NORMAL POST-RACE ANTIMYOSIN MYOCARDIAL SCINTIGRAPHY IN ASYMPTOMATIC MARATHON RUNNERS WITH ELEVATED SERUM CREATINE-KINASE-MB-ISOENZYME AND TROPONIN-T LEVELS - EVIDENCE AGAINST SILENT MYOCARDIAL-CELL NECROSIS

Recent epidemiologic studies confirm that heavy physical exertion can trigger myocardial infarction. Diagnosis of acute myocardial injury in marathon runners is complicated by elevations of serum creatine kinas e MB isoenzyme activity in asymptomatic finishers with normal post-rac e infarct-avid myocardial scintigraphy. Such isoenzyme elevations can arise from exertional rhabdomyolysis of skeletal muscle biochemically altered by training, from silent injury to the myocardium or from a co mbined tissue source, To assess silent myocardial cell necrosis in mar athon runners, we performed quantitative antimyosin myocardial scintig raphy after competition with serum immunoassays for creatine kinase MB isoenzyme and troponin T. Therefore, 8 male marathon runners with a m ean age of 52 years underwent quantitative antimyosin myocardial scint igraphy immediately following the 1988 and 1993 Boston Marathons. Seru m immunoassays for creatine kinase MB isoenzyme by a chemiluminescent method (CLIA) and troponin T by an enzyme-linked immunosorbent assay w ere performed in 4 runners after the 1993 race, Quantitative antimyosi n myocardial scintigraphy was normal in all runners including 3 who pa rticipated after both races 5 years apart. Post-race serum creatine ki nase MB isoenzyme and/or troponin T levels were in a range otherwise d iagnostic of acute myocardial infarction in 3 of 4 subjects. Normal qu antitative antimyosin myocardial imaging in asymptomatic marathon runn ers excludes silent myocardial cell necrosis as the source of elevated serum protein markers. Such imaging may be the optimal diagnostic mod ality for detection of myocardial cell necrosis in symptomatic athlete s when results of conventional testing are inconclusive.