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Catheter Ablation for Atrial Flutter: Current Concepts and Results
Author(s) -
TOUBOUL PAUL,
SAOUDI NADIR,
ATALLAH GEORGES,
KIRKORIAN GILBERT
Publication year - 1992
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1992.tb01942.x
Subject(s) - medicine , atrial flutter , cardiology , coronary sinus , ablation , catheter ablation , reentry , atrial fibrillation , interatrial septum , atrium (architecture) , anesthesia , left atrium
Ablation of Atrial Flutter . The role of a macroreentrant mechanism within the right atrium is currently accepted in the genesis of human atrial flutter. Fractionated potentials are recordable in various parts of the atrium, suggesting slow conduction areas. Transient entrainment may be helpful in identifying those areas belonging to the reentrant circuit. Using such criteria, the Koch triangle appears to be a critical zone to ablate. Our personal experience includes 16 patients with drug refractory type I atrial flutter who underwent direct catheter ablation of the atrial tissue. In every case, careful mapping of endocardial depolarization during flutter revealed a counterclockwise circus movement within the right atrium, the impulse ascending along the interatrial septum and swinging toward the anterolateral wall of the atrium. Areas of prolonged, fragmented electrograms could usually be detected in the inferior and posteroseptal parts of the right atrium in the vicinity of the coronary sinus os. Transient entrainment was used to provide evidence that these slow conduction areas belonged to the circuit. Under general anesthesia, unipolar shocks of 2 to 2.5 J/kg were delivered to these sites. Immediate ventricular fibrillation occurred in one patient, which required cardioversion, and another subject developed permanent complete atrioventricular block necessitating a VVIR pacemaker. Early relapses affected 50% of the patients: they always led to repeat ablation and additional prescription of antiarrhythmic drugs. Eight patients are currently asymptomatic: five without treatment and three on drugs (mean follow‐up 34 months). In the others, cardiac arrhythmias have persisted: identical flutter in half of them, or newly developed paroxysmal atrial fibrillation. In the arrhythmia‐free subjects, atrial flutter remained electrically inducible in 40% of the cases. In conclusion, efficacy of catheter ablation for refractory atrial flutter is still modest. Further progress may depend on a better understanding of human atrial flutter and also on new modes of ablation (radiofrequency current).