Search PubMed⌕ Search

Biomedical subjects

D J Wilber

Publications and source records attributed to D J Wilber.

At least 37 records · Page 2Linked to original sources
PubMed1995

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↗
PubMed1995

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↗
PubMed1993

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↗
PubMed1993

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↗
PubMed1992

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↗
PubMed1992

Local activation variability during monomorphic ventricular tachycardia in the dog.

OBJECTIVE: The aim was to determine the beat to beat variability in local activation time during sustained monomorphic ventricular tachycardia in a canine model of experimental myocardial infarction. METHODS: A digital template matching algorithm was developed for detecting subtle beat to beat variability in local activation timing at each of multiple ventricular sites. Ten electrically induced sustained ventricular tachycardia episodes, mean cycle length 211 (SD 40) ms, were endocardially and epicardially mapped in mongrel dogs weighing 15-20 kg. Digitised data were analysed for beat to beat local activation time variability. Similar data recorded during ventricular pacing at comparable rates and during sinus rhythm served as controls. RESULTS: The overall mean variability of local activation time for all 10 ventricular tachycardias was 3.2(1.6) ms, range 1.8(1.1) ms to 4.7(2.8) ms, in contrast to the overall mean variability of 0.2(0.4) ms (p = 0.0001) for ventricular pacing and 0.7(0.6) ms (p = 0.0001) for sinus rhythm. Oscillations in local activation time manifested alternans type periodicity during seven of 10 ventricular tachycardias independent of any alternans in local electrogram morphology. CONCLUSIONS: During sustained, monomorphic ventricular tachycardia, beat to beat variability and alternans type oscillations in local activation time are common and may be an intrinsic property of re-entry since they are negligibly small during ventricular pacing.

Animals↗
PubMed1992

Atrial flutter--update on the mechanism and treatment.

Atrial flutter is a common and usually benign but symptomatic supraventricular tachycardia. There is a striking similarity between patients with atrial flutter suggesting a common substrate despite the presence or absence of underlying heart disease. In man, the mechanism is a single reentrant circuit originating in the right atrium whose center appears to be functional within the anatomical constraints of the right atrium. The reentrant circuit of atrial flutter contains an area of slow conduction in the inferior right atrium but the size and exact location is uncertain. Drug therapy directed at terminating and preventing atrial flutter has been available for many years. The efficacy and safety of this therapy is not as well tested as is the same therapy for atrial fibrillation. The most effective way to terminate atrial flutter is a nonpharmacological approach. Several nonpharmacological methods provide new treatment options in the management of patients with drug resistant or hemodynamically unstable atrial flutter. The use of anticoagulation for this disorder is still evolving. There is a risk of clinically apparent thromboemboli in some patients with atrial flutter although the risk appears less than that for atrial fibrillation. In the future, refinements and improvements in therapy for atrial flutter will likely be derived from a better understanding of its mechanism.

Animals↗
PubMed1992

Radiofrequency catheter ablation of an automatic atrial tachycardia in an adult.

Automatic atrial tachycardia (AAT) is often refractory to medical management. While surgical ablation and isolation procedures such as atrioventricular node ablation have been useful in the management of AAT, important limitations remain. Reported experience with catheter ablation of AAT is limited. This report describes the successful application of transvenous radiofrequency catheter ablation in an adult with AAT. Potential limitations of catheter ablation in the management of AAT are discussed.

Adult↗
PubMed1991

Immediate reproducibility of electrically induced sustained monomorphic ventricular tachycardia before and during antiarrhythmic therapy.

The immediate reproducibility of sustained ventricular tachycardia induction was evaluated prospectively during 106 studies performed in 53 patients with clinical sustained monomorphic ventricular tachycardia. Programmed electrical stimulation was performed twice, using the same protocol during 53 drug-free studies and 53 subsequent studies on antiarrhythmic therapy. Sustained monomorphic ventricular tachycardia was reproduced in 104 (98%) of the 106 studies. There was no significant difference in the incidence of reproducible tachycardia in the drug-free state compared with that observed during treatment with different classes of antiarrhythmic drugs. An increase in the number of extrastimuli was required to reinitiate the tachycardia in 9 (11%) of 83 studies in which single or double extrastimuli were initially required to induce the tachycardia. In 39 (37%) of 104 studies with reproducible tachycardia induction, the two tachycardias significantly differed in electrocardiographic (ECG) configuration and cycle length. These observations suggest that the overall reproducibility of ventricular tachycardia induction is sufficiently high to provide a reliable marker for evaluating the efficacy of therapeutic interventions. However, specific tachycardia characteristics such as cycle length and ECG configuration are more variable even within the same study and may be less useful in assessing the effects of subsequent interventions.

Anti-Arrhythmia Agents↗
PubMed1991

Control of refractory ventricular tachycardia with biventricular assist devices.

A 65-year-old man developed incessant ventricular tachycardia following coronary artery bypass grafting while being weaned from cardiopulmonary bypass. The arrhythmia was refractory to procainamide, lidocaine, bretylium, and magnesium. Ventricular tachycardia subsided following reinitiation of cardiopulmonary bypass. Ultimately, the patient required ventricular assist devices to control his arrhythmia. This case is unique as the ventricular assist devices were used not for hemodynamic support, but for arrhythmia control. The mechanism of arrhythmia suppression may be related to contraction-excitation coupling.

Aged↗
PubMed1991

Localization of breakthrough site of canine monomorphic ventricular tachycardia by pacemapping. A vectorial approach.

