Effects of iatrogenic myocardial injury on coronary microvascular function in patients undergoing radiofrequency catheter ablation of atrial fibrillation

Hong Euy Lim, Cheol Ung Choi, Jin Oh Na, Jongil 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, Young Hoon Kim

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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.

Original languageEnglish
Pages (from-to)318-326
Number of pages9
JournalCirculation: Arrhythmia and Electrophysiology
Volume6
Issue number2
DOIs
Publication statusPublished - 2013 Apr 1

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Catheter Ablation
Atrial Fibrillation
Activated-Leukocyte Cell Adhesion Molecule
Wounds and Injuries
Phospholipases
Lipoproteins
Cardiac Arrhythmias
Nitric Oxide
Recurrence
Blood Vessels
Echocardiography
Coronary Vessels
Myocardium

Keywords

  • Atrial fibrillation
  • Catheter ablation
  • Coronary microvascular function
  • Index of microvascular resistance

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

@article{bd418e535db2472d834d496b64a33f48,
title = "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.",
keywords = "Atrial fibrillation, Catheter ablation, Coronary microvascular function, Index of microvascular resistance",
author = "Lim, {Hong Euy} and Choi, {Cheol Ung} and Na, {Jin Oh} and Jongil Choi and Kim, {Seong Hwan} and Kim, {Jin Won} and Kim, {Eung Ju} and Han, {Seong Woo} and Park, {Sang Weon} and Seung-Woon Rha and Park, {Chang Gyu} and Seo, {Hong Seog} and Oh, {Dong Joo} and Chun Hwang and Kim, {Young Hoon}",
year = "2013",
month = "4",
day = "1",
doi = "10.1161/CIRCEP.113.000282",
language = "English",
volume = "6",
pages = "318--326",
journal = "Circulation: Arrhythmia and Electrophysiology",
issn = "1941-3149",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Effects of iatrogenic myocardial injury on coronary microvascular function in patients undergoing radiofrequency catheter ablation of atrial fibrillation

AU - Lim, Hong Euy

AU - Choi, Cheol Ung

AU - Na, Jin Oh

AU - Choi, Jongil

AU - Kim, Seong Hwan

AU - Kim, Jin Won

AU - Kim, Eung Ju

AU - Han, Seong Woo

AU - Park, Sang Weon

AU - Rha, Seung-Woon

AU - Park, Chang Gyu

AU - Seo, Hong Seog

AU - Oh, Dong Joo

AU - Hwang, Chun

AU - Kim, Young Hoon

PY - 2013/4/1

Y1 - 2013/4/1

N2 - 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.

AB - 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.

KW - Atrial fibrillation

KW - Catheter ablation

KW - Coronary microvascular function

KW - Index of microvascular resistance

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U2 - 10.1161/CIRCEP.113.000282

DO - 10.1161/CIRCEP.113.000282

M3 - Article

C2 - 23476035

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JO - Circulation: Arrhythmia and Electrophysiology

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