Ventricular Tachycardia Associated With Flecainide

Muhiddin, Khulood A.; Nathan, Anthony W.; Hellestrand, K; Banim, SeamusO.; Camm, A. John

doi:10.1016/s0140-6736(82)91238-7

Cited by 21 publications

(7 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Repolarization properties with most Class IC agents are paradoxical in ventricular and Purkinje fibers, with marked shortening of refractoriness in the latter and either no effect of lengthening in the former. These divergent effects contribute to the antiarrhythmic potency of Class IC agents, but have recently been suggested to cause proarrhythmia as well [157].…”

Section: Characteristics Of Proarrhythmia After Drug-lnduced Qt Prolomentioning

confidence: 99%

“…However, this "balance" may not be achieved in all parts of the heart, especially not in the diseased heart. As a consequence, heterogeneities in the recovery of excitability may be enhanced and may facilitate focal reexcitation and arrhythmogenic effects without affecting the QT interval [157,177].…”

Section: Characteristics Of Proarrhythmia After Drug-lnduced Qt Prolomentioning

confidence: 99%

See 1 more Smart Citation

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

Zehender

Hohnloser

Just

1991

Cardiovasc Drug Ther

View full text Add to dashboard Cite

The antiarrhythmic principle of drug-induced QT-interval prolongation is well known. However, with the widespread use of the presently known and new Class III antiarrhythmic agents under investigation, and the growing number of agents not primarily designed as antiarrhythmic drugs that potentially cause QT prolongation, we have also become aware of the proarrhythmic hazards associated with many of these agents. The proarrhythmic risk differs markedly from one agent to another and interferes with many individual clinical variables (e.g., hypokalemia, sinus bradycardia). This paper summarizes the present data on the proarrhythmic risk of drug-induced QT prolongation, including the value and problems of the rate-corrected QT interval, the mechanisms involved in the genesis of proarrhythmia, and the clinical cofactors that facilitate the occurrence of proarrhythmic events. In addition, an extensive database provides information on the known proarrhythmic risk of all currently used QT-prolonging agents.

show abstract

Section: Characteristics Of Proarrhythmia After Drug-lnduced Qt Prolomentioning

confidence: 99%

Section: Characteristics Of Proarrhythmia After Drug-lnduced Qt Prolomentioning

confidence: 99%

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

Zehender

Hohnloser

Just

1991

Cardiovasc Drug Ther

View full text Add to dashboard Cite

show abstract

“…On the other hand, have reported ventricular arrhythmias associated with its use which they sugges-ted may be related to slow intraventricular conduction rather than repolarization changes. Ventricular tachycardia from a similar mechanism was reported in association with flecainide treatment (Muhiddin et al, 1982). Nathan et al (1984) reported 6 further cases of cardiac arrhythmias associated with flecainide therapy.…”

Section: Absence Of Adverse Effectsmentioning

confidence: 52%

Is there an ideal antiarrhythmic drug? A review — with particular reference to class I antiarrhythmic agents

Muhiddin

Turner

1985

Postgraduate Medical Journal

View full text Add to dashboard Cite

“…However, clinical trial results indicated that in patients with structural heart disease susceptible to ventricular arrhythmias, fl ecainide might in fact be pro-arrhythmogenic [61,62] . Recently, there has been a resurgence of enthusiasm for the use of fl ecainide in a select group of CPVT patients with genetic predisposition to ventricular arrhythmias and SCD.…”

Section: Wwwchinapharcom Mccauley MD Et Almentioning

confidence: 99%

Targeting ryanodine receptors for anti-arrhythmic therapy

McCauley

Wehrens

2011

Acta Pharmacol Sin

View full text Add to dashboard Cite

Antiarrhythmic drugs are a group of pharmaceuticals that suppress or prevent abnormal heart rhythms, which are often associated with substantial morbidity and mortality. Current antiarrhythmic drugs that typically target plasma membrane ion channels have limited clinical success and in some cases have been described as being pro-arrhythmic. However, recent studies suggest that pathological release of calcium (Ca 2+ ) from the sarcoplasmic reticulum via cardiac ryanodine receptors (RyR2) could represent a promising target for antiarrhythmic therapy. Diastolic SR Ca 2+ release has been linked to arrhythmogenesis in both the inherited arrhythmia syndrome 'catecholaminergic polymorphic ventricular tachycardia' and acquired forms of heart disease (eg, atrial fi brillation, heart failure). Several classes of pharmaceuticals have been shown to reduce abnormal RyR2 activity and may confer protection against triggered arrhythmias through reduction of SR Ca 2+ leak. In this review, we will evaluate the current pharmacological methods for stabilizing RyR2 and suggest treatment modalities based on current evidence of molecular mechanisms.

show abstract

Ventricular Tachycardia Associated With Flecainide

Cited by 21 publications

References 9 publications

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

Is there an ideal antiarrhythmic drug? A review — with particular reference to class I antiarrhythmic agents

Targeting ryanodine receptors for anti-arrhythmic therapy

Contact Info

Product

Resources

About