Abstract
New-onset atrial fibrillation (NOAF) is common after acute myocardial infarction (AMI) and associated with short and long-term mortality. We aimed to elucidate the pathophysiological mechanisms involved. To investigate the relationship between circulating biomarkers (Galectin 3, GDF-15), heart rate variability parameters (pNN50, SDNN) using continuous electrographic monitoring (CEM) and the occurrence of NOAF during AMI. From the RICO survey, all consecutive patients with AMI admitted in the coronary care unit (CCU) of Dijon between May 2017 to February 2018 were prospectively included. Patient with prior AF were excluded. Clinical data, plasma biomarkers and HRV parameters were analyzed to build predictive models of NOAF. Among the 380 analyzed patients, 47 (12%) developed AF during AMI. AF was asymptomatic in 90% of them. Median age was 67 years, 31% were women. AF patients had higher levels of Gal-3 (23.8 vs 12.5 ng/mL, P = 0.003) and GDF-15 (3238 vs 1980 pg/mL, P < 0.001). HRV parameters were available for 202 patients (175 SR, 27 AF) and we found that AF patients had higher SDNN values (73 vs 34ms, P < 0.001) and pNN50 values (28% vs 5%, P < 0.001) than sinus rhythm (SR) patients. 2 multivariate models of AF prediction were built, the model 1 including the whole population: GDF-15 > 1789 pg/mL (OR 3.69 (1.54–8.86), P = 0.004), STEMI (OR 3.50 (1.59–7.69), P = 0.002), Gal-3 > 16.8 ng/mL (OR 2.64 (1.30–5.37), P = 0.008) and CKD-EPI < 60 mL/min (OR 2.57 (1.15–5.65), P = 0.004) and the model 2 limited to the patients in who HRV parameters were available ( n = 202): SDNN (OR 11.88 (3.71–37.97), P < 0.001), Gal-3 > 16.8 ng/mL (OR 6.95 (2.18–22.18), P = 0.001), GDF-15 > 1789 pg/mL (OR 4.64 (1.44–14.89), P = 0.010) and STEMI (OR 4.09 (1.25–13.37), P = 0.020). Our study highlights by a multimodal approach the involvement of inflammation, autonomic nervous system dysfunction and underlying atrial myopathy in the pathogenesis of NOAF after AMI.
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