Importance of abortive shock capability with electrogram storage in cardioverter-defibrillator devices.

OBJECTIVES: This study evaluates the ability of a third-generation cardioverter-defibrillator to abort energy delivery and the importance of electrogram storage in analyzing the aborted events. BACKGROUND: In the Cadence Tiered Therapy Defibrillator, when a tachycardia satisfies detection criteria for cardioversion or defibrillation therapy, high voltage capacitors begin charging. The Cadence defibrillator continues monitoring the rhythm during charging and if the rate decreases to below the rate triggering therapy, charging is terminated. This event is registered as an aborted shock. The defibrillator also has the ability to store intracardiac electrogram recordings of the electrical events that precipitate device therapy or aborted shocks. METHODS: During a mean follow-up interval of 10 +/- 7 months, 55 aborted events were registered by the Cadence defibrillator in 18 of the 49 patients who received it. Thirty-two stored ventricular electrograms of events leading to aborted shocks were available for analysis in 15 patients. RESULTS: Intracardiac electrogram recordings demonstrated the probable electrical events leading to these aborted shocks included nonsustained ventricular tachycardia (n = 10), nonsustained rapid polymorphic ventricular tachycardia/ventricular fibrillation (n = 2), atrial fibrillation (n = 5), supraventricular tachycardia (n = 2) and electrical noise (n = 13). Eleven patients had a therapeutic intervention initiated as a consequence of the diagnostic information provided by analysis of intracardiac electrogram recordings. Four of the 15 patients had no changes made. During a follow-up period of 9 +/- 5 months after therapy was altered, no patient had subsequent aborted shocks. Five patients have had seven appropriate shocks for sustained ventricular tachycardias. CONCLUSIONS: The ability of Cadence defibrillator to continue tachycardia sensing during capacitor charging and to abort shock therapy for self-terminating events prevented unnecessary shocks in 18 (37%) of the 49 patients. Intracardiac electrogram recordings were critical for instituting appropriate therapy that may have prevented unnecessary device charging and inappropriate discharges.

Unique sensing errors in third-generation implantable cardioverter-defibrillators.

OBJECTIVES: Third-generation cardioverter-defibrillators appear to be susceptible to unique sensing errors. This study was performed to determine the incidence and types of sensing errors in combination therapy implantable devices. BACKGROUND: One of the advantages offered by third-generation implantable cardioverter-defibrillators is the combination of bradycardia and antitachycardia pacing and cardioversion-defibrillation capabilities in a single device. The potential for unique sensing errors, those caused by the conflicts presented by combining bradycardia and tachycardia sensing and therapy algorithms in the same device, has not been previously addressed. METHODS: To determine the incidence of important sensing errors, 61 patients with a combination therapy device (Cadence [Ventritex] and PCD [Medtronic]) were studied for a 25-month period. In addition to surface electrocardiographic recordings during implantation and routine device testing, real-time and stored electrograms recorded from the rate-sensing leads (Cadence) and real-time marker channel recordings (PCD) were reviewed to diagnose sensing errors that resulted in symptoms, device inefficacy or delivery of inappropriate therapy. After recognition, specific reprogramming steps were performed in an attempt to avoid recurrent sensing errors. RESULTS: A total of 13 sensing errors were diagnosed in 12 patients (19.7%); the incidence was similar in both devices. Five distinct categories of sensing errors were identified. After device reprogramming, only one recurrent error occurred in 98 patient-months of follow-up. CONCLUSIONS: Important sensing errors occur in approximately 20% of patients with third-generation combination therapy cardioverter-defibrillators. Prompt diagnosis of sensing errors can lead to specific reprogramming steps to avoid recurrent errors.

Relationship of steady-state serum concentrations of amiodarone and desethylamiodarone to therapeutic efficacy and adverse effects.

