Presence of obesity is associated with lower mortality in elderly patients with implantable cardioverter defibrillator.

BACKGROUND: Higher body mass index (BMI) is associated with greater prevalence of cardiovascular risk factors, yet an inverse relationship between obesity and survival after cardiovascular events has been described. It is unclear whether a similar relationship exists for patients with implantable cardioverter defibrillators (ICDs) at high risk for mortality. We aimed to assess the impact of BMI on mortality and cardiovascular hospitalization in patients with ICD. METHODS: Patients who underwent ICD implantation in 2010-2011 were divided into normal (<25 kg m-2), overweight (25-29.9 kg m-2) and obese (⩾30 kg m-2) groups based on BMI. Clinical parameters were compared and long-term outcomes were determined using χ2 test, Wilcoxon's rank-sum test, logistic regression models and Kaplan-Meier curves. RESULTS: Of 904 patients (mean age 67±13 years), 26% had normal BMI, 32% were overweight and 42% were obese. No significant baseline differences in ventricular ejection fraction, ICD for primary or secondary prevention, history of heart failure, syncope or cardiac arrest existed. Despite a greater prevalence of diabetes, hypertension and prior myocardial infarction, the obese and overweight groups had lower mortality (10.1% and 7.9%, respectively) than the normal group (22.9%, P<0.001). On multivariate logistic regression, BMI in the obese and overweight range (odds ratio (OR): 0.35; 95% confidence interval (CI): 0.21-0.58 and OR: 0.25; 95% CI: 0.13-0.40, respectively) was protective against mortality, whereas history of diabetes (OR: 2.01; 95% CI: 1.30-3.09), myocardial infarction (OR: 1.76; 95% CI: 1.11-2.80), heart failure (OR: 3.88; 95% CI: 1.56-9.66), stroke (OR: 3.19; 95% CI: 1.63-6.23) and history of cardiac arrest (OR: 2.65; 95% CI: 1.37-5.15) were independent risk factors for higher mortality. CONCLUSIONS: A paradoxical relationship between BMI and mortality risk is present in elderly patients with ICD at high risk of sudden death with a lower mortality in obese or overweight patients than in those with normal BMI.

Bundle branch reentry: a mechanism of ventricular tachycardia in the absence of myocardial or valvular dysfunction.

OBJECTIVES: The aim of this study was to present bundle branch reentry as the mechanism of sustained ventricular tachycardia in the absence of myocardial or valvular dysfunction. BACKGROUND: Previous reports have documented the relation between structural heart disease and bundle branch reentrant ventricular tachycardia. Myocardial or valvular dysfunction has thus far been recognized as the only anatomic substrate for the development of this tachycardia. METHODS: Three patients with a wide QRS complex tachycardia underwent noninvasive and invasive cardiac evaluation and electrophysiologic studies to identify the substrate and mechanism of tachycardia. Catheter ablation of the right bundle branch using radiofrequency current was performed in each patient. RESULTS: The patients were all men (aged 54, 34 and 72 years) who presented with presyncope, palpitation and cardiac arrest, respectively. Electrocardiography during sinus rhythm revealed nonspecific intraventricular conduction delay in all three patients. Cardiac evaluation revealed no evidence of myocardial or valvular dysfunction in any patient. The baseline HV interval was prolonged in each patient (90, 100 and 75 ms, respectively). Programmed right ventricular stimulation initiated bundle branch reentrant tachycardia with typical left (three patients) and right (one patient) bundle branch block pattern. Catheter ablation of the right bundle branch using radiofrequency current abolished bundle branch reentry in all three patients. After 26-, 13- and 8-month follow-up periods, complete right bundle branch block persisted, and all three patients remained asymptomatic without antiarrhythmic drugs. CONCLUSIONS: Sustained bundle branch reentry can be a clinical arrhythmia in patients with no identifiable myocardial or valvular dysfunction except for isolated conduction abnormalities in the His-Purkinje system. This mechanism of tachycardia should be recognized during electrophysiologic evaluation, given the seriousness of this arrhythmia and the availability of the effective treatment.

Slow pathway ablation in patients with atrioventricular node reentrant tachycardia and a prolonged PR interval.

