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Cardiac device infections (CDIs) represent a serious complication after the implantation of pacemakers and defibrillators. In addition to antimicrobials, complete hardware removal, mostly with percutaneous lead extraction (PLE), is necessary to limit recurrences. However, CDI diagnosis is often difficult and is sometimes delayed, and scarce data exist on how the timing of PLE may affect clinical outcomes. In this study, the in-hospital outcomes of 52 consecutive patients with CDIs who underwent PLE were retrospectively analyze. Co-morbidities such as diabetes mellitus, congestive heart failure, renal insufficiency, and end-stage renal disease were highly prevalent in the study cohort. Patients were divided into group A (bacteremia or device endocarditis) and group B (localized pocket infection). In-hospital mortality was 29% in group A and 5% in group B (p = 0.02) and was due mostly to sepsis. Hospital stays were shorter in group B patients (5.7 vs 21.7 days, p0.001). Presentation with hypotension was more commonly observed in group A patients and was associated with higher in-hospital mortality, whereas pocket findings correlated with better survival. Postoperative courses after PLE were uneventful in most patients, and no fatal complications were observed. PLE was performed significantly earlier in group B patients (hospitalization day 1.3 vs 7.6, p0.001). PLE performed within 3 hospitalization days was associated with lower in-hospital mortality (p = 0.01). In conclusion, PLE performed within 3 days from admission is associated with shorter hospitalization and better survival. A timely diagnosis is crucial, particularly in the absence of local findings, because early treatment with PLE is likely to prevent the catastrophic outcomes of unrelenting CDIs.

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 (p0.001). 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.

Objectives We sought to evaluate approaches used to control rate, the effectiveness of rate control, and switches from one drug class to another in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study. Background The AFFIRM study showed that atrial fibrillation (AF) can be treated effectively with rate control and anticoagulation, but drug efficacy to control rate remains uncertain. Methods Patients (n = 2,027) randomized to rate control in the AFFIRM study were given rate-controlling drugs by their treating physicians. Standardized rate-control efficacy criteria developed a priori included resting heart rate and 6-min walk tests and/or ambulatory electrocardiographic results. Results Average follow-up was 3.5 ± 1.3 years. Initial treatment included a beta-adrenergic blocker (beta-blocker) alone in 24%, a calcium channel blocker alone in 17%, digoxin alone in 16%, a beta-blocker and digoxin in 14%, or a calcium channel blocker and digoxin in 14% of patients. Overall rate control was achieved in 70% of patients given beta-blockers as the first drug (with or without digoxin), 54% with calcium channel blockers (with or without digoxin), and 58% with digoxin alone. Adequate overall rate control was achieved in 58% of patients with the first drug or combination. Multivariate analysis revealed an association between first drug class and several clinical variables. There were more changes to beta-blockers than to the other two-drug classes (p Conclusions Rate control in AF is possible in the majority of patients with AF. Beta-blockers were the most effective drugs. To achieve the goal of adequate rate control in all patients, frequent medication changes and drug combinations were needed.

Background: CVT-510, N-(3(R)-tetrahydrofuranyl)-6-aminopurine riboside, is a selective A,-adenosine receptor agonist with potential potent antiarrhythmic effects in tachycardias involving the atrioventricular (AV) node. This study, the first in humans, was designed to determine the effects of CVT-5 10 on AV nodal conduction and hemodynamics. Methods and Results: Patients in sinus rhythm with normal AV nodal function at electrophysiologic study (n = 32) received a single intravenous bolus of CVT-5 10. AH and HV intervals were measured during sinus rhythm and during atrial pacing at 1, 5, 10, 15, 20, 30, 45, and 60 minutes after the bolus. Increasing doses of CVT-510 (0.3 to 10 pg/kg) caused a dosedependent increase in the AH interval. At 1 minute, a dose of 10,ug/kg increased the AH interval during sinus rhythm from 93 ± 23 msec to 114 ± 37 msec, p = 0.01 and from 114 ± 31 msec to 146 ± 44 msec during atrial pacing at 600 msec, p = 0.003). The AH interval returned to baseline by 20 minutes. CVT-510 at doses of 0.3 to 10,ug/kg had no effect on sinus rate, HV interval, or systemic blood pressure, and was not associated with serious adverse effects. At doses of 15 and 30 pg/kg, CVT-510 produced transient second/third degree AV heart block in all four patients treated. One of these patients also had a prolonged sedative effect that was reversed with aminophylline. Conclusions: CVT-510 promptly prolongs AV nodal conduction and does not affect sinus rate or blood pressure. Selective stimulation of the A,-adenosine receptor by CVT-510 may be useful for immediate control of heart rate in atrial fibrillation/flutter and to convert paroxysmal supraventricular tachycardia to sinus rhythm, while avoiding vasodilatation mediated by the A2-adenosine receptor, as well as the vasodepressor and negative inotropic effects associated with 3-adrenergic receptor blockade and/or calcium channel blockers.

OBJECTIVES We compared the efficacy of a novel rectilinear biphasic waveform, consisting of a constant current first phase, with a damped sine wave monophasic waveform during transthoracic defibrillation. BACKGROUND Multiple studies have shown that for endocardial defibrillation, biphasic waveforms have a greater efficacy than monophasic waveforms. More recently, a 130-J truncated exponential biphasic waveform was shown to have equivalent efficacy to a 200-J damped sine wave monophasic waveform for transthoracic ventricular defibrillation. However, the optimal type of biphasic waveform is unknown. METHODS In this prospective, randomized, multicenter trial, 184 patients who underwent ventricular defibrillation were randomized to receive a 200-J damped sine wave monophasic or 120-J rectilinear biphasic shock. RESULTS First-shock efficacy of the biphasic waveform was significantly greater than that of the monophasic waveform (99% vs. 93%, p = 0.05) and was achieved with nearly 60% less delivered current (14 ± 1 vs. 33 ± 7 A, p CONCLUSIONS This study demonstrates a superior efficacy of rectilinear biphasic shocks as compared with monophasic shocks for transthoracic ventricular defibrillation, particularly in patients with a high transthoracic impedance. More important, biphasic shocks defibrillated with nearly 60% less current. The combination of increased efficacy and decreased current requirements suggests that biphasic shocks as compared with monophasic shocks are advantageous for transthoracic ventricular defibrillation.

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.

