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Obstructive Sleep Apnea and Atrial Fibrillation

Current data from both cross-sectional and case–control studies support the independent association between obstructive sleep apnea (OSA) and atrial fibrillation (AF), while other empirical evidence indicates that OSA may increase the occurrence of intermittent AF following ablation/cardioversion. A recent meta-analysis also reported that OSA strongly predicted AF occurrence after coronary artery bypass grafting. Obstructive sleep apnea per se may have significant cardiovascular consequences. The relation between OSA and hypertension has been already established, while it is also linked to arterial stiffness, congestive heart failure, coronary heart disease (CHD), and arrhythmias, such as AF. Mean platelet volume (MPV) reflects increased platelet activation, and, consequently, inflammation and thrombosis. Elevated MPV has been previously associated with the presence and severity of CHD and stroke. Obstructive sleep apnea has been associated with platelet activation. Hence, it might be considered as a prothrombotic condition. The connection between AF and thromboembolism is well established. The study of Akyuz et al examined the connection between MPV, AF, and OSA, as indicated by apnea hypopnoea index (AHI). The authors compared patients with OSA having concomitant AF (n 1⁄4 40) to patients with OSA exhibiting normal sinus rhythm (NSR; n 1⁄4 50). Mean platelet volume was significantly higher in patients with AF than in patients with NSR (9.8 + 0.6 vs 8.4 + 0.6 fL, P < .001). The importance of this finding is enhanced by the observation that a high odds ratio (OR) for the presence of AF is associated with higher MPV and AHI levels (OR 1⁄4 2.41; 95% confidence interval [CI], 1.36-5.26, P < .004 and OR 1⁄4 1.91; 95% CI, 1.26-3.32, P 1⁄4 .02, respectively). Additionally, the authors reported that an elevated MPV of 9.4 fL can be used as a cutoff point for the presence of AF with 70% sensitivity and 63% specificity. The study of Akyuz et al has limitations, as acknowledged by the authors. First, it is a single-centre study with a retrospective design, including a small number of participants. Second, it only used a single marker of platelet function. Third, due to limited number of participants with AF, the participants could not be stratified according to OSA severity, precluding further subgroup analysis. Based on the recent above-mentioned findings, we are beginning to appreciate that the presence of AF in patients with OSA may be associated with increased MPV as well as AHI severity. These findings suggest that patients having OSA with increased MPV need to be screened for the presence of AF by a thorough cardiologic evaluation. More importantly, MPV might prove to be a useful biomarker for the timely identification of patients with OSA carrying an excessively high thromboembolic risk. Finally, additional issues still need to be addressed. These include the identification of MPV cutoff points valid enough to discriminate patients at risk for AF and the potential existence of a reverse pathway, enabling the detection of OSA among patients with AF, with the use of diagnostic tools. The latter may be the Epworth Sleepiness Scale and the Berlin Questionnaire, along with physical examination, and, if indicated, polysomnography. Large prospective randomized studies are now warranted to clarify these questions.