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Background The most important factor for improving out-of-hospital ventricular fibrillation survival rates is early defibrillation. This can be achieved if small, lightweight, inexpensive automatic external defibrillators are widely disseminated. Because automatic external defibrillator size and cost are directly affected by defibrillation waveform shape and because of the favorable experience with truncated biphasic waveforms in implantable cardioverter-defibrillators, we compared the efficacy of a truncated biphasic waveform with that of a standard damped sine monophasic waveform for transthoracic defibrillation. Methods and Results The principal goal of this multicenter, prospective, randomized, blinded study was to compare the first-shock transthoracic defibrillation efficacy of a 130-J truncated biphasic waveform with that of a standard 200-J monophasic damped sine wave pulse using anterior thoracic pads in the course of implantable cardioverter-defibrillator testing. Pad-pad ECGs were also examined after transthoracic defibrillation. After the elimination of data for 24 patients who did not meet all protocol criteria, the results from 294 patients were analyzed. The 130-J truncated biphasic pulse and the 200-J damped sine wave monophasic pulse resulted in first-shock efficacy rates of 86% and 86%, respectively ( P =.97). ST-segment levels measured 10 seconds after the shock in 151 patients in sinus rhythm were −0.26±1.58 and −1.86±1.93 mm for the 130- and 200-J shocks, respectively ( P Conclusions We found that 130-J biphasic truncated transthoracic shocks defibrillate as well as the 200-J monophasic damped sine wave shocks that are traditionally used in standard transthoracic defibrillators and result in fewer ECG abnormalities after the shock.

Background Oral amiodarone effectively suppresses ventricular arrhythmias; however, full activity may take days or weeks. In patients with frequent, life-threatening ventricular arrhythmias, this delay is not acceptable. Thus, in these patients, the speed and dosing accuracy of an intravenous formulation would be beneficial. The goal of this study was to demonstrate the efficacy of intravenous amiodarone in patients with refractory, recurrent hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation by determining a dose response among three regimens. Methods and Results A total of 342 patients were enrolled at 46 medical centers in the United States. Patients received one of three randomized, double-blind dose regimens delivering 125, 500, or 1000 mg during the first 24 hours. Supplemental infusions (150 mg) of intravenous amiodarone could be given to treat breakthrough ventricular arrhythmias. The key efficacy end points were the arrhythmia event rate, time to first arrhythmic event, and number of supplemental infusions administered. The event rate decreased with increasing doses: median values were 0.07, 0.04, and 0.02 events per hour for the 125-, 500-, and 1000-mg dose groups, respectively, representing a significant decrease from baseline event rates ( P =.043), and approached significance in the overall test for trend ( P =.067). There was a significant dose-related increase in the time to first event (trend test P =.025) and a significant dose-related decrease in the number of supplemental boluses per hour (trend test P =.043). Hypotension was the most common (26%) treatment-emergent adverse event during intravenous amiodarone therapy; there was no dose-response relationship. Seventy-eight percent of the patients survived to at least 48 hours. Conclusions Intravenous amiodarone is effective for the treatment of recurrent, life-threatening ventricular tachyarrhythmias.

