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D J Wilber

Publications and source records attributed to D J Wilber.

At least 19 recordsLinked to original sources

Retrograde fast pathway ablation for atrioventricular nodal reentry associated with markedly prolonged PR intervals.

Three patients with typical atrioventricular nodal reentrant tachycardia (AVNRT) and markedly prolonged PR intervals (>300 ms) without dual pathway physiology at baseline or during isoproterenol infusion underwent successful fast pathway ablation and remained asymptomatic without recurrent AVNRT, atrioventricular block, or symptomatic bradycardia for a mean of 19 months. In patients with recurrent AVNRT and markedly prolonged PR intervals, selective ablation of the retrograde fast pathway can eliminate AVNRT without further impairment of anterograde atrioventricular nodal function.

Adrenergic beta-Agonists

Atrial fibrillation after radiofrequency ablation of type I atrial flutter: time to onset, determinants, and clinical course.

BACKGROUND: The occurrence of atrial fibrillation after ablation of type I atrial flutter remains an important clinical problem. To gain further insight into the pathogenesis and significance of postablation atrial fibrillation, we examined the time to onset, determinants, and clinical course of atrial fibrillation after ablation of type I flutter in a large patient cohort. METHODS AND RESULTS: Of 110 consecutive patients with ablation of type I atrial flutter, atrial fibrillation was documented in 28 (25%) during a mean follow-up of 20.1+/-9.2 months (cumulative probability of 12% at 1 month, 23% at 1 year, and 30% at 2 years). Among 17 clinical and procedural variables, only a history of spontaneous atrial fibrillation (relative risk 3.9, 95% confidence intervals 1.8 to 8.8, P=0.001) and left ventricular ejection fraction <50% (relative risk 3.8, 95% confidence intervals 1.7 to 8.5, P=0.001) were significant and independent predictors of subsequent atrial fibrillation. The presence of both these characteristics identified a high-risk group with a 74% occurrence of atrial fibrillation. Patients with only 1 of these characteristics were at intermediate risk (20%), and those with neither characteristic were at lowest risk (10%). The determinants and clinical course of atrial fibrillation did not differ between an early (< or = 1 month) compared with a later onset. Atrial fibrillation was persistent and recurrent, requiring long-term therapy in 18 patients, including 12 of 19 (63%) with prior atrial fibrillation and left ventricular dysfunction. CONCLUSIONS: Atrial fibrillation after type I flutter ablation is primarily determined by the presence of a preexisting structural and electrophysiological substrate. These data should be considered in planning postablation management. The persistent risk of atrial fibrillation in this population also suggests a potentially important role for atrial fibrillation as a trigger rather than a consequence of type I atrial flutter.

Aged

Electroanatomic imaging using magnetic catheter tracking in the diagnosis and treatment of atrial arrhythmias.

Recent data emphasize the importance of structural factors in the pathophysiology of atrial arrhythmias. As a consequence, catheter ablation increasingly has become an anatomically oriented procedure. A recently developed magnetic catheter tracking system provides spatially precise and realistic three-dimensional reconstructions of endocardial geometry. A variety of electrophysiologic data can be superimposed on these reconstructions, including activation sequence, electrogram amplitude and morphologic features, response to pacing maneuvers, and sites of planned or delivered radiofrequency energy ablation. These features enhance the ability to analyze and visualize arrhythmia mechanisms, plan and execute appropriate ablation strategies, and provide new opportunities for physiologic research.

Atrial Fibrillation

Radiofrequency catheter ablation of atrioventricular nodal reentry tachycardia utilizing nonfluoroscopic electroanatomical mapping.

