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Cellular and Clinical Electrophysiology of Verapamil‐Sensitive Ventricular Tachycardias
Author(s) -
LAUER MICHAEL R.,
BING LIEM L.,
YOUNG CHARLIE,
SUNG RUEY J.
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.tb00992.x
Subject(s) - medicine , cardiology , reentry , verapamil , ventricular tachycardia , coronary artery disease , tachycardia , myocardial infarction , electrophysiology , procainamide , amiodarone , anesthesia , atrial fibrillation , calcium
Verapamil‐Sensitive Ventricular Tachycardias. Ventricular tachycardia (VT) due to reentry is often associated with organic structural heart disease, such as coronary artery disease with previous myocardiai infarction, and primary or secondary cardiomyopathy. Treatment of this form of VT generally requires the use of potent antiarrhythmic drugs such as procainamide, quinidine, and amiodarone, or nonpharmacologic interventions such as endocardial resection and implantation of cardioverter defibrillators. Some forms of VT, typically occurring in younger patients and not associated with structural heart disease, may be due to a mechanism other than reentry and may be terminated or prevented by Ca 2+ channel or beta blockers. Because these tachycardias are often so effectively treated with these rather benign agents, all patients with sustained VT undergoing an electrophysiologic study should be carefully evaluated to rule out the possibility of having these forms of VT. These tachycardias may be induced by treadmill exercise testing, programmed electrical stimulation, and/or catecbolamine infusion. While it appears that the mechanisms of these tachycardias may be caused by triggered activity related to afterdepolarizations or enhanced automaticity, there is evidence that some may in fact be due to reentry involving Ca 2+ ‐dependent slow conduction. The cellular mechanisms of triggered activity and enbanced automaticity, and their relation to clinical ventricular arrhythmias, are discussed. ( J Cardiovasc Electrophysiol, Vol. 3. pp. 500–514 October 1992 )