive medication and may not benefit those without excessive daytime sleepiness (EDS) or with longstanding controlled hypertension or mild OSA.

Data to support efficacy include the following:

●PAP reduces blood pressure measurements – The reduction in systemic blood pressure due to PAP therapy is usually small. In a 2014 meta-analysis that included 30 randomized trials and over 1900 patients, PAP therapy was associated with a mean net lowering in systolic blood pressure of 2.6 mmHg [60]. While this reduction is modest, it has been shown to be clinically significant in the prevention of cardiovascular events in patients with non-OSA [64]. However, the same clinical significance has not been shown in OSA patients.

Uncontrolled hypertension, severity of OSA, and presence of EDS may predict a blood pressure response to PAP.

•Several meta-analyses using patient-level data found that the presence of uncontrolled hypertension at baseline was an important predictor of reduction in blood pressure with PAP therapy [62,63]. One trial reported that PAP therapy lowered systolic blood pressure by 2 to 3 mmHg in normotensive patients and 6 to 7 mmHg in hypertensive patients [25].

•Another study reported a greater decrease in blood pressure among those with more severe OSA compared with those who have moderate or mild OSA [48].

•Most studies that show benefit are limited to OSA patients with EDS. Studies that have evaluated patients without EDS have found no reduction in the blood pressure or incidence of hypertension following the initiation of PAP [19,65-67].

The antihypertensive benefit of PAP therapy appears to be long-lasting in patients with moderate to severe OSA treated with PAP therapy. However, PAP withdrawal may be associated with a rebound increase in blood pressure [68].

Although the impact of PAP therapy on reducing systemic blood pressure has been fairly consistent, findings have not been universal [65,66,69-71]. The conflicting results may be due to methodological differences among the trials, including differences in study populations (symptomatic versus asymptomatic, OSA severity), cointerventions (eg, antihypertensive regimens), PAP adherence rates, sample sizes, outcome measures (single time point or 24-hour blood pressure), and durations of follow-up [19,48,65-68,72-74].

●The impact of PAP therapy appears to be less than that of antihypertensive medication – In a randomized crossover trial of 23 patients with both untreated hypertension and untreated OSA, antihypertensive medication lowered mean 24-hour blood pressure significantly more than PAP therapy (-9 versus -2.1 mmHg) [75]. Moreover, for patients whose blood pressure was not controlled with PAP or antihypertensive medication, an extended trial of treatment that combined the two therapies showed further significant reduction in blood pressure.

●Non-PAP therapies also decrease blood pressure – The effects of alternative therapies (eg, oral appliances or upper airway surgery) on blood pressure are less well studied but suggest similar benefit [57,59,76-78]. As examples:

•One meta-analysis of 51 studies of OSA patients with hypertension reported that compared with patients on placebo or not receiving therapy, mandibular advancement devices were associated with a significant reduction in systolic blood pressure (SBP; -2.1 mmHg, 95% CI -0.8 to -3.4) and diastolic blood pressure (DBP; -1.9 mmHg, 95% CI -0.5 to -3.2) [59]. In addition, the level SBP and DBP reduction was similar to that reported in patients treated with continuous PAP. (See "Oral appliances in the treatment of obstructive sleep apnea in adults".)

•A randomized trial of 181 OSA patients with hypertension demonstrated a more pronounced reduction of systolic and mean artery pressures with six months of PAP therapy plus a weight loss intervention compared with either approach alone [76].

•Weight loss alone induced by tirzepatide has also resulted in significant improvement in blood pressure control. These data are described separately. (See "Obstructive sleep apnea: Overview of management in adults", section on 'Weight loss pharmacotherapy'.)

•Limited data show that hypoglossal nerve stimulation does not significantly reduce blood pressure compared with PAP therapy [79].(See "Hypoglossal nerve stimulation for adult patients with obstructive sleep apnea".)

CARDIAC ARRHYTHMIAS —

In OSA, the most common sustained arrhythmia reported is atrial fibrillation (AF). Other rhythm disturbances occur less commonly [80].

Atrial fibrillation — There is a strong association between OSA and AF, but the impact of positive airway pressure (PAP) therapy on AF burden is unclear.

Clinical evidence — Evidence supports an increased risk of AF and AF recurrence in OSA, particularly in patients with severe disease.