The advent of catheter ablation stimulated extensive research into anatomical localization of the pathways involved in atrioventricular nodal reentrant tachycardia (AVNRT). Conventional electrophysiological methods that attempt to correlate intracardiac electrograms with two-dimensional fluoroscopic anatomy are limited by the relative inaccuracy and poor reproducibility of this technique, and the requirement for high levels of radiation exposure. A new method of nonfluoroscopic electroanatomical mapping utilizes magnetic field sensing with a specialized catheter to construct three-dimensional electroanatomical endocardial maps of selected heart chambers with spatial resolution of < 1 mm. This system can be used in patients undergoing catheter ablation for AVNRT to create accurate maps of Koch's triangle and to guide application of radiofrequency energy. Initial experience in 14 patients suggests efficacy and safety comparable to conventional mapping and ablation techniques. Further evaluation may confirm the potential benefits of this system with respect to success rates, complications, procedure time, and radiation exposure.

Atrioventricular Node

What can we expect from prophylactic implantable defibrillators?

Death due to ventricular tachyarrhythmia (VT) remains an important public health problem; patients with prior myocardial infarction (MI) constitute the largest identifiable population for prophylactic interventions. Targeting of progressively higher-risk subgroups of post-MI survivors carries inevitable tradeoffs with respect to the global impact of interventions on overall mortality. Therapy with aspirin, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors comprise the benchmark against which all additional interventions, including implantable defibrillators, must be measured. Initial enthusiasm for empiric amiodarone therapy has been tempered by the limited benefit demonstrated in recent randomized trials. Trials of other class III antiarrhythmic drugs, including both d,l-sotalol and d-sotalol, have also failed to demonstrate survival benefit. The Multicenter Automatic Defibrillator Implantation Trial (MADIT) demonstrated significantly improved survival associated with defibrillators in a small subgroup of post-MI survivors with a high short-term risk of death. The ultimate number and optimal criteria for selection of patients who may benefit from prophylactic defibrillator therapy after MI will undergo continued evolution as new data from current and ongoing trials become available.

Amiodarone

Therapeutic options in atrial flutter and fibrillation.

Newer antiarrhythmic agents can control atrial flutter and fibrillation in many patients, although individual episodes may require cardioversion. Catheter ablation is often curative for refractory flutter. Ablation of atrial fibrillation is more difficult, because of its different mechanism. Surgical and catheter-based ablation procedures have been pioneered for fibrillation but remain experimental.

Aged

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.

Animals

Adenosine-sensitive bundle branch reentry.

INTRODUCTION: Bundle branch reentry is an uncommon mechanism for ventricular tachycardia. More infrequently, both fascicles of the left bundle may provide the substrate for such macroreentrant bundle branch circuits, so-called interfascicular reentry. The effect of adenosine on bundle branch reentrant mechanisms of tachycardia is unknown. METHODS AND RESULTS: A 59-year-old man with no apparent structural heart disease and history of frequent symptomatic wide complex tachycardias was referred to our center for further electrophysiologic evaluation. During electrophysiologic study, a similar tachycardia was reproducibly initiated only during isoproterenol infusion, which had the characteristics of bundle branch reentry, possibly using a left interfascicular mechanism. Intravenous adenosine reproducibly terminated the tachycardia. Application of radiofrequency energy to the breakout site from the left posterior fascicle prevented subsequent tachycardia induction and rendered the patient free of spontaneous tachycardia during long-term follow-up. CONCLUSIONS: Patients with ventricular tachycardia involving a bundle branch reentrant circuit may be sensitive to adenosine. These results suggest that adenosine may not only inhibit catecholamine-mediated triggered activity but also some catecholamine-mediated reentrant ventricular arrhythmias.

Adenosine

Current-based transthoracic defibrillation.

