Summary
Recent data with encainide and flecainide (CAST study) question the benefit of reducing premature ventricular contractions in survivors of myocardial infarction. Proarrhythmic mechanisms might include excessive slowing of conduction. In patients with supraventricular tachycardias, proarrhythmic effects of Class 1c agents are very uncommon.
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References
Hauswirth O, Singh BN. Ionic mechanisms in heart muscle in relation to the genesis and the pharmacologic control of cardiac arrhythmias.Pharmac Rev 1978;30:5–63.
Singh BN, Courtney K. On the classification of antiarrhythmic mechanisms: Experimental and clinical correlations. In: Zipes DP, Jalife J (eds).Cardiac Electrophysiology: From the Cell to the Bedside. Philadelphia: WB Saunders, 1989, in press.
Singh BN. Effects of anti-arrhythmic compounds on the cardiac action potential: Basis for the interpretation of their anti-arrhythmic actions. In: Zipes DP (ed).Progress in Cardiology. Philadelphia: Lea and Febiger, 1987:37–86.
Antonaccio MJ, Gomoll A, Byrne J. Encainide.Cardiovascular Drugs and Therapy 1989;3(5).
Campbell TJ. Kinetics of onset of rate-dependent effects of Class I drugs are important in determining their effects on refractoriness in guinea pig ventricle and provide a theoretical basis for their subclassification.Cardiovasc Res 1983;17:344–352.
The Encainide-Ventricular Tachycardia Study Group. Treatment of life-threatening ventricular tachycardia with encainide hydrochloride in patients with left ventricular dysfunction.Am J Cardiol 1988;62:571–575.
The CAPS Investigators. The Cardiac Arrhythmia Pilot Study.Am J Cardiol 1986;57:91–95.
The Cardiac Arrhythmia Pilot Study (CAPS) Investigators. Effects of encainide, flecainide, imipramine and moricizine on ventricular arrhythmias during the year after myocardial infarction.Am J Cardiol 1988;61:501–509.
Feld GK, Venkatesh N, Singh BN. Pharmacologic conversion and suppression of experimental canine atrial flutter: Differing effects of d-sotalol, quinidine and lidocaine and the significance of changes in refractoriness and conduction.Circ 1986;74:197–204.
Singh BN, Vaughan Williams EM. A third class of antiarrhythmic action. Effects on atrial and ventricular intracellular potentials and other pharmacologic actions on cardiac muscle of MJ1999 and AH 3474.Br J Pharmacol 1970;39:675–685.
Singh BN, Vaughan Williams EM. The effect of amiodarone, a new anti-anginal drug, on cardiac muscle.Br J Pharmacol 1970;39:357–367.
Singh BN, Nademanee K. Control of arrhythmias by selective lengthening of cardiac repolarization: Theoretical considerations and clinical observations.Am Heart J 1985;109:421–430.
Singh BN (ed.).Control of Cardiac Arrhytmias by Lengthening Repolarization. Mount Kisco, NY: Futura Publishing, 1988;1–577.
Singh BN. When is QT prolongation anti-arrhythmic and when is it pro-arrhythmic? (editorial).Am J Cardiol 1989;63:867–869.
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Supported in part by funds from the American Heart Association of the Greater Los Angeles Affiliate and the Medical Research Funds of the Veterans Administration.
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Singh, B.N. Controlling cardiac arrhythmias: To delay conduction or to prolong refractoriness. Cardiovasc Drug Ther 3, 671–674 (1989). https://doi.org/10.1007/BF01857618
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DOI: https://doi.org/10.1007/BF01857618