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Other OSA comorbidities
Road traffic accidents
Several cross-sectional studies using driving simulators showed worse driving performance and increased risk of road traffic accidents in patients with OSA [143]. In a sample of 913 employed adults whose motor vehicle accident history was obtained from a statewide database covering the period 1988–1993, men with OSA (AHI≥5) were more likely to have at least one accident in 5 years compared to those without OSA (age and miles driven adjusted OR 4.2 for AHI 5–15, and 3.4 for AHI>15) [10,144]. Men and women combined with AHI>15 (vs. no OSA) were significantly more likely to have multiple accidents in 5 years (OR 7.3) [10,144]. Similar results were found in another case-control study from Spain [145]. Interestingly, neither of these two studies showed a relationship between reported sleepiness and the road traffic accidents nor was there a dose relation between OSA severity and the likelihood of involvement in an accident.
Cardiovascular mortality and morbidity
OSA has been associated with sustained hypertension and lack of the normal nocturnal dipping of blood pressure (BP). Nondipping of BP in OSA patients was examined prospectively in a subsample of 328 adults enrolled in the Wisconsin Sleep Cohort Study who completed 2 or more 24-hour ambulatory BP studies over an average of 7.2 years [146]. After adjustment for many confounders, the adjusted OR (95% CI) of incident systolic nondipping for baseline AHI 5–14.9 and ≥15, vs. AHI<5, were 3.1 (1.3–7.7) and 4.4 (1.2–16.3), respectively [146]. In a cross-sectional analysis of 6132 middle-aged and older persons (aged ≥ 40 years) from the Sleep Heart Health Study, the OR (95%CI) for hypertension for the highest vs. the lowest category of AHI was 1.37 (1.03–1.83, p=0.005) after adjustment for BMI, neck circumference, waist-to-hip ratio (WHR), alcohol, and smoking [147]. The associations of hypertension with OSA were seen in men and women, older and younger, all ethnic groups, and among normal-weight and overweight individuals [147]. In another prospective study based on the Wisconsin Sleep Cohort Study, the relation between OSA and hypertension in 709 participants over 4 years was examined [148]. After adjustment, and relative to an AHI of 0 at baseline, the OR for the presence of hypertension at follow-up were 1.42 (95% CI: 1.13–1.78), 2.03 (1.29–3.17) and 2.89 (1.46–5.64) for an AHI of 0.1–4.9, 5.0–14.9, and ≥15.0, respectively (p=0.002 for the trend) [148].
Several cross-sectional and case-control studies showed an association between OSA and cardiovascular disease (CVD) [10]. Three prospective studies used more accurate methods to diagnose OSA (i.e., polysomnography) [149–151]. In a study of a 182 consecutive middle-aged men free of CVD at baseline who were followed for 7 years, the incidence of CVD was 36.7% of patients with OSA vs. 6.6% of subjects without OSA (p<0.001) [149]. OSA was an independent predictor of CVD (OR 4.9; 95% CI 1.8–13.6) after adjustment for confounders [149]. CPAP treatment was associated with lower incidence of CVD compared to those untreated (56.8% vs. 6.7%, p<0.001) [149]. In another prospective study in which men with OSA were followed for a mean of 10.1 years, patients with untreated severe OSA had a higher incidence of fatal CVD and nonfatal CVD than did untreated patients with mild-moderate OSA, simple snorers, patients treated with CPAP, and healthy participants [150]. After adjustment for confounders, untreated severe OSA significantly increased the risk of fatal (OR 2.87; 95% CI 1.17–7.51) and nonfatal (3.17; 1.12–7.51) CVD compared with healthy participants [150]. In another important prospective study, 1022 patients were followed up for a median of 3.4 years [151]. After adjustment for confounders, OSA was significantly associated with stroke or death (hazard ratio (HR), 1.97; 95% CI 1.12–3.48; p=0.01) [151]. Furthermore, in patients with stable coronary artery disease, patients with OSA had larger atherosclerotic plaque volume as assessed by intravascular ultrasound and AHI correlated positively with the plaque volume measured by US (r=0.6, p=0.01) [152] or CT angiogram (r=0.4, p=0.02) [153]. The role of nocturnal events in OSA in the development of myocardial infarction is further supported by a study that showed patients with OSA were more likely to develop acute myocardial infarction between 12AM and 6AM compared to patients matched for comorbidities but who did not have OSA (32% vs. 7%, p=0.01) [154].
The impact of OSA on mortality was examined in the Wisconsin Sleep Cohort Study [155] and the Sleep Heart Health Study [156]. In 18-year follow-up, there was a step-wise reduction in survival with worsening OSA.The adjusted hazard ratio (HR; 95% CI) for all-cause mortality with severe vs. no OSA was 2.7 (1.3–5.7) after adjustment for possible confounders [155]. In 6441 men and women who were followed up for 8.2 years; compared to those without OSA (AHI<5 events per hour), the HR for all-cause mortality in those with mild, moderate, and severe OSA were 0.93 (95% CI 0.80–1.08), 1.17 (95% CI 0.97–1.42), and 1.46 (95% CI 1.14–1.86), respectively, after adjustment for age, sex, race, smoking status, BMI, and prevalent medical conditions [156]. Measures of intermittent hypoxemia, but not sleep fragmentation, were independently associated with all-cause mortality [156].