Does Ischemic Preconditioning Occur with Obstructive Sleep Apnea (OSA)? Comparing the Severity of Myocardial Necrosis Between the Patients with OSA and Without OSA After an Acute ST Elevation Myocardial Infarction

Document Type


Publication Date



Rationale: Ischemic preconditioning refers to the protection conferred to ischemic myocardium by preceding brief periods of sub-lethal ischemia. In animal models, this phenomenon is well described; however, limited literature is available describing it in humans. We investigated if intermittent nocturnal hypoxia associated with obstructive sleep apnea (OSA) can cause “ischemic preconditioning” of the myocardium and thus decrease the severity of myocardial necrosis in the event of acute ST elevation myocardial infarction (STEMI).

Method: A retrospective analysis of patients (n=277) admitted with STEMI between January 2009 to December 2013 to Lankenau Medical Center was done. A cohort of patients with OSA (diagnosed with polysomnography) (n1=22) was identified. Subsequently, a matching cohort of patients without OSA (control) was identified based on age, sex, previously known coronary artery disease (CAD) and the culprit vessel causing STEMI (n2=39). Unpaired T-test was performed to assess the statistical significance of difference between the means of biomarkers of myocardial injury (peak troponin levels, CK, CK-MB, left ventricular ejection fraction-LB-EF) and length of stay (LOS). A chi-square test of independence was performed to examine the relation between groups (case and control) and mortality.

Results: OSA was identified in 7.9% of the entire cohort of STEMI patients (22/277), 77% were male (17/22) and an average age of 66 years. An unpaired T-test was performed for analysis of means. Troponin levels were not significantly different between the groups (mean 32.68+/-29.73 ng/ml for cases vs. 45.13+/-73 np/ml for control; p=0.4979). CK levels were not significantly different (mean 1767+/-2136 u/l for cases vs. 2437.82+/-2536.3 u/l for control; p=0.4548). CK-MB levels were not statistically significantly different (mean 115.7+/-75.99 ng/ml for cases vs. 284.07+/-325.69 ng/ml for controls ; p=0.1402). LV-EF was not significantly different (mean = 47.9545%+/-13.0693 for cases vs. 46.7273%+/-15.0687 for controls; p=0.9551). Similarly, LOS was not significantly different between cases and controls (mean 5.32+/-4.5 days and 4.2+/-4.4 days, respectively; p=0.3506). The mortality rate was not significantly different between the two groups.

Conclusion: Based on our analysis, OSA does not change the severity of myocardial necrosis as assessed by biomarkers and ejection fraction. However, while not statistically significant, biomarkers were higher in patients without OSA compared to those with OSA, which raises the possibility of ischemic preconditioning. Prospective studies aiming at better screening for OSA among the patients with STEMI, and use echocardiography in addition to biomarkers might provide more evidence to further assess the possibility of ischemic preconditioning associated with OSA.


American Thoracic Society International Conference (ATS)


Denver, CO