Sotalol is an antiarrhythmic agent with combined beta-blocking and class III antiarrhythmic properties. This study was designed to assess the safety and efficacy of sotalol in terminating supraventircular tachycardia (SVT), atrial fibrillation (AFib), and atrial flutter (AFI). Ninety-three patients with spontaneous or induced SVT ( p = 45) or AF (AFib or AFI; n = 48) with a ventricular rate of ≥120 beats/min were studied. In the first phase, the double-blind phase, patients were randomly assigned to receive placebo or intrevenous (iv) sotalol, 1.0 or 1.5 mg/kg. If SVT or AF did not convert to sinus rhythm or if the ventricular rate did not slow to p p p not snigificant [NS] vs placebo), and 2 (13%) of 16 who received 1.5 mg/kg sotalol ( p = NS vs placebo); in these groups, a >20% reduction of ventricular rate without conversion to sinus rhythm occurred in 0 (0%) of 14, 13 (72%), of 18 ( p p p = NS vs placebo), and 10% of those who received 1.5 mg/kg iv sotalol ( p = NS vs placebo). Most of these events were mild to moderate, but all were transient and clinically manageable. In conclusion, iv sotalol is safe and effective for acute termination of SVT and for acute slowing of ventricular rate during AF but not for termination of AF at doses to 1.5 mg/kg.

The use of MAP recording techniques has been said to have bridged the gap between basic in vitro investigation of the transmembrane action potential and observations made in situ from the beating heart. With regard to antiarrhythmic agents, MAP recordings are particularly useful in evaluating drugs which prolong repolarization. The simultaneous measurement of MAP and ERP at the same site permits the comparison of drug effects on repolarization and refractoriness. The ability to safely and reliably record the MAP contributes importantly to the evaluation and classification of antiarrhythmic drug effects in vivo and may ultimately lead to more rational selection of drug therapy for individual patients. Antiarrhythmic drug effects demonstrated with MAP recordings have generally shown good agreement with the Vaughan Williams classification of electrophysiological actions. An important key to drug efficacy may be that some drugs prolong refractoriness beyond their effect on repolarization. Conversely, a potential explanation for proarrhythmia may lie in slowing of conduction without the concomitant protective effect of postrepolarization refractoriness. The phenomenon of use dependence, which has been demonstrated for many drugs, suggests why an agent that prevents induction of arrhythmia during programmed stimulation in the electrophysiology laboratory may not prevent spontaneous arrhythmia initiation at slower heart rates. The paramount task of clinical electrophysiology is the successful treatment of rhythm disturbances. The more detailed and quantitative evaluation of drug effects afforded by MAP recordings may ultimately result in the more effective use of antiarrhythmic drugs in general and to more precise tailoring of therapy for individual patients.

The evaluation of survivors of sudden cardiac death with serial electrophysiologic studies involves a lengthy and expensive hospitalization, especially when an automatic implantable cardioverter-defibrillator is ultimately necessary. The cost efficacy of this conventional approach was therefore compared with direct implantation of a cardioverter-defibrillator after the first electrophysiologic study. Thirty-two survivors of sudden death who had inducible ventricular tachycardia during their initial electrophysiologic study underwent serial drug trials. At discharge 12 (37%) were taking an antiarrhythmic drug found to prevent induction of ventricular tachycardia and 20 underwent cardioverter-defibrillator implantation after serial drug trials proved ineffective. The average length of hospitalization for this group that had undergone serial drug testing was 20.2 +/- 9.3 days at an average cost of $48,900 +/- $31,600. Seven survivors of sudden death had no inducible ventricular tachycardia during their initial electrophysiologic study and underwent direct cardioverter-defibrillator implantation. Their average length of hospitalization was 12.6 +/- 6.2 days at an average cost of $40,400 +/- $8,300. It is concluded that automatic implantable cardioverter-defibrillator implantation as an early intervention is not more costly and indeed may be cost-effective compared with therapy guided by serial electrophysiologic testing. As antitachycardia devices become more versatile, long lived and easier to implant, earlier implantation is likely to compare even more favorably with drug therapy.

OBJECTIVE To assess the safety and efficacy of intravenous adenosine in terminating acute episodes of paroxysmal supraventricular tachycardia. DESIGN Two prospective, double-blind, randomized, placebo-controlled trials to evaluate dose response in patients receiving adenosine and to compare the effects of adenosine with those of verapamil. PATIENTS A total of 359 patients with a tachycardia electrocardiographically consistent with paroxysmal supraventricular tachycardia were entered into the two protocols. Patients subsequently found to have arrhythmias other than paroxysmal supraventricular tachycardia were excluded from the efficacy analysis. INTERVENTIONS The first protocol compared sequential intravenous bolus doses of 3, 6, 9, and 12 mg of adenosine to equal volumes of saline. In the second protocol, patients received either 6 mg and, if necessary, 12 mg of adenosine or 5 mg and, if necessary, 7.5 mg of verapamil. MEASUREMENTS AND MAIN RESULTS When data are expressed in terms of cumulative response in eligible patients, intravenous adenosine terminated acute episodes of paroxysmal supraventricular tachycardia in 35.2%, 62.3%, 80.2%, and 91.4% of patients who received maximum doses of 3, 6, 9, and 12 mg, respectively, in a four-dose sequence, whereas 8.9%, 10.7%, 14.3%, and 16.1% of patients responded to four sequential placebo doses (P less than 0.0001). In the second trial, cumulative response rates after 6 mg followed, if necessary, by 12 mg of adenosine were 57.4% and 93.4%, and after 5 mg followed, if necessary, by 7.5 mg of verapamil were 81.3% and 91.4%. The average time after injection to termination of tachycardia by adenosine was 30 seconds. Adenosine caused adverse effects in 36% of patients, but they lasted less than 1 minute and were usually mild. CONCLUSIONS Adenosine in graded doses up to 12 mg rapidly and effectively terminates acute episodes of paroxysmal supraventricular tachycardia in which the atrioventricular node is an integral part of the re-entrant circuit. The overall efficacy of adenosine is similar to that of verapamil, but its onset of action is more rapid. Adverse reactions to adenosine are common but are minor and brief.