OBJECTIVES: We sought to assess the safety and efficacy of selective slow pathway ablation using radiogfrequency energy and a transcatheter technique in patients with a prolonged PR interval and atrioventricular (AV) node reentrant tachycardia. BACKGROUND: Although both fast and slow AV node pathways can be ablated in patients with AV node reentrant tachycardia, slow pathway ablation, by obviating the risk of AV block, appears to be safer. However, the safety and efficacy of selective slow pathway ablation using transcatheter radiofrequency energy in patients with a prolonged PR interval during sinus rhythm are unclear. METHODS: The seven study patients with a prolonged PR interval (mean +/- SD 237 +/- 26 ms) comprised three women and four men with a mean age of 31 +/- 15 years. The slow pathway was targeted in all seven patients at the posterior/inferior interatrial septal aspect of the tricuspid annulus. Two patients presented with the uncommon variety of AV node reentrant tachycardia after initial fast pathway ablation; in the remaining five patients, the AV node reentrant tachycardia was of the common variety. RESULTS: A single radiofrequency pulse at 30 W successfully abolished the slow pathway in both the anterograde and the retrograde direction in the two patients with uncommon AV node reentrant tachycardia. A mean of 5 +/- 3 radiofrequency pulses were required in the remaining five patients with reentrant tachycardia of the common variety. The postablation PR interval and AH interval remained unchanged. The shortest cycle length of 1:1 AV conduction was prolonged significantly (from 327 +/- 31 to 440 +/- 59 ms, p < 0.01, as was the AV node effective refractory period (from 244 +/- 35 to 344 +/- 43 ms, p < 0.01). During a mean follow-up interval of 20 +/- 6 months, no patient developed symptoms suggestive of AV node reentrant tachycardia or had evidence of second- or third-degree AV block. CONCLUSIONS: These data suggest that the AV node slow pathway can be ablated in patients with AV node reentrant tachycardia who demonstrate a prolonged PR interval during sinus rhythm.

Efficacy of the implantable cardioverter-defibrillator in the elderly.

OBJECTIVES: We sought to assess the effect of advanced age on the outcome of patients with an implantable cardioverter-defibrillator (ICD). BACKGROUND: ICDs are effective in preventing sudden cardiac death in susceptible patients, but their beneficial effect on survival is attenuated by the high rate of nonsudden cardiac death in those treated. Although advanced age is an important variable in determining cardiovascular mortality, its impact on the outcome of patients with an ICD has been inadequately studied. METHODS: We performed multivariate analysis of a data base consisting of 769 consecutive patients with an ICD. Seventy-four patients > or = 75 years old at ICD implantation (Group 1) were compared with the remaining 695 patients (Group 2). RESULTS: The two groups were similar in clinical presentation, left ventricular function and gender distribution. The mean follow-up time was 29 and 42 months, respectively, for patients in Group 1 and Group 2. Actuarial survival at 4 years was 57% in Group 1 versus 78% in Group 2 (p = 0.0001). This difference was primarily due to a higher rate of nonsudden cardiac death in Group 1. On multivariate analysis, age > or = 75 years, New York Heart Association functional class III, left ventricular ejection fraction < 30% and appropriate shocks during follow-up were independently associated with increased mortality (odds ratio 3.56, 1.8, 1.6 and 1.39, respectively). CONCLUSIONS: Among patients with similar functional class and ejection fraction, the mortality risk is increased threefold in those > or = 75 years old at the time of ICD implantation. Extrapolation of results from younger patients is likely to overestimate ICD benefit in the elderly.

Preliminary experience with a hybrid nonthoracotomy defibrillating system that includes a biphasic device: comparison with a standard monophasic device using the same lead system.

