Interleukin-6 Mediated Non-ischemic Injury To Cardiac Myocytes During Marathon Running

Abstract

Since the fatal collapse of the legendary Pheidippides in 490 BC, mechanisms contributing to sudden cardiac death as shown to occur in 1 per 50,000 marathon runners during races are poorly understood. PURPOSE To explore the role of an acute inflammatory response to exertional rhabdomyolysis in the triggering of acute cardiac events. METHODS measurement of total creatine kinase, interleukin (IL)-6, C reactive protein (CRP), creatine kinase MB (CK-MB), cardiac troponin T (cTnT) and ischemia modified albumin (IMATM) by the albumin cobalt binding ACB ± TM Test in 46 asymptomatic middle-aged marathon runners before and sequentially after the 2001–02 Boston Marathons. RESULTS A 15-fold post-race rise in CK was accompanied by 40- and 20- fold increases in IL-6 and C-reactive protein respectively. There was a transient increase in cTnT to diagnostically indeterminate levels with no change in IMA by the ACB Test despite a 14-fold increase in CK-MB (Table 1).TableCONCLUSIONS These findings are consistent with non-ischemic injury to cardiomyocytes without necrosis perhaps due to IL-6 mediated leakage of cytosolic cTnT. Strategies for primary prevention of exertional cardiac events including the Pheidippides factor and the diagnostic assessment of such runners for acute coronary syndromes are considered. Supported by NIH Grants PO1- DA14528, K05-DA00101, K05-DA0064.