Aggravation and provocation of ventricular arrhythmias by antiarrhythmic drugs.

Velebit, V; Podrid, Philip J.; Lown, Bernard; Cohen, Bernice H.; Graboys, Thomas B.

doi:10.1161/01.cir.65.5.886

Cited by 614 publications

(88 citation statements)

References 30 publications

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“…In the majority of patients only a specific drug proves effective, while electrophysiologically similar agents are frequently devoid of effect or may aggravate arrhythmia. "' 32 Our findings suggest the following: (1) Among patients who have experienced recurrent malignant ventricular arrhythmias, maximal exercise testing is safe. It is associated with a 2.3% incidence of sustained arrhythmias requiring prompt intervention for which cardioversion is required during 1.2% of tests in 5.7% of patients.…”

Section: Circulationmentioning

confidence: 76%

Safety of maximal exercise testing in patients at high risk for ventricular arrhythmia.

Young¹,

Lampert²,

Graboys³

et al. 1984

Circulation

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Section: Circulationmentioning

confidence: 76%

Safety of maximal exercise testing in patients at high risk for ventricular arrhythmia.

Young¹,

Lampert²,

Graboys³

et al. 1984

Circulation

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“…Provocation of venricular arrhythmias is increasingly becoming a clinically recognised feature of antiarrhythmic agents, such arrhythmias often occurring within the therapeutic plasma range of the drug (Velebit et al, 1982;Goldstein et al, 1984). The pro-arrhythmic activity of BWA256C, observed at plasma concentrations 3-4 fold greater than those displaying antiarrhythmic activity, further demonstrates the need for caution when using these agents in the medical management of patients with life threatening arrhythmias.…”

Section: Discussionmentioning

confidence: 99%

BW A256C, a chemically novel class 1 antiarrhythmic agent. A comparison of in vitro and in vivo activity with other class 1 antiarrhythmic agents

Allan¹,

Donoghue

Follenfant

et al. 1986

British J Pharmacology

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1 BW A256C (5(3)-amino-6-(2,3-dichlorophenyl)-2,3(2,5)-dihydro-3(5)-imino-2-isopropyl-1,2,4-triazine) is a novel class 1 antiarrhythmic agent designed to combine the features ofpotency with reduced central nervous system penetration. 2 BW A256C reduced the maximum rate of depolarization of guinea-pig ventricle and dog Purkinje fibres in vitro (EC5o, 2.2 x 10-6 M and 1.8 x 10-6 M, respectively), being significantly more potent than quinidine, lidocaine, disopyramide and flecainide. BW A256C was also more potent than these agents at inhibiting aconitine-induced arrhythmias in anaesthetized rats; however, unlike these agents, BW A256C was devoid of hypotensive activity at antiarrhythmic doses. 3 In anaesthetized dogs, intravenous administration of BW A256C (0.25-1 mg kg-') caused a dosedependent suppression of ventricular arrhythmias that occurred on reperfusion of an occluded coronary artery. 4In conscious dogs, intravenous infusion (total dose, 1.5 mg kg 1) or oral administration of BW A256C (1.25-5mg kg-') caused dose-dependent suppression of the ventricular ectopic activity that occurred following 20-24 h of permanent coronary artery ligation. 5In the conscious dog, BWA256C was approximately 7 times more potent and was also longer acting than flecainide. 6 Administration of BW A256C was not associated with any evidence of peripheral or CNS toxicity. However, plasma levels 3-4 times greater than the antiarrhythmic levels were associated with a proarrhythmic activity.

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“…Worsening of pre-existing ventricular arrhythmias or the development of new ventricular arrhythmias following the introduction of an "antiarrhythmic" drug have been described with most agents currently in use (Velebit et al, 1982 A further mechanism of provocation of ventricular arrhythmias is drug interaction. Amiodarone, in combination with other drugs known to prolong the QT interval, has been reported to favor the development of polymorphic ventricular tachycardia (Bmchier and Fauchier, 1978; Kern et al, 1981).…”

Section: Aggravation Of Ventricular Arrhythmiasmentioning

confidence: 99%

Serious adverse effects of amiodarones

McGovern

Garan

Ruskin

1984

Clinical Cardiology

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Summary:Amiodarone is an effective antiarrhythmic drug which has been used successfully to treat a variety of cardiac arrhythmias. Early reports emphasized both the striking efficacy of this agent and the relative paucity of side effects necessitating discontinuing treatment with this drug. As amiodarone has been used more widely and in more diverse patient populations, reports of serious thyroid, pulmonary, cardiovascular, and other adverse reactions have appeared in the literature. In this paper, we review the serious adverse effects that have been reported to date. The incidence of these reactions varies considerably in different series, and cannot be explained solely by different doses employed or by varying methods of drug administration. The final role of amiodarone in the therapy of cardiac arrhythmias cannot be determined until the long-term toxicity has been more thoroughly investigated.

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Aggravation and provocation of ventricular arrhythmias by antiarrhythmic drugs.

Cited by 614 publications

References 30 publications

Safety of maximal exercise testing in patients at high risk for ventricular arrhythmia.

Safety of maximal exercise testing in patients at high risk for ventricular arrhythmia.

BW A256C, a chemically novel class 1 antiarrhythmic agent. A comparison of in vitro and in vivo activity with other class 1 antiarrhythmic agents

Serious adverse effects of amiodarones

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