The relationship of steady-state serum levels of amiodarone and its major metabolite, desethylamiodarone, to therapeutic and toxic effects was evaluated in 111 patients treated for supraventricular and ventricular arrhythmias. All patients were treated for more than two months (mean 10 +/- 7), and repeated serum levels determined at least two months apart were within 0.5 mg/liter of each other. Effective control of arrhythmias during steady-state therapy was achieved in 91 patients (82 percent of the study populations); recurrent arrhythmias or sudden death did not correlate with levels. An adverse drug effect necessitating cessation of therapy and/or concomitant medical therapy for the adverse effect occurred in 12 patients (11 percent); an additional 33 patients (30 percent) had an adverse effect that did not require change in therapy. The mean serum concentrations of amiodarone and desethylamiodarone associated with adverse drug effects were higher (2.6 +/- 1.2 mg/liter and 2.0 +/- 0.8 mg/liter) than those in patients without adverse effects (2.1 +/- 1.0 mg/liter and 1.5 +/- 0.7 mg/liter), p less than 0.05. An amiodarone serum concentration of 2.5 mg/liter or more had a positive predictive value of 76 percent for identifying patients with an adverse effect. The level of desethyl metabolite of amiodarone correlated directly with the serum amiodarone concentration (r = 0.82). Measurement of desethylamiodarone did not increase the sensitivity or specificity of the amiodarone level alone in the identification of patients at risk for adverse drug effects.

Value of Holter monitoring in identifying risk for sustained ventricular arrhythmia recurrence on amiodarone.

Seventy-four patients with sustained ventricular tachyarrhythmias had 22 +/- 3 hours of Holter monitoring before and after 11 +/- 6 days of amiodarone treatment. On control Holter recordings, 55 patients (group I) had frequent (more than 10 extrasystoles per hour) and/or complex (at least couplets) ventricular ectopic activity (VEA), and 19 patients (group II) had infrequent and simple VEA. A positive Holter monitor response to amiodarone was defined as a decrease in VEA by more than 85% and abolition of all complex VEA. In group I, 34 patients (62%) had a positive Holter monitor response. In group II, 16 patients (84%) had persistent, infrequent and simple VEA and 3 had frequent and/or complex VEA. During a mean follow-up of 13 +/- 12 months, 22 patients (30%) had ventricular tachycardia (VT) or sudden death. In group I, VT or sudden death occurred in 6 of 34 (18%) patients with a positive Holter monitor response and 11 of 21 (52%) with a negative Holter monitor response (p less than 0.01), and in group II, VT or sudden death occurred in 5 of 16 patients (31%) with persistent, infrequent and simple VEA. All episodes of VT or sudden death occurred after at least 2 weeks of amiodarone therapy (mean 5 +/- 6 months). The predictive accuracy of a positive Holter monitor response as an indicator for subsequent prevention of sustained ventricular tachyarrhythmias and sudden cardiac death was 82% and for a negative Holter monitor response as an indicator of tachyarrhythmia or sudden death recurrence on therapy it was 52%.(ABSTRACT TRUNCATED AT 250 WORDS)

Prognostic factors in nonsustained ventricular tachycardia.

Electrophysiologic studies were performed in 83 consecutive patients with spontaneous nonsustained ventricular tachycardia (VT). VT was inducible in 52 patients (nonsustained VT only in 37 patients, nonsustained and sustained VT in 13 and sustained VT only in 2). During a follow-up of 3 to 111 months (mean 33), 10 patients died suddenly, 5 with coronary artery disease (CAD) and 5 with dilated cardiomyopathy. All patients with sudden death had an ejection fraction less than or equal to 0.40. Sudden death occurred in 4 of 15 patients with inducible sustained VT, 2 of 37 patients with only nonsustained VT and 4 of 31 patients without inducible VT. One patient with dilated cardiomyopathy and VT inducible only by isoproterenol died suddenly. Three of 5 patients with CAD who had sudden death had had inducible sustained VT, but 3 of 5 patients with cardiomyopathy who had sudden death had no inducible VT. Multivariate analysis revealed that patients with inducible sustained VT or an ejection fraction less than or equal to 0.40 had a 3-fold increased risk of sudden death, and patients with both factors had a 7-fold increased risk of sudden death. This study demonstrates that patients with nonsustained VT with an ejection fraction greater than 0.40 have an uncomplicated course; however, noninducibility does not predict such a course, particularly in patients with cardiomyopathy. The most powerful predictor of risk for sudden cardiac death is a left ventricular ejection fraction less than or equal to 0.40, but the presence of inducible sustained VT is an independent risk factor for sudden death.

