In the report by Parashar et al, it was recently concluded that cardiospecific troponin was not independently associated with new-onset atrial fibrillation (AF) after acute myocardial infarction. Several lines of evidence now attest that the concentrations of cardiospecific troponins and d -dimer are increased in patients with AF and that their values are significantly associated with a worse prognosis including stroke, death, and thromboembolic events. Nevertheless, no information is available on the relation between these 2 biomarkers in patients with new-onset AF.

In this retrospective investigation, clinical and laboratory data about all consecutive patients admitted to the local emergency department (ED) for new-onset AF (i.e., symptoms lasting <48 hours at presentation) over the past 6 months were retrieved from the hospital database. In all patients, d -dimer was measured with an immunoturbidimetric assay (HemosIL D-dimer HS for ACL TOP; Instrumentation Laboratory, Bedford, Massachusetts), whereas troponin I (TnI) was assessed using Beckman Coulter AccuTnI on Unicel DxI (Beckman Coulter, Brea, California). The diagnostic threshold of the d -dimer assay is 243 ng/ml, whereas the limit of detection and the ninety-ninth percentile of the upper reference limit values of AccuTnI are 0.01 μg/L and 0.03 μg/L, respectively. Results of testing are reported as median and interquartile range (IQR). The differences between groups were assessed by the Wilcoxon-Mann-Whitney test, and the relation among variables was tested with both univariate and multivariate regression analyses, using Analyse-it (Analyse-it Software Ltd, Leeds, United Kingdom). The investigation was performed in accord with the Declaration of Helsinki and under the terms of all relevant local legislation.

Overall, 271 cases of new-onset AF were observed in the ED throughout the study period (134 men and 137 women; age range 22 to 93 years). The frequency of increased values was 20% for d -dimer (55 of 271) and 18% for TnI (49 of 271). A highly significant correlation was found between d -dimer and TnI in univariate analysis (r = 0.39, p <0.001), and the significance of the association was not attenuated in multivariate analysis after adjustment for age and gender (p <0.001). When the study population was stratified according to d -dimer values below (n = 216) or above (n = 55) the diagnostic cutoff, TnI values of patients with d -dimer ≥243 ng/ml (0.020 μg/L, IQR 0.015 to 0.035 μg/L) were significantly greater than those of patients with d -dimer <243 ng/ml (0.012 μg/L, IQR 0.010 to 0.020 μg/L, p = 0.004). Similarly, when the study population was stratified according to TnI values below (n = 222) or above (n = 49) the ninety-ninth percentile of upper reference limit concentration, d -dimer values of patients with TnI ≥0.03 μg/L (213 ng/ml, IQR 136 to 342 ng/ml) were significantly greater than those of patients with TnI <0.03 μg/L (108 ng/ml, 56 to 181 ng/ml, p <0.001). The odds ratio for increased d -dimer values in patients with TnI ≥0.03 μg/L compared with those with TnI below such limit was 3.7 (95% confidence interval 1.9 to 7.2, p <0.001).

The results of this retrospective investigation on a cohort of subjects presenting to the ED with new-onset AF attest that a significant number of these patients have increased values of TnI and d -dimer on admission. Moreover, we found that a significant relation exists between these biomarkers, and this finding may have relevant physiopathological and clinical implications. First, the mutual relation existing between d -dimer and cardiospecific troponin suggests that troponin elevations may often be accompanied by activation of blood coagulation, as mirrored by the presence of abnormal d -dimer values (odds ratio 3.7). It is hence conceivable that myocardial injury, as reflected by increased TnI values, could trigger the activation of the coagulation cascade, which is then mirrored by d -dimer elevation. Because an increased d -dimer is associated with greater thromboembolic risk, the concomitant measurement of these 2 biomarkers on ED admission may help identify a particular subset of patients at increased risk of worse prognosis, who may be tightly monitored or targeted with a more aggressive antithrombotic therapy.