●Increased risk of AF in OSA – Studies have found an increased, up to fourfold, prevalence of AF in patients with OSA compared with patients without OSA [81-83]. The association appears to be independent of obesity and other confounding variables, although this finding has not been universal [84]. In a study of 400 patients with moderate to severe OSA, the prevalence of AF was 3 percent, which was approximately threefold higher than the expected prevalence in the general population. In another large cross-sectional study, there was an increased prevalence of AF in patients with sleep-disordered breathing by polysomnography compared with those without sleep-disordered breathing, which was independent of age, sex, body mass index, and prevalent cardiovascular disease (5 versus 1 percent; odds ratio 4, 95% CI 1-15.7) [81].

The risk of incident AF also appears to be higher in OSA. In a large clinic-based cohort, nocturnal hypoxemia predicted a threefold increased risk of incident AF in those <65 years of age, even after adjusting for obesity [85]. Another retrospective cohort study of nearly 7000 middle-aged adults demonstrated that those with an apnea-hypopnea index (AHI) >5 events per hour had a 55 percent increased risk of incident AF over a median follow-up period of 12 years [86]. Prospective data involving older male patients support an approximate twofold increase in odds of AF associated with baseline central sleep apnea (CSA) or Cheyne-Stokes respirations over a 6.5-year mean follow-up period [81].

OSA also appears to be a risk factor for recurrent AF after cardioversion or ablation. In a meta-analysis of six observational studies, a diagnosis of OSA increased the risk of recurrent AF after radiofrequency catheter ablation by 25 percent [87]. Other meta-analyses have shown up to a 57 percent risk of recurrence [88-91].

Although not definitive, support for an immediate causal temporal relationship of respiratory events (mainly hypopneas) preceding paroxysms of AF has been demonstrated [92]. These findings suggest that discrete episodes of upper airway compromise may lead to proximate arrhythmia generation.

●Possible dose response – Rates appear more prevalent in those with severe OSA. A study comprised of nearly 3000 older male patients reported that increasing severity of OSA was associated with increasing prevalence of AF [93]. Such findings were more pronounced in CSA compared with OSA.

●Risk of OSA higher in those with AF – Cohort studies report that the prevalence of OSA in patients with AF is much higher than in the general population, with estimates ranging from 30 to 80 percent [82,94]. Most, but not all, studies have also found that the association is independent of shared risks factors, such as increased age, obesity, hypertension, and heart failure. (See "Epidemiology, risk factors, and prevention of atrial fibrillation", section on 'Obstructive sleep apnea'.)

Impact of treatment — Whether treatment of OSA improves AF burden and other outcomes is unclear and data are conflicting.

One meta-analysis reported a 42 percent reduction in the risk of AF with PAP therapy (pooled risk ratio 0.58, 95% CI 0.47-0.7) [89], the benefit of which was greatest in those who also underwent cardioversion or ablation [90,91]. (See "Atrial fibrillation: Catheter ablation", section on 'Prevention of recurrence'.)

In contrast, a randomized trial of nonsleepy patients with mild OSA (AHI >5) and another meta-analysis of mixed severity OSA patients reported no reduction in AF recurrence following cardioversion in response to PAP therapy [88,95]. Another trial of minimally symptomatic patients with moderate to severe OSA (AHI >15) also identified no difference in three-month AF burden with PAP therapy compared with supportive care [96].

The effect of therapies other than PAP (eg, oral appliances, pharmacotherapy, surgery, tracheostomy) on the risk of AF and AF recurrence following therapy is unknown.

Other arrhythmias — OSA is associated with nocturnal cardiac arrhythmias other than AF. These arrhythmias may be associated with respiratory events during sleep and improve with PAP therapy.

Clinical evidence — Nocturnal cardiac arrhythmias other than AF that occur during sleep in patients with OSA include the following:

●Bradyarrhythmias – Limited data report conduction delay arrhythmias including atrioventricular (AV) block, bradycardia-tachycardia, sinus pauses, and asystole in patients with OSA.

Older studies reported that bradyarrhythmias occur in up to 18 percent of patients with severe OSA (ie, AHI >30 events per hour) and lower oxygen saturation nadirs during sleep [97]. Anecdotally, bradyarrhythmias appear to be more common during rapid eye movement sleep and, in extreme cases, asystole can last longer than 10 seconds. (See "Permanent cardiac pacing: Overview of devices and indications".)

In one study, 15 patients with OSA and asystole who underwent electrophysiology exams all had normal (or only slightly abnormal) sinus and AV node function [98], suggesting that respiratory events are the primary reason for OSA-induced nocturnal arrhythmias.

●Ventricular arrhythmias – Ventricular ectopy and ventricular tachyarrhythmias have also been associated with OSA [99].

