Affiliation:
1. From the Department of Cardiology (D.B., F.O., M.A., S.E., K.-H.K.), AK St. Georg, Hamburg, Germany; Department of Rhythmology (T.A., R.W.), Bad Krozingen, Germany; and the Wichita Institute for Clinical Research, Wichita, Kan (J.E.V.-M.).
Abstract
Background—
We report on 4 patients (aged 57 to 77 years; 3 men) who developed drug-refractory, repetitive ventricular tachyarrhythmias after acute myocardial infarction (MI). All episodes of ventricular arrhythmias were triggered by monomorphic ventricular premature beats (VPBs) with a right bundle-branch block morphology (RBBB).
Methods and Results—
Left ventricular (LV) mapping was performed to attempt radiofrequency (RF) ablation of the triggering VPBs. Activation mapping of the clinical VPBs demonstrated the earliest activation in the anteromedial LV in 1 patient and in the inferomedial LV in 2 patients. Short, high-frequency, low-amplitude potentials were recorded that preceded the onset of each extrasystole by a maximum of 126 to 160 ms. At the same site, a Purkinje potential was documented that preceded the onset of the QRS complex by 23 to 26 ms during sinus rhythm. In 1 patient, only pace mapping was attempted to identify areas of interest in the LV. Six to 30 RF applications abolished all local Purkinje potentials at the site of earliest activation and/or perfect pace mapping and suppressed VPBs in all patients. No episode of ventricular tachycardia or fibrillation has recurred for 33, 14, 6, and 5 months in patients 1, 2, 3, and 4, respectively.
Conclusions—
Incessant ventricular tachyarrhythmias after MI may be triggered by VPBs. RF ablation of the triggering VPBs is feasible and can prevent drug-resistant electrical storm, even after acute MI. Catheter ablation of the triggering VPBs may be used as a bailout therapy in these patients.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine
Cited by
242 articles.
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