Thirty-three patients with ventricular tachycardia (VT) (3 or more beats, less than 30 seconds in duration, rate more than 100 per minute) on 24-hour Holter monitoring and no history of clinical arrhythmia (presyncope, syncope or sudden death) were studied using programmed electrical stimulation (PES). PES induced VT in 14 patients (42%), sustained VT in 7 (21%) and nonsustained VT in 7 (21%). Inducible VT was associated with underlying heart disease in 9 of 19 patients with coronary artery disease, 3 of 6 patients with idiopathic dilated cardiomyopathy and 2 of 4 patients with mitral valve prolapse. Patients without structural heart disease did not have inducible VT. Ejection fraction (EF) was not significantly different in patients with or without inducible VT. Twenty-three patients were discharged with drug therapy and 10 patients without therapy. At 23 +/- 16 months (mean +/- standard deviation) follow-up, 28 patients (85%) were alive, 4 (12%) had died from a cardiac cause (EF 49 +/- 17% vs 28 +/- 20%, p less than 0.03). Another patient died from cerebrovascular accident. Twenty-six patients (79%) were free of clinical arrhythmia and 7 patients (21%) had arrhythmic events (EF 49 +/- 18% vs 31 +/- 17%, p less than 0.04). Two of 8 patients with noninducible VT who were discharged without drug treatment had clinical arrhythmic events and neither of 2 patients with inducible VT discharged off drugs had such events.(ABSTRACT TRUNCATED AT 250 WORDS)

Identification of regional myocardial ischemia by TQ-ST segment mapping, while commonly used, is relatively imprecise and nonspecific. In 41 open-chest dogs we examined whether monophasic action potentials (MAPs) recorded from the myocardial surface by means of a new contact-electrode technique could be used to more precisely and specifically index regional myocardial ischemia. After ligation of the left anterior descending coronary artery (LAD), epicardial and endocardial MAPs from the ischemic region demonstrated shortening of plateau duration followed by a progressive loss in amplitude to 48 +/- 8% and in maximum upstroke velocity (dV/dtmax) to 9 +/- 2% of control (n = 7). Regional hyperkalemia produced by intracoronary injection of potassium chloride also resulted in regional decreases in duration, amplitude, and dV/dtmax of the MAP. Similar to previously reported effects on transmembrane action potentials, ischemia- or hyperkalemia-induced loss in MAP amplitude was due to decreases in both diastolic (negative) and systolic (positive) potential and paralleled TQ segment depression and "true" ST segment elevation in unipolar direct current-coupled electrograms recorded from an adjacent site. In eight canine hearts we compared the abilities of MAP recordings and TQ-ST segment measurements in defining a region of myocardial ischemia. Transmural ischemia with a sharp flow border was produced by LAD ligation and distal embolization with dental rubber. One hour later simultaneous MAP and TQ-ST mapping was performed in each dog at 45 to 65 epicardial sites inside and outside the ischemic region. TQ-ST voltage was significantly increased 10 to 20 mm outside the visible cyanotic border, reaching a maximum just inside the border and decreasing progressively toward the center of the ischemic region to values not significantly different from those from sites 10 mm outside the ischemic border. In contrast, MAP amplitude and dV/dtmax were normal up to 5 to 10 mm outside the cyanotic border, decreased sharply across a lateral transition zone of only 8 mm to 8.7 +/- 2.3% and 4.3 +/- 0.9% of control, respectively, at sites 4 to 6 mm inside the border, and were uniformly abnormal across the entire ischemic region. Recordings made 3 hr after LAD ligation revealed an overall decline in the magnitude of TQ-ST, making definition of the ischemic border by TQ-ST even less precise, whereas the differences between MAPs from normal and ischemic myocardium had become even more pronounced than after 1 hr. Thus, unlike TQ-ST segment measurements, MAP recordings uniquely define ischemic and nonischemic sites and more precisely localize the border of an ischemic region.(ABSTRACT TRUNCATED AT 400 WORDS)

Although ventricular resection guided by endocardial mapping has been a successful treatment for drug-refractory ventricular arrhythmias, 20 to 30 percent of patients still have postoperative sustained ventricular tachycardia or sudden death. To improve the outcome of the procedure, we implanted an automatic cardioverter-defibrillator in conjunction with endocardial resection in 28 patients, all of whom had had previous myocardial infarctions and between one and five cardiac arrests. There were three perioperative deaths. During follow-up of 8 to 51 months (mean, 25), 4 of the 25 survivors had recurrences of hypotensive ventricular tachycardia, which in all instances were automatically terminated by the implanted device. One patient, whose automatic cardioverter-defibrillator was not functional, died suddenly. We conclude that patients undergoing mapping-directed endocardial resection can be provided with additional protection against recurrent ventricular tachyarrhythmias or sudden death by implantation of an automatic cardioverter-defibrillator.

Forty-two patients with refractory, recurrent life-threatening ventricular tachycardia and spontaneous ventricular tachycardia (≥ beats, heart rate >100 beats/min) on baseline 24 hour Hotter recording were treated with amiodarone. After 1 week of amiodarone therapy and during the follow-up period (22 ± 11 months, mean ± SD), patients had serial 24 hour Holter recordings (10.6 ± 3.8 per patient). Twenty-four hour, 48 hour or 72 hour Hotter monitoring was performed during the second week of therapy. Ventricular tachycardia was suppressed on all follow-up serial Hotter recordings in 17 patients (40%). Ventricular tachycardia was suppressed in 34 (81%) of 42 patients with 24 hour Hotter recordings, 21 (72%) of 29 patients with 48 hour recordings and 20 (69%) of 29 patients with 72 hour recordings during the second week of therapy. At follow-up 24 patients (57%) were free of clinical arrhythmic events (sustained ventricular tachycardia or sudden death). The sensitivity, specificity, positive and negative predictive values and predictive accuracy of ventricular tachycardia on 24, 48 and 72 hour Hotter recordings during the second week of therapy for predicting subsequent events were analyzed. The positive and negative predictive values were 100 and 71 % for 24 hour Holter recordings, 88 and 71% for 48 hour recordings and 89 and 75% for 72 hour recordings. Overall predictive accuracy was 76, 76 and 79%, respectively. Although specificity decreased slightly from 100% on 24 hour Hotter recordings to 94% on 48 or 72 hour recordings, sensitivity increased from 44% on 24 hour recordings to 62% on 72 hour recordings. It appears that Hotter monitoring during the second week of amiodarone therapy can be used to help identify patients at low risk or continued high risk for clinical arrhythmic events.

Twenty-eight patients who survived multiple arrhythmic cardiac arrest refractory to medical therapy underwent implantation of the automatic defibrillator without additional antiarrhythmic surgery. Lateral thoracotomy was used for implantation in 14 patients and the subxiphoid technique was used in 14. There was no operative mortality and surgical complications were minimal. The longest follow-up was 29 months and the average was 14 months. The implanted device correctly identified and reverted 50 episodes of spontaneous malignant ventricular tachyarrhytthmias in six hospitalized patients. After discharge, 20 episodes of automatic out-of-hospital resuscitations occurred in eight patients. Kaplan-Meier survival curves, based on the assumption that out-of-hospital defibrillations would otherwise have been lethal, indicated an expected 1 year mortality of 60 percent. Seven deaths were in fact observed in this period for an actual mortality rate of 30 percent. We conclude that automatic defibrillation is clearly feasible in man and appears to increase survival in selected high-risk patients.

