Abstract 18566: How is the Presence of Obstructive Sleep Apnea Associated with Vasospastic Angina?

Abstract

Background: Vasospastic angina (VSA) is characterized by transient vasoconstriction of the epicardial coronary arteries leading to myocardial ischemia. It characteristically occurs from midnight to early morning. Obstructive sleep apnea (OSA) is caused by obstruction of the upper air passage during sleep, which leads to hypopnea. Although OSA may have an influence on VSA, the association between these two conditions remains unclear. To clarify this relationship, the frequency of OSA (Study 1) and the association between OSA and anginal attacks (Study 2) were investigated. Methods: (Study 1) Eighty-seven patients (41 men, mean age 67 years) were included in whom spasm-provocation testing for evaluation of chest symptoms was performed. VSA was defined as >90% narrowing of the epicardial coronary arteries on the angiogram during a spasm-provocation test, accompanied by chest pain and/or ST-segment deviation on ECG. Polysomnography (PSG) was performed in all patients. The presence of OSA was verified using the apnea hypopnea index (AHI) >15/h. The frequency of OSA in VSA patients (VSA group, n = 58) was compared with that in patients in whom negative spasm-provocation testing (non-VSA group, n = 29) was performed. (Study 2) Seventy-seven VSA outpatients were examined in whom PSG was performed (45 OSA, 32 non-OSA), and these patients followed up for at least a year. The number of anginal attacks per month was evaluated. The presence of intractable VSA was defined as uncontrollable angina even after administration of two types of coronary vasodilators. Results: (Study 1) No difference was observed in AHI (VSA group: 15.2 ± 1.3/h, non-VSA group: 12.8 ± 1.8/h) and the frequency of OSA (VSA group: 25/58, 43%, non-VSA group: 9/29, 31%) between the two groups. (Study 2) The number of anginal attacks tended to be higher in the OSA group (2.9 ± 0.6/months) than in the non-OSA group (1.3 ± 0.8/months, p = 0.09). The frequency of intractable VSA was higher in the OSA group (47%) than in the non-OSA group (19%, p < 0.05). Logistic regression analysis demonstrated that the presence of OSA was the significant factor responsible for intractable VSA. Conclusions: These results suggest that although OSA may not be involved in the pathogenesis of VSA, it may be a deteriorating factor of VSA.