Repetitive, monomorphic ventricular tachycardia: clinical and electrophysiologic characteristics in patients with and patients without organic heart disease.

The clinical and electrophysiologic characteristics of 6 patients who had repetitive monomorphic ventricular tachycardia (VT) after a remote myocardial infarction (group A) were compared with those of 22 patients who had this arrhythmia without structural heart disease (group B). VT had a right bundle branch block morphologic pattern in 5 of 6 group A patients and a left bundle branch block morphologic pattern in all group B patients. Endocardial catheter activation mapping was performed in 4 group A patients and in 9 group B patients during VT. In all group A patients, the site of VT origin was on the border of the previous infarction; in all group B patients VT originated at the right ventricular outflow tract. Pacing and programmed stimulation induced VT in 5 of 6 group A patients and 7 of 22 group B patients (p = 0.03). Isoproterenol infusion provoked VT in 4 group A patients and 9 group B patients. Type I antiarrhythmic agents suppressed VT in 4 group A patients and in 14 group B patients, whereas propranolol suppressed VT in 3 of 3 group A patients tested and in 12 of 20 group B patients. Verapamil suppressed spontaneous VT in 1 group A patient and in 4 group B patients. During a mean follow-up of 19 months for group A and 40 months for group B, no patient had died suddenly or had cardiac arrest.

Shock occurrence and survival in 241 patients with implantable cardioverter-defibrillator therapy.

BACKGROUND: The purpose of this study was to determine the influence of clinical characteristics on shock occurrence and survival in 241 patients with implantable cardioverter-defibrillator (ICD) therapy. METHODS AND RESULTS: Two hundred forty-one consecutive patients underwent ICD implantation between November 1982 and November 1991 and were subsequently followed for 26 +/- 22 months (intention-to-treat analysis). Actuarial incidence of "appropriate" shocks was 13%, 42%, and 63%, and the incidence of any spontaneous shocks was 15%, 51%, and 76% at 1, 3, and 5 years of follow-up, respectively. Poor left ventricular function (ejection fraction < or = 30%) was associated with an earlier occurrence of both appropriate and any spontaneous ICD shocks (p = 0.001). Appropriate and any spontaneous shocks occurred significantly later in patients who presented with cardiac arrest and in patients in whom only ventricular fibrillation but no uniform ventricular tachycardia was induced during preoperative programmed stimulation. In addition, amiodarone treatment at implant was associated with later occurrence of any spontaneous shocks. Cumulative survival from all-cause mortality including perioperative mortality was 84%, 62%, and 57%, and survival from arrhythmic death was 97%, 89%, and 83% at 1, 3, and 5 years, respectively. Ejection fraction < or = 30% was the best predictor of both total arrhythmic death (p = 0.019) and total mortality (p = 0.003). Antiarrhythmic therapy with class 1 agents at implant was also associated with a higher total mortality during follow-up (p = 0.023) but not with total arrhythmic death. Age, sex, underlying heart disease, clinical presentation, and preoperative response to programmed stimulation did not predict long-term survival. In addition, survival curves were similar for patients with and without spontaneous shocks. CONCLUSIONS: The majority of patients receive shocks during long-term follow-up. The occurrence of appropriate or any spontaneous shocks during follow-up is not associated with increased arrhythmic or total mortality consistent with effective prevention of sudden cardiac death with ICD therapy in this high-risk patient population. Although low ejection fraction is the strongest predictor of both shock occurrence and mortality during follow-up, no easy algorithm can be derived from the analyzed clinical characteristics to predict which patients will benefit most from ICD implantation.

Comparison of simultaneous versus sequential defibrillation pulsing techniques using a nonthoracotomy system.

