A question of causation: since Western diets predispose to CAD in the young, how did the authors distinguish CAD as the SCD cause -- given its high incidence in the population -- versus a finding on molecular autopsy for a pathologic gene or myocarditis? I recently dealt with a case of a 34-year-old white male who likely had a missed aortic dissection (chest pain for 7 hours despite negative EKGs x5 on telemetry and negative troponins x3; no CTA; d-dimer in the 4000s, but no actual autopsy due to organ donation), but histology of the heart showed diffuse granulomas/giant cells and coronary artery occlusion up to 80-90% with some areas of fibrosis. He coded with PEA. His cause of death on his death certificate read, "PEA: arrhythmia, cardiomyopathy, and hypertension." We felt it was a missed aortic dissection that likely ruptured with hemoperitoneum and exsanguination, and others argued it was CAD and/or the granulomatous myocarditis that killed him -- we felt the granulomas were an incidental finding. I raise this question because all 3 causes -- CAD, myocarditis, and possible aortic dissection -- appear as SCD causes in the paper (see page 2446, Figure 2, graph C).
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