Marathon running transiently increases the risk of sudden cardiac death. Some previous studies have suggested that this is due to relatively advanced but asymptomatic atherosclerosis. Other theories suggest that potentiation of inflammation and the coagulation cascade, by extremes of exertion, is more important. We present a clinical case of a young, previously fit athlete who felt chest discomfort eight miles into a marathon but finished the race. Shortly after completion he felt very unwell and had chest pain. Ambulance electrocardiograms showed evidence of an evolving anterior myocardial infarction. Invasive assessment with coronary angiography and intravascular ultrasound was able to show the mechanism of thrombosis. Fissuring of a small rim of atherosclerosis potentiated a large pro-thrombotic response, the patient was also found to have sickle cell trait. Medical treatment with blood thinning drugs was able to restore normality to the vessel over a period of two weeks, without the need for angioplasty or stent implantation.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4536480 | PMC |
http://dx.doi.org/10.3978/j.issn.2223-3652.2015.05.03 | DOI Listing |
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