In learn more addition, it might be just the results of ASM, not cause, which is very important limitation of this study. Nevertheless, we could confirm that ASM was not caused by myocardial ischemia. According to a large scale review of 3923 cases by Reynolds et al.,5) the incidence of ASM was 40%, and valve surgery was more likely to cause ASM compared to CBS. In the present study, the incidence of ASM was 74%, almost

two-fold what was previously Inhibitors,research,lifescience,medical reported, but we did not observe an association between the type of surgery and the occurrence of ASM. The same mechanism may be responsible for ASM in both CBS and HVS. In the literature, it is described that ASM occurs immediately after surgery and usually tends to resolve with time, Inhibitors,research,lifescience,medical although it can persist indefinitely in some patients.23) In consensus with this statement, our data showed ASM disappeared over time in most patients without clinically detectable pericardial constriction. Only 3 patients in our study sample had clinically significant transient constrictions probably because of the use of steroids; in 2 of these patients, ASM disappeared over time. In summary, ASM is frequent after OHS, however, ASM does not seem to have any clinical significance and will likely disappear over time. Further, we demonstrated that decreased postoperative

Inhibitors,research,lifescience,medical systolic VRad of the antero-septum and anterior wall is associated with the occurrence of ASM. Limitations Echocardiographic Inhibitors,research,lifescience,medical views are relatively poorer after HVS than those after CBS. Therefore, the occurrence of ASM after HVS might be underestimated. Although data from all the patients

were available immediately after the operation, data from the 3–6-month and 1-year follow-up visits were only available for 40–45% of the patients each group. In addition, we performed VVI analysis Inhibitors,research,lifescience,medical before and immediately after surgery in only a limited number of patients (approximately 40 patients), and we were unable to identify reversal of systolic VRad of the antero-septum and anterior wall when ASM disappeared. Lastly, we usually use diuretics peri-OHS; thus, some patients with constrictive physiology may not have been revealed. However, this limitation may not be clinically Thymidine kinase relevant, even in patients with ASM, because the majority of study patients did not require prolonged diuretic administration after OHS. Conclusion Even though ASM was common in patients immediately after cardiac surgery, it disappeared over time without causing clinically detectable pericardial constriction. Furthermore, ASM might not be caused by myocardial ischemia, but we demonstrated that a decreased postoperative systolic VRad of the antero-septum and anterior wall is associated with ASM after cardiac surgery. Acknowledgements This study was supported by the Korean National Research Foundation and funded with a grant from the Korean Government (MEST) (No. 2012027176).