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The link between minor troponin (cardiac troponin I [cTnI]) elevations and atrial fibrillation (AF) is still debated.A total of 948 patients with AF lasting less than 48 hours participated in the study and were required to undergo 1-month and 12-month follow-up. The exclusion criteria were represented by younger than 18 years, the presence of hemodynamic instability, or severe comorbidity. Primary end point was the composite of ischemic vascular events inclusive of stroke, acute coronary syndrome, revascularization, and death.In the short term, 4 patients (5%) of 78 with abnormal cTnI reached the primary end point (P = .001 vs others). Conversely, in the long term, 13 patients (17%) with abnormal cTnI, 21 (10%) with known ischemic vascular disease, and 50 (5%) aged patients (75 ± 10 years) reached the primary end point (P < .001, P < .001, and P = .002, respectively). At multivariate analysis, abnormal cTnI (hazard ratio [HR], 2.84; 95% confidence interval, 1.38-5.84; P = .005), known ischemic vascular disease (HR, 2.03; 95% confidence interval, 1.11-3.70; P = .021), and age (HR, 1.05; 95 confidence interval, 1.02-1.08; P = .002) were predictors of the primary end point. Minimal or minor cTnI elevation (<0.45 or ≥ 0.45 ng/mL, respectively) showed no differences when associated with the primary end point. The C-statistic demonstrated the significant prognostic value of older age and known ischemic vascular disease, beyond troponin. Clinical parameters inclusive of heart rate, blood pressure, and risk factors for arteriosclerosis showed no relationship with adverse events. Readmission rate did not differ between groups.In patients with acute AF, minor cTnI elevations link to short-term adverse events. Known ischemic vascular disease and older age showed prognostic value only in the long term.