The defibrillation threshold (DFT) using simultaneous (SIML) versus sequential (SEQ) pathways for shock delivery was compared in 16 patients with an implanted cardioverter defibrillator. All patients had three-lead nonthoracotomy systems (NTL) using a left chest subcutaneous patch, a right ventricular endocardial lead, and a lead in the coronary sinus (n = 5) or superior vena cava (n = 11). The DFT were determined 2-44 days (17 +/- 17 days) after implantation. The DFT was defined as the lowest energy shock that resulted in successful defibrillation. The first pathway tested was SIML in 12 and SEQ in 4 patients with output beginning at or above the intraoperative DFT, routinely 18 J. The second pathway was tested beginning 2-4 J above the DFT of the first tested pathway. All shocks were delivered in 2-4 J decrement or increment steps. The SEQ pathway shocks resulted in a significantly lower DFT than SIML pathway shocks (14 +/- 6 vs 18 +/- 6 J; P < 0.01). There was no difference in the time delay after ventricular fibrillation initiation before shock delivery for the successful defibrillation between SIML versus SEQ pathways (7 +/- 2 secs for both pathways). In 7 of 16 patients, defibrillation using SEQ pathway resulted in a > 5 J lowering of DFT, while only one patient had > 5 J lowering of DFT using SIML shocks (P < 0.05). These results have important implications for selecting the optimal pathway for implantable cardioverter defibrillator therapy with a multilead NTL system.

Early postoperative increase in defibrillation threshold with nonthoracotomy system in humans.

The stability of the defibrillation threshold (DFT) early after implantation of an implantable cardioverter defibrillator was evaluated in 15 patients. All but one patient had a three lead nonthoracotomy system using a subcutaneous patch, a right ventricular endocardial lead, and a lead in coronary sinus (n = 5) or superior vena cava (n = 9). Shocks were delivered using simultaneous in nine, sequential in three, and single pathway (coronary sinus not used) in one patient. DFTs were measured at implant (n = 15), 2-8 days postoperation (postop, n = 15), and 4-6 weeks later (n = 8). The DFT was defined as the lowest energy shock that resulted in successful defibrillation. The DFT was assessed with output beginning at 18 joules or 2-4 joules above the implant DFT. All shocks were delivered in 2- to 4-joule increments or decrements. DFTs were significantly higher postoperatively than DFTs at implant (22.7 +/- 7.0 J vs 16.9 +/- 3.9 J; P < 0.05). Eight of 15 patients had DFT determined at all three study periods. In these patients, DFT increased at postop (22.8 +/- 8.3 J vs 16.4 +/- 3.9 J at implant; P < 0.05) and returned to baseline at 4-6 weeks (16 +/- 7.1 J vs 16.4 +/- 3.9 J at implant; P = N.S.). Thus, in patients with a multilead nonthoracotomy system, a DFT rise was observed early after implant. The DFT appears to return to baseline in 4-6 weeks. These results have important implications for programming energy output after implantable cardioverter defibrillator implantation.

Amiodarone versus amiodarone and a type IA agent for treatment of patients with rapid ventricular tachycardia.

Induction of rapid ventricular tachycardia or fibrillation during therapy with amiodarone is associated with an increased risk of sudden death. To determine whether the addition of a type IA antiarrhythmic agent to therapy would improve outcome, 37 patients in whom ventricular tachyarrhythmia of a cycle length less than 350 msec was induced after 14 +/- 2 days of amiodarone were randomly assigned to therapy with amiodarone alone (group 1, 20 patients) or amiodarone plus type IA agent (group 2, 17 patients). Type IA therapy consisted of procainamide in 13 patients and quinidine in four procainamide-intolerant patients. To assess the short-term effects of a type IA agent on inducibility of ventricular tachyarrhythmia, cycle length, and hemodynamic tolerance, 16 of 20 patients in group 1 and all patients in group 2 underwent repeat programmed stimulation after the intravenous administration of procainamide during amiodarone therapy (mean procainamide serum concentration 7.2 +/- 2.0 micrograms/ml). Procainamide prevented induction of sustained arrhythmia in only two of 33 patients. Procainamide increased the cycle length of induced ventricular tachycardia from 283 +/- 30 to 352 +/- 46 msec (p less than .001). After the addition of procainamide, 16 of 31 patients vs 10 of 37 patients on amiodarone alone had an induced arrhythmia that was tolerated hemodynamically (p less than .05). There were no differences between groups 1 and 2 with respect to patient or arrhythmia characteristics, response to short-term procainamide, or duration of follow-up. The mean follow-up for all patients was 14 +/- 10 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Implantable cardioverter-defibrillator therapy in the absence of significant symptoms. Rhythm diagnosis and management aided by stored electrogram analysis.

