Atrial fibrillation (AF) recurs within the first year after successful cardioversion in about 50% of patients . Predictors of recurrence may help in planning the frequency of planned clinical visits, in modulating therapy and in better understanding the pathophysiology of the disease. Whilst several studies have reported increased concentrations of cardiovascular markers in patients with AF [2–7], few studies have assessed the predictive roles of these markers in patients in sinus rhythm at high risk of AF [8, 9]. Given the complexity of studies in this field because of the heterogeneity of populations and the limitations in terms of sample size, it can be concluded that in general natriuretic peptides are elevated during AF and predict AF recurrence or first occurrence in patients with various comorbidities , hypertension  and heart failure , or those who have undergone cardiac surgery . Major limitations of these studies include small sample size (<100 patients) and/or retrospective design.
GISSI-AF, a trial to determine the effect of valsartan in preventing recurrence of AF in patients in sinus rhythm , appeared to be a suitable setting to investigate how different biomarkers would predict recurrence of AF. Accordingly, six different cardiovascular markers were assayed in 382 patients enrolled in the GISSI-AF trial. High-sensitivity cardiac troponin T (hsTnT) and N-terminal probrain natriuretic peptide (NT-proBNP) were measured as sensitive and specific markers of cardiac injury/strain/filling pressures. Mid-regional proatrial natriuretic peptide (MR-proANP) was assayed as it is considered to best reflect atrial strain, a determinant of AF. Amongst the three vasoactive peptides, C-terminal proendothelin-1 (CT-proET-1) was measured because of the relation between endothelin and new-onset AF in heart failure  and because of its possible role in the pathogenesis of AF [14, 15]. Mid-regional proadrenomedullin (MR-proADM) and C-terminal provasopressin (copeptin) have been found to be related to the altered haemodynamics and volume load in heart failure [16, 17].