Key result
Radiofrequency catheter ablation provoked coronary microvascular dysfunction, with an IMR change cutoff of 9.3 mm Hg/s predicting AF recurrence with 56.7% sensitivity and 91.2% specificity (P=0.028).
Why the study?
Does radiofrequency catheter ablation for atrial fibrillation cause coronary microvascular dysfunction and systemic inflammation?
Observational (n=83)
Does radiofrequency catheter ablation for atrial fibrillation cause coronary microvascular dysfunction and systemic inflammation?
Myocardial damage from radiofrequency catheter ablation for atrial fibrillation induces transient coronary microvascular and diastolic dysfunction, which may contribute to early arrhythmia recurrence.
May link ablation-induced microvascular dysfunction to recurrence; leaves open whether mitigation reduces events.
BACKGROUND: Iatrogenic myocardial injury by radiofrequency catheter ablation (RFCA) releases proinflammatory substances from damaged myocardium, and these may contribute to endothelial dysfunction in systemic vascular structure. The aim of this study is to evaluate the effect of nonischemic myocardial damage on coronary microvascular function in patients undergoing atrial fibrillation (AF) ablation. METHODS AND RESULTS: We included 49 patients who underwent AF ablation (paroxysmal AF=25, persistent AF=24) and 34 controls. Immediately before and after RFCA, index of microvascular resistance (IMR) was assessed at left anterior descending coronary artery, and blood samples were obtained for analyses of nitric oxide (NO), activated leukocyte cell adhesion molecule, and lipoprotein-associated phospholipase. Transthoracic echocardiography was performed at baseline, 1 day, 1 month, and 3 months after RFCA. Compared with baseline, IMR, activated leukocyte cell adhesion molecule, and lipoprotein-associated phospholipase increased and NO decreased after RFCA. In 36 subjects with increasing IMR, E/E' ratio increased at 1 day and returned to baseline level at 3 months after RFCA. Changes in activated leukocyte cell adhesion molecule and lipoprotein-associated phospholipase between baseline and after RFCA were independently related to the increase in IMR. In 14 subjects (28.6%), arrhythmia recurred. Using a cutoff value of 9.3 mm Hg/s, sensitivity was 56.7% and specificity was 91.2% for IMR change in predicting AF recurrence (P=0.028). CONCLUSIONS: Myocardial damage by RFCA provoked coronary microvascular dysfunction through systemic proinflammatory reaction that may contribute to transient diastolic dysfunction. This phenomenon may represent a mechanism for early recurrence of arrhythmia after RFCA. CLINICAL TRIAL REGISTRATION: URL: http://cris.cdc.go.kr. Unique identifier: KCT0000030.
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Lim et al. (2013) conducted an observational in Atrial fibrillation (n=83). Radiofrequency catheter ablation (RFCA) vs. Controls was evaluated on IMR change in predicting AF recurrence (p=0.028). Radiofrequency catheter ablation provoked coronary microvascular dysfunction, with an IMR change cutoff of 9.3 mm Hg/s predicting AF recurrence with 56.7% sensitivity and 91.2% specificity (P=0.028).
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