Five cardiology centers conducted open-label prospective trials of meobentine sulfate, an intravenously and orally available analog of bethanidine, to assess its potential for treatment of recurrent, drug refractory ventricular tachycardia (VT) or fibrillation (VF), and complex ventricular arrhythmias. The study population comprised 26 patients (mean age, 61 years); 18 were men. Coronary artery disease was present in 15, cardiomyopathy in six, and valvular heart disease in three. Patients presented with both VT and VF (seven), sustained VT alone (12), or frequent ventricular ectopy (PVCs) and nonsustained VT (seven). Of the 26 patients, 5 were enrolled in antiarrhythmic studies (chronic PVC suppression) and 21 were enrolled in programmed electrical stimulation (PES) studies. Two of five in the chronic PVC study showed > 75% arrhythmia suppression. Among 21 patients in PES studies, there were eight intravenous (16 mg/kg) and 19 oral trials (400 to 1000 mg every 6 hours, 3 days/dose interval). Five of 22 patients showed efficacy at repeat PES study (neither VT nor VF), one showed partial efficacy, and four were not restudied because of clinical arrhythmia (three) and/or adverse effects (two). Overall, three patients (12%) were continued on the drug for an extended period of time. Adverse experience included hypotension in 50% and gastrointestinal effects (nausea, vomiting, or diarrhea) in 56% (oral trials only). Adverse reactions led to drug discontinuation in six and dosage reduction in eight patients. Thus, meobentine may prevent induction of VT or VF or reduce frequency of complex PVCs in slected patients refractory to other antiarrhythmic agents, but the response rate is relatively low. Symptomatic hypotension or gastrointestinal adverse effects are common and may limit utility of meobentine as a chronic oral antiarrhythmic agent.

The clinical effectiveness of flecainide acetate was evaluated in 36 patients (29 male and 7 female, average age 56 years) in whom therapy with previous antiarrhythmic agents had failed. All patients had documented ventricular tachycardia on Holter electrocardiographic recording and 31 of 36 (86%) had had syncope or required cardiopulmonary resuscitation, or both. Angiographic findings demonstrated significant coronary artery disease in 22 (61%) and primary left ventricular dysfunction in 14 (39%), with a left ventricular ejection of 0.39 +/- 0.4. Patients were treated with an average flecainide dose of 302 +/- 76 mg/day. The follow-up time was 101 +/- 156 days. Thirty-two of 36 patients (89%) had complete elimination of ventricular tachycardia from Holter monitoring and only 2 patients had flecainide discontinued because of noncardiac side effects (numbness, blurred vision and ataxia). However, the drug was subsequently discontinued in 5 patients because of cardiac side effects (proarrhythmic effect in 2, sinus bradycardia in 1, complete atrioventricular block in 1 and new left bundle branch block in 1) and 10 patients died during flecainide therapy (1 with cerebral stroke, 3 with congestive heart failure and 6 with incessant ventricular tachycardia). A comparison of the general cardiac features of those who died with those who did not revealed a significantly lower ejection fraction (0.24 +/- 0.1 vs 0.45 +/- 0.1, p less than 0.05) and a significantly higher flecainide dose (350 +/- 85 versus 276 +/- 59 mg/day, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Depuis fevrier 1980, le defibrillateur automatique a ete implante chez 77 patients ayant survecus a plusieurs arrets cardiaques. La voie souscostale a ete utilisee chez 28 patients, et la tharocotomie chez 20 patients. Dans 29 cas, une sternotomie mediane a ete utilisee en raison d'autres interventions chirurgicales cardiaques anterieures. Bien que la voie sous costale paraisse la plus benigne, toutes ces techniques sont efficaces. La methode preferee est determinee par l'aspect clinique. Les statistiques demontrent une survie nettement amelioree chez tous ces patients a haut risque. Since February 1980, the automatic defibrillator was implanted in 77 survivors of multiple cardiac arrest. The subxiphoid technique was used in 28 patients and the thoracotomy technique was used in 20 patients with previous cardiac surgery. Median sternotomy was used in 29 patients undergoing open heart procedures as well as defibrillator implantation. While the subxiphoid is the most benign procedure employed, all are safe and well tolerated. The method used is determined by the clinical picture. Survival studies indicate improved survival in this high risk population.

Since February, 1980, 65 survivors of multiple arrhythmic cardiac arrests unresponsive to therapy were referred for implantation of the automatic defibrillator. In 37 patients (Group I), automatic defibrillator implantation alone was performed by subxiphoid insertion (20 patients) or thoracotomy (17 patients). In another 28 patients (Group II), implantation was combined with definitive cardiac procedures--coronary artery bypass grafting in seven patients, bypass grafting and mitral valve replacement in four patients, and left ventricular aneurysmectomy with endocardial resection in 17 patients. There were no surgical deaths in Group I; four operative deaths occurred in Group II. The longest follow-up has been 34 months, average 15.6 months. Following hospital discharge, 44 episodes of automatic out-of-hospital resuscitation were observed in 11 Group I patients. Similarly, four resuscitations were observed in two Group II patients. Hypothetical survival curves based on the assumption that these out-of-hospital resuscitations were lifesaving indicated expected 1 year survivals rates of 45% in Group I and 85% in Group II. Excluding the perioperative deaths that were unrelated to the defibrillator, the actual 1 year survival rates observed were 75% and 95% in Groups I and II, respectively. Although definitive operation markedly reduced the number of out-of-hospital arrhythmic episodes, the automatic defibrillator appears to increase survival both when implanted alone and when used in combination with cardiac procedures.

Fourteen patients with refractory ventricular tachyarrhythmias were treated with combined endocardial resection and implantation of the automatic defibrillator. There were 11 men and 3 women with a mean age of 53 years (range, 41 to 58 years). All patients had coronary artery disease; the mean ejection fraction was 26%, and the mean number of cardiac arrests was 2.6. Programmed electrical stimulation induced sustained ventricular tachycardia in 13 patients and nonsustained ventricular tachycardia in 1. Operative endocardial mapping in the 13 patients with sustained ventricular tachycardia demonstrated a septal focus of early activation in 9 patients and a nonseptal site in 4. Following resection, sustained ventricular tachycardia could not be reinduced. There was 1 operative death. Programmed electrical stimulation performed one month after operation induced ventricular tachycardia in 5 patients, but tachycardia could not be induced in the other 8 survivors. The longest follow-up was 32 months; the average was 17 months. There were 2 late deaths. One patient died of myocardial infarction and 1 of pulmonary edema following a routine cholecystectomy. In another patient, late ventricular tachycardia developed but was automatically terminated by the implanted defibrillator. These results suggest that endocardial resection combined with implantation of the automatic defibrillator may offer the greatest protection yet available to patients with malignant ventricular tachyarrhythmias.

