Development of an automaton model of rotational activity driving atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is difficult to treat effectively, owing to uncertainty in where to best ablate to eliminate arrhythmogenic substrate. A model providing insight into the electrical activation events would be useful to guide catheter ablation strategy. Method A two-dimensional, 576×576 node automaton was developed to simulate atrial electrical activity. The substrate field was altered by the presence of differing refractory period at varying locations. Fibrosis was added in the form of short, randomly positioned lines of conduction block. Larger areas of block were used to simulate ablation lesions. Anisotropy was imposed in a 2:1 ratio. A premature electrical impulse from one of four grid corners was utilized to initiate activation. RESULTS: Rotational activity was uninducible when refractory patch dimensions were less than 20×20mm. For larger refractory regions, a single premature stimulus was capable of inducing an average of 1.19±1.10 rotors, which often formed near the patch edges. A maximum of 5 rotors formed when refractory patch dimensions approached the size of the entire left atrial virtual field. Rotors formed along a refractory patch edge, after wavefront arrival was delayed at turning points or due to the presence of a fiber cluster of sufficient size. However, rotational activity could also occur around a large fiber cluster without the need of spatially variable refractoriness. When obstacles to conduction were lacking in size, nascent rotors drifted and either extinguished, or stabilized upon anchoring at a sufficiently large fiber cluster elsewhere in the field. Transient rotors terminated when traversing a region with differing refractory periods, if no obstacle to conduction was present to sufficiently delay wavefront arrival beyond the longest refractory period. Other rotors were annihilated when a nearby rotor with faster spin rate gradually interrupted the activation pathway. Elimination of anchors by removal, or by simulated ablation over a sufficient region, prevented rotor onset at a particular location where it would otherwise form. CONCLUSIONS: The presence of obstacles to conduction and spatial differences in refractory period are important parameters for initiating and maintaining rotational activity in this simulation of an atrial substrate.

Long-term infection rates associated with the pectoral versus abdominal approach to cardioverter- defibrillator implants.

Infection is an uncommon (0% to 6.7%) but serious complication after implantable cardioverter-defibrillator (ICD) implantation. All ICD primary implants, replacements, or revisions performed at the Massachusetts General Hospital between April 1983 and May 1999 were reviewed. A total of 21 ICD-related infections (1.2%) were identified among 1,700 procedures affecting 1.8% of the 1,170 patients who underwent a primary implant, a generator change, or a revision of their systems. The mean follow-up time was 35 +/- 33 months. Of the 959 patients with long-term follow-up, 19 of the 584 patients (3.2%) with abdominal and 2 of the 375 patients (0.5%) with pectoral systems developed ICD-related infections (p = 0.03). There was no significant difference between the infection rate among the 959 primary ICD implants and the 447 replacements or system revisions. Only 5 of the patients (24%) had systemic signs of infection, including fever (T>100.5) and elevated white blood count >12,000. Cultures from the wound revealed staphylococcal species in 16 patients (76%). Nineteen patients were treated with removal of the entire ICD system in addition to intravenous antibiotics for 2 to 4 weeks. A decrease in the incidence of ICD-related infection has occurred since the advent of transvenous pectoral systems. The main organism responsible for ICD infection is Staphylococcus. The mainstay of ICD infection management consists of complete removal of the entire implanted system.

Long-term clinical outcome of patients with prior myocardial infarction after palliative radiofrequency catheter ablation for frequent ventricular tachycardia.

Patients with coronary artery disease and hemodynamically tolerated, highly frequent, sustained monomorphic ventricular tachycardia (VT) may undergo radiofrequency catheter ablation (RFCA) for elimination of > or = 1 morphologically distinct VTs. The purpose of this study was to evaluate the long-term clinical benefit following RFCA as a palliative treatment of highly frequent or incessant ischemic VT. Fifty-five patients underwent RFCA of 62 VTs. The target VT was successfully ablated in 82% of patients. Complication and perioperative mortality rates were 7.2% and 1.8%, respectively. At 5 years, total mortality was 51% and probability of freedom from all ventricular tachyarrhythmias was 28%. All patients had highly frequent or incessant drug-refractory VT before RFCA. Clinical benefit was defined as either freedom from all ventricular tachyarrhythmias, or a reduction in frequency of recurrence from > 1 episode per month before RFCA to < or = 1 episode per year of any ventricular tachyarrhythmia, including all appropriate implantable cardioverter defibrillator (ICD) therapies. By this definition, 54% of the patients continued to benefit from RFCA at 5 years. Of 19 variables analyzed with a Cox univariate model, only the presence of a left ventricular aneurysm and a previously implanted ICD were predictive of any ventricular arrhythmia recurrence. However, at 5 years over half of the surviving patients still continued to benefit from RFCA of their clinical VT. Because the overall rate of any ventricular tachyarrhythmia occurrence during follow-up is high, additional protection, such as an ICD, is required.