BACKGROUND: This report describes the value of stored ventricular electrogram analysis in the diagnosis and management of patients experiencing minimal or no symptoms before implantable cardioverter-defibrillator (ICD) therapy. METHODS AND RESULTS: The study population included 48 patients who received the Cadence Tiered Therapy Defibrillator System, an investigational third-generation ICD with ventricular electrogram storage capabilities. Criteria for arrhythmia diagnosis were based on analysis of the electrogram rate, RR interval variability, and morphology. Twenty-nine of the 48 patients (60%) experienced at least one episode of antitachycardia pacing or shock (one shock or more in 25 of 29 patients) that was preceded by minimal or no symptoms during a mean follow-up of 15.1 +/- 7.8 months. There were 194 tachycardia episodes registered by the device, including 101 for which ventricular electrograms were stored and available for analysis. Of the 101 stored electrograms, 74 were classified as ventricular tachycardia (VT), 24 as non-VT rhythms (atrial fibrillation, 13; supraventricular tachycardia, six; rate-sensing lead disruption, four; T wave oversensing, one), and only three as indeterminate rhythms. Based on the electrogram analysis, changes in tachycardia detection criteria and/or antiarrhythmic drug regimens were implemented and were associated with a reduction in the number of device responses for non-VT rhythms from 24 during the initial study period to three during 11.0 +/- 7.2 months of additional follow-up. CONCLUSIONS: ICD responses in the absence of symptoms are relatively common in third-generation devices with antitachycardia pacing capabilities. Despite potential limitations such as the effect of bundle branch block on the electrogram morphology during supraventricular tachycardia, the availability of electrogram storage capabilities allowed a presumptive diagnosis of the events precipitating asymptomatic device responses. Device reprogramming based on analysis of stored electrograms was associated with a dramatic reduction in the incidence of ICD responses for non-VT rhythms.

Nonsustained ventricular tachycardia in patients with coronary artery disease: role of electrophysiologic study.

Sixty-two consecutive patients with chronic coronary artery disease referred for evaluation of nonsustained ventricular tachycardia (VT) underwent electrophysiologic studies. Sustained VT was induced by one to three ventricular extrastimuli in 28 patients (45%). Therapy was guided by the results of electrophysiologic testing in 44 patients: 19 patients without inducible sustained VT received no antiarrhythmic therapy, and 25 patients with inducible sustained or symptomatic nonsustained VT received therapy guided by the results of electrophysiologic studies. The results of electrophysiologic studies were ignored by physicians for a second group of 18 patients: four had inducible sustained VT but received no antiarrhythmic therapy, and 14 had inducible sustained or nonsustained VT and received antiarrhythmic therapy not guided by results of electrophysiologic testing. After a mean follow-up period of 28 months, 11 patients had died suddenly. Seven of the 11 patients who died suddenly had inducible sustained VT. Three of 44 patients in the group receiving therapy guided by electrophysiologic studies died suddenly versus eight of 18 in the group receiving therapy not guided by electrophysiologic studies (p = .001). Only one of 19 patients without inducible sustained VT who were not treated experienced sudden death. Two of four patients with inducible sustained VT who did not receive antiarrhythmic therapy died suddenly. Multivariate analysis of the relationship of induced arrhythmias, left ventricular ejection fraction, site of myocardial infarction, history of syncope, or type of antiarrhythmic therapy to outcome revealed a greater than twofold increased risk for sudden cardiac death in patients whose therapy was not guided by results of electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy of antitachycardia pacing in patients presenting with cardiac arrest.

