Effects of Iatrogenic Myocardial Injury on Coronary Microvascular Function in Patients Undergoing Radiofrequency Catheter Ablation of Atrial Fibrillation

Abstract

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.