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Dr. Mutlu is Chief Fellow and Dr. Rubinstein is Professor of Medicine, Section of Respiratory and Critical Care Medicine, Department of Medicine, University of Illinois, Chicago, IL.
Correspondence to: Israel Rubinstein, MD, FCCP, Section of Respiratory and Critical Care Medicine (M/C 787), Department of Medicine, University of Illinois at Chicago, 840 S Wood St, Chicago, IL 60612-7323; e-mail: IRubinst{at}uic.edu
It is well established that obstructive sleep apnea syndrome (OSAS) is associated with an increased risk for developing cardiovascular complications, most notably ischemic heart disease (IHD).1 Moreover, some investigators consider OSAS to be an independent risk factor for IHD because the incidence of OSAS is twofold to threefold higher in patients with IHD relative to age- and gender-matched healthy individuals, and because OSAS is often present in patients who have experienced acute coronary artery events.2 3 4 However, despite the negative impact of OSAS on myocardial oxygenation and its frequent association with IHD, a direct causal relationship between OSAS and IHD has yet to be firmly established.
In this issue of CHEST, Mooe et al (see page 1597) have attempted to evaluate the contribution of OSAS to nocturnal myocardial ischemia by studying a relatively large cohort of patients with IHD. Left ventricular ejection fraction was normal in the majority of patients, and most had two-vessel coronary artery disease. The patients underwent overnight polysomnography and 24-h Holter monitoring. While 60% of patients had OSAS, the majority of patients had a mild form of the disease with a mean respiratory disturbance index of 10. Ischemia was considered to be temporally related to OSAS if it occurred within 2 min after a respiratory event. Although ST-segment depression was recorded in 31% of patients during sleep, particularly in men and in patients with more frequent respiratory events, the majority of these phenomena were not preceded by a respiratory event. Apnea-associated ST-segment depression was often preceded by a significant increase in heart rate, several consecutive apneas, and severe arterial oxygen desaturation.
The results of this study are intriguing and illustrate the complexity of the proposed association between OSAS and nocturnal myocardial ischemia in patients with IHD. They do not substantiate previous studies reporting a relatively high prevalence of OSAS-associated nocturnal myocardial ischemia in patients with both IHD and OSAS. Although the reasons underlying these discrepant results are uncertain, they may be related, in part, to the heterogeneity of the patient populations being studied. Unlike Mooe et al, other investigators studied patients with moderate to severe OSAS5 6 7 or patients with a relatively higher incidence of nocturnal angina pectoris.5 8 However, these studies did not evaluate nocturnal chest pain as an independent predictor of OSA-associated nocturnal myocardial ischemia.
Collectively, these data suggest that patients with IHD and mild OSAS are not at increased risk of developing OSAS-associated nocturnal myocardial ischemia. However, we propose that in patients presenting with nocturnal angina pectoris the presence of underlying OSAS should be sought. Moreover, an increase in heart rate during a respiratory event may contribute to the pathogenesis of OSAS-associated nocturnal myocardial ischemia. Further studies to elucidate the mechanisms whereby OSAS modulates myocardial ischemia during sleep are warranted.
References
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