The efficacy of antitachycardia pacing (ATP) incorporated into implantable cardioverter defibrillators (ICDs) was assessed in 29 consecutive survivors of cardiac arrest, not attributable to acute myocardial infarction, ischemia, or drug and electrolyte effects. The cohort included 25 men and 4 women with a mean age of 65 years and a mean left ventricular ejection fraction of 29%. Seventeen patients had coronary artery disease, 11 had nonischemic dilated cardiomyopathy, and 1 had long QT syndrome. Programmed stimulation yielded monomorphic ventricular tachycardia (VT) in 17 patients, polymorphic VT in 6, and no inducible VT in 6. During a mean follow-up of 22 months, a total of 91 episodes of monomorphic VT occurred, 73 of which were successfully pace terminated (83%). Monomorphic VT amenable to pace termination recurred only in the group that had this arrhythmia inducible. The recurrent arrhythmias in the 12 patients having either no inducible VT or polymorphic VT were all rapid VTs, having a cycle length < 220 ms; and therefore, not amenable to pace termination. These results suggest that ATP incorporated into ICDs is useful in survivors of cardiac arrest and may significantly reduce the number of shocks that these patients would otherwise receive. Programmed stimulation may also help to define those patients who would receive the maximum benefit from ATP.

Acute and chronic cycle length dependent increase in ventricular pacing threshold.

Several factors have been shown to influence ventricular pacing threshold in humans, including pacing lead location (endocardial vs epicardial), lead maturation, and antiarrhythmic agents. To determine whether ventricular pacing rate has a significant influence on acute and chronic pacing thresholds, we measured pacing thresholds in 16 patients receiving an implantable antitachycardia pacemaker cardioverter defibrillator (Cadence). Ventricular pacing thresholds were determined using the device programmer at cycle lengths of 600, 400 and 300 msec at the time of implantation; prior to hospital discharge at 3-14 days; and during follow-up outpatient visits at 6-8 weeks, 3 months, and 6 months to 1 year. Eleven patients had an epicardial lead system and five an endocardial lead system. Eleven patients were being treated with antiarrhythmic drug therapy. Device output ranged from 1-10 V and was adjustable in 1-V increments (pulse width was held constant at 1 msec). A cycle length dependent increase in pacing threshold (defined as a > or = 1-V increase in threshold at 400 or 300 msec relative to 600 msec) was observed in 10/16 patients during 12/72 pacing trials at 400 msec, and in 15/16 patients during 31/67 trials at 300 msec. In trials in which an increase in pacing threshold occurred, the magnitude of the increase at 400 msec relative to 600 msec was only 1 V in all 12 trials, but at 300 msec the increase ranged from 4-9 V in 7/31 (23%) trials.(ABSTRACT TRUNCATED AT 250 WORDS)

The automatic implantable cardioverter-defibrillator: efficacy, complications, and device failures.

Twenty-six patients with refractory ventricular arrhythmias received the automatic implantable cardioverter-defibrillator. A patch lead only was placed during arrhythmia surgery in 7 other patients. During 13 +/- 6 (SD) months, the device discharged in 10 patients because of a sustained ventricular arrhythmia. No sudden deaths occurred. There were 31 complications in 17 patients, including postoperative refractory heart failure, coronary artery erosion, subclavian vein thrombosis, postoperative stroke after conversion of atrial fibrillation, atelectasis with pneumonia, symptomatic pleural effusions, and infection at the generator site. The cardioverter-defibrillator discharged in 9 asymptomatic patients, failed to terminate ventricular fibrillation during postoperative testing in 3 patients, and had premature battery failure in 4 patients. Tachycardia slowing during chronic amiodarone therapy and unipolar ventricular pacing during ventricular fibrillation precluded or delayed arrhythmia sensing. Thus, the cardioverter-defibrillator can be life saving, but its potential complications and interactions with antiarrhythmic drugs and pacemakers must be considered at patient selection.