Effect of Prior Coronary Artery Disease on Troponin Kinetics and Its Prognostic Association in Acute Pulmonary Embolism.

Troponin is prognostic in acute pulmonary embolism (PE), but whether prior coronary artery disease (CAD) modifies troponin levels, kinetics, or prognostic value is unclear. We conducted a retrospective cohort study using the Medical Information Mart for Intensive Care IV database (2008 to 2022) in adults with primary acute PE and ≥1 conventional troponin within 72 hours, excluding those with concurrent STEMI or NSTEMI so that troponin elevation reflected PE rather than acute coronary syndrome. CTEPH was also excluded. Prior CAD was defined as documented chronic ischemic heart disease, prior coronary revascularization, or remote myocardial infarction. Troponin-outcome models compared first troponin, peak, delta, and time-to-peak by prior CAD status. Clinical-outcome models tested first troponin, prior CAD, and their interaction across mortality, hemodynamic decompensation, advanced PE therapy, discharge home, length of stay, and peak lactate. All models adjusted for demographics, comorbidities, creatinine, and the simplified Pulmonary Embolism Severity Index. Among 1,942 patients (17.9% prior CAD), first troponin did not differ by CAD status after adjustment (β = 0.13 per 0.1 ng/ml [-0.04, 0.30], p = 0.145), and no kinetic outcome differed (all p >0.4). Higher first troponin was associated with higher mortality and worse outcomes overall (5 of 6 measures, all p ≤0.048). Prior CAD did not modify these associations (interaction p ≥0.129), except for lactate (β = 0.32 mmol/L, p <0.001). In conclusion, troponin elevation in acute PE is not altered by underlying coronary disease and carries the same prognostic value regardless of prior CAD.