Mechanism of sustained monomorphic ventricular tachycardia in systemic sclerosis.

Three patients with advanced systemic sclerosis and recurrent or incessant monomorphic ventricular tachycardia underwent cardiac electrophysiologic studies. Biventricular transcatheter mapping showed findings most compatible with a reentrant mechanism, which was effectively treated with transcatheter ablation.

T-wave alternans and dispersion of the QT interval as risk stratification markers in patients susceptible to sustained ventricular arrhythmias.

T-wave alternans and QT dispersion were compared as predictors of the outcome of electrophysiologic study and arrhythmia-free survival in patients undergoing electrophysiologic evaluation. T-wave alternans was a highly significant predictor of these 2 outcome variables, whereas QT dispersion was not.

Transvenous single lead atrial defibrillation: efficacy and risk of ventricular fibrillation in an ischemic canine model.

Transvenous atrial defibrillation with multiple atrial lead systems has been shown to be effective in models without the potential for ventricular arrhythmias. The specific aim of this study was to evaluate the efficacy and safety of transvenous single lead atrial defibrillation in a canine model of ischemic cardiomyopathy. Ten dogs had ischemic cardiomyopathy induced by repeated intracoronary microsphere injections. The mean LV ejection fraction decreased from 71% +/- 9% to 38% +/- 14% (P = 0.003). Spontaneous atrial fibrillation (AF) developed in four dogs, and in six AF was induced electrically. Atrial defibrillation thresholds (ADFTs) were determined with synchronous low energy shocks using a transvenous tripolar lead with two defibrillation coils (right ventricle, superior vena cava) and an integrated sensing lead (RV coil vs electrode tip). The ADFTs derived by logistic regression were compared at 50% and 90% probability of success (ED50, ED90): ED50 was 2.4 +/- 1.7 J and 2.9 +/- 2.1 J, respectively, for 5- and 10-ms monophasic shocks, and 1.8 +/- 0.9 J, respectively, for 5- and 10-ms biphasic shocks. Immediately after 3 of 2,179 (0.1%) synchronized shocks, ventricular fibrillation (VF) developed. VF was induced in 3 of 1,062 (0.3%) shocks with integrated sensing (RV coil vs electrode tip) compared to 0 of 1,117 shocks when a separate bipolar RV sensing electrode was used for synchronization. In our canine model of ischemic cardiomyopathy, low energy atrial defibrillation via a transvenous single lead system was highly effective. However, there was a small but definite risk of VF induction, which seemed to be greater when an integrated as opposed to a true bipolar RV sensing was used.

Prognostic significance of electrical alternans versus signal averaged electrocardiography in predicting the outcome of electrophysiological testing and arrhythmia-free survival.

OBJECTIVE: To investigate the accuracy of signal averaged electrocardiography (SAECG) and measurement of microvolt level T wave alternans as predictors of susceptibility to ventricular arrhythmias. DESIGN: Analysis of new data from a previously published prospective investigation. SETTING: Electrophysiology laboratory of a major referral hospital. PATIENTS AND INTERVENTIONS: 43 patients, not on class I or class III antiarrhythmic drug treatment, undergoing invasive electrophysiological testing had SAECG and T wave alternans measurements. The SAECG was considered positive in the presence of one (SAECG-I) or two (SAECG-II) of three standard criteria. T wave alternans was considered positive if the alternans ratio exceeded 3.0. MAIN OUTCOME MEASURES: Inducibility of sustained ventricular tachycardia or fibrillation during electrophysiological testing, and 20 month arrhythmia-free survival. RESULTS: The accuracy of T wave alternans in predicting the outcome of electrophysiological testing was 84% (p < 0.0001). Neither SAECG-I (accuracy 60%; p < 0.29) nor SAECG-II (accuracy 71%; p < 0.10) was a statistically significant predictor of electrophysiological testing. SAECG, T wave alternans, electrophysiological testing, and follow up data were available in 36 patients while not on class I or III antiarrhythmic agents. The accuracy of T wave alternans in predicting the outcome of arrhythmia-free survival was 86% (p < 0.030). Neither SAECG-I (accuracy 65%; p < 0.21) nor SAECG-II (accuracy 71%; p < 0.48) was a statistically significant predictor of arrhythmia-free survival. CONCLUSIONS: T wave alternans was a highly significant predictor of the outcome of electrophysiological testing and arrhythmia-free survival, while SAECG was not a statistically significant predictor. Although these results need to be confirmed in prospective clinical studies, they suggest that T wave alternans may serve as a non-invasive probe for screening high risk populations for malignant ventricular arrhythmias.

