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DRAFT — PENDING SOURCE VERIFICATIONUnder physician review; not for operational use. Summary AI-drafted from the abstract; awaiting physician sign-off.
Paper ✓ verified

Pheidippides Redux: Reducing Risk for Acute Cardiac Events During Marathon Running[1]

Summary

Review of mechanisms and prevention of acute cardiac events during marathon running, from the Boston Marathon's longtime medical investigator. Marathon running transiently raises absolute and relative risk of sudden cardiac death (up to 17-fold over resting baseline in previously sedentary middle-aged men), attenuated by training-induced cardioprotection in experienced runners. During races, exertional rhabdomyolysis is common, with neutrophilia and inflammatory biomarkers (IL-6, CRP) and a prothrombotic hemostatic imbalance including in vivo platelet activation. Plaque rupture from atherothrombosis triggers exertional events in low-risk runners as in high-risk patients. Discusses prophylactic aspirin as a candidate risk-reduction strategy.

So what

The mechanistic companion to Kim/RACER: where the registry counts arrests, Siegel explains the physiology — transient exertional prothrombotic state meeting vulnerable plaque — and why the risk concentrates in undertrained middle-aged men. The prophylactic-aspirin proposal remains contested (see the four published replies), so cite as hypothesis, not guidance. For race medical directors the practical content is the risk profile: the highest-risk runner is the inexperienced one, which argues for education and screening at registration rather than only finish-line response.

Key findings

  • Marathon transiently raises SCD risk up to 17-fold in sedentary middle-aged men
  • Training confers cardioprotection - experienced runners lower risk
  • Race physiology: rhabdomyolysis, IL-6/CRP inflammation, platelet activation (prothrombotic)
  • Mechanism: plaque rupture/atherothrombosis, as in high-risk patients
  • Prophylactic aspirin proposed but contested (four published replies)

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Domains

Endurance