New Antiarrhythmic Drugs for Ventricular Arrhythmias: Do They Work

  • B. N. Singh
Conference paper


In the early 1960s, at the time Coronary Care Units (CCUs) were conceived and being set up as a way to reduce arrhythmia mortality by detecting, treating, and preventing ventricular arrhythmias, there were very few antiarrhythmic drugs available to the clinician — quinidine, procainamide, and lidocaine (1). Disopyramide was being developed and had not attained established usage. Digoxin was regarded as being an antiarrhythmic compound but its use in controlling ventricular tachyarrhythmias was never established. Thus, the field of antiarrhythmic drugs was dominated by drugs that acted fundamentally by delaying conduction via inhibition of sodium-channel activity. This was considered as having several major consequences. First, the delay in conduction and often complete block in certain tissues was thought to convert unidirectional to bidirectional block, thereby terminating and preventing reentrant tachycardia. Second, the block in conduction might be expected to markedly suppress premature ventricular contractions (PVCs) by preventing their propagation. It was consistent with the observation that the greater the propensity of a compound (e.g., class I agent) to block conduction, the higher its suppressant effect on PVCs. Third, it was realized that the refractory period of the ventricular myocardium may be prolonged by the blocking of sodium-channel activity by delaying its reactivation. Thus, the change in refractory period was time dependent when affected by drugs that selectively blocked sodium channels. It so happened that in the case of quinidine, the archetype of antiarrhythmic drugs, as well as in the case of procainamide and disopyramide, there was the additional property of lengthening repolarization, which in itself could prolong the refractory period and they constitute a discrete antifibrillatory mechanism. On the other hand, there has always been the theoretical possibility that excessive delay in conduction induced by sodium-channel blockers may create the substrate for reentrant ventricular tachycardia/ventricular fibrillation (VT/VF) as a proarrhythmic reaction (2, 3).


Ventricular Arrhythmia Antiarrhythmic Drug Total Mortality Block Sodium Channel Program Electrical Stimulation 
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Copyright information

© Springer-Verlag Italia, Milano 1996

Authors and Affiliations

  • B. N. Singh
    • 1
  1. 1.Department of Cardiology, Veterans Affairs Medical Center of West Los Angeles, and the Department of MedicineUCLA School of MedicineLos AngelesUSA

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