Reproducible induction of "atypical" torsades de pointes by programmed electrical stimulation: a novel form of sotalol-induced proarrhythmia?

We present a patient with sotalol-induced polymorphic ventricular tachycardia that was seen only with programmed ventricular stimulation. Electrophysiologic studies performed prior to initiation of sotalol therapy revealed inducible monomorphic ventricular tachycardia. Possible underlying electrophysiologic mechanisms are discussed.

The treatment of patients with infected implantable cardioverter-defibrillator systems.

OBJECTIVE: The purpose of this study was to evaluate the treatment of patients with infected implantable cardioverter-defibrillator systems. METHODS: Retrospective analysis was done of the cases of 21 patients treated for implantable cardioverter-defibrillator infection during an 11-year period. RESULTS: Of 723 cardioverter-defibrillator implantations (550 primary implants, 173 replacements), nine (1.2%) were complicated by early postoperative device-related infections. Late infections developed in two patients 19 and 22 months, respectively, after implantation. Ten other patients were transferred to our institution for treatment of cardioverter-defibrillator infection. The time from implantation to overt infection was 2.2 +/- 1.3 months, excluding the two late infections. The responsible organisms were Staphylococcus aureus (9), Staphylococcus epidermidis (6), Streptococcus hemolyticus (1), gram-negative bacteria (3), Candida albicans (1), and Corynebacterium (1). All patients were treated with intravenous antibiotic drugs. Total system removal was done in 15 patients and partial removal in 2; in 4, the cardioverter-defibrillator system was not explanted. There were no perioperative deaths. A new implantable cardioverter-defibrillator system was reimplanted in 7 patients after 2 to 6 weeks of antibiotic therapy. Ten patients were treated without reimplantation (2 arrhythmia operation, 8 antiarrhythmic drugs). Four patients (3 patients without explantation and 1 with partial system removal) were treated with maintenance long-term antibiotic therapy. During a mean follow-up of 21 +/- 2.8 months, no patient had clinical recurrence of infection. One patient treated with antiarrhythmic drugs without system reimplantation died suddenly. CONCLUSIONS: Infections that involve implantable cardioverter-defibrillator systems can be safely managed by removing the entire system with reimplantation after intravenous antibiotic therapy. In selected patients in whom the risk for system explantation is high and anticipated life expectancy is short, long-term antibiotic therapy to suppress low-virulence infections may represent an acceptable alternative.

Mechanisms underlying different surface ECG morphologies of recurrent monomorphic ventricular tachycardia and their modification by procainamide.

INTRODUCTION: Distinct surface ECG morphologies (ECGMs), from one episode to the next, of recurrent monomorphic ventricular tachycardia (VT) in the same patient complicate endocardial catheter mapping and the success of ablative therapy. This study investigates the incidence and mechanisms of multiple ECGMs during recurrent monomorphic VTs in a canine model of experimental myocardial infarction (MI). METHODS AND RESULTS: Computerized ECG analysis and simultaneous endocardial and epicardial activation mapping with a 64 bipolar electrode array were used to analyze the relation between site of VT origin, local activation sequence, and surface ECGM in 72 VT episodes induced in 9 of 17 dogs with experimental MI. Pairwise comparisons of all VTs induced in the same animal were done in drug-free state (47 VTs) and after intravenous procainamide (25 VTs). In drug-free state, VT pairs with similar surface ECGMs manifested endocardial breakthrough sites (BSs) within a distance < 10 mm in 46 (100%) of 46 VT pairs compared to 43 (45%) of 95 VT pairs with different surface ECGMs (P < 0.0001). Of all 89 VT pairs with endocardial BSs within < 10 mm, similar endocardial activation patterns were found in 34 (74%) of 46 pairs with similar ECGMs in contrast to 6 (14%) of 43 pairs with different ECGMs (P < 0.001). Similar comparisons of VT pairs induced after intravenous procainamide administration showed that the endocardial BSs were located within < 10 mm in 9 (75%) of 12 VT pairs with similar and in 17 (49%) of 95 with different surface ECGMs, respectively (P = NS). CONCLUSIONS: In the same heart, similar surface ECGMs of recurrent VT are highly predictive of closely spaced endocardial BSs in drug-free state, but not after procainamide administration. Nearly half of the VTs with different surface ECGMs still originate from closely spaced endocardial BSs but commonly manifest a change in the endocardial activation spread from this site. Thus, assumptions about different mechanisms and sites of VT origin based on different surface ECGMs should be made with caution.