In an observational study, 228 patients with a sleep-related breathing disorder (respiratory disturbance index ≥30 events per hour of sleep) were compared with 338 patients without OSA [81]. The sleep-related breathing disorder group had a higher prevalence of nocturnal nonsustained ventricular tachycardia (5.3 versus 1.2 percent) and complex ventricular ectopy (25 versus 14.5 percent; eg, bigeminy, trigeminy, and quadrigeminy). These relationships persisted after adjustment for confounding variables.

The severity of OSA and degree of hypoxemia may contribute to these arrhythmias. In a large cohort of older male patients, severity of OSA versus CSA appeared to be more closely related to ventricular arrhythmias than AF, as did the extent of hypoxemia [93].

The biologic plausibility of the relationship of OSA with clinically significant ventricular arrhythmias is also supported by data in patients with congenital long QT syndrome that demonstrate further QT segment prolongation in those with concomitant OSA [100]. (See "Congenital long QT syndrome: Diagnosis".)

Impact of treatment — Preliminary data in patients with OSA support a possible role for PAP therapy in abolishing nocturnal asystole and improving other arrhythmias [98,101,102].

In a prospective cohort study of 23 patients with moderate or severe OSA, PAP reduced the incidence of nocturnal arrhythmias from 47 to 0 percent over a period of six months [101]. A randomized trial in patients with heart failure and OSA demonstrated a 58 percent reduction in the frequency of ventricular premature beats in patients treated with PAP compared with no reduction in those not treated with PAP therapy [103].

However, it is unknown whether nocturnal arrhythmia suppression improves mortality and there are few data about the impact of therapy on arrhythmias other than ventricular arrhythmia, bradycardia, or asystole.

The effect of therapies other than PAP (eg, oral appliances, pharmacotherapy, surgery, tracheostomy) on nocturnal arrhythmias is unknown.

HEART FAILURE —

Sleep-disordered breathing, which includes both OSA and central sleep apnea, is commonly observed in patients with heart failure. This is discussed in further detail separately. (See "Sleep-disordered breathing in heart failure".)

SUDDEN CARDIAC DEATH —

Limited data suggest that severe or untreated OSA may increase risk of sudden cardiac death (SCD), usually from fatal cardiac arrhythmias [18,104,105]. Positive airway pressure (PAP) therapy may be preventative.

A longitudinal study of 107 patients with OSA who were followed for seven years found that the rate of SCD was increased in patients who had discontinued PAP therapy compared with those who were adherent to PAP (7 versus 0 percent) [18]. Patients with OSA appeared to have a nocturnal predilection to SCD (midnight to 6 AM), with an approximately threefold increased risk, compared with the general population and those without OSA [105].

In a large, observational study of over 10,000 individuals referred for diagnostic polysomnography, nearly 80 percent of whom met criteria for OSA, several indicators of OSA severity were associated with increased risk of incident SCD [104]. These include nadir nocturnal oxygen saturation apnea-hypopnea index ≥20 events per hour of sleep, ventricular ectopy, and nonsustained ventricular tachycardia [104]. However, these OSA factors were of a much lower magnitude of risk than established factors, such as coronary heart disease, cardiomyopathy, and heart failure. (See "Overview of sudden cardiac arrest and sudden cardiac death".)

Limited data suggest that PAP therapy prevents SCD [18].

PULMONARY HYPERTENSION

Clinical evidence — The prevalence of pulmonary hypertension (PH) in patients with moderate to severe OSA is approximately 20 percent [106,107]. In the absence of coexisting lung disease, PH is typically mild. Risk factors for PH include comorbid lung disease, daytime hypoxemia, increasing apnea-hypopnea index (AHI), and comorbid obesity hypoventilation syndrome. (See "Clinical manifestations and diagnosis of obesity hypoventilation syndrome".)

The presence of PH may indicate poorer prognosis in patients with OSA compared with OSA without PH. An observational study of 83 patients with OSA reported that compared with those who did not have PH, those with PH had lower survival rates at one year (93 versus 100 percent), four years (75 versus 90 percent), and eight years (43 versus 76 percent) [108].

OSA-associated PH has also been associated with decreased functional capacity and quality of life [109,110].

Data suggest that nocturnal hypoxia, rather than higher AHI, is associated with right ventricular dysfunction and increased mortality in OSA-associated group 1 pulmonary arterial hypertension [111,112].

Impact of treatment — While treatment with positive airway pressure (PAP) reduces pulmonary artery pressure in many patients, the reduction is modest, and evidence of improved patient-important outcomes is lacking.

In patients with OSA, PAP therapy has been shown to reduce systolic pulmonary artery pressure (sPAP) and pulmonary vascular resistance (PVR) over a period of three to four months [113,114]. In one trial of 23 patients with OSA, therapeutic PAP reduced the estimated sPAP from 29 to 24 mmHg [114]. The extent of reduction was greatest among patients who had OSA plus PH at baseline compared with those who did not have PH at baseline.