This study examines in a prospective, multicenter trial the feasibility and advantage of current-based, transthoracic defibrillation. Current-based, damped, sinusoidal waveform shocks of 18, 25, 30, 35, or 40 amperes (A) were administered beginning with 25 A for polymorphic ventricular tachycardia (VT) and ventricular fibrillation (VF) or 18 A for monomorphic VT; success rates were compared with those of energy-based shocks beginning at 200 J for VF/polymorphic VT and 100 J for VT. The current-based shocks were delivered from custom-modified defibrillators that determined impedance in advance of any shock using a "test-pulse" technique; the capacitor then charged to the exact energy necessary to deliver the operator-selected current against the impedance determined by the defibrillator. Three hundred sixty-two patients received > 1 shock for VF, polymorphic VT, or monomorphic VT: 569 current- based shocks and 420 energy-based shocks. Current-based shocks of 35/40 A achieved success rates of up to 74% for VF/polymorphic VT; 30 A shocks terminated 88% of monomorphic VT episodes. Energy-based shocks of 300 J terminated 72% of VF/polymorphic VT; 200-J shocks terminated 89% of monomorphic VT. We could not demonstrate a significant increase in the success rate of current-based shocks over energy-based shocks for patients with high transthoracic impedance; this may be due to inadequate sample size. Thus, current-based defibrillation is clinically feasible and effective. A larger study will be needed to test whether current-based defibrillation is superior to energy-based defibrillation.

Electric Countershock

Multicenter comparison of truncated biphasic shocks and standard damped sine wave monophasic shocks for transthoracic ventricular defibrillation. Transthoracic Investigators.

BACKGROUND: The most important factor for improving out-of-hospital ventricular fibrillation survival rates is early defibrillation. This can be achieved if small, lightweight, inexpensive automatic external defibrillators are widely disseminated. Because automatic external defibrillator size and cost are directly affected by defibrillation waveform shape and because of the favorable experience with truncated biphasic waveforms in implantable cardioverter-defibrillators, we compared the efficacy of a truncated biphasic waveform with that of a standard damped sine monophasic waveform for transthoracic defibrillation. METHODS AND RESULTS: The principal goal of this multicenter, prospective, randomized, blinded study was to compare the first-shock transthoracic defibrillation efficacy of a 130-J truncated biphasic waveform with that of a standard 200-J monophasic damped sine wave pulse using anterior thoracic pads in the course of implantable cardioverter-defibrillator testing. Pad-pad ECGs were also examined after transthoracic defibrillation. After the elimination of data for 24 patients who did not meet all protocol criteria, the results from 294 patients were analyzed. The 130-J truncated biphasic pulse and the 200-J damped sine wave monophasic pulse resulted in first-shock efficacy rates of 86% and 86%, respectively (P = .97). ST-segment levels measured 10 seconds after the shock in 151 patients in sinus rhythm were -0.26 +/- 1.58 and -1.86 +/- 1.93 mm for the 130- and 200-J shocks, respectively (P < .0001). CONCLUSIONS: We found that 130-J biphasic truncated transthoracic shocks defibrillate as well as the 200-J monophasic damped sine wave shocks that are traditionally used in standard transthoracic defibrillators and result in fewer ECG abnormalities after the shock.

Adolescent

Evaluation and treatment of nonsustained ventricular tachycardia.

The clinical significance of nonsustained ventricular tachycardia continues to undergo reevaluation as clinicians attempt to optimize screening strategies for identifying high-risk patients and to evaluate the efficacy of therapeutic interventions. The utility of ambulatory monitoring and programmed stimulation as screening tools in the patient who has suffered an infarction remains unsettled; ongoing clinical trials may help resolve these issues. New data suggest that the survival benefit associated with angiotensin-converting enzyme inhibition is unrelated to effects on spontaneous arrhythmias, similar to results previously reported for beta-blockers. Randomized clinical trials of prophylactic amiodarone in patients with congestive heart failure and nonsustained ventricular tachycardia have produced conflicting results. A strong relationship between polymorphic nonsustained ventricular tachycardia and sudden death in patients without structural heart disease or QT prolongation has been reported. The significance of nonsustained ventricular tachycardia in dilated cardiomyopathy and hypertrophic cardiomyopathy has also been reassessed.

Amiodarone

Catheter ablation of the mitral isthmus for ventricular tachycardia associated with inferior infarction.

