Comparison of sotalol with digoxinquinidine for conversion of acute atrial fibrillation to sinus rhythm (the sotalol-digoxin-quinidine trial)

Comparison of sotalol with digoxinquinidine for conversion of acute atrial fibrillation to sinus rhythm (the sotalol-digoxin-quinidine trial)

276 Editor’s comment: This is not a new concept, but a surprising number of injuries would have been missed in the setting of altered mental status or...

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276 Editor’s comment: This is not a new concept, but a surprising number of injuries would have been missed in the setting of altered mental status or distracting injury.

0 EFFICACY AND SAFETY OF D-SOTALOL, A PURE CLASS IH ANTIARRHYTHMIC COMPOUND, IN PATIENTS WITH SYMPTOMATIC COMPLEX VENTRICULAR ECTOPY. Hohnloser SH, Meinertz T, Stubbs P, et al. Circulation. 1995;92:1517- 1525. This prospective, double-blind, placebo-controlled study was conducted to evaluate d-Sotalol, a pure Class III antidysrythmic agent. 233 patients with more than 30 premature ventricular contractions (PVCS)/HR randomly received placebo or d-sotalol at 50,100 or 200 mg given twice daily. Dose dependent efficacy was electrocardiographically assessedby QT and QTc durations indicating class III activity. A d-sotalol induced decreasein PVCs was observed,which reachedstatistical significance at the 200 mg dosage. These patients had 311 PVCs/hr during baseline Holter monitering and 135 per hour during active treatment (p < .05). This group consisted of only 8 patients or 14% meeting the primary efficacy criterion of more than a 75% reduction in PVCs. At the statistically significant high dose of 200 mg BID there was one sudden death and one nonfatal cardiac arrest, which occured in patients with advanced organic heart disease. [Aviva Jacoby, MD]

q COMPARISON OF SOTALOL WITH DIGOXINQUINIDINE FOR CONVERSION OF ACUTE ATRIAL FIBRILLATION TO SINUS RHYTHM (THE SOTALOL-DIGOXIN-QUINIDINE TRIAL). Halinen 0, Huttunen M, Paakinen S, et al. American Journal of Cardiology 1995;76:495-8. The objective of this prospective study was to compare the efficacy of sotalol with that of digitalis and quinidine in converting acute atria1fibrillation ( AF) to sinus rhythm (SR) in the emergency department. Sixty-one patients with recent onset AF lasting < 48 hours were randomized into 2 treatment groups. In the digitalis-quinidine group (n = 28)) intravenous digoxin up to 0.75 mg was given initially if needed to decrease the heart rate to under 100 beats per minute (bpm), then quinidine was given orally 200 mg every 2 hours until cardioversion to sinus rhythm occurred or until a total of 600 mg was reached. In the sotalol group (n = 33), 80 mg of sotalol was given orally and again at 2 hour and 4 hour intervals if AF persisted with a heart rate over 80 bpm to a maximum of 320 mg. The study was initially scheduled for 260 patients but was cut short after interim analysis was performed. Homogeneity of the patients groups were analyzed with Student’s t test of chi-square tests. Results were analyzed with the Mann-Whitney U test. Conversion to SR occurred in 52% of patients taking sotalol and 86% of patients taking quinidine. Time to SR with sotalol was 10.2 +I- 7.6 hours and with quinidine 4.0 i-l- 2.9 hours (p < 0.01). Treatment was discontinued in 48% of patients taking sotalol becauseof asymptomatic bradycardia

The Journal of Emergency Medicine

or hypotension. The authors conclude that oral sotalol does not appear to be as effective as quinidine for conversion ot [Christy M. Rosa, MD, UCSD ] paroxysmal AF. Editor’s comment: Sotolol may be effective in suppressing ventricular ectopy, but does not appear to have acute indication at this time.

0 RANDOMIZED, DOUBLE BLIND COMPARISON OF RETEPLASE DOUBLE BOLUS ADMINISTRATION WITH STREPTOKINASE IN ACUTE MYOCARDIAL INFARCTION (INJECT): TRIAL TO INVESTIGATE EQUIVALENCE. International Joint Efficacy Comparison of Thrombolytics The Lancet, Vol. 346, pp. 329-335. This study evaluated whether reteplase, a new thrombolytic, was at least equivalent to a standard dosing of streptokinase. The authors designed the study to determine if reteplase has the sameeffect on survival. Reteplaseis a recombinant plasminogen activator that has only the kringle-2 and the protease domain of tissue plasminogen activator (tPA) Reteplasehas a longer half-life than tPA, which allows bolus administration. A total of 6010 patients with symptoms and electrocardiograms consistent with an acute myocardial infarction were enrolled into the study. Patients were randomized, in a double blind fashion, to receive either streptokinase 1.5 MU IV over 60 min or reteplase 2 boluses of 10 MU given 30 min apart. Treatment was started up to 12 hrs after the onset of symptoms. All patients received heparin IV for at least 24 hrs. The primary end point for this study was 35 day survival outcome. There were 270 deaths in the reteplase cohort and 285 deaths in the streptokinase group, a statistically insignificant difference. Bleeding events were similar for the two treatment groups. There were significantly fewer cases of recurrent atrial fibrillation, asystole, cardiogenic shock, and heart failure in the reteplase group. This study demonstrates that reteplase is as effective as streptokinase in decreasing the 35 day mortality in the treatment of AMI. [Paolo Berger, MD]

0 BRAIN COMPUTERIZED TOMOGRAPHY AFTER HYPERBARIC OXYGEN THERAPY FOR CARBON MONOXIDE POISONING. Pracyk JB, Stolp BW, Fife CE, et al. Undersea and Hyperbaric Medicine, 1995;22 ( 1) : l-7. In a review of 40 selected patients, the results of computed tomography (CT) were compared with clinical outcome after serious carbon monoxide (CO) exposure. All patients had suffered loss of consciousnessduring CO exposure and were treated with hyperbaric oxygen (HBO) therapy. Computed tomographic studies were performed when patient condition permitted. A neuroradiologist blinded to the clinical outcome confirmed the radiographic findings. CT abnormalities included globus pallidus hypodensities (9 patients), subcortical white matter hypodensities (4), cerebral cortical lesions ( 1) , cerebral edema ( 1), hippocampal lesions ( 1) , and complete loss of gray-white differentiation