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Verapamil-sensitive left ventricular tachycardia in patients with coronary artery disease: clinical and
C Sorbera1, M Cohen, V Kuznetsov
1Division of Cardiology, Westchester Medical Center, New York Medical College, Valhalla, New York 10595, USA.
Insights
Verapamil effectively treated left ventricular tachycardia in patients with severe coronary artery disease. This suggests triggered activity in the Purkinje system, responsive to calcium channel blockers, is a key mechanism.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Patients with severe coronary artery disease and myocardial infarction often present with complex ventricular arrhythmias.
- Left ventricular tachycardia (LVT) in this population can be challenging to manage, impacting cardiac function and prognosis.
Observation:
- Three male patients with severe coronary artery disease, prior myocardial infarction, and significant left ventricular dysfunction (mean EF 34%) experienced verapamil-sensitive LVT.
- The LVT exhibited a right bundle branch block/left axis deviation morphology and was sustained by isoproterenol.
- One patient had incessant LVT post-coronary bypass surgery.
Findings:
- Electrophysiological studies suggested triggered activity, potentially in the Purkinje system, as the mechanism, differing from typical reentry mechanisms seen in non-ischemic VT.
- Verapamil successfully terminated the LVT in all patients.
- Adenosine, beta-blockers, and Class I/III antiarrhythmics were ineffective.
- Radiofrequency ablation guided by Purkinje potentials was successful.
Implications:
- Verapamil-sensitive LVT in ischemic heart disease may arise from triggered activity, responsive to calcium channel blockade.
- This finding expands the understanding of VT mechanisms in patients with structural heart disease.
- Targeting Purkinje system activity with calcium channel blockers or ablation offers a potential therapeutic strategy.
Abstract:
This is a retrospective review of three male patients with verapamil-sensitive left ventricular tachycardia, severe coronary artery disease, and past myocardial infarction. Each patient had severe left ventricular dysfunction (mean ejection fraction 34%). Each tachycardia had a right bundle branch block/left axis deviation morphology, which was sustained with isoproterenol. One patient had incessant tachycardia 3 days after coronary bypass surgery. Electrophysiology and clinical parameters were suggestive of triggered activity rather than reentry. Each tachycardia was terminated with verapamil but failed with adenosine, beta blockers, and class I/III antiarrhythmics. Prior cases of verapamil-sensitive ventricular tachycardia have been seen in patients without organic heart disease, and the putative mechanism appears to be reentry. These patients with ischemic coronary artery disease may exhibit a mechanism of triggered activity in the Purkinje system region, which is responsive to calcium channel blockade. Successful radiofrequency ablation was guided by Purkinje potentials.
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