BACKGROUND: Intraoperative mapping studies suggest that an isthmus of myocardium between the mitral valve annulus and the border of inferior myocardial infarction may play a role in the genesis of ventricular tachycardia. We examined the frequency with which a slow conduction zone within the mitral isthmus was critical to the maintenance of ventricular tachycardia associated with remote inferior infarction in patients undergoing catheter ablation. METHODS AND RESULTS: In 4 of 12 patients, a critical zone of slow conduction was identified within the mitral isthmus. In each of these patients, two characteristic and morphologically distinct tachycardias were induced: a left bundle (rS in V1, R in V6), left superior axis morphology and a right bundle (R in V1, QS in V6), right superior axis morphology (cycle length, 610 to 320 ms). In each patient, a zone of slow conduction, shared by both morphologies, was characterized by diastolic potentials with electrogram-QRS intervals of 85 to 161 ms (21% to 47% of tachycardia cycle length) and entrainment with concealed fusion during pacing associated with stimulus-QRS intervals of 81 to 400 ms (20% to 91% of tachycardia cycle length). In each patient, a single radiofrequency energy application at the shared site of slow conduction eliminated inducibility of both morphologies. During follow-up of 1 to 11 months, no patient had recurrent tachycardia. CONCLUSIONS: The mitral isthmus contains a critical region of slow conduction in some patients with ventricular tachycardia after inferior myocardial infarction, providing a vulnerable and anatomically localized target for catheter ablation. Characteristic tachycardia morphologies may provide clinical markers for this underlying mechanism.

Cardiac Catheterization

Dose-ranging study of intravenous amiodarone in patients with life-threatening ventricular tachyarrhythmias. The Intravenous Amiodarone Multicenter Investigators Group.

BACKGROUND: Oral amiodarone effectively suppresses ventricular arrhythmias; however, full activity may take days or weeks. In patients with frequent, life-threatening ventricular arrhythmias, this delay is not acceptable. Thus, in these patients, the speed and dosing accuracy of an intravenous formulation would be beneficial. The goal of this study was to demonstrate the efficacy of intravenous amiodarone in patients with refractory, recurrent hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation by determining a dose response among three regimens. METHODS AND RESULTS: A total of 342 patients were enrolled at 46 medical centers in the United States. Patients received one of three randomized, double-blind dose regimens delivering 125, 500, or 1000 mg during the first 24 hours. Supplemental infusions (150 mg) of intravenous amiodarone could be given to treat breakthrough ventricular arrhythmias. The key efficacy end points were the arrhythmia event rate, time to first arrhythmic event, and number of supplemental infusions administered. The event rate decreased with increasing doses: median values were 0.07, 0.04, and 0.02 events per hour for the 125-, 500-, and 1000-mg dose groups, respectively, representing a significant decrease from baseline event rates (P = .043), and approached significance in the overall test for trend (P = .067). There was a significant dose-related increase in the time to first event (trend test P = .025) and a significant dose-related decrease in the number of supplemental boluses per hour (trend test P = .043). Hypotension was the most common (26%) treatment-emergent adverse event during intravenous amiodarone therapy; there was no dose-response relationship. Seventy-eight percent of the patients survived to at least 48 hours. CONCLUSIONS: Intravenous amiodarone is effective for the treatment of recurrent, life-threatening ventricular tachyarrhythmias.

Amiodarone

Predictors of defibrillation energy requirements with nonepicardial lead systems.

The determinants of high defibrillation energy requirements (DER) using nonepicardial lead systems (NELS) have not been well characterized. The goal of this study was to examine prospectively the influence of clinical, radiographic, echocardiographic, and procedural variables on DER during NELS placement. Data from 100 consecutive patients undergoing attempted NELS implantation were analyzed. Transvenous leads, subcutaneous patches, and monophasic shock devices from two manufacturers were used. Leads were successfully positioned for testing in 95% of patients. An adequate DER (< or = 25 J) was obtained in 73 of 95 (77%) of patients. Univariate analysis identified amiodarone therapy and left ventricular mass as predictors of high DER. With multivariate analysis, amiodarone therapy was the sole significant predictor of high DER (P = 0.002, odds ratio 5.46). The 22 patients with high NELS DER also had high epicardial DER (mean 24 +/- 9 J). The two patch epicardial DER was > 25 joules in 12 of 22 patients. Thus, adequate DER with monophasic shock waveforms can be obtained in most patients undergoing NELS testing. However, amiodarone therapy significantly increases the probability of obtaining high DER.

