1952
DOI: 10.1016/0002-8703(52)90028-8
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Ventricular tachycardia following the administration of quinidine

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Cited by 21 publications
(9 citation statements)
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“…How ever, it has been pointed out that were this the case the incidence of non fatal arterial embolism should be higher following conversion than it is in most series of cases (lOS, 106). It has been shown both experimentally and clinically that quinidine itself can produce ventricular arrhythmias, and it is now believed that at least certain of these fatalities are due to ventricular standstill or '\Tentricular fibrillation produced by the quinidine (107,108,109). If this is true, the use of procaine amide may prove to be no safer in this regard, because Grumbach (110) has shown in animal experiments that it [and potassium and most other agents which are used for their irri tability depressing properties (111)]' will also produce ventricular arrhy thmias under certain circumstances.…”
Section: Arrhythmiasmentioning
confidence: 99%
“…How ever, it has been pointed out that were this the case the incidence of non fatal arterial embolism should be higher following conversion than it is in most series of cases (lOS, 106). It has been shown both experimentally and clinically that quinidine itself can produce ventricular arrhythmias, and it is now believed that at least certain of these fatalities are due to ventricular standstill or '\Tentricular fibrillation produced by the quinidine (107,108,109). If this is true, the use of procaine amide may prove to be no safer in this regard, because Grumbach (110) has shown in animal experiments that it [and potassium and most other agents which are used for their irri tability depressing properties (111)]' will also produce ventricular arrhy thmias under certain circumstances.…”
Section: Arrhythmiasmentioning
confidence: 99%
“…In occasional patients, this dosing tactic resulted in a wide-complex, relatively slow VT (Wetherbee et al 1951). This approach to AF management was supplanted by electrical cardioversion, but similar VTs were noted with the introduction of the potent sodium channel blockers encainide and flecainide (Winkle et al 1981;Oetgen et al 1983).…”
Section: Clinical Featuresmentioning
confidence: 99%
“…One feature of treatment with these agents was that arrhythmia suppression was routinely accompanied by obvious and striking prolongation of P wave, PR interval, and QRS durations, evidence of marked conduction slowing across the heart. Such ECG changes had been seen with the aggressive use of high dose of quinidine to convert atrial fibrillation, 6 where they were considered a sign of drug toxicity, occasionally preceding the development of ventricular tachycardia (VT). Even during the early development of encainide and flecainide, case reports emerged that occasional patients appeared to develop “paradoxical” worsening of ventricular arrhythmias, including patients who developed incessant sustained monomorphic or polymorphic VT, some of whom who could not be resuscitated.…”
Section: Learning From Historymentioning
confidence: 99%