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RESEARCH PRODUCT

015: Relation between platelet activation and inflammation indexes measured on admission and new onset atrial fibrillation in patients with acute myocardial infarction

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ObjectivePlatelet activation is present in atrial fibrillation (AF), but there is some debate whether this is due to AF itself and/or to underlying cardiovascular diseases. We aim to determine the association between a marker of platelet reactivity (mean platelet volume (MPV)) and systemic inflammation (CRP) measured on admission, and new onset episode of AF in patients with MI.Patients and methodsProspective cohort of 4994 consecutive patients with AMI. Patients with paroxysmal or persistent AF were excluded.Results426 (8.5%) patients were diagnosed with a new onset of AF during the in-hospital-stay (mean stay 3±2 days). These patients were older (75 vs 65, p<0.001), predominantly male, and prevalence of hypertension and diabetes was greater. Also less smoker were found among this group. Despite similar reperfusion strategies, clinical presentation with heart failure and increased heart rate (HR) was more frequently found in patients with AF. Left ventricular ejection fraction (LVEF) was significantly depressed in AF patients (47 vs. 55, p<0.001), among with increased NT-proBNP, admission MPV (8.9 vs. 8.6, p<0.001) and CRP (10.7 vs 5.7, p<0.001). Backward logistic regression analysis (model 1) found that age [OR=1.04, 95%CI (1.031–1.050), p<0.001)], HR [OR=1.016, 95%CI (1.011–1.021), p<0.001)], LVEF [OR=0.979, 95%CI (0.970–0.987), p<0.001)] and MPV [OR=1.182, 95%CI (1.064–1.312), p<0.001)] were independent predictors of AF occurrence. A second backward regression analysis (model 2= model 1+CRP) found that age [OR=1.036, 95%CI (1.026–1.046), p<0.001)], HR [OR=1.013, 95%CI (1.008–1.018), p<0.001)], LVEF [OR=0.977, 95%CI (0.968–0.987), p<0.001)] and CRP [OR=1.003, 95%CI (1.001–1.005), p=0.006)] were independent predictors of AF occurrence after MI.ConclusionsThis study suggested that new onset of AF early after MI is rather linked to inflammation induced by myocardial damage or the existing atherosclerotic burden than platelet activation.