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Figures

Fig. 1

The chart of time to clinical evaluation, management, and main outcomes at 1-year follow-up in patients presenting with recent-onset AF.

Fig. 2

Event-free survival in the entire cohort (a-c) and propensity-matched cohort (A-C) based on troponin rise on the 1-month (a and A), 1-year (b and B), and 10-year (c and C) follow-up. Black line indicates patients with troponin rise; gray dot line, patients without troponin rise. P < .001.

Fig. 3

Coronary atherosclerosis in patients with or without troponin rise (P < .001). Degrees of atherosclerosis are as follows: critical, coronary stenosis greater than or equal to 70%, black bars; subcritical, coronary stenosis greater than or equal to 30% to 69%, gray bars; and “coronary disease free,” stenosis less than 30%, light bars.

Fig. 4

Receiver operating characteristic curve analysis for patients presenting with troponin rise to detect the optimal cutoff value in sensitivity/specificity ratio to revascularization. ROC Area, 0.658; SE, 0.069; 95% CI, 0.523 to 0.792.

Abstract

Background

The relationship between troponin and atrial fibrillation (AF) without acute coronary syndrome is still unclear. We sought to investigate the presence of coronary atherosclerosis and adverse outcomes in patients with AF.

Methods

Consecutive patients with recent-onset AF and without severe comorbidities were enrolled between 2004 and 2013. Patients with a troponin rise or with adverse outcomes were considered for coronary angiography and revascularization when “critical” stenosis (≥70%) was recognized. Propensity score matching was performed to adjust for baseline characteristics; after matching, no differences existed between the groups of patients with or without troponin rise. The primary end point was the composite of acute coronary syndrome, revascularization, and cardiac death at 1- and 12-month follow-ups.

Results

Of 3627 patients enrolled, 3541 completed the study; 202 (6%) showed troponin rise; and 91 (3%), an adverse outcome. In the entire cohort, on multivariate analysis, the odds ratio for the occurrence of the primary end point of troponin rise was 14 (95% confidence interval [CI], 10-23; P < .001), and that of known coronary artery disease was 3 (CI, 2-5; P = .001). In the matching cohort, the odds ratio of troponin rise was 10 (CI, 4-22; P < .001), and that of TIMI score greater than 2 was 4 (CI, 2-9; P ≤ .001). In the entire cohort, patients with or without troponin rise achieved the primary end point in 38 (19%) and 43 (1%) patients, respectively (P < .001). Stroke occurred in 4 (2%) and 20 (1%), respectively (P = .018). Critical stenosis and revascularization account for 23 (12%) and 15 (1%), respectively (P < .001). In the matching cohort, results were confirmed, but incidence of stroke was comparable.

Conclusions

Patients with recent-onset AF and troponin rise showed higher prevalence of coronary atherosclerosis and adverse cardiac events. Stroke per se did not succeed in justifying the high morbidity. Thus, beyond stroke, coronary atherosclerosis might have a pivotal role in poor outcomes.

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?The authors declare no potential conflicts of interest.

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