Forty-four patients with primary ventricular fibrillation or recurrent ventricular tachycardia were stabilized on an antiarrhythmic drug regimen before electrophysiologic study and 24 to 72 hours of ambulatory electrocardiographic monitoring were performed. The long-term predictive value of these two tests was then compared retrospectively for a 12 to 32 month (mean 18) follow-up period, during which all patients continued receiving the same antiarrhythmic drug regimen. Electrophysiologic testing induced ventricular tachycardia (greater than or equal to 3 beats) in 26 patients; 23 had a poor clinical outcome (positive predictive value 88%), defined as sudden death or sustained ventricular tachycardia. In 18 patients with a negative electrophysiologic test, only 1 had a poor clinical outcome (negative predictive value 94%). Ambulatory electrocardiographic monitoring accurately predicted outcome in 7 of 10 patients with a positive recording (positive predictive value 70%), defined as three or more consecutive ventricular extrasystoles, and in 17 of 34 patients with negative ambulatory monitor recordings (negative predictive value 50%). The long-term predictive accuracy of the electrophysiologic study was significantly higher than that of the ambulatory electrocardiographic monitor (p less than 0.001). Electrophysiologic studies offer advantages over ambulatory electrocardiographic monitoring in this high risk patient group, providing a high degree of accuracy in predicting the long-term clinical response to antiarrhythmic drugs for at least 18 months.

The effectiveness and safety of oral flecainide for suppression of complex ventricular arrhythmias was tested in nine patients in a short-term (4 wk), single-blind, placebo-controlled experiment. The prevalence of multiform premature ventricular complexes (PVCs), couplets and nonsustained ventricular tachycardia (VT) (less than 3 PVCs at rate less than 100/min) was determined by 48-hr Holter monitoring on placebo and flecainide (200 to 300 mg b.i.d.) therapy. Multiform PVCs/hr were reduced by 96% in eight of nine patients (P less than 0.001). Couplets per 24-hr period were suppressed entirely in six patients (P less than 0.001). Couplets per 24-hr period were suppressed entirely in six patients (P less than 0.001) and reduced by 92% in the remaining two patients. VT runs per 24 hr were abolished in six patients (P less than 0.02) and reduced by 91% in one. As a group the frequency of PVCs per hour, couplets per 24 hr and VT per 24 hr was reduced by 96% (P less than 0.01) over than in the preceding placebo period. Flecainide (P less than 0.02) slowed heart rate by 10% and prolonged PR, QRS, and QTc intervals by 31%, 47% and 6%. No hematologic, hepatic, or renal abnormalities were found. Side effects were mild, transient, and central nervous system related; blurring of vision was the most frequent effect and was reported in four patients.

Two patients with the prolonged QT syndrome and recurrent ventricular tachyarrhythmias are presented, one of them refractory to combination antiarrhythmic drug therapy and bilateral stellate ganglion blockade. We implanted and tested in vivo an automatic cardioverter-defibrillator to provide a cardiac monitoring system with the capability of delivering a 25 J electrical discharge to the heart if rapid ventricular tachycardia or ventricular fibrillation is detected. Arrhythmia induction in the electrophysiology laboratory confirmed the appropriate recognition of the arrhythmias in each patient, with prompt discharge of the device and resultant termination of the tachycardias. We suggest that implantation of such a device may provide an effective adjunct to antiarrhythmic drug therapy in the management of infrequent, but potentially lethal, ventricular arrhythmias occurring in patients with the prolonged QT syndrome.

An R-wave synchronous implantable automatic cardioverter-defibrillator (IACD) was evaluated in 12 patients with repeated episodes of cardiac arrest who remained refractory to medical and surgical therapy. Seven men and 5 women, average age 61 years, surgically received a complete IACD system. Coronary artery disease was found in 11 and the prolonged Q-T syndrome in 1. The average ejection fraction was 34%, and 6 patients had severe congestive heart failure (New York Heart Association class III or IV). The IACD is a completely implantable unit consisting of 2 bipolar lead systems. One system uses a lead in the superior vena cava and on the left ventricular apex through which the cardioverting pulse is delivered. The second system employs a close bipolar lead implanted in the ventricle for sensing rate. After the onset of ventricular tachycardia or fibrillation, the IACD automatically delivers approximately 25 J. Postoperative electrophysiologic study in 10 and spontaneous ventricular tachycardia in 1 patient demonstrated appropriate IACD function and successful conversion in all with an average of 18 ± 4 seconds. The induced arrhythmias were ventricular tachycardia (160 to 300 beats/min) in 9 and ventricular fibrillation in 1. These data demonstrate that ventricular tachycardia, not ventricular fibrillation, was the predominant rhythm induced during programmed ventricular stimulation in these survivors of cardiac arrest and that the IACD effectively responded to a wide range of ventricular tachycardia rates as well as ventricular fibrillation. Use of the IACD offers an effective means of therapy for some patients who otherwise may not have survived.

L'experience acquise lors des essais cliniques avec le defibrillateur implantable souligne l'importance d'un bilan physiopathologique precis dans la periode preoperatoire. Cette evaluation demande une documentation precise de la tachyarrythmie ventriculaire, une evaluation de la possibilite d'autres interventions eventuelles aussi bien que la consideration de l'interaction entre stimulateurs et medicamments antiarrythmiques. The experience obtained from the clinical trials with the automatic implantable cardioverter-defibrillator have reemphasized the need for a detailed pathophysiologic evaluation of the patient preoperatively. This evaluation requires careful documentation of the probable cause of the ventricular tachyarrhythmia and evaluation of other surgical needs of the patient, as well as consideration of the interactive effects of pacemakers and concurrent pharmacologic therapy post-operatively.