OBJECTIVES: This study analyzed the advantage of combining a biphasic device with a transvenous system and compared the results with those obtained with a standard monophasic device. BACKGROUND: Available lead systems use monophasic pulses and may require lengthy intraoperative testing to achieve adequate defibrillation threshold in a conspicuous number of patients. The option of biphasic waveform may provide further benefits. However, clinical experience with a permanent implant is lacking. METHODS: Fifty-five patients underwent testing and received a permanent implant using the Endotak lead system associated with a CPI monophasic device. The remaining 36 patients received a permanent implant with the Endotak lead system connected to a biphasic device. In both groups a subcutaneous patch was combined when needed to obtain acceptable defibrillation thresholds. RESULTS: Biphasic pulses resulted in lower mean (+/- SD) defibrillation thresholds (monophasic 15 +/- 4.7 J vs. biphasic 12 +/- 5 J, p = 0.03) and a better implantation rate (100% biphasic vs. 89% monophasic, p = 0.07). Biphasic pulses allowed implantation with less ventricular fibrillation induction (7.4 +/- 3.2 vs. 3.5 +/- 1.8, p < 0.01) and a mean shorter procedure time (168 +/- 39 vs. 111 +/- 30 min, p < 0.01). With the biphasic waveform a greater proportion of patients met the implantation criteria with the lead system alone (83% vs. 45%, p < 0.01). When needed, the left prepectoral location of the patch electrode was always sufficient in left subscapular position was required in 15 patients in the monophasic group. Implantation of the biphasic device was associated with a shorter mean hospital stay (3.8 +/- 0.8 vs. 5.4 +/- 2.2 days, p < 0.01). CONCLUSIONS: Incorporation of a biphasic device in a transvenous implantable cardioverter-defibrillator uniformly increases the efficacy of the system and the ease of implantation.

Distribution of atrial electrogram types during atrial fibrillation: effect of rapid atrial pacing and intercaval junction ablation.

OBJECTIVES: This study examined the anatomic distribution types and possible determinant of atrial electrogram types during atrial fibrillation. BACKGROUND: Different types of atrial electrograms during atrial fibrillation have been observed and classified, but their anatomic distribution patterns, determinants and potential usefulness in guiding future catheter ablation are unknown. METHODS: Two animal models of atrial fibrillation were used: the sterile pericarditis model (n = 10) and the rapid atrial pacing model (400 beats/min for 6 weeks, n = 6). The atrial electrogram of atrial fibrillation and the atrial effective refractory period were obtained from multiple sites of the right and left atrium. In addition, decremental rapid atrial stimulation was applied to the site of shortest and longest atrial effective refractory periods until atrial fibrillation induction in a subgroup of nine dogs. Ablation of the intercaval junction was performed using the radiofrequency catheter technique in dogs with atrial fibrillation duration > 1 min. RESULTS: In both models, organized atrial electrograms (type I) were predominantly observed at the left atrial sites and the right atrial appendage, whereas disorganized atrial electrograms (type III) were mainly observed at the right posterolateral atrium. The distribution of the atrial electrogram types closely followed that of the atrial effective refractory period, with the shortest atrial effective refractory period corresponding to organized atrial electrograms (type I) and the longest atrial effective refractory period corresponding to disorganized atrial electrograms (type III). The correlation of atrial electrogram type with the atrial effective refractory period was further demonstrated by the effect of rapid atrial stimulation. When rapid atrial stimulation was applied to the site with the shortest atrial effective refractory period, disorganized atrial electrograms were observed at sites with the longest atrial effective refractory period, whereas 1:1 atrial capture was still present at the stimulation site. Ablation of the intercaval junction made atrial fibrillation noninducible or tended to shorten the atrial fibrillation duration (from 26.4 +/- 24.2 to 8.8 +/- 22.6 min in the pericarditis group, p = 0.02, and from 33.7 +/- 29.2 to 12.1 +/- 23.8 min in the rapid pacing group, p = 0.09) but did not change the atrial electrogram types during atrial fibrillation. CONCLUSIONS: Various types of atrial electrograms are present at different locations during atrial fibrillation. The atrial electrogram characteristics of atrial fibrillation at a specific location are related to the atrial effective refractory period, with short effective refractory periods associated with organized atrial electrograms and long effective refractory periods associated with disorganized electrograms.

Feasibility of atrial fibrillation detection and use of a preceding synchronization interval as a criterion for shock delivery in humans with atrial fibrillation.