Surgical weight loss in OSA may also result in improved pulmonary hemodynamics [115]. The impact of other therapies on PH is unknown (eg, oral appliances, pharmacotherapy, other surgery, tracheostomy).

PH-specific therapy is discussed in detail separately. (See "Treatment of pulmonary arterial hypertension (group 1) in adults: Pulmonary hypertension-specific therapy" and "Pulmonary hypertension due to lung disease and/or hypoxemia (group 3 pulmonary hypertension): Treatment and prognosis".)

VENOUS THROMBOEMBOLISM —

OSA may be a risk factor for venous thromboembolism (VTE).

Several reviews have reported that OSA may be an independent risk factor for VTE and that the risk may be two- to threefold higher than in those without OSA [116,117].

Perhaps explaining this association is the observation in patients with OSA of increased hypercoagulable markers (including fibrinogen and plasminogen activator inhibitor-1) in the morning relative to the evening, even in those with mild OSA [118].

The impact of treatment with PAP therapy is unknown.

SOCIETY GUIDELINE LINKS —

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Sleep-related breathing disorders in adults".)

SUMMARY AND RECOMMENDATIONS

●Definition and pathophysiology – Obstructive sleep apnea (OSA) is a disorder characterized by repetitive episodes of apnea or hypopnea due to upper airway obstruction during sleep. The resulting hemodynamic, autonomic, inflammatory, and metabolic effects of this abnormal breathing and arousal pattern may contribute to the pathogenesis of a range of cardiovascular diseases. (See 'Pathophysiology' above.)

●Acute cardiovascular events – OSA, particularly when severe, is an established risk factor for acute cardiovascular events (eg, acute myocardial infarction, stroke) and cardiovascular mortality. However, there is no convincing evidence that treatment of OSA with positive airway pressure (PAP) is associated with a reduction in acute cardiovascular events or cardiovascular mortality. It remains unclear whether considering larger sample sizes of specific populations with longer duration of follow-up and adequate adherence may enhance the ability to detect significant cardiovascular benefit. (See 'Acute cardiovascular events' above.)

●Hypertension – There is an increased prevalence of hypertension in patients with OSA with a dose-response effect between the severity of OSA and the likelihood of hypertension. While PAP therapy can lower blood pressure by modest (and even clinically significant) levels, this benefit has not been shown to lower the rate of associated cardiovascular events. (See 'Hypertension' above.)

●Arrhythmias – In OSA, the most strongly associated sustained arrhythmia is atrial fibrillation (AF). Other rhythm disturbances occur less commonly and may be associated with respiratory events during sleep.

•AF – Patients with OSA have an increased prevalence of AF. OSA is also a risk factor for recurrence after AF-specific therapy (eg, cardioversion, ablation). Limited observational data are conflicting regarding the impact of PAP therapy on AF burden and AF recurrence. (See 'Atrial fibrillation' above.)

•Other arrhythmias – Anecdotal and limited evidence describe OSA as a risk factor for bradyarrhythmia (including sinus pauses and asystole) and ventricular arrhythmias (including ectopy and tachyarrhythmias), especially during respiratory events during sleep. These events may improve with PAP therapy. (See 'Other arrhythmias' above.)

•Sudden cardiac death (SCD) – Limited data suggest that severe or untreated OSA may increase risk of SCD usually from fatal cardiac arrhythmias. PAP therapy may be preventive. (See 'Sudden cardiac death' above.)

●Heart failure – Sleep-disordered breathing is common in patients with heart failure. Further details regarding the relationship between OSA and heart failure are provided separately. (See "Sleep-disordered breathing in heart failure".)

●Others

•Pulmonary hypertension (PH) – PH is present in approximately 20 percent of patients with moderate to severe OSA and may be associated with decreased survival. While treatment targeting OSA with PAP reduces systolic pulmonary artery hypertension in many patients, the reduction is modest and evidence of improved patient-important outcomes, such as mortality, is lacking. (See 'Pulmonary hypertension' above.)

•Venous thromboembolism – OSA may be a risk factor for venous thromboembolism. The impact of treatment with PAP therapy is unknown.

ACKNOWLEDGMENTS —

The UpToDate editorial staff acknowledges Renaud Tamisier, MD, and J Woodrow Weiss, MD, who contributed to earlier versions of this topic review.

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Topic 7705 Version 55.0

خرید پکیج

Obstructive sleep apnea and cardiovascular disease in adults

References