Cibenzoline, a new antiarrhythmic agent, was tested in 26 patients who had symptomatic ventricular tachycardia (24 patients) or premature ventricular complexes (2 patients) unresponsive to conventional drugs. Cibenzoline was given orally every 8 hours to maximal doses of 65 mg in 2 patients, 81.25 mg in 22 patients and 97.5 mg in 2 patients. Cibenzoline abolished spontaneous episodes of ventricular tachycardia in 8 of 16 patients with ventricular tachycardia during a 72 hour control electrocardiographic recording, and 7 of 22 patients had greater than 83% decrease in premature ventricular complexes compared with control. The PR interval increased 14% (p < 0.001), QRS duration increased 17% (p < 0.001), QT interval did not change and mean ejection fraction in 10 patients did not change.Electrophysiologic studies were performed on 10 patients in the control period and during maximal cibenzoline dosage. Cibenzoline did not affect electrophysiologic properties of the atrium or atrioventricular (AV) node. It prolonged the ventricular effective (223 ± 16 to 241 ± 22 ms, p < 0.02) and functional (247 ± 18 to 264 ± 25 ms, p < 0.02) refractory periods. At control electrophysiologic studies, ventricular tachycardia was induced in 9 of 10 patients (mean cycle length 210 ± 31 ms). Cibenzoline therapy prevented ventricular tachycardia induction in two patients, and in the other seven patients the mean ventricular tachycardia cycle length increased from 210 to 260 ms. The one patient with no ventricular arrhythmia induced during the control study still had no arrhythmia induced while receiving cibenzoline. Among six patients receiving cibenzoline during follow-up, one patient died of recurrent myocardial infarction, two patients stopped taking cibenzoline because of recurrent veutricular tachycardia and three patients have continued taking cibenzoline for 10 ± 4 months with control of symptomatic arrhythmias.Thus, cibenzoliue suppressed ventricular tachycardia and premature veutricular complexes in some patients unresponsive to conventional drugs and was well tolerated. Cibenzoline significantly prolonged ventricular effective and functional refractory periods and had minimal negative hemodynamic effects.

The purpose of this study was to test the hypothesis that vagal efferent nerves travel in the left ventricular subendocardium in a base to apex direction. Efferent vagal stimulation during constant background isoproterenol infusion prolonged left ventricular endocardial and epicardial effective refractory periods in a control state and after a left ventriculotomy performed while dogs were supported by cardiopulmonary bypass. After a 2 mm deep endocardial circumferential incision, efferent vagal stimulation still prolonged the effective refractory period at an endocardial site basal to the encircling endocardial incision, but no longer prolonged the effective refractory period at the endocardium or immediately overlying epicardium apical to the incision. Interpretation of these data suggests that efferent vagal fibers travel in the superficial subendocardium of the canine left ventricle in a base to apex direction, penetrating upward to innervate the epicardium. Conceivably, a lesion such as a subendocardial myocardial infarction could selectively interrupt efferent vagal innervation, leaving sympathetic innervation unopposed. This may be a source of some arrhythmias.

Objectives. We sought to determine the response rate and safety of intravenous amiodarone in patients with ventricular tachyarrhythmias refractory to standard therapies. Background. Numerous small retrospective reports suggest a response of refractory ventricular tachyarrhythmias to intravenous amiodarone, yet no controlled prospective trials exist. Methods. Two hundred seventy-three patients with recurrent hypotensive ventricular tachyarrhythmias refractory to lidocaine, procainamide and bretylium were randomized to receive one of three doses of intravenous amiodarone: 525, 1,050 or 2,100 mg/24 h (mean [±SE] dose 743.7 ± 418.7, 1,175.2 ± 483.7, 1,921.2 ± 688.8 mg, respectively) by continuous infusion over 24 h. Results. Of the 273 patients, 110 (40.3% response rate) survived 24 h without another hypotensive ventricular tachyarrhythmic event while being treated with intravenous amiodarone as a single agent (primary end point). A significant difference in the time to first recurrence of ventricular tachyarrhythmia (post hoc analysis) over the first 12 h was observed when the combined 1,050- and 2,100-mg dose groups were compared with the 525-mg dose group (p = 0.046). The number of supplemental (150 mg) infusions of intravenous amiodarone (given for breakthrough destabilizing tachyarrhythmias) during hours 0 to 6 (prespecified secondary end point) was significantly greater in the 525-mg dose group than in the 2,100-mg dose group (1.09 ± 1.57 vs. 0.51 ± 0.97, p = 0.0043). However, there was no clear dose-response relation observed in this trial with respect to success rates (primary end point), time to first recurrence of tachyarrhythmia (post hoc analysis) or mortality (secondary end point) over 24 h. Conclusions. Intravenous amiodarone is a relatively safe therapy for ventricular tachyarrhythmias refractory to other medications.