OBJECTIVES: This study assessed the feasibility of detecting atrial fibrillation (AF) and delivery of appropriately timed R wave shocks using an implantable atrial defibrillator. BACKGROUND: For atrial defibrillation therapy to be feasible in an implantable form, AF must be detected in a specific fashion, and the risk of ventricular proarrhythmia should be minimized. METHODS: Eleven patients with AF underwent testing with an implantable atrial defibrillator (METRIX 3000 Automatic Atrial Defibrillator, InControl, Inc.). Wideband electrograms (EGMs) were recorded from the right ventricular (RV) bipolar catheter and from the multipolar catheters located in the right atrium (RA) and coronary sinus (CS). Atrial fibrillation detection was performed using two serial algorithms-quiet interval analysis and baseline crossing analysis-that detect atrial activity on the RA-CS channel. Ventricular sensing using a minimal preceding synchronization interval of 500 ms as a criterion for synchronous shock delivery was performed from filtered RV and RV-CS EGMs. RESULTS: The AF detection algorithms were applied to 53 AF data segments and 18 normal sinus rhythm data segments. Atrial fibrillation was detected appropriately in 49 instances, and the specificity for detecting AF and normal sinus rhythm was 100%. Synchronization criterion efficacy was assessed by delivering shock markers and shocks. Of the 2,025 R waves processed, 557 (27.5%) were marked as suitable for shock delivery. In addition, 69 therapeutic and 11 test shocks were delivered during AF. All shock markers and shocks were delivered synchronously with the R wave, and the synchronization criterion was never violated. CONCLUSIONS: Atrial fibrillation can be detected in a specific fashion using the RA-CS lead configuration and serial detection algorithms for atrial sensing. The delivery of properly timed shocks is feasible and should minimize the risk of ventricular proarrhythmia.

Physics and engineering of transcatheter cardiac tissue ablation.

Ablation of arrhythmogenic cardiac tissues has emerged as one of the most important advances in cardiac electrophysiology. With the introduction of transcatheter ablation, the treatment of ventricular tachycardia, Wolff-Parkinson-White syndrome and other cardiac arrhythmias has progressed from an expensive and painful surgical therapy accompanied by a long recovery period to the less expensive, less traumatic transcatheter approach. The feasibility of cardiac ablation, along with the increasing number of physicians using the technique, requires understanding of the anatomic and electrophysiologic bases of transcatheter ablation as well as the different technologies, their limitations and complications. This report provides an overview of the physical, scientific and technical aspects of cardiac ablation performed with the methods currently available and a summary of the limitations of each method and expected future technologic developments in this growing field. Emphasis is placed on radiofrequency and direct current energies, the primary methods now used. Methods such as cryoablation and laser, and microwave and chemical ablation are discussed with less detail because the method of delivering energy for these ablative procedures has not been fully developed.

Use of intravenous esmolol to predict efficacy of oral beta-adrenergic blocker therapy in patients with neurocardiogenic syncope.

The usefulness of esmolol in predicting the efficacy of treatment with an oral beta-adrenergic blocking agent was evaluated in 27 consecutive patients with neurocardiogenic syncope. Seventeen patients had a positive head-up tilt test response at baseline and 10 patients required intravenous isoproterenol for provocation of hypotension. All patients were then given a continuous esmolol infusion (500 micrograms/kg per min loading dose for 3 min followed by 300 micrograms/kg per min maintenance dose) and rechallenged with a head-up tilt test at baseline or with isoproterenol. Of the 17 patients with a positive baseline tilt test response, 11 continued to have a positive response to esmolol challenge. Sixteen patients (including all 10 patients with a positive tilt test response with isoproterenol) exhibited a negative response to upright tilt during esmolol infusion. Irrespective of their response to esmolol infusion, all patients had a follow-up tilt test with oral metoprolol after an interval of greater than or equal to 5 half-lives of the drug. All 16 patients (100%) with a negative tilt test response during esmolol infusion had a negative tilt test response with oral metoprolol. Of the 11 patients with a positive tilt test response during esmolol infusion, 10 (90%) continued to have a positive response with oral metoprolol. It is concluded that in the electrophysiology laboratory, esmolol can accurately predict the outcome of a head-up tilt response to oral metoprolol. This information may be helpful in formulating a therapeutic strategy at the initial head-up tilt test in patients with neurocardiogenic syncope.

Recurrence of neurocardiogenic syncope without pharmacologic interventions.

