The treatment of quinidine-induced ventricular fibrillation by closed-chest resuscitation and external defibrillation

Rainier-Pope, C; Schrire, V.; Beck, Walter; Barnard, C. N.

doi:10.1016/0002-8703(62)90002-9

Cited by 25 publications

(5 citation statements)

References 51 publications

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“…Proved ventricular fibrillations as a toxic effect of quinidine therapy has been reported on numerous occasions (Davis and Sprague, 1928;Sokolow, 1951 ;Selzer and Wray, 1964;Davies, Leak, and Oram, 1965). Rainier-Pope et al (1962) make the point that in their two patients, as in ours, the attacks were heralded by frequent ventricular ectopic beats.…”

Section: Commentsupporting

confidence: 50%

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Unilateral Renal Vein Thrombosis with Nephrotic Syndrome

Khokhani¹,

Raghavan²,

Sant³

et al. 1966

BMJ

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Section: Commentsupporting

confidence: 50%

“…Molar sodium lactate (Bellet, 1963), sympathomimetics (Rokseth and Storstein, 1963;Linenthal and Zoll, 1963), calcium sodium versenate (Luchi et al, 1963), and external massage and direct-current shock (Rainier-Pope et al, 1962) are among the remedies that have been used either clinically or experimentally. In our patient the E.C.G.…”

Section: Commentmentioning

confidence: 99%

Unilateral Renal Vein Thrombosis with Nephrotic Syndrome

Khokhani¹,

Raghavan²,

Sant³

et al. 1966

BMJ

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“…Clinically, the phenomenon of quinidine-induced syncope was first described by Frey et al [64] and was suggested to be related to malignant arrhythmias by Rainer-Pope et al [182] and proven by Selzer et al [203] and others (115,183,228,101]. The incidence of quinidine-induced syncopal arrhythmias is related to the treated arrhythmias [217].…”

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

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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.

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“…AVT was found to be induced mainly by quinidinel [8][9][10][11][12][13] and by other antiarrhythmic and cardiac drugs such as procainamide,"l 1" disopyramide,'5' 18 lidocainell and prenylamine. "1 Occasionally, other drugs such as phenothiazines,'7 as well as hypokalemia,4 7 hypomagnesemia, ' 18 electrical ventricular stimulation,19 congenital QT prolongation syndrome,20 or acute central nervous system damage2' may precipitate AVT.…”

mentioning

confidence: 99%