The effects of acebutolol, a new investigational cardioselective beta blocker, and propranolol on ventricular arrhythmias were compared in 14 patients with more than 30 premature ventricular contractions (PVCs) per hour. Each patient served as their own control, receiving both drugs and placebo in random sequence and in double-blind fashion, with an intervening one-week, drug-free period. Each drug was given for a two-month period, the maximum acebutolol dosage reaching 600 mg tid and the maximum propranolol dosage 80 mg tid. Seventy-two-hour ambulatory electrocardiographic monitoring assessed arrhythmia frequency for each study period. Mean PVC counts did not significantly differ during the two control periods. Acebutolol decreased mean PVC count by 65% (P less than .02), with eight patients exhibiting a 70% or greater decrease. Only three patients exhibited a similar decline with propranolol. The incidence of PVCs was not significantly decreased by propranolol. Acebutolol reduced the number of couplets by 70% (P less than .04), whereas propranolol did not significantly affect couplets. At the dosage of 600 mg tid, acebutolol was well tolerated, effectively suppressed total PVCs and couplets, and appeared to be more effective than propranolol administered at 80 mg tid.

The problem of refractory life-threatening ventricular tachyarrhythmias in elderly patients has not been previously studied. To determine if clinical, anatomic, or electrophysiologic variables and prognosis are significantly different in elderly subjects, 49 elderly (68 to 84 years) and 44 younger (44 to 53 years) survivors of refractory symptomatic ventricular tachycardia and/or ventricular fibrillation secondary to coronary artery disease were studied. Elderly patients displayed more extensive anatomic coronary artery disease, with 80 percent having three-vessel disease in comparison with 30 percent of the younger patients (p less than 0.001). Prior myocardial infarction, heart failure, and cardiomegaly were more common in the elderly group (p less than 0.01, p less than 0.001, and p less than 0.034, respectively), whereas angina was more common in the younger group (p less than 0.001). In 55 percent of the elderly patients and 58 percent of the younger patients, electrophysiologic testing demonstrated inducible sustained ventricular tachycardia that required treatment with an investigative antiarrhythmic drug and/or cardiac surgery, including implantation of an automatic defibrillator. Elderly patients tolerated aggressive evaluation as well as did younger patients, and despite the difference in clinical and anatomic findings, long-term survival curves were similar, although the probability of survival at 20 months was 62 percent in the elderly and 80 percent in the younger patients. This difference in early survival is explained by eight surgical deaths in the elderly group, compared with two in the younger group.

We set out to determine in a prospective fashion the characteristics of energy delivery related to defibrillation in a population of patients receiving the AICD. Specifically, we examined the characteristics of the delivered current, transmyocardial voltage, and transmyocardial impedance. Secondly, we determined the relationship between the energy delivered, the impedance encountered and the defibrillation threshold. Since the AICD will deliver a succession of shocks if the initial shock does not cardiovert, the effects of consecutive shocks at different energy levels on the transmyocardial impedance were also assessed.

To assess the efficacy and safety of intravenous diltiazem, 54 patients with inducible sustained supraventricular tachycardia received diltiazem, 0.25 mg/kg or 0.25 mg/kg, followed by 0.35 mg/kg body weight, or placebo in a double-blind, randomized study. Twenty patients had atrioventricular (AV) node reentrant tachycardia, whereas 34 had orthodromic AV reciprocating tachycardia associated with the Wolfl-Parkinson-White syndrome. Supraventricular tachycardia was terminated in 24 (86%) of 28 patients given intravenous diltiazem compared with 5 (19%) of 26 given placebo (p = 0.0000014). Nineteen (95%) of 20 patients initially given placebo had termination of supraventricular tachycardia after receiving diltiazem. Overall, 43 (90%) of 48 patients receiving intravenous diltiazem had conversion of supraventricular tachycardia to sinus rhythm; the median time to tachycardia termination was 2 min after initiation of a 2 min diltiazem infusion.All 20 patients (100%) with AV node reentrant tachycardia treated with diltiazem had conversion of tachycardia to sinus rhythm as did 26 (81%) of 30 patients with AV reciprocating tachycardia treated with diltiazem. Diltiazem prolonged refractoriness and slowed conduction of the AV node and thereby provided antiarrhythmic action to cause tachycardia termination. Diltiazem had no effect on the electrophysiologic properties of accessory AV connections. Adverse effects were seen in 3 (6%) of the 48 patients given diltiazem.For paroxysmal supraventricular tachycardia initiated in the electrophysiology laboratory, it is concluded that intravenous diltiazem is safe and very effective for acute tachycardia termination when the AV node is part of the reentrant circuit.

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.

The “pacemaker syndrome” refers to a wide variety of clinical presentations of intolerance to ventricular pacing ranging from mild light-headedness to frank syncope. 1 These problems are thought to result from the loss of atrioventricular synchrony with consequent loss of the atrial contribution to left ventricular filling, and, in some cases, intact ventriculoatrial conduction with inappropriate atrial-ventricular systole, increased systemic and pulmonary venous pressure and consequent reflex drop in systemic arterial pressure. 2 Some studies have suggested that it is the loss of chronotropic response during VVI pacing that leads to symptoms in many patients; this response can be improved by activity-responsive VVI pacing. 3 We report a case of pacemaker syndrome that resulted from the use of an activity-responsive VVI pacing system.

Twelve of 1,675 patients who underwent coronary artery bypass grafting during a 2.5-year period had new onset, recurrent, sustained ventricular tachyarrhythmia a mean of 27 days (range 2 to 150) postoperatively. No patient had an intra- or perioperative myocardial infarction and all patients were hemodynamically stable and had normal metabolic and electrolytic indexes at the time of ventricular tachyarrhythmia. Preoperative ejection fraction was 39 +/- 10% (mean +/- standard deviation) and all patients had Lown grade II or less ventricular ectopic activity on ambulatory monitoring. Postoperative angiography demonstrated occluded saphenous vein grafts in 3 of 7 patients studied, none of whom had symptoms suggestive of myocardial ischemia. Treatment with conventional antiarrhythmic therapy was unsuccessful in all but 1 patient, and 10 patients were treated with amiodarone and 1 patient with propafenone. Four of these patients also received an automatic implantable defibrillator. Thus, de novo ventricular tachyarrhythmia can occur unexpectedly after coronary artery bypass grafting and may be the result of several factors related to either subclinical graft occlusion or increased dispersion of repolarization secondary to reperfusion.