In 54 patients with positive tilt and who refused medical therapy, we observed a significant decrease in the frequency of syncopal spells after diagnosis and counseling. However, symptoms were reported at follow-up by 64.8% of the patients and were predicted by the frequency and total number of syncope episodes before upright tilt.

Relevance of asystole during head-up tilt testing.

The prognosis of patients manifesting prolonged asystole during head-up tilt testing is unclear. In 209 consecutive patients with a history of syncope and positive head-up tilt tests, 19 had asystole lasting > 5 seconds (mean duration 15 +/- 10) (group 1a). When compared with patients without asystole (group 1b), group 1a patients were younger (32 +/- 12 vs 47 +/- 21 years, p < 0.005), but clinical manifestations were not any more dramatic (the number of episodes of syncope [7 +/- 5 vs 8 +/- 6 episodes, p = NS] and injury during syncope [2 vs 13 patients, p = NS] were similar). During follow-up (mean 2 +/- 1 year), with the patient taking pharmacologic therapy such as beta blockers, ephedrine, theophylline, or disopyramide, the recurrence rate was 11% and 8% in groups 1a and 1b (p = NS). No patient in the asystole group underwent pacemaker implantation. Additionally, of 75 normal volunteers (group 2) with no history of syncope undergoing tilt tests to define its specificity, 3 had asystole (mean duration 10 seconds). During > 1 year of follow-up, despite no treatment, all 3 are symptom free. Thus, asystole during head-up tilt testing does not predict either a more malignant outcome or a poor response to pharmacologic therapy. Moreover, an asystolic response does not enhance the specificity of the head-up tilt test because it may be present in asymptomatic "normal" volunteers.

Feasibility of concomitant implantation of permanent transvenous pacemaker and defibrillator systems.

In 17 patients (14 men and 3 women aged 69 +/- 10 years), a transvenous pacemaker was implanted before (8 patients), following (7 patients), or simultaneously (2 patients) with the insertion of a transvenous defibrillator. Indications included malignant ventricular arrhythmias and symptomatic bradycardia in all patients. All patients had structural heart disease. All pacemakers were non-programmable bipolar, either single chamber (n = 7) or dual chamber (n = 10). Eleven pacemakers were rate responsive. The Transvene system was implanted in 7 patients (Pacer-Cardioverter-Defibrillator in 6 patients and the Cadence defibrillator in 1). The Endotak lead system was implanted in 10 patients (Ventak in 7 patients and the Cadence in 3). The mean defibrillation threshold was 16 +/- 5 J. Repositioning of the pacemaker leads eliminated undersensing of ventricular fibrillation by the defibrillator, which occurred during asynchronous pacing in 2 patients. During a mean follow-up of 11 +/- 6 months, 2 patients died because of pump failure and 7 patients received defibrillator therapy for ventricular arrhythmias. No significant complications were noted. Successful concomitant implantation of transvenous pacemakers and defibrillators was thus accomplished in 17 patients, which suggests that insertion of a second transvenous device can be safely accomplished.

Unmasking the trifascicular left intraventricular conduction system by ablation of the right bundle branch.

Twenty-five patients underwent transcatheter right bundle ablation either for bundle branch reentrant tachycardias or inadvertent or deliberate right bundle ablation during atrioventricular junctional ablation for rate control. Electrophysiologic data and 12-lead electrocardiograms before and after right bundle ablation were available in all patients. Eleven of the patients had no significant intraventricular conduction abnormalities by surface electrocardiograms (group I), whereas 14 patients had underlying intraventricular conduction delays (group II). All group I patients had typical electrocardiographic changes of right bundle branch block after right bundle ablation, with minimal changes in initial or mean QRS axis. In group II, 5 patients had an initial 40 ms QRS axis shift of > 45 degrees, in 7 patients the mean QRS axis changed significantly (leftward in 4 and rightward in 3), and a qR pattern in V1 was seen in 12 of 14 patients including 2 with structurally normal hearts. These changes, namely new Q waves, and rightward and leftward axis shifts are most likely the result of septal fascicular, left posterior fascicular, and left anterior fascicular delay/block, which were exposed by exclusive conduction via a diseased left bundle and its fascicles. The trifascicular nature of left intraventricular conduction is more apparent when diseased and unmasked by concomitant block in the right bundle branch.

