1966
DOI: 10.1136/bmj.1.5502.1522
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Quinidine-induced Paroxysmal Ventricular Fibrillation Treated with Propranolol

Abstract: This report describes such a case. The diagnosis of renal vein thrombosis was suspected from the renal histopathology and radioisotope renography and was confirmed by inferior vena cavography.CASE REPORTA 19-year-old youth who worked in a grain shop was referred to us for puffiness of the face and swelling of the feet of five months' duration. The onset was insidious and was not preceded by pain in the loins. There was no history of respiratory symptoms suggestive of pulmonary embolism.

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Cited by 20 publications
(2 citation statements)
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“…We are, therefore, of the opinion that combined treatment with pro pranolol and quinidine is indicated in patients with atrial fibrillation because of the incidence of successful outcome, because sinus rhythm can be maintained, because it is excellently tolerated, and because propranolol, with its depressant effect on ventricular myocardial excitability [Seaton, 1966], provides a safeguard against the possibility of quinidine-induced syncope due to ventricular fibrillation.…”
Section: Discussionmentioning
confidence: 99%
“…We are, therefore, of the opinion that combined treatment with pro pranolol and quinidine is indicated in patients with atrial fibrillation because of the incidence of successful outcome, because sinus rhythm can be maintained, because it is excellently tolerated, and because propranolol, with its depressant effect on ventricular myocardial excitability [Seaton, 1966], provides a safeguard against the possibility of quinidine-induced syncope due to ventricular fibrillation.…”
Section: Discussionmentioning
confidence: 99%
“…(Tachycardie Ventriculaire en Torsades en Torsades de Pointe-Κοιλιακή ταχυκαρδία δίκην ριπι- 31,32,85,101,112,113) Ή έμφάνισις μεμονωμένων έκτακτων συστολών καί ώς συνέπεια αύ-των ή έμφάνισις της ώς άνω επικινδύνου διαταραχής του κοιλιακού ρυθ μού, κατόπιν χορηγήσεως κινιδίνης, πιθανώτατα δεν οφείλεται εις τήν αϋξησιν τοϋ αυτοματισμού των κυττάρων των μυοκαρδιακών ινών, γνωστού οντος οτι ή ουσία δρα εν τω προκειμένω κατασταλτικώς.Τα ΗΚΓ/φικα ευρήματα της έν λόγω κοιλιακής ταχυκαρδίας και τα εν γένει αυτής χαρακτηριστικά συνηγορούν υπέρ τής απόψεως οτι καί επί ταύτης υφίσταται μηχανισμός έπανεισόδου, αλλ' ούτος είναι διάφορος του υπολόγου τής κλασσικής κοιλιακής ταχυκαρδίας καί οτι συνδέεται πιθα νότατα μετά τής ύπο τής κινιδίνης προκαλούμενης διάχυτου διαταραχής τής αγωγής καί συνεπεία ταύτης ανομοιογενούς αυξήσεως τής άνερεθίστου περιόδου των κυττάρων των διαφόρων μυοκαρδιακών ινών (άσυγχρονισμος κοιλιακής έπαναπολώσεως). <13 '34 • 35 • 36 • 40 ' 59 • 9Μ18)…”
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