Parasympathetic blockade shortens the duration of the Q-T interval and ventricular effective refractory period independent of heart rate change. Since relative parasympathetic effect increases during sleep, it was determined whether sleep was associated with a change in the Q-T interval. Fifteen patients receiving no drugs underwent 3 to 6 days of continuous electrocardiographic recordings. Tracings were sampled every 30 minutes and recorded at a paper speed of 25 mm/s. This provided 12,000 Q-T and R-R intervals that were measured. Comparison of R-R intervals that had similar durations during sleep and awake states revealed that the duration of the Q-T interval was longer during sleep in all 15 patients (p less than 0.001). Eight patients had sufficient range of overlap of R-R intervals to compare linear regression lines of Q-T intervals recorded while awake with Q-T intervals recorded while asleep. The regression lines during sleep exhibited a mean intercept change of 38 +/- 37 ms and mean slope change of -0.021 +/- 0.040 ms when compared with the regression lines during the awake state. The difference in Q-T interval between awake and sleep states was 19 +/- 7 ms when calculated at a heart rate of 60 beats/min. These statistical comparisons of the relationship of the Q-T interval to R-R interval indicate that the Q-T interval is longer during sleep than during the awake state at the same heart rate. Prolongation of the Q-T interval during sleep may reflect increased vagal tone or sympathetic withdrawal. These changes in repolarization may be related to the diurnal variation of some ventricular arrhythmias.

Sustained ventricular tachycardia was induced in dogs following occlusion-reperfusion of the left anterior descending coronary artery. While dogs were supported by cardiopulmonary bypass, the left ventricle was opened and the endocardium was mapped during electrically induced ventricular tachycardia to determine the earliest site of ventricular activation. Phenol (carbolic acid) application at that site necrosed myocardium to a depth of 1 to 3 mm and prevented electrical reinduction of ventricular tachycardia in 9 of 15 dogs. These data suggest that chemical ablation may be used as an alternate means to destroy areas of myocardium involved in the genesis or maintenance of ventricular tachycardia, particularly if these areas cannot be resected surgically because of their size or location.

Twenty-six patients had ventricular tachycardia initiated at control electrophysiologic study and had a repeat study during oral propafenone therapy. Ten patients had had sustained ventricular tachycardia, 6 cardiac arrest and 10 symptomatic, nonsustained ventricular tachycardia. Twenty-two patients had heart disease, 18 of whom had coronary artery disease. During propafenone therapy, ventricular tachycardia could not be initiated during programmed ventricular stimulation in 5 patients, and in 21 patients the cycle length of induced ventricular tachycardia increased from 246 +/- 42 ms at control to 355 +/- 96 ms (p less than 0.001). Seventeen patients were discharged with propafenone therapy and have been followed for a mean of 11 months. No symptomatic ventricular tachycardia recurred in the 5 patients without inducible ventricular tachycardia during drug treatment. Six of 12 patients with inducible ventricular tachycardia during the drug study have remained asymptomatic. In conclusion, propafenone substantially prolongs the cycle length of ventricular tachycardia, and initiation of ventricular tachycardia by programmed ventricular stimulation at drug study does not preclude a favorable clinical outcome.

The purpose of this study was to test the efficacy, safety, and patient tolerance of transvenous cardioversion and defibrillation in patients who had recurrent ventricular tachyarrhythmias. In five of seven patients, a truncated exponential shock of 0.025 to 2.0 joules synchronized to the QRS complex terminated 47 episodes of recurrent sustained ventricular tachycardia (VT). Cardioversion threshold was less than or equal to 0.25 joule in three patients and 0.75 to 2.0 joules in two patients. Shocks of 0.75 joule and 2.0 joule failed to terminate VT in one patient each; higher energies were not tried because of hemodynamic decompensation. In one patient, a shock of 25 joules terminated ventricular fibrillation (VF) on three occasions, and in another patient a shock of 1.0 joule terminated atrial fibrillation on one occasion. Shocks less than or equal to 0.5 joule were well tolerated by the awake unsedated patient. One hundred forty of 141 synchronized shocks (including subthreshold shocks) produced no repetitive ventricular activity. In one seriously ill patient who had received multiple antiarrhythmic drugs and required balloon counterpulsation for hemodynamic support, on a single occasion each a synchronized transvenous shock and a synchronized conventional transthoracic shock produced ventricular flutter and ventricular fibrillation (VF), respectively. We conclude that synchronized transvenous cardioversion by a catheter electrode offers promise as a new therapeutic approach.