Circulatory and catecholamine changes during head-up tilt testing in neurocardiogenic (vasovagal) syncope.

Changes in heart rate, arterial pressure, norepinephrine and epinephrine levels were compared in 19 consecutive patients (10 men and 9 women, mean age 46 +/- 16 years) with neurocardiogenic syncope and 11 age- and sex-matched control subjects (5 men and 6 women, mean age 49 +/- 15 years) during head-up tilt testing. Norepinephrine and epinephrine levels were measured at the baseline supine position, in the initial upright position, every 90 seconds during the 70 degrees upright tilt, at the time of termination due to hypotension and syncope (or at 15 minutes in control subjects), and at 40 seconds and 1 minute and 40 seconds in the supine position after terminating the head-up tilt test. Baseline norepinephrine, epinephrine and heart rate were slightly higher in patients. Despite a significant decrease in mean arterial pressure during head-up tilt testing in patients (51 +/- 20 mm Hg; p < 0.001), norepinephrine levels in patients and control subjects at the time of terminating the head-up tilt test were comparable (459 +/- 204 vs 473 +/- 172 pg/ml). A fivefold increase in epinephrine levels (73 +/- 53 to 345 +/- 260 pg/ml; p < 0.01) were seen in patients, whereas control subjects had insignificant change (38 +/- 16 to 65 +/- 44 pg/ml). It is concluded that diminished neuronal sympathetic activity and enhanced adrenomedullary activity is demonstrated during head-up tilt testing in patients with neurocardiogenic syncope.

Use of sublingual nitroglycerin during head-up tilt-table testing in patients >60 years of age.

Previous work had demonstrated a reduced specificity associated with head-up tilt protocols using high-dose isoproterenol in patients between 20 and 50 years of age. We evaluated the specificity of head-up tilt testing using different isoproterenol infusion doses and administration of nitroglycerin in patients aged >60 years. In addition, whether the same protocols have impact on the sensitivity of the test was also assessed. One hundred sixty subjects were included in this study. Seventy-six were volunteers randomized to either head-up tilt test with low-dose, 3- and 5-microg/min of isoproterenol (group I) or to a protocol including 0.4 mg of sublingual nitroglycerin (group II). In addition, after an upright tilt drug-free state, 58 patients with a history of syncope underwent repeat head-up tilt with increasing doses of isoproterenol infusion, followed by sublingual nitroglycerin if the test result remained negative. The remaining 33 patients were subjected to the nitroglycerin protocol after the drug-free state phase. In the control groups, the incidence of false-positive responses was 88% and 95%, respectively. In patients with syncope after a negative test result during 5 microg of isoproterenol infusion, nitroglycerin administration increased the number of positive responses from 45% to 79%. The percentage of positive tilt in patients undergoing nitroglycerin administration after the drug-free state part of the protocol was 78%. Administration of nitroglycerin was the most significant predictor of a positive upright tilt in patients with syncope. In subjects aged >60 years, head-up tilt protocols with high-dose isoproterenol infusion and nitroglycerin maintained an adequate specificity. In this subset of patients, nitroglycerin seemed to provide a better sensitivity than isoproterenol.

Comparison of outcome of implantable cardioverter defibrillator implantation in patients with severe versus moderately severe left ventricular dysfunction secondary to atherosclerotic coronary artery disease.

This study was undertaken to assess the feasibility and clinical outcome of implantable cardioverter-defibrillators (ICDs) among patients with coronary artery disease and left ventricular ejection fraction (LVEF) of <20%. The morbidity, mortality, and the long-term survival of 117 patients with LVEF of <20% (group 1) were compared with 321 patients with LVEF of 20% to 40% (group 2). Mortality in the first 30 days after ICD implantation was 0% for group 1 and 0.6% in group 2. Actuarial survival (all cause) at the end of 2, 4, and 5 years were 83%, 70%, and 62%, respectively, in group 1 and 90%, 80%, and 71% in group 2 (p = 0.05). Fifty-five patients (47%) in group 1 and 126 patients (39%) in group 2 received appropriate shocks during follow up. Among the patients in group 1, the overall survival at 2 years after an appropriate shock from an ICD was 92% for patients <60 years of age, 77% for patients ages 60 to 69, and 53% for patients >70 years old. Although the overall survival of patients in group 1 was slightly lower compared with those in group 2, in a multivariate analysis, the EF was not an independent predictor of poor survival. The ICD can be implanted with acceptable operative morbidity and mortality in selected patients with LVEF of <20%.