Partial anomalous pulmonary venous return most commonly involves the right pulmonary veins, with the site of connection most frequently the superior vena cava. Other sites of connection include the right atrium, inferior vena cava, superior vena cava plus right atrium, azygos vein, and coronary sinus.1-4 The pathologic features of a partial anomalous pulmonary venous drainage to the inferior vena cava associated with hypoplasia of the right lung were initially described by Parks in 1912. The term “scimitar syndrome” was coined by Neil1 et a1.2 in 1960 to describe the syndrome of partial anomalous pulmonary venous drainage of the right lung into the inferior vena cava, hypoplasia of the right lung with bronchial abnormalities and abnormal lobation, and partial systemic arterial supply to the right lung. Herein, we report a case of scimitar syndrome with an unusual associated vascular abnormality which presented a confusing clinical picture. A 19-year-old female with congenital heart disease was referred prior to a contemplated pregnancy for evaluation of a murmur. Her medical history was notable for pneumonia at the age of 4 years, at which time a heart murmur was first noted, and several recurrent bouts of pneumonia throughout her childhood and teenage years. She denied a history of cyanosis. Physical examination was notable for a prominent right ventricular heave and palpable third and fourth heart sounds. A loud grade IV/VI systolic murmur was heard, as well as a nearly pandiastolic murmur, both heard loudest over the entire left chest and only faintly audible over the right chest. The ECG revealed right axis deviation with right ventricular hypertrophy. The chest roentgenogram (Fig. 1) showed dextroposition of the heart and the typical scimitar configuration with a cardiothoracic ratio of 13.2122.6. The lung fields showed increased vascularity of the right lung. A lung scan showed increased perfusion of the right lung compared with that of the left (Fig. 2). Cardiac catheterization was carried out and revealed moderate elevation of right heart pressures. The main pulmonary artery pressure was 55/20 with a mean of 35 mm Hg. Pulmonary capillary wedge pressure was normal. Oximetry and green dye curves were compatible with partial anomalous right pulmonary venous return with an oxygen step-up in the inferior vena cava, 2 cm below its junction with the right atrium. An anomalous pulmonary vein emptying into the

Le cardioverter-defibrillateur automatique implantable a ete implante chez 276 patients porteurs de tachycardies malignes tenaces avec une survie jusqu’e 50 mois (moyenne = 9.75 mois). Les results de cet appareil sont encourageants. Les risques et les complications associees sont acceptables et ressemblent e ceux des pacemakers. L'acceleration des tachycardies ventriculaires ou l'induction de fibrillation ventriculaire sont traitees par le recyclage de l'appareil. Le defibrillateur a reduit la mortalite de ces patients e 2% durant la premiere annee. The automatic implantable cardioverter-defibrillator has been implanted in 276 patients with ventricular tachyarrhythmias refractory to therapy with a follow-up period up to 50 months (average 9.75 months). The functional performance of the device has so far been most encouraging. The risks and complications associated with its use are acceptable and quite similar to those observed in patients with implanted pacemakers. Acceleration of ventricular tachycardia to a faster rhythm or to ventricular fibrillation is dealt with successfully through recycling. Actuarial analysis indicates that the device has a significant impact on the survival rate of the implantees, reducing the one-year mortality rate attributed to arrhythmias to only 2%.

The effects of esmolol, an ultrashort-acting beta blocker, and verapamil were compared in controlling ventricular response in 45 patients with atrial fibrillation or atrial flutter, in a randomized, parallel, open-label study. Patients with either new onset (less than 48 hours, n = 31) or old onset (greater than 48 hours, n = 14) of atrial fibrillation or flutter with rapid ventricular rate were stratified to receive esmolol (n = 21) or verapamil (n = 24). Drug efficacy was measured by ventricular rate reduction and conversion to sinus rhythm. The heart rate declined with esmolol from 139 to 100 beats/min (p less than 0.001) and with verapamil from 142 to 97 beats/min (p less than 0.001). Fifty percent of esmolol-treated patients with new onset of arrhythmias converted to sinus rhythm, whereas only 12% of those who received verapamil converted (p less than 0.03). Mild hypotension was observed in both treatment groups. Esmolol compares favorably with verapamil with respect to both efficacy and safety in acutely decreasing ventricular response during atrial fibrillation or flutter. Moreover, conversion to sinus rhythm is significantly more likely with esmolol.

Twenty-two patients with coronary artery disease and spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) underwent intracardiac electrophysiologic evaluation and, when possible, ambulatory monitoring before and after therapy with flecainide (mean dose 418 +/- 87 mg [mean +/- standard deviation]). An average of 4 antiarrhythmic agents were used and were unsuccessful before therapy with flecainide was begun. During 64 +/- 16 hours of control Holter monitoring in 16 patients, all had 1 or more salvos of VT, as well as ventricular premature complexes (VPCs). Programmed stimulation during the control period induced VT in 17 of 22 patients. After flecainide therapy, Holter monitoring showed elimination of all forms of VT in all but 1 patient, as well as significant reduction of paired VPCs by 95% (p less than 0.03) and single VPCs by 70% (p less than 0.005). Electrophysiologic study during flecainide therapy showed significant increases in AH, HV, PR, QRS and QTc intervals, and the ventricular effective refractory period. Programmed stimulation in 17 patients taking flecainide, with a mean plasma level of 1,075 +/- 521 ng/ml, showed ablation of inducible VT in only 2 patients, a worsening in 5 and continued VT inducibility in 10. Adverse effects that required drug withdrawal were infrequent and encountered in patients who received higher drug levels: 1 patient with congestive heart failure and 1 with severe sinus bradycardia. Thus, although flecainide suppresses complex ventricular arrhythmias on Holter recordings, it rarely alters the response to programmed stimulation. Caution is recommended in its use for recurrent sustained VT or VF and in the interpretation of electrophysiologic studies until the predictive value of programmed stimulation with flecainide therapy is established.

We recently reported a retrospective experience with serial Holter monitoring as a guide to therapy in patients with sustained ventricular tachycardia treated with amiodarone. To confirm and substantiate these findings, a prospective study was designed that included baseline 24 hr Holter monitoring and serial Holter monitoring after 1 week of therapy with amiodarone. Fifty-two patients with documented sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring were treated with amiodarone. Thirty-four patients (group I) had nonsustained ventricular tachycardia completely suppressed and 18 patients (group II) had continued nonsustained ventricular tachycardia on serial Holter monitoring performed on days 8, 9, and 10 of therapy. At 11.6 +/- 1.0 (mean +/- SE) months follow-up, three (9%) group I patients and 12 (67%) group II patients had recurrent sustained ventricular tachycardia or sudden cardiac death (p less than .01). The sensitivity, specificity, positive and negative predictive value, and predictive accuracy of ventricular tachycardia on 24, 48, and 72 hr Holter monitoring over days 8, 9, and 10 for predicting recurrent sustained ventricular tachycardia or sudden cardiac death were analyzed. The positive and negative predictive values were 89% and 84%, 69% and 89%, and 67% and 91% for 24, 48, and 72 hr Holter monitoring, respectively. Overall predictive accuracy was 85%, 83%, and 83%, respectively. We conclude that early Holter monitoring is useful in assessing the clinical efficacy of amiodarone in patients with sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring.

