Our study demonstrated that age, AHI, basal oxygen saturation, oxygen desaturation index and presence of diabetes mellitus were associated with CAC in patients with OSAS. However, even after controlling these parameters, age and AHI were the only independent predictors of subclinical atherosclerosis in patients with OSAS.
Obstructive sleep apnea which occurs in approximately 9–24% of the general population  is an emerging cardiovascular risk factor [4, 5]. The Sleep Heart Health Study showed a modest increase in the odds ratio of CAD in patients with severe OSAS compared to controls . Hung et al.  also reported that in patients with myocardial infarction, OSAS was a strong risk factor as obesity, smoking and hypertension. In a group of 23 OSAS patients without symptoms or history of CAD, about one-third showed asymptomatic ST-segment depression during sleep, but only one patient was found to have positive exercise stress test result, suggesting a low prevalence of symptomatic CAD in OSAS . Therefore determination of subclinical atherosclerosis in patients with OSAS can be important in order to prevent the adverse cardiovascular events.
Although in recent studies [20, 21] increased cardiovascular morbidity have been confirmed in patients with OSAS, the occurrence of other cardiovascular risk factors often limited the assessment of an independent pathogenetic role for OSAS. Whereas in our study, although there was no difference in regard to the presence of cardiovascular risk factors, when patients were evaluated according to the severity of OSAS we found that the number of patients who had coronary calcification were higher in the group with higher AHI and the patients with higher AHI had significantly higher coronary calcium score compared to patients with lower AHI. On the other hand , when OSAS patients were evaluated according to the presence of coronary calcium, it was found that patients with coronary calcium were significantly older and had marginally significant higher prevalence of diabetes mellitus with higher AHI. Our study showed that the severity of OSAS was related to subclinical atherosclerosis irrespective of the presence of other cardiovascular risk factors except for age. Thus, it may be suggested that the presence of OSAS is a marker of subclinical atherosclerosis dependent on increasing age and the severity of subclinical atherosclerosis correlates with the severity of OSAS.
A recent study conducted by Sorajja et al. revealed that increasing severity of OSAS was related to an increase in the severity of CAC independent from other risk factors . To confirm this study, our results showed that the risk of subclinical atherosclerosis was increasing with a sensitivity of 77.8% when AHI > 16 which is an indicator of moderate-to-severe OSAS. Besides, Kepez et al. observed that the relationship between the severity of OSAS and the increase in cardiovascular risk was dependent only on the age of patients . On the contrary, our results demonstrate that the level of AHI and advanced age are independently associated with the development of CAC. Regardless of the severity of OSAS, patient’s age > 45 becomes an indicator of cardiovascular risk with the sensitivity of 88.9%. An additional ROC analysis also showed that considering the age > 45 and AHI > 16 together in patients with OSAS, specificity increased with unchanged sensitivity for predicting subclinical atherosclerosis (87% sensitivity, 70.6% specificity).
Although the mechanisms underlying cardiovascular disease in patients with OSAS are still poorly understood, endothelial dysfunction, oxidative stress, and inflammation are long-term consequences that mediate cardiovascular disease in patients with OSAS [24–27]. An important mechanism of atherosclerosis in OSAS is inflammation resulting in endothelial dysfunction . Several mediators that have been implicated in the pathogenesis of atherosclerosis are abnormal in patients with OSAS. C-reactive protein, a marker of systemic inflammation, and endothelin-1, a potent long-acting vasoconstricting substance are shown to be elevated in OSAS . Moreover, intermittent hypoxia and reperfusion during repetitive episodes of nocturnal apnea may be involved in the generation of highly reactive oxygen radicals, as well as in ischemia-reperfusion injury to the vascular wall, resulting in increased risk for atherosclerosis [26, 27].