Sudden cardiac death.

SCD continues to be an important cause of death and morbidity. Despite expanding insight into the mechanisms causing SCD, the population at high risk is not being effectively identified. Although there is still much to do in the management phase of SCD (predicting the efficacy of various therapies), recent clinical trials have helped define the relative risks and benefits of therapies in preventing SCD. Trials are underway to determine whether treating other patient populations, including asymptomatic patients after MI, will improve survival rate. The approach to reducing mortality rate will always be multifaceted; primary prevention of coronary artery disease and prompt salvage of jeopardized myocardium are 2 important aspects of this approach. In addition to interventions for MI, such as myocardial revascularization when indicated, simple and easily administered therapies that are likely to remain the most effective prophylactic interventions are aspirin, ACE inhibitors, beta-blockers, and cholesterol-lowering agents. However, the MADIT and AVID data clearly demonstrate a role for ICD therapy in a subgroup of patients who have VT/VF and are at risk of cardiac arrest. Even though the absolute magnitude of benefit associated with ICDs is still to be determined, the AVID study and other recent reports provide convincing evidence that patients who have VT/VF fare better with ICDs than with antiarrhythmic drug therapy. For the high-risk population described in this article, in addition to aggressive anti-ischemic and heart failure therapy, ICDs are now a mainstay of life-saving treatment. Still to be surmounted is the challenge of identifying patients who have nonischemic substrates and of providing them with the appropriate therapy. Guided by genetic studies and new insight into the mechanisms of such problems as congenital long QT syndrome, life-saving and life-enhancing therapies may soon be available for the management of SCD.

Atrioventricular nodal reentrant tachycardia. Electrophysiologic characteristics, therapeutic interventions, and specific reference to anatomic boundary of the reentrant circuit.

Over the past several decades there has been enormous progress in the understanding of many electrophysiologic characteristics of the AVNRT circuit. Although a great number of questions have been resolved, several pertinent issues require further investigation. Medical treatment remains the most widely used therapeutic intervention for acute or short-term management of patients with recurrent AVNRT. However, nonpharmacologic approaches, particularly transcatheter modification of the AV node, have increasingly become popular for long-term management. Radiofrequency energy has been safe and effective for transcatheter ablative techniques. It seems highly likely that in the next several years, selective transcatheter ablation of the AV nodal (slow or fast) pathway, by providing permanent cure, will become the modality of choice in symptomatic patients with AVNRT.

Neurocardiogenic syncope. Diagnosis, mechanisms, and treatment.

Neurocardiogenic syncope is a common medical problem that can be identified easily by history and the findings of the head-up tilt test. Depressor reflexes from the heart causing sympathetic withdrawal that, in turn, lead to peripheral vasodilatation and hypotension may have an important role in the pathogenesis of neurocardiogenic dysfunction. Once a diagnosis of neurocardiogenic syncope has been made, specific therapeutic strategies can usually prevent recurrent syncope. However, the natural history of neurocardiogenic syncope has not been studied. Double-blind placebo-controlled studies or drug withdrawal trials are needed to assess whether all patients with neurocardiogenic syncope need lifelong therapy.

Implantable cardioverter-defibrillator therapy for prevention of sudden cardiac death.

Patients with known symptomatic VT or VF are at high risk for sudden cardiac death. Various therapeutic choices can be used to reduce the incidence of arrhythmic sudden cardiac death. These include beta-blockers, class I and III antiarrhythmic agents, VT focal ablations, and ICD therapy. The overall incidence of sudden cardiac death in ICD recipients is less than 2% per year, a rate of survival not achieved with any of the available antiarrhythmic agents. VT surgical therapy can produce comparable survival results, but the minimal operative mortality is higher than that with ICD therapy. In patients with noninducible VT/VF or inducible polymorphic VT, and in those refractory to or intolerant of antiarrhythmic agents and poor left ventricular function, ICD therapy may be the only realistic option.