Belinda T. Flores

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.

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)

Relation of the intraoperative defibrillation threshold to successful postoperative defibrillation with an automatic implantable cardioverter defibrillator

To determine the relation between the intraoperative defibrillation threshold and successful postoperative termination of induced ventricular fibrillation (VF) with the automatic implantable cardioverter defibrillator (AICD), 33 patients who underwent AICD implantation were studied. The defibrillation threshold, determined after at least 10 seconds of VF, was 5 J in 2, 10 J in 6, 15 J in 10, 20 J in 10 and 25 J in 5 patients. The AICD energy rating on the first discharge was 28 +/- 1.8 J. Defibrillation of induced VF was demonstrated postoperatively in 29 of 33 (88%) patients. The AICD terminated VF postoperatively in all 18 patients with a defibrillation threshold less than or equal to 15 J. Only 11 of the 15 (73%) patients with a defibrillation threshold greater than or equal to 20 J (p less than 0.04) had VF terminated postoperatively. In all 4 patients in whom the AICD failed to terminate induced VF, the energy difference between the AICD rating and the defibrillation threshold was less than or equal to 10 J. Among the 14 patients with a difference of less than or equal to 10 J between the AICD energy rating and the defibrillation threshold, there were no significant differences between the 4 patients with and the 10 without successful VF termination with respect to the duration of VF induced postoperatively or the AICD lead system. In summary, failure to terminate VF with the AICD is not uncommon (27%) when the defibrillation threshold approaches the energy delivering capacity of the AICD.(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.

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

BackgroundThe 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 ResultsTwo 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

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

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%o, and 83% at 1, 3, and 5 years, respectively. Ejection fraction

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

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. ConclusionThe 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.

Hazards of intravenous verapamil for sustained ventricular tachycardia

BackgroundThis report describes the value of stored ventricular electrogram analysis in the diagnosis and management of patients experiencing minimal or no symptoms before implantable cardioverterdefibrillator (ICD) therapy Methods and ResultsThe 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. ConclusionICD 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.

Unique sensing errors in third-generation implantable cardioverter-defibrillators

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.

Usefulness of electrophysiologic study to determine the clinical tolerance of arrhythmia recurrences during amiodarone therapy

In 11 of 25 patients (44%) with sustained ventricular tachycardia (VT) who received intravenous verapamil (5 to 10 mg), acute severe hypotension or loss of consciousness developed, necessitating immediate cardioversion. Comparison of these 11 patients with the 14 who did not have adverse effects after verapamil revealed no significant difference in age, heart disease, ejection fraction, blood pressure before verapamil administration, other oral or intravenous drugs use, verapamil dose or VT characteristics (rate and morphologic pattern). Although most patients with severe adverse effects after verapamil had prior myocardial infarction, deterioration also occurred in patients without coronary disease and in patients with a normal left ventricular ejection fraction. VT terminated after verapamil infusion in 6 patients. No single electrocardiographic morphologic pattern characterized these patients. A control group of 25 patients presenting with hemodynamically stable VT who received other antiarrhythmic agents was examined. Hypotension developed in only 1 patient during acute therapy and did not require emergency cardioversion. Thus, although verapamil may terminate VT, severe adverse effects occur much more often. Use of verapamil to differentiate supraventricular tachycardia with aberrant conduction from ventricular tachycardia is hazardous.