Transient right bundle branch block causing R wave attenuation postdefibrillation.

Transient and significant decrease in R wave amplitude, associated with transient right bundle branch block, was noted to occur after defibrillation in a defibrillator patient. The mechanism is probably stunning of the right bundle branch, causing right intraventricular conduction delay and decrease in signal amplitude reaching the endocardial sensing dipoles.

Internal atrial defibrillation: lessons learnt from experimental studies.

Following the introduction of a transvenous biatrial electrode configuration and a biphasic waveform for internal atrial defibrillation in patients in 1992, it was realized that the standard principles of efficient defibrillation derived from decades of ventricular defibrillation research would not provide painless atrial defibrillation in conscious patients. Over the last five years extensive experimental studies have addressed the risk of ventricular proarrhythmia from synchronized atrial shocks with reassuring results and the influence of the preceding R-R interval on the safety of atrial shocks has been established. Experimental atrial defibrillation research is now aimed at developing waveforms which are less painful and at exploring hybrid therapies including percutaneous right atrial compartmentalization by catheter ablation prior to atrial defibrillation and attempts at multisite pace-entrainment prior to and immediately following the delivery of perithreshold shocks.

A perspective on the ESVEM trial current knowledge: sotalol should not be the first-line agent in the management of ventricular arrhythmias.

The Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial has recently shown the superiority of sotalol over class-1 agents in lowering the rate of recurrence of ventricular tachyarrhythmias. However, this study was not placebo-controlled, and amiodarone was not included as one of the antiarrhythmic drugs in the trial. Randomized comparative trials between sotalol and amiodarone are available, but the results are inconclusive mainly because of small sample sizes. Because of the specific pharmacokinetics of amiodarone, sotalol has become the first-line agent in the management of ventricular arrhythmias. Because this policy is based on expediency rather than follow-up data, the long-term efficacy, morbidity, and safety of sotalol should be compared with those of amiodarone as well as of nonpharmacological treatment modes for ventricular tachyarrhythmias, such as implantable cardioverter defibrillator therapy in prospective trials. Until these issues are resolved, it is incorrect to say that sotalol should be the first-line agent in the management of ventricular arrhythmias.

A perspective on the ESVEM trial and current knowledge: catheter ablation for ventricular tachyarrhythmias.

Although an effective and potentially curative technique for treating idiopathic ventricular tachycardia, map-guided transcatheter radiofrequency ablation is far from optimal for ventricular tachyarrhythmias in patients with advanced ischemic or other types of organic heart disease. First, this technique can be applied only to a minority of patients with structural heart disease, who can tolerate relatively long episodes of induced ventricular tachycardia necessary for mapping and successful ablation. Second, the success rate is lower and recurrence higher in patients with organic heart disease. Finally, for patients who lose consciousness during tachycardia or who present with prehospital cardiac arrest, transcatheter radiofrequency ablation is inappropriate as definitive treatment. At best, it is palliative and may be used to suppress relatively slow, frequent, or incessant ventricular tachycardias but does not obviate the need for other therapies such as cardioverter-defibrillator implantation or antiarrhythmic drug therapy.

Comparison of cycle lengths between induced and spontaneous sustained ventricular tachycardia during concordant antiarrhythmic therapy associated with healed myocardial infarction.

We propose that in clinical practice, whenever possible, the VT detection interval should be selected by adding >60 ms to the induced maximal VT cycle length in order to ensure a high sensitivity for the detection of future spontaneous VT episodes.

Influence of the implantable cardioverter/defibrillator on sudden death and total mortality in patients evaluated for cardiac transplantation.

