New insights on the pathogenesis of atrial fibrillation in acute myocardial infarction: Data from the “ObseRvatoire des Infarctus de Côte d’Or” (RICO) survey

Abstract

Atrial fibrillation (AF) is common after acute myocardial infarction (AMI), and associated with mortality. However, there is an unmet need in the understanding of the pathophysiology of AF in AMI. Heart rate variability (HRV) reflects the cardiovascular response to the autonomic nervous system (ANS). We investigated the relationship between ANS parameters and the occurrence of AF during AMI. From the RICO survey, all consecutive patients hospitalized for AMI in our university hospital between June 2001 and November 2014 were prospectively analysed by Holter ECG < 48 h following admission. HRV was measured using temporal and spectral analysis. Among the 2035 included patients, 168 (8.2%) developed AF during AMI. Compared to the sinus-rhythm group, patients who developed AF were older (77 ± vs. 64 ± y, P < 0.001), had more frequent hypertension (114 vs. 924, P < 0.001) and lower LVEF (47% vs. 55%, P < 0.001). On ANS Holter parameters, AF patients had higher pNN50 values (11% vs. 4%, P < 0.001) as for mean heart rate (73 ± vs. 66 ± bpm, P < 0.001). There was a marked difference regarding the sympathovagal balance as assessed by the median LH/HF ratio: 2.75 (1.46–4.58; P < 0.001) in sinus rhythm-group, compared to 0.88 (0.57–2.00); P < 0.001, respectively in AF-group. In ROC curve analysis, the optimal LF/HF cut-off for AF prediction was at 1.735. In our population, 75% of AF patients had a LF/HF ratio < 1.735, as compared to 30% of patients in the sinus-rhythm group. By multivariate analysis, low LF/HF [OR 3.562 (2.202–5.763)] was the strongest predictor of AF, beyond age [OR (95%CI) 1.040 (1.018–1.062)], and mean sinus-rhythm rate on Holter recording [OR 1.031 (1.016-1.045)]. Our large prospective HRV analysis in AMI shows that low LF-HF ratio is a major predictor of AF. Our study strongly suggests that AF in AMI primarily occurs on previous underlying atrial electrical remodelling, rather than acute sympathovagal imbalance.