Cardiac troponin I: prothrombotic risk marker in non-valvular atrial fibrillation

Evidence of a link between small rises in cardiac troponin I (cTnI) and an increased risk of thromboembolic events (TE) in atrial fibrillation (AF) is currently scarce.

We aimed to assess the relation between cTnI and findings of an increased thromboembolic risk in patients with non-valvular AF using transesophageal echocardiography.

We have included 245 patients performing transthoracic and transesophageal echocardiogram, alongside with laboratory assessment (including cTnI) in a cross-sectional survey. Changes associated to TE were sought on transesophageal echocardiogram: left atrial or left atrial appendage thrombus, dense spontaneous echocardiographic contrast, low flow velocities in the left atrial appendage and protuberant aortic plaques. Comparisons were performed according to the baseline concentration of cTnI, regarding the prevalence of these changes. We have added cTnI to CHADS2 and CHA2DS2-VASc scores in order to assess its capability to refine risk stratification using transesophageal markers as surrogate endpoints and assessed it by means of ROC-curve analysis and Net Reclassification Improvement (NRI).

A direct relation between rising concentrations of cTnI and a higher prevalence of transesophageal echocardiogram changes was found. Furthermore, the addition of cTnI to CHADS2 and CHA2DS2-VASc scores improved their ability to predict changes associated to TE on transesophageal echocardiography both through ROC-curve analysis and NRI.

cTnI seems to be associated to thromboembolic risk in patients with AF. The possible role of cTnI in the refinement of risk stratification schemes needs to be tested in further prospective studies using clinical endpoints.