Amiodarone

Use of multiple patches during implantation of epicardial defibrillator systems.

During implantation of epicardial automatic defibrillator systems, occasional patients have difficulty in obtaining adequate defibrillation thresholds. Of 236 consecutive patients undergoing implantation of epicardial defibrillator systems, 18 patients received a 3-patch (n = 15) or 4-patch (n = 3) defibrillator system. Twelve patients who received a multiple-patch defibrillator system had a best 2-patch defibrillation energy requirement of > or = 30 J; in the remaining 6 patients less stringent clinical criteria were used in the decision to add a third defibrillator patch (defibrillation energy requirement > 18 J in 4 patients, and > 20 J in 2 patients). Technically, multiple-patch systems were made possible with either the use of Y-connectors or defibrillators allowing output to 3 patches. In 3 patients, addition of a third epicardial patch still resulted in a defibrillation energy requirement of > or = 30 J; in these 3 patients, addition of a fourth patch resulted in a defibrillation energy requirement of < or = 20 J. All patients receiving a multiple-patch defibrillator system had a reduction in defibrillation energy requirement, and 12 patients had a reduction in defibrillation energy requirement of > or = 10 J over the best 2-patch defibrillation energy requirement. In the patients who eventually had placement of a multiple-patch system, the best 2-patch defibrillation energy requirement was > 18 J in 4 patients, > 20 J in 2 patients, > or = 30 J in 9 patients, and > 40 J in 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents

Adenosine-sensitive ventricular tachycardia. Clinical characteristics and response to catheter ablation.

BACKGROUND: Sustained ventricular tachycardia in the absence of structural heart disease may have diverse mechanisms. Termination of the tachycardia by adenosine suggests triggered automaticity as the etiology in many of these patients. We examined the clinical characteristics, electrophysiological responses, and results of catheter ablation in this patient subgroup. METHODS AND RESULTS: Intravenous adenosine terminated sustained ventricular tachycardia in seven of 14 consecutive patients without evidence of structural heart disease. In each of these patients, the tachycardia had a left bundle branch block, inferior-axis QRS configuration and occurred predominantly during stress or exertion. A morphologically similar sustained tachycardia was induced in six of seven patients during programmed ventricular stimulation, although day-to-day reproducibility was poor. Signal-averaged ECGs were normal in all patients. Imaging with 123I-metaiodobenzylguanidine did not reveal focal abnormalities in any of five patients. A discrete site of origin was identified in the free wall of the pulmonary infundibulum in all patients. Limited application of direct current shocks (two patients) or radiofrequency energy (five patients) resulted in long-term abolition of spontaneous and inducible ventricular tachycardia in all patients. CONCLUSIONS: Adenosine-sensitive ventricular tachycardia appears to arise from relatively discrete sites predominantly located in the free wall of the pulmonary infundibulum. The localized nature of this tachycardia renders it amenable to long-term cure by catheter ablation techniques.

Adenosine

Palpitations and arrhythmias. Separating the benign from the dangerous.

Palpitations are a nonspecific symptom and do not necessarily imply serious heart disease. The vast majority of palpitations are benign. Goals in evaluation include detecting and identifying an arrhythmia, clarifying symptom severity, and defining the extent of underlying heart disease. If palpitations are infrequent and not accompanied by angina, congestive heart failure, or syncope, outpatient transtelephonic monitoring yields useful clinical information in most patients and is more cost-effective than Holter monitoring. Patients with major symptoms require hospitalization for aggressive cardiac evaluation and, possibly, electrophysiologic testing to guide treatment.

Arrhythmias, Cardiac