Abstract
Objective: The impact of the co-occurrence of hypertension and obstructive sleep apnea (OSA) on the risk of long-term cardiovascular disease (CVD) outcomes has not been extensively studied in the Asian population, and the residual effect of OSA on CVD in patients under antihypertensive treatment is not clear. The study aimed to explore the impact of OSA on the risk of CVD outcomes in a large-scale Asian cohort under antihypertensive treatment using retrospective design. Design and method: Hypertensive patients who underwent polysomnography (PSG) test in January 2011 to December 2013 were recruited from the UROSAH cohort, which was conducted in Hypertension Center of People's Hospital. OSA was defined as apnea hypopnea index over 5. Outcomes were extended major adverse cardiovascular and cerebrovascular events (MACCE), including the first occurrence of nonfatal myocardial infarction, nonfatal stroke, revascularization, rehospitalization due to unstable angina or heart failure and all-cause death. Cox regression analysis was performed to explore the effect of OSA and hypertension coexistence on MACCE. Results: A total of 3329 hypertension patients were enrolled, of whom 2585 patients (about 77.7%) suffered from OSA. During a median follow-up period of 7.0 years, 415 patients developed extended MACCE. The incidence of extended MACCE was significantly greater in patients with OSA than those without OSA (hazard ratio [HR]: 1.59; 95% confidence interval [CI]: 1.27-1.99; P<0.001). Overall, patients with OSA had an increased risk of cardiac events of 57% compared to those without OSA [HR (95%CI): 1.57 (1.04-2.39), P=0.034] and the association did not change in further sensitivity analysis. Particularly in uncontrolled hypertension, OSA was found to have a 93% increased risk of cardiac events, compared with patients without OSA (P=0.036). Conclusions: Untreated OSA seemed to be a factor affecting the prognosis of cardiac events in hypertensive patients, although the association between OSA and cardiac events would be attenuated by the pharmacological-induced blood pressure control, which highlights the need to treat OSA.
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