Verapamil eliminates the hierarchical nature of activation frequencies from the pulmonary veins to the atria during paroxysmal atrial fibrillation

• Published in: Heart rhythm Vol. 7; no. 5; p. 577
• Main Authors: Kushiyama, Yasunori, Osaka, Toshiyuki, Yokoyama, Eriko, Hasebe, Hideyuki, Kuroda, Yusuke, Kamiya, Kaichiro, Kodama, Itsuo
• Format: Journal Article
• Language: English
• Published: United States 01.05.2010
• Subjects: Analysis of Variance; Anti-Arrhythmia Agents - adverse effects; Anti-Arrhythmia Agents - therapeutic use; Atrial Fibrillation - chemically induced; Atrial Fibrillation - etiology; Atrial Fibrillation - pathology; Atrial Fibrillation - surgery; Catheter Ablation; Coronary Sinus - drug effects; Coronary Sinus - innervation; Coronary Sinus - pathology; Electrocardiography; Female; Fourier Analysis; Heart Atria - drug effects; Heart Atria - innervation; Heart Atria - pathology; Heart Conduction System - drug effects; Heart Conduction System - pathology; Heart Rate - drug effects; Humans; Male; Middle Aged; Prospective Studies; Pulmonary Veins - drug effects; Pulmonary Veins - innervation; Pulmonary Veins - pathology; Verapamil - adverse effects; Verapamil - therapeutic use
• ISSN: 1556-3871
• DOI: 10.1016/j.hrthm.2010.01.008

There is evidence that verapamil promotes the persistence of paroxysmal atrial fibrillation (AF). Little is known about the underlying mechanisms. The purpose of this study was to determine the effect of verapamil on dominant frequencies (DFs) in the pulmonary veins (PVs) and atria during paroxysmal AF with reference to its potential arrhythmogenicity. Forty-three patients with paroxysmal AF were studied. Bipolar electrograms were recorded simultaneously during AF from the right atrial free wall (RAFW), coronary sinus (CS) and three PVs, or two PVs and the left atrial appendage (LAA). The DFs were obtained by fast Fourier transform analysis before and after infusion of verapamil (0.1 mg/kg, intravenously). At baseline, the maximum DF among the PVs (6.9 +/- 0.9 Hz) was significantly higher than the DF in the RAFW (6.2 +/- 0.7 Hz), CS (5.7 +/- 0.5 Hz), or LAA (5.9 +/- 0.7 Hz) (P<.01); there was a substantial PV-to-atrial DF gradient (RAFW 0.7 +/- 0.9, CS 1.1 +/- 0.7, LAA 0.7 +/- 0.9 Hz). Verapamil increased the atrial DF to 6.9 +/- 0.8, 6.6 +/- 0.7, and 7.2 +/- 1.0 Hz in the RAFW, CS, and LAA, respectively (P<.0001) but did not affect the maximum PV DF (7.1 +/- 0.7 Hz). The PV-to-atrial DF gradient was eliminated after verapamil (RAFW 0.2 +/- 0.8, CS 0.5 +/- 0.6, LAA -0.4 +/- 0.8 Hz; P<.01 vs. baseline). Verapamil increases the activation frequency in the atria but not in the PVs, eliminating the PV-to-atrial DF gradient during paroxysmal AF.