BACKGROUND: The precision and limitations of ventricular pacemapping as a method to localize the site of earliest breakthrough of ventricular tachycardia (VT) were investigated in a canine model of experimental myocardial infarction. METHODS AND RESULTS: Forty-one episodes of VT induced in 10 animals were mapped using a standard grid of 64 endocardial and epicardial bipolar electrodes to determine the site of earliest endocardial or epicardial breakthrough of activation during VT. Each of these 64 recording sites was also used for ventricular pacing during sinus rhythm at cycle lengths comparable to those of the VTs. Orthogonal X, Y, and Z Frank electrocardiographic (ECG) leads were recorded during all episodes of VT and ventricular pacing from all sites after the chest was closed in all animals. Surface ECG waveforms corresponding to each VT and each ventricular pacing were compared pairwise by measuring the Euclidean metric difference between the VT and ventricular pacing vectors with the orthogonal ECG leads as their X, Y, and Z components. The pacing site that generated the vector most similar to VT vector (smallest vectorial difference) was defined as the predicted breakthrough site. This predicted site of breakthrough was identical to the actual site of breakthrough determined by activation sequence mapping during VT for only nine VTs (22%). However, for an additional 27 VTs (66%), the observed and predicted breakthrough locations were at adjacent (1 cm or less apart) recording sites. For five VTs (12%), the two sites were remote, the distance between them exceeding 1 cm. CONCLUSIONS: In this model, locating the breakthrough site by pacemapping is exact in only a small minority of VTs. However, when orthogonal surface ECG leads are used for comparison, pacemapping can predict the site of earliest breakthrough during VT with a 1-cm resolution in the majority of VTs.

Animals↗
PubMed1990

Electrophysiological testing and nonsustained ventricular tachycardia. Use and limitations in patients with coronary artery disease and impaired ventricular function.

Electrophysiological testing was performed in 100 consecutive patients with spontaneous asymptomatic nonsustained ventricular tachycardia, chronic coronary artery disease, and ejection fraction of less than 40%. Fifty-seven patients without inducible sustained ventricular arrhythmias were discharged on no antiarrhythmic therapy. Sustained monomorphic ventricular tachycardia was induced in 37 patients, and polymorphic ventricular tachycardia or ventricular fibrillation was induced in six patients. Of the 43 patients with inducible sustained ventricular arrhythmias, three had spontaneous cardiac arrest during serial drug testing and were excluded from further analysis. Twenty patients were discharged on drug therapy, resulting in suppression of inducible sustained ventricular arrhythmias. The remaining 20 patients with persistently inducible sustained arrhythmias were discharged on drug therapy, resulting in maximal rate slowing of the induced tachycardia. During a mean follow-up of 16.7 months, there were 10 recurrent cardiac arrests or sudden deaths. The 1- and 2-year actuarial incidence of these events was 2% and 6%, respectively, in patients without inducible sustained ventricular arrhythmias; 0% and 11%, respectively, in patients in whom inducible arrhythmias were suppressed; and 34% and 50%, respectively, in patients with persistently inducible sustained ventricular arrhythmias. Multivariate Cox analysis identified only the persistence of inducible sustained ventricular arrhythmias as a significant independent predictor of sudden death or recurrent sustained arrhythmias (p less than 0.001; relative risk, 3.5; 95% confidence intervals, 2.1-4.9). In this population, therapeutic intervention to prevent sudden death is unnecessary in patients without inducible sustained ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Catecholamine sensitive right ventricular outflow tract tachycardia: intraoperative mapping and ablation of a free-wall focus.

A patient with catecholamine-sensitive right ventricular outflow tract tachycardia refractory to pharmacological therapy underwent intraoperative mapping and cryoablation. Epicardial and endocardial mapping demonstrated earliest ventricular activation in the free-wall of the outflow tract, and cryoablation of the area resulted in surgical cure. No histologic abnormalities at the site of tachycardia origin were detected. Catecholamine sensitivity does not appear to result from a diffuse myocardial process, and permanent ablation of the tachycardia in this group of patients with a regional procedure is feasible.

Catecholamines↗
PubMed1989

Coronary revascularization and implantation of the automatic cardioverter/defibrillator: reliability of immediate intraoperative testing.

Concomitant coronary revascularization and implantation of the automatic cardioverter/defibrillator is an increasingly common procedure. To determine whether cardioversion/defibrillation thresholds measured after weaning patients from cardiopulmonary bypass are sufficient to justify immediate implantation of the pulse generator, we prospectively compared postpump values to those obtained 1 week later in five patients. R-wave amplitudes during both sinus rhythm and ventricular tachycardia, lead impedance, defibrillation thresholds and cardioversion thresholds remained stable or improved from the postpump to the 1 week values. Five other patients had the generator implanted at the time of revascularization. Immediate postbypass cardioversion thresholds (mean 10 +/- 8 joules) in these ten patients did not significantly differ from those of 20 nonpump implantations (VT mean 7 +/- joules; VF 15 +/- 4 joules and defibrillation thresholds mean 17 +/- 6 joules). These findings suggest that the residual effects of cardioplegia, core-cooling and operative ischemia have no significant effects on intraoperative testing of implanted defibrillators. This clinical experience supports the practice of immediate implantation of the pulse generator at the time of revascularization.

Cardiopulmonary Bypass↗
PubMed1988

Out-of-hospital cardiac arrest. Use of electrophysiologic testing in the prediction of long-term outcome.

We examined the role of electrophysiologic testing in the prediction of long-term outcome in 166 survivors of out-of-hospital cardiac arrest not associated with acute myocardial infarction. Ventricular arrhythmias were inducible in 131 patients (79 percent) at base line and were suppressