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Because many episodes of ventricular fibrillation (VF) are believed to be triggered by ventricular tachycardia (VT), patients who present with VT or VF are usually grouped together in discussions of natural history and treatment. However, there are significant differences in the clinical profiles of these 2 patient groups, and some studies have suggested differences in their response to therapy. We examined arrhythmias occurring spontaneously in 449 patients assigned to implantable cardioverter-defibrillator (ICD) therapy in the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial to determine whether patients who receive an ICD after VT have arrhythmias during follow-up that are different from patients who present with VF. ICD printouts were analyzed both by a committee blinded to the patients' original presenting arrhythmia and by the local investigator. During 31 +/- 14 months of follow-up, 2,673 therapies were reported. Patients who were enrolled in the AVID trial after an episode of VT were more likely to have an episode of VT (73.5% vs 30.1%, p <0.001), and were less likely to have an episode of VF (18.3% vs 28.0%, p = 0.013) than patients enrolled after an episode of VF. Adjustment for differences in ejection fraction, previous infarction, and beta-blocker and antiarrhythmic therapy did not appreciably change the results. Ventricular arrhythmia recurrence during follow-up is different in patients who originally present with VT than in those who originally present with VF. These findings suggest there are important differences in the electrophysiologic characteristics of these 2 patient populations. [ABSTRACT FROM AUTHOR]

We compared 2 studies of implantable cardiac defibrillators (ICDs) to determine the effects of device mode on outcomes. The Antiarrhythmics Versus Implantable Defibrillators (AVID) trial (1993 to 1997) demonstrated improved survival with the ICD compared with antiarrhythmic drug therapy. The Dual-chamber And VVI Implantable Defibrillator (DAVID) trial (2000 to 2002) showed that VVI pacing at 40 beats/min in patients with ICDs reduced the combined end point of death and hospitalization for congestive heart failure compared with DDDR pacing at 70 beats/min. Patients in the AVID trial (631 of 1,016) and the DAVID trial (221 of 506) meeting common inclusion and all exclusion criteria were studied. The major end points were the time to death, and the composite end point of time to death or hospitalization for congestive heart failure. Patients in the AVID and DAVID trials were similar, but more AVID patients had coronary artery disease (p = 0.04), history of myocardial infarction (p = 0.005), and previous ventricular arrhythmias (p = 0.03). DAVID patients underwent more previous revascularization procedures (coronary artery bypass surgery, p = 0.03; percutaneous coronary intervention, p = 0.001), and were more often taking beta-blocking drugs at hospital discharge (p <0.001). The backup VVI ICD groups in both studies had similar outcomes (p = 0.4), even when corrected for the previous demographic differences. The time-to- composite end point was similar in AVID patients treated with antiarrhythmic drugs and DAVID patients treated with DDDR ICDs (p = 0.6). Despite improved pharmacologic therapy and revascularization, outcomes have not improved with backup VVI pacing ICDs. If DDDR ICDs had been used in the AVID trial, benefit from ICDs for patients with serious ventricular arrhythmias could have been missed.

In the Atrial Fibrillation Follow-up Investigation of Rhythm Management study, preexisting pulmonary disease did not preclude the use of amiodarone. Preexisting pulmonary disease was associated with a higher risk of pulmonary death and had a higher risk of diagnosed amiodarone pulmonary toxicity. However, use of amiodarone in the presence of preexisting pulmonary disease did not increase pulmonary death and all-cause mortality rates. Cautious use of amiodarone to treat atrial fibrillation appears acceptable in elderly patients with atrial fibrillation, even if preexisting pulmonary disease is present.

Whether patients with serious ventricular arrhythmias should be treated first with antiarrhythmic drugs or an implantable cardioverter-defibrillator (ICD) is not known. Many patients are ultimately treated with both an antiarrhythmic drug and on ICD. Early studies reported that 40-70% of patients who received an ICD were ultimately treated with an antiarrhythmic drug, although fewer patients are now being treated with both modalities. The beneficial interactions between antiarrhythmic drugs and an ICD are slowing of ventricular tachycardia, which yields improved hemodynamic tolerance; improved antitachycardia pacing and low energy cardioversion success; lowering of antiarrhythmic drug doses, which reduces the risk of side effects; limiting the number of arrhythmia episodes, which minimizes patients discomfort and prolongs ICD battery life; and preventing or slowing supraventricular tachyarrhythmias, which reduces the number of inappropriate shocks from the ICD. The disadvantages of combining pharmacologic therapy and the use of an ICD are the cost and side effects of both therapies. Adverse interactions between an ICD and antiarrhythmic drugs include slowed ventricular tachycardia, which may lead to failure to detect the arrhythmia; increased defibrillation and pacing thresholds; worsened hemodynamic tolerance of ventricular tachycardia; lengthened PR, QRS, or QT intervals causing multiple counting; and decreased size of the intracardiac electrogram, leading to failure to detect the ventricular tachycardia or fibrillation. Caution must be used when combining pharmacologic therapy with an ICD. Repeat electrophysiologic testing is frequently necessary after the initiation of antiarrhythmic drug therapy in a patient with an ICD to ensure successful therapy with the ICD.

Holter data from the 17,609 postmyocardial infarction patients in the CAST Registry were analyzed to study the effect of age on VPC and VT incidence and frequency. Multivariable analysis demonstrated that age is an important independent predictor of increased ventricular ectopy, with the median rate of VPCs/hour increasing from 0.4 (patients aged < 50 years) to 4.0 (patients aged 75 to 80 years), and the prevalence of VT increasing from 7.3% (patients aged < 50 years) to 15.3% (patients aged 75 to 80 years).

All transthoracic defibrillators on the US market use nominally monophasic shock waveforms. However, biphasic waveforms have a lower defibrillation threshold than monophasic waveforms for transthoracic defibrillation of animals and for defibrillation of humans by implantable cardioverter defibrillators. The relative efficacies of Edmark monophasic and Gurvich biphasic transthoracic cardioversion waveforms (200 J into 50 omega) were compared for transthoracic cardioversion in 171 patients undergoing electrophysiologic study for evaluation of ventricular arrhythmias. Patients were randomized in a blinded fashion to receive either a monophasic or a biphasic waveform for the initial shock for conversion of induced ventricular arrhythmias (ventricular fibrillation [VF] = 53, monomorphic ventricular tachycardia [VT] = 80, polymorphic VT = 30, ventricular flutter = 8). Delivered energies for the Edmark and Gurvich waveforms were 215 +/- 11 and 171 +/- 11 J, respectively. There were no significant differences in patient characteristics, use of antiarrhythmic agents, arrhythmia cycle length, or duration of arrhythmia prior to shock for monophasic and biphasic waveform groups. The first shock for all arrhythmias was successful in 75 of 88 patients (85.2%) for the monophasic waveform compared with 81 of 83 patients (97.6%) for the biphasic waveform, p = 0.0054. The first shock for VF was successful in 22 of 28 patients (78.6%) for the monophasic waveform compared with 25 of 25 (100%) for the biphasic waveform, p = 0.0241. The Gurvich biphasic waveforms delivering a mean of 171 J were superior to Edmark monophasic waveforms delivering a mean of 215 J for transthoracic cardioversion of arrhythmias of short duration. This finding may have important implications for the development of future transthoracic defibrillators.

The Antiarrhythmics Versus Implantable Defibrillators (AVID) study compares a strategy of initial treatment with an implantable cardioverter-defibrillator (ICD) to a strategy of initial treatment with an antiarrhythmic drug to prevent death in patients with a history of ventricular fibrillation or hemodynamically compromising ventricular tachycardia, or both. Neither arrhythmia can have been due to a transient or correctable cause. The principle exclusions are a contraindication to amiodarone therapy and inability to undergo ICD implantation. Antiarrhythmic drug therapy includes empiric amiodarone and guided sotalol. The ICDs allowed are advanced generation devices, and most are implanted transvenously. The primary end point of the study is total mortality. Secondary end points are cost and quality of life. The study was designed in 2 phases. The pilot phase enrolled 200 patients between June 1993 and June 1994. Data collected during the pilot phase confirmed that the trial is feasible. An additional 1,000 patients will be enrolled between June 1994 and March 1997. It is anticipated that all 1,200 patients will be followed until September 1998, and will be included in the intention-to-treat analysis.

The Cardiac Arrest in Seattle: Conventional Versus Amiodarone Drug Evaluation (CASCADE) study evaluated antiarrhythmic drug therapy in patients who had survived an episode of out-of-hospital ventricular fibrillation (VF) and who were thought to be at high risk for recurrence of VF. Therapy with empiric amiodarone was compared to therapy with other antiarrhythmic agents, guided by electrophysiologic testing and/or Holter recording. The study evaluated the endpoints of (1) cardiac death, (2) cardiac arrest from ventricular fibrillation with resuscitation, and (3) complete syncope followed by a shock from an automatic implanted defibrillator that restored consciousness. The study comprised 228 patients, 113 treated with amiodarone and 115 treated with conventional antiarrhythmic drug therapy. Most patients had coronary artery disease with a prior myocardial infarction, and one half of the population had a history of congestive heart failure. The mean left ventricular ejection fraction was 35%. Survival was better in patients treated with amiodarone than in patients treated with other antiarrhythmic agents. Patients treated with amiodarone were less likely to receive a shock from an implanted defibrillator, and syncope followed by a shock from a defibrillator was less common in patients treated with amiodarone. However, overall mortality was high, and side effects of therapy were common. Patients treated with amiodarone, even at the low doses used in this study, were still at risk for thyroid dysfunction (both hyperthyroidism and hypothyroidism) and for pulmonary toxicity.

In a retrospective survey of 1,195 survivors of out-of-hospital ventricular fibrillation, 43 patients were identified in whom left ventricular ejection fraction was greater than or equal to 0.50 and in whom no coronary artery stenosis of greater than or equal to 50% luminal diameter were present. Thirteen (30%) of these patients had hypokinesia on left ventriculography, and 20 patients (47%) had a persistently abnormal electrocardiogram. Seven patients (16%) had recurrent out-of-hospital cardiac arrest during an average follow-up of 86 +/- 54 months. The presence of either wall motion or electrocardiographic abnormalities defined patients with a several-fold higher risk of recurrent cardiac arrest than those without such abnormalities. The risk for recurrent cardiac arrest within 5 years was 30% in those with abnormal electrocardiograms versus 5% in the others (p less than 0.03). Age was an independent predictor of recurrent cardiac arrest in this group (p less than 0.01); surprisingly, recurrent cardiac arrest was occurring more often among younger patients. Although cardiac arrest is unusual in patients without major structural heart disease, its recurrence in such survivors is common. Patients at relatively high risk for recurrent ventricular fibrillation can be identified by their youth and by abnormalities detected on the surface 12-lead electrocardiogram or by contrast left ventriculography.

The results of signal-averaged electrocardiography and programmed electrical stimulation were evaluated in 25 patients with recurrent sustained ventricular tachycardia (VT) and 46 patients with a history of out-of-hospital ventricular fibrillation (VF) to characterize the electrophysiologic substrate responsible for these different clinical arrhythmia presentations. Patients with VT had a higher incidence of late potentials (VT 83%, VF 50%, p = 0.005). Significant differences between these groups were also noted in response to programmed electrical stimulation. A sustained ventricular arrhythmia was induced in 24 of 25 (96%) patients with a history of VT but in only 27 of 46 (59%) of VF patients (p = 0.005). In addition, VF was induced in 11 (24%) patients in the VF group but in none of the patients in the VT group (p = 0.005). When the 2 groups were compared on the basis of select clinical characteristics, no significant difference in age, sex, presence of coronary artery disease or ejection fraction was noted. The frequency of prior myocardial infarction was significantly higher in the VT group (VT 20 of 25, 80%; VF 24 of 46, 52%; p = 0.03). Finally, no significant relation between the presence of late potentials and induced arrhythmias was noted in either group. The inability of signal-averaged electrocardiography to predict inducibility in VF patients may represent a significant limitation of this technique in identifying patients at risk for sudden cardiac death.

Ventricular fibrillation (VF) is the first recorded arrhythmia in 75% of patients who have a sudden cardiovascular collapse. Rarely (1%) does sustained ventricular tachycardia (VT) alone cause collapse and unconsciousness. Whether all VF begins as VT is unknown. Early application of cardiopulmonary resuscitation and rapid defibrillation are essential to ensure survival and satisfactory neurologic recovery. During the last 2 years in Seattle, the initial resuscitation rate for VF was 269 of 447 patients (60%), with 114 of 447 patients (26%) surviving long-term. Survivors of VF have a high overall risk of recurrent VF, with many univariate risk factors identified: evidence of poor left ventricular function (history of congestive heart failure, prior myocardial infarction [MI] or low ejection fraction), extensive coronary artery disease, absence of a new MI (either Q wave or non-Q wave) with VF, male gender, advanced age, complex or high-frequency ventricular ectopy on Holter recording, inducibility at electrophysiologic study, exercise-induced angina or hypotension, and smoking. Classification of cardiac deaths as arrhythmic or nonarrhythmic is important in interpreting the therapeutic response. However, because many patients have chronic symptoms, timing of the onset of a new event is difficult. Furthermore, accurate timing of an event does not guarantee correct classification. Sudden death is not necessarily arrhythmic, nor is all arrhythmic death sudden. Total cardiac mortality may be a simpler and more relevant end point to measure the overall effect of antiarrhythmic therapy.

Although myocardial ischemia may occur in thyrotoxic patients with normal coronary arteries, the mechanism remains unclear. This report describes a woman with hyperthyroidism who had ventricular fibrillation during an apisode of myocardial ischemia. The event was documented with continuous ambulatory electrocardiography. Subsequent angiography revealed normal coronary anatomy with spasm of the right coronary artery that disappeared after ingestion of one sublingual nitroglycerin tablet. The angina, electrocardiographic evidence of myocardial ischemia, ventricular arrhythmias and the patient's need for nitroglycerin were eliminated after she became euthyroid. These findings suggest that coronary spasm may be associated with myocardial ischemia and arrhythmias in a hyperthyroid patient.

Myocardial size and contractility were measured by gated radionuclide ventriculography in 70 patients before and a mean of 66 days after beginning amiodarone therapy. The mean dose of amiodarone at the time of the second study was 481 mg. The mean left ventricular (LV) ejection fraction (EF) increased slightly, from 40% to 43% (p = 0.001). The mean right ventricular EF remained unchanged (38% to 39%, difference not significant [NS]). The LV end-diastolic volume (count-based method) increased by 9% (p = 0.01), but no change could be demonstrated for end-systolic volume (4%, NS). The LV stroke volume increased 19% (p = 0.001), but cardiac output remained unchanged (5%, NS) because the heart rate decreased by 9 beats/min (p = 0.001). The right ventricular end-diastolic volume increased by 12% (p = 0.01) and end-systolic volume increased by 11% (p = 0.03). Stroke volume increased by 18% (p = 0.005). There was no significant correlation between the change in LVEF and the pre-amiodarone LVEF, the time interval between studies, or with indexes of amiodarone effect (change in heart rate, QRS, QTc, TSH, amiodarone dosage). In 5 patients (7%), LVEF decreased significantly, requiring discontinuation of amiodarone therapy in 1 patient. At the time of the second study congestive heart failure was manifest in 19%, and there was a trend suggesting that congestive heart failure was more likely if the initial LVEF was less than or equal to 35% (p = 0.10). Thus, amiodarone may rarely adversely affect contractility, although myocardial contractility is typically unchanged. There is an associated small increase in the size of both ventricles.

The Cardiac Arrhythmia Pilot Study (CAPS) was a randomized, double-blind trial of antiarrhythmic drugs (encainide, flecainide, moricizine, imipramine and placebo) in 502 patients with an ejection fraction greater than 0.20 and at least 10 ventricular premature complexes/hour, 6 to 60 days after acute myocardial infarction. Patients were followed for 1 year and the incidence of new or worsened congestive heart failure (CHF) was evaluated. Heart failure in the 1-year follow-up was gauged by the development (in order of increasing severity) of new symptoms (grade 1), the need for a change in therapy, including addition of digitalis, addition or increase of dose of diuretics or afterload reduction agents or discontinuation of beta-blocking agents (grade 2), or by hospitalization (grade 3). Sixty-one of 502 patients (12%) required hospitalization for CHF in the 1-year follow-up. One hundred five of 403 patients (26%) in the active treatment group and 18 of 99 patients (18%) in the placebo group (difference not significant) developed CHF requiring hospitalization or a change in therapy or both. Although patients with severely impaired ejection fraction were excluded, new or worsened CHF was common in follow-up during CAPS.

Coughing has been shown to be helpful in altering the bradycardia and hypotension that may occur after intracoronary injections of contrast medium and can enable a patient to maintain consciousness during episodes of ventricular fibrillation and asystole. This report describes a patient with ischemic heart disease in whom 33 episodes of drug-refractory ventricular tachycardia were converted to normal sinus rhythm after abrupt forceful coughs were performed on command. When the patient was unable to cough as directed, external electric countershock was necessary to terminate the arrhythmia. These findings suggest that the cough may in isolated cases be effective in the conversion of potentially fatal ventricular tachyarrhythmias.

Serum levels of quinidine or procainamide were measured in patients who had amiodarone added to their antiarrhythmic regimen. Dosages of quinidine or procainamide were held constant. Eleven of 11 patients had an increase in the serum quinidine level, and 11 of 12 other patients had an increase in the serum procainamide level. The dose requirement to maintain a stable plasma level of quinidine or procainamide decreased by 37% and 20%, respectively. Clinical toxicity occasionally occurred with the increase in serum levels of quinidine and procainamide, and the dose of these drugs should be decreased when amiodarone is administered concurrently.

The effect of initially ineffective defibrillation pulses on subsequent defibrillation success is not known. Therefore, the voltage, current and energy at the defibrillation threshold were compared with the defibrillation rescue pulse voltage, current and energy that terminated ventricular fibrillation when an ineffective pulse just below the defibrillation threshold had been used initially. This lower amplitude ineffective pulse was termed a "subdefibrillation threshold" pulse. The pulse that restored sinus rhythm after the subdefibrillation threshold pulse was delivered was termed the "subdefibrillation threshold rescue pulse." This comparison was undertaken, intraoperatively, in 14 out-of-hospital cardiac arrest survivors using a sequential-pulse catheter-patch defibrillation system. Each of the 14 patients required higher voltage, current, delivered energy and stored energy for defibrillation with the subdefibrillation threshold rescue pulse than with the defibrillation threshold pulse. The defibrillation threshold voltage was 451 +/- 127 volts compared with a subdefibrillation threshold rescue voltage of 585 +/- 147 volts (p less than 0.00002). The defibrillation threshold current was 5.5 +/- 2.4 amps compared with a subdefibrillation threshold rescue current of 7.2 +/- 2.7 amps (p less than 0.00001). Delivered and stored energies were 10.9 +/- 7.4 and 12.3 +/- 7.2J, respectively, for the defibrillation threshold pulse and were 17.6 +/- 9.4 J (p less than 0.00002) and 20.5 +/- 9.3 J (p less than 0.00005), respectively, for the subdefibrillation threshold rescue pulse. It is concluded that the risk of requiring considerably higher energies than anticipated for defibrillation must be incurred, should defibrillation fail because of an initially insufficient defibrillation pulse.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of electrode polarity on defibrillation thresholds in humans is unknown. This prospective, randomized evaluation of electrode polarity on defibrillation thresholds was performed in 21 survivors of ventricular fibrillation (VF) undergoing cardiac surgery. Defibrillation was always performed with 2 identical large rectangular, wire mesh electrodes positioned over the anterior wall of the right ventricle and the posterolateral wall of the left ventricle. The initial electrode polarity for the left ventricular (LV) electrode was chosen randomly for determination of the defibrillation threshold. Subsequently, electrode polarity was reversed. The defibrillation threshold was defined as the lowest pulse amplitude that would effectively terminate VF with a single discharge delivered 10 seconds after initiation of an episode of VF with alternating current. For each defibrillation pulse, voltage, current, resistance and delivered energy were recorded. Of the 21 patients, 15 (71%) had a lower defibrillation threshold when the LV electrode was positive, 2 patients (10%) had a lower defibrillation threshold when the LV electrode was negative and 4 patients (19%) had equal defibrillation thresholds (within 0.5 J) regardless of polarity. The mean leading edge defibrillation threshold voltage was 370 +/- 88 volts when the LV electrode was negative and 320 +/- 109 volts (14% less) when the LV electrode was positive (p = 0.014). Mean leading edge defibrillation threshold current was 9.3 +/- 3.1 amps when the LV electrode was negative compared to 7.7 +/- 3.1 amps (17% less) when the LV electrode was positive (p = 0.0033). There were no differences in resistance with the 2 configurations.(ABSTRACT TRUNCATED AT 250 WORDS)

The Cardiac Arrhythmia Pilot Study (CAPS) was a randomized, double-blind trial of antiarrhythmic drugs (encainide, flecainide, moricizine, imipramine and placebo) in 502 patients with at least 10 ventricular premature complexes/hour, 6 to 60 days after acute myocardial infarction. CAPS tested the feasibility of performing a larger study to determine if suppression of ventricular ectopic activity after acute myocardial infarction could improve survival. Patients in CAPS were followed for 1 year. All death or cardiac arrest events were evaluated by at least 2 investigators using a classification scheme that characterized the underlying mechanism as cardiac arrhythmic, cardiac nonarrhythmic or noncardiac. Forty-five patients (9%) died or had cardiac arrest during the 1-year follow-up, 29 (64%) within 1 hour from the onset of symptoms and 16 greater than 1 hour from the onset of symptoms. Twenty-three deaths (51%) were classified as arrhythmic, 19 (42%) as nonarrhythmic and 3 (7%) as noncardiac. Acute myocardial ischemia or infarction was associated with the death/cardiac arrest event in 16 patients (36%), 8 in the arrhythmic death group. Discrepancies in classification among reviewers were particularly common in patients with long-standing symptoms of congestive heart failure, in whom it was frequently difficult to identify the precise moment of the onset of symptoms in the death/cardiac arrest event. Using only the temporal relation of symptoms to categorize deaths or cardiac arrests, the mechanism of 12 (27%) of the 45 patients was in disagreement with the classification based on the Events Committee review. Classification of death as sudden or nonsudden is not equivalent to the classification of death as arrhythmic or nonarrhythmic.

The acute electrophysiologic effects of intravenous aprindine were evaluated in 48 patients to assess the effect on conduction times and refractoriness in patients with severe cardiac disease and arrhythmias. The patients had not responded to conventional antiarrhythmic medications or had been unable to tolerate effective doses of conventional medications because of side effects. Eleven patients had an abnormal H-V interval, 9 had prolonged QRS duration and 22 had evidence of severe left ventricular dysfunction. Aprindine prolonged conduction transiently in the atria, the atrioventricular (A-V) node, the His-Purkinje system and the ventricles. The refractory times of the atria, the A-V node and the ventricles increased insignificantly, both functionally and statistically. Atrioventricular block did not develop in any patient, and side effects were minor. Thus, aprindine can be safely administered intravenously (10 to 15 mg/min) to severely ill patients with arrhythmias that are refractory to other medications even in the presence of underlying conduction system and myocardial disease.

Nineteen patients with posterior accessory pathways and disabling, refractory arrhythmias, underwent catheter ablation using standard defibrillator pulses at energy settings of 150 to 400 J. Accessory pathway ablation was successful in 13 of 19 (68%). Effective catheter ablation correlated with local ventriculoatrial (VA) intervals determined from the coronary sinus catheter at the site of earliest retrograde atrial activation during orthodromic reciprocating tachycardia. In 12 of the 13 successfully ablated patients, the local VA interval was less than 80 ms. In 4 of the 6 unsuccessfully treated patients, the local VA interval was greater than or equal to 80 ms, p less than 0.01. Transient abnormalities noted with the procedure included sinus bradycardia (3 patients), atrioventricular block (5), accelerated junctional rhythm (3), ectopic atrial tachycardia (2), myocardial depression (1), "ischemic" appearing T-wave inversions (10) and hemodynamically insignificant small pericardial effusions (5) Creatine kinase-MB increased from 3 +/- 2 U/liter to 26 +/- 18 U/liter (p less than 0.001), 4 to 8 hours after ablation. In addition, electrical shorts occurring during the ablation procedure in 2 patients were identified and corrected only with oscilloscopic monitoring of voltage and current waveforms. Significant adverse sequelae were seen in 4 patients. Three patients required sternotomy for control of cardiac tamponade secondary to a ruptured coronary sinus and 1 patient had a small posterior left ventricular infarction related to spasm of a right coronary artery extension branch. Coronary sinus rupture correlated with the ratio of catheter diameter to coronary sinus diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

This study evaluated the ability of 24 new standard tripolar and quadripolar U.S. Catheter Instruments catheters to withstand a single damped sinusoidal shock delivered by a standard defibrillator. The schema for energy delivery was meant to simulate possible clinical practices. Delivered peak voltage and current were measured during each shock. Each electrode was examined for pitting and changes in line resistance as a consequence of the shock. Electrode pitting occurred on all selected anodal poles. However, it also was found on "unsolicited" electrodes from 7 catheters, indicating that current had followed unanticipated routes. Electrode line resistance was unmeasurable in 6 of these 7 inappropriately pitted electrodes. Delivered peak voltage and postshock catheter dielectric strength depended on the manner of energy delivery. To simulate a posterior septal accessory pathway ablation procedure, a shock was delivered to 2 proximal (anodal) poles in 16 quadripolar catheters (8 received 200 J and 8 received 360 J). Delivered peak voltage was 3,125 +/- 362 V for the 200-J shock and 4,100 +/- 160 V for the 360-J shock. Postshock catheter dielectric strength for the 200- and 360-J shock was 1,425 +/- 826 V and 601 +/- 707 V, respectively. This was significantly lower than peak delivered voltage (p less than 0.001 for either energy). To simulate His bundle or ventricular tachycardia focus ablation, 8 tripolar catheters each received a single 200-J shock to the tip electrode. This resulted in a delivered peak voltage of 2,900 +/- 351 V, compared with a postshock dielectric strength of 1,325 +/- 1,320 V (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Sixteen survivors of cardiac arrest underwent intraoperative comparison of the effectiveness of sequential-pulse and single-pulse defibrillation. Defibrillation was tested alternately with the single-pulse or sequential-pulse technique 10 seconds into an episode of ventricular fibrillation that was induced with alternating current. The sequential-pulse defibrillation technique using truncated exponential pulses was performed with a right ventricular endocardial catheter and a left ventricular epicardial patch electrode. The first pulse was delivered between the right ventricular apical and the superior vena caval electrode on the right ventricular endocardial catheter. The second pulse was delivered between the right ventricular apical electrode and the left ventricular patch electrode 0.2 ms after termination of the first pulse. Single-pulse defibrillation was performed with a standard intracardiac defibrillation system in which a single truncated exponential pulse was delivered across 2 epicardial patch electrodes positioned over the anterolateral right ventricle and the posterolateral left ventricle. During defibrillation threshold determination, voltage and current waveforms were recorded and integrated to determine delivered energy. Average defibrillation threshold leading-edge voltage for the sequential pulse technique was 496 +/- 140 V, compared with 365 +/- 157 V for the single-pulse technique (p less than 0.005). Defibrillation threshold leading-edge current for the sequential-pulse technique was 6.0 +/- 2.3 A, compared with 10.6 +/- 5.1 A for the single-pulse method (p less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

The repetitive ventricular response, defined as the production of two or more ventricular premature complexes in response to a single ventricular pacing stimulus, is common in patients with serious ventricular arrhythmias. Twenty-seven patients with refractory ventricular tachycardia were studied to determine whether acute suppression of the repetitive ventricular response by aprindine predicts long-term effectiveness of this agent. Twenty-three of the 27 patients had the repetitive ventricular response before intravenous administration of aprindine, whereas only 6 had the response after aprindine. All patients were maintained on a regimen of oral aprindine and evaluated repeatedly for a mean of 12 months. Twenty of the 21 patients who had no repetitive ventricular response after intravenous aprindine manifested clinical improvement compared with only 1 of the 6 in whom the repetitive response was present after aprindine (P less than 0.0005). Aprindine is a useful agent in refractory ventricular tachycardia, and the absence of the repetitive ventricular response after its intravenous administration predicts long-term clinical responsiveness to the oral form.

The electrophysiologic characteristics of the repetitive ventricular response that followed an electrically induced single premature ventricular complex were evaluated to determine its mechanism during atrial pacing or sinus rhythm in 30 patients. Seven patients had preexisting bundle branch block. His bundle or right bundle branch deflections did not precede the repetitive complex in 29 of the 30 patients, which implies that the proximal His-Purkinje system was not involved in the reentry circuit. In 24 of 30 patients the QRS axis ot the repetitive complex was divergent 45 degrees or more from the stimulated complex. In 22 of 30 patients the reprtitive complex had a right bundle branch block configuration. In 14 of 18 patients with two or more repetitive complexes, the QRS pattern changed from beat to beat, which implies that either the reentry pathway or conduction was changing. Thus, the repetitive ventricular response, which can be associated with clinically important ventricular arrhythmias, probably represents intraventricular rather than proximal His-Purkinje system reentry.