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Clinical Trial
Journal Article
Clinical prediction of cavotricuspid isthmus dependence in patients referred for catheter ablation of "typical" atrial flutter.
Journal of Cardiovascular Electrophysiology 2005 September
INTRODUCTION: Typical atrial flutter (AFL) can be cured by catheter ablation of the cavotricuspid isthmus (CTI). The surface electrocardiogram (ECG) is not always diagnostic of isthmus dependence of AFL. The aim of this study was to evaluate clinical parameters for the prediction of isthmus-dependent AFL.
METHODS AND RESULTS: Sixty consecutive adult patients without suspected atriotomy-related AFL, congenital heart disease, or previous AFL ablation, referred for catheter ablation of presumed typical AFL were studied. All patients had distinct flutter waves in the inferior leads, suggestive of CTI-dependent AFL, either on presentation to the electrophysiology (EP) lab or documented on prior ECG. Electrophysiology study was performed in the standard fashion. Patients who presented to the EP laboratory not in AFL underwent arrhythmia induction with a burst pacing protocol. A clinical history of persistent AFL (P = 0.0001) and existence of AFL on presentation to the EP laboratory (P = 0.0001) were strong predictors of CTI dependence. History of atrial fibrillation (P = 0.19), structural heart disease (P = 0.6), hypertension (P = 0.4), and previous cardiac surgery (P = 0.5), as well as the nature of AFL-related symptoms (P = 0.5), were not predictors of CTI-dependent AFL documented during EP study.
CONCLUSION: In patients with ECG suggestive of typical AFL, the presence of persistent rather than paroxysmal AFL and presentation to the EP laboratory in AFL are strong predictors of CTI-dependent AFL. A paroxysmal pattern of AFL predicts noninducibility of CTI-dependent AFL during EP study. CTI ablation may therefore be less effective in these patients.
METHODS AND RESULTS: Sixty consecutive adult patients without suspected atriotomy-related AFL, congenital heart disease, or previous AFL ablation, referred for catheter ablation of presumed typical AFL were studied. All patients had distinct flutter waves in the inferior leads, suggestive of CTI-dependent AFL, either on presentation to the electrophysiology (EP) lab or documented on prior ECG. Electrophysiology study was performed in the standard fashion. Patients who presented to the EP laboratory not in AFL underwent arrhythmia induction with a burst pacing protocol. A clinical history of persistent AFL (P = 0.0001) and existence of AFL on presentation to the EP laboratory (P = 0.0001) were strong predictors of CTI dependence. History of atrial fibrillation (P = 0.19), structural heart disease (P = 0.6), hypertension (P = 0.4), and previous cardiac surgery (P = 0.5), as well as the nature of AFL-related symptoms (P = 0.5), were not predictors of CTI-dependent AFL documented during EP study.
CONCLUSION: In patients with ECG suggestive of typical AFL, the presence of persistent rather than paroxysmal AFL and presentation to the EP laboratory in AFL are strong predictors of CTI-dependent AFL. A paroxysmal pattern of AFL predicts noninducibility of CTI-dependent AFL during EP study. CTI ablation may therefore be less effective in these patients.
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