BACKGROUND: Implantable cardioverter/defibrillators (ICDs) may reduce sudden tachyarrhythmic death in patients with severe left ventricular dysfunction. It is uncertain whether this improves survival, particularly in patients awaiting cardiac transplantation. METHODS AND RESULTS: The effect of treatment for spontaneous ventricular arrhythmias (ICD [n = 59], antiarrhythmic drugs [n = 53], or no antiarrhythmic treatment [n = 179]) on total mortality and mode of cardiac death was analyzed in 291 consecutive patients evaluated for cardiac transplantation between January 1986 and January 1995. There were 109 deaths (37.4%) (63 [21.6%] sudden, 40 [13.7%] nonsudden, and 6 [2.1%] noncardiac) during mean follow-up of 15 months (range, 1 to 118 months). Baseline clinical variables, medical therapies for heart failure, and actuarial rates of transplantation were similar between treatment groups. Kaplan-Meier sudden death rates were lowest in the ICD group, intermediate in the no antiarrhythmic treatment group, and highest in the drug treatment group throughout follow-up (12-month sudden death rates, 9.2%, 16.0%, and 34.7%, respectively; P = .004). Total mortality and nonsudden death rates did not differ. Cox proportional-hazards model revealed that antiarrhythmic drug treatment was associated with sudden death (relative risk, 2.1; 95% CI, 1.04 to 3.39; P = .04) and ICD was associated with nonsudden death (relative risk, 2.26; 95% CI, 1.12 to 4.62; P = .02). CONCLUSIONS: Sudden death rates were lowest in patients treated with ICDs compared with drug treatment or no antiarrhythmic treatment. However, although ICDs reduced sudden death in selected high-risk patients with severe left ventricular dysfunction, the effect on long-term survival was limited, principally by high nonsudden death rates.

Malfunction of implantable cardioverter defibrillators placed by a nonthoracotomy approach: frequency of malfunction and value of chest radiography in determining cause.

OBJECTIVE: The purpose of this study was to determine the frequency of system malfunction in patients with nonthoracotomy implantable cardioverter defibrillators and to assess the role of chest radiography in detecting and determining the cause of malfunction. MATERIALS AND METHODS: The study population consisted of 300 consecutive patients in whom implantable cardioverter defibrillators were implanted using an initial nonthoracotomy approach between September 1990 and October 1994. Transvenous electrodes were placed via the subclavian or cephalic vein under local anesthetic. Intraoperative testing, pulse generator implantation, and, if necessary, subcutaneous patch or extrapericardial patch placement via thoracotomy were done in the operating room under general anesthetic. Follow-up consisted of routine device interrogation every 2-3 months and annual chest radiography. Chest radiographs were obtained more often if patients were symptomatic or if results of device interrogation were abnormal. RESULTS: Patients were followed up for a mean +/- SD of 19 +/- 14 months following implantation. Implantable cardioverter-defibrillator malfunction occurred in 17 patients (6%) during the follow-up period. Of these, 12 (71%) had component abnormalities on chest radiographs. Patients with radiographically apparent implantable cardioverter-defibrillator abnormalities presented in two discrete time periods after device implantation, early (mean, 35 +/- 14 days) and late (mean, 18 +/- 5 months). CONCLUSION: Malfunction of nonthoracotomy implantable cardioverter-defibrillator systems develops infrequently after device implantation. In most cases, the cause can be identified on chest radiographs.

Subclavian crush syndrome complicating transvenous cardioverter defibrillator systems.

UNLABELLED: Subclavian crush syndrome, described with pacemaker leads implanted via subclavian puncture, may occur when conductor fractures and insulation breaches develop by compression of a lead between the first rib and clavicle. We reviewed our experience in 164 patients who underwent intended implantation of transvenous defibrillator systems to determine the clinical relevance of subclavian crush syndrome in defibrillator patients. Venous access was obtained via subclavian puncture in 114 patients (70%) and via cephalic cut-down in 50 patients (30%). Nonthoracotomy lead systems, with or without subcutaneous patch, were successfully implanted in 131 of 164 patients (79.9%). Thoracotomy was required in 32 patients (19.5%) and subxiphoid patch in 1 patient (0.6%). Over a mean of 12.9 months (range 1-62 months), 3 patients (1.8%) required revision of the rate sensing lead/coil or superior vena cava coil after development of lead compression fractures in the region of the clavicle and first rib. In all 3 patients the leads had been implanted via subclavian puncture (2.6% of patients in whom the subclavian technique was utilized). Two patients presented with spurious shocks. One patient was asymptomatic. CONCLUSIONS: When venous access is obtained via subclavian puncture, subclavian crush syndrome may develop in patients with transvenous defibrillator systems. Patients may be asymptomatic and lead fractures may go unrecognized. When implanting transvenous defibrillator systems, strong consideration should be given to obtaining venous access primarily via the cephalic cut-down technique.