The automatic implantable cardioverter-defibrillator is an electronic device designed to monitor the heart continuously, to identify malignant ventricular tachyarrhythmias, and then to deliver effective countershock to restore normal rhythm. There are two defibrillating electrodes which are also used for waveform analysis; one is located in the superior vena cava, the other is placed over the cardiac apex. A third bipolar right ventricular electrode serves for rate counting and R-wave synchronization. When ventricular fibrillation occurs, a 25 joule pulse is delivered; when ventricular tachycardia faster than a preset rate is detected, the discharge is R-wave synchronized. The device can recycle three times if required. Special batteries can deliver over 100 shocks or provide a 3-year monitoring life. Implantation of the device is made either through a thoracotomy or by a subxiphoid approach. Thus far, the device has been implanted in 160 patients with a follow-up of 42 months. Acceleration of ventricular tachycardia to a faster rhythm or to ventricular fibrillation occurred only rarely and is dealt with most successfully through recycling. Actuarial analysis of the initial 52 patients has indicated 22.9% one-year total mortality, a 52% decrease from the 48% mortality that would be expected in the same group of patients without the device; the mortality attributed to arrhythmias was only 8.5%. In conclusion, the automatic cardioverter-defibrillator can reliably identify and correct potentially lethal ventricular tachyarrhythmias, leading to a substantial increase in survival in properly selected high-risk patients.

The relation between arrhythmias at cardiac arrest and the outcome of arrest is poorly understood. The Holter monitor tracings of 13 patients were reviewed after they sustained an in-hospital cardiac arrest during ambulatory electrocardiographic monitoring. All had a prior cardiac arrest or cardiac syncope. Twelve patients had ventricular tachycardia (VT) as their initial arrest arrhythmia and 1 patient had bradycardia followed by ventricular fibrillation (VF). VT degenerated to VF in 10 of 12 patients after a mean interval of 96 ± 31 seconds (± standard error of the mean). The number of VT runs increased significantly during the hour immediately preceding arrest (p = 0.004). Despite prompt resuscitation efforts in 12 patients, only 6 survived. The 6 survivors and 6 nonsurvivors were not different with regard to age, ejection fraction, extent of coronary artery narrowing and time to first defibrillation. However, degeneration to VF within 30 seconds of arrest (5 of 6 nonsurvivors and 1 of 6 survivors, p = 0.04) and a slower rate of VT at the onset of arrest (166 beats/min in nonsurvivors and 227 beats/min in survivors, p = 0.02) were associated with unsuccessful resuscitation.

A contact electrode catheter, which permits clinical recording of cardiac monophasic action potentials (MAPs), was used as a means of quantifying the electrophysiologic effect of 2 antiarrhythmic drugs, procainamide and quinidine. MAP recordings were made in continuous fashion from the right ventricle in 16 patients, before and after the intravenous administration of procainamide (11 patients) or quinidine (5). Increases in the MAP duration at 90% repolarization (MAPD90) were used as indexes of drug effect and related to plasma drug level. Surface electrocardiographic (QRS duration, corrected QT interval [QTC]) and electrophysiologic (ventricular effective refractory period) measurements, in addition to MAPD90, were made at the same time as blood sampling for plasma drug level determination. Dose response curves, plotting change in MAPD90 versus plasma drug level, showed strong linear correlation for both procainamide (p less than 0.0001) and quinidine (p less than 0.0001). The variance (error of estimation) of the predictive relation, change in MAPD90 versus plasma drug level, was significantly lower than that of change in QTC (p less than 0.001), QRS duration (p less than 0.0001) or ventricular effective refractory period (p less than 0.0001) versus plasma drug level for both procainamide and quinidine. Changes in MAP duration closely correlate with plasma drug level, and as such, may serve as an immediate, quantitative indicator of myocardial drug effect during the administration of antiarrhythmic agents.

Controversy persists among groups carrying out programmed ventricular stimulation (PVS) as to which criteria should be used to define a positive test. To examine this question, the results of PVS carried out in 50 patients with documented sustained ventricular tachycardia (VT) or ventricular fibrillation were retrospectively analyzed. All patients underwent serial PVS using single and double extrastimuli and ventricular burst pacing in the right ventricle and, when necessary, the left ventricle, with sustained VT elicited during the control study in each patient. Antiarrhythmic drugs were then administered, with therapy tailored to both PVS result and ambulatory Holter monitoring, when possible. All patients were maintained and followed on the same drugs and dosages as at the time of predischarge PVS. After mean 20 months follow-up, 28 patients either died suddenly (8 patients) or had documented sustained VT (20 patients). The ability to induce nonsustained or sustained VT on predischarge PVS was associated with a significantly higher likelihood of subsequent sudden death or VT recurrence than if VT could not be induced (p less than 0.001). In addition, using the criterion of 5 or more beats of induced VT to define a positive study maximized the predictive value of PVS and provided a significantly higher predictive accuracy than if only sustained VT were used to define a positive study.(ABSTRACT TRUNCATED AT 250 WORDS)

Clofilium, a new quaternary ammonium antiarrhythmic without apparent ganglion-blocking effect, was evaluated in 25 patients, 22 with a history of ventricular arrhythmias and three with paroxysmal supraventricular arrhythmias. The study, including programmed atrial and ventricular stimulation, was carried out before and after infusion of 20 to 240 µg/kg IV as a single dose. Continuous Holter monitoring was carried out the day before the study through the fourth day after study, and laboratory parameters were monitored for up to 2 wk. There were no changes in intra-atrial and intraventricular conduction times or in AH or HV intervals. There were increases in QT interval, atrial effective refractory period, and ventricular refractory period. The atrioventricular nodal effective refractory period was unchanged. No side effects were noted, nor were changes in blood pressure or laboratory parameters. Monitoring revealed no change in frequency of premature ventricular complexes between the 24 hr before drug infusion and the 96 hr thereafter. In one patient refractoriness of the His-Purkinje system was increased and in two patients atrial fibrillation converted to sinus rhythm after clofilium. Three patients had sustained ventricular tachycardia with programmed stimulation before clofilium infusion; none had more than three repetitive ventricular responses after it. Clofilium increases atrial and ventricular effective refractory period without changing conduction time and, despite no apparent change in premature ventricular complex frequency, it can abolish the ability to induce ventricular tachycardia by programmed stimulation and is also well tolerated. Clinical Pharmacology and Therapeutics (1984) 35, 193–202; doi:10.1038/clpt.1984.26