• Hong Euy Lim, Cheol Ung Choi, Jin Oh Na, Jong-Il Choi, Seong Hwan Kim, Jin Won Kim, Eung Ju Kim, Seong Woo Han, Sang Weon Park, Seung-Woon Rha, Chang Gyu Park, Hong Seog Seo, Dong Joo Oh, Chun Hwang, and Young-Hoon Kim.
• Cardiovascular Center, Division of Cardiology, Department of Internal Medicine, Korea University Guro Hospital, Korea University College of Medicine, Seoul, Republic of Korea.
• Circ Arrhythm Electrophysiol. 2013 Apr 1; 6 (2): 318-26.

BackgroundIatrogenic 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 ResultsWe 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).ConclusionsMyocardial 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 RegistrationURL: http://cris.cdc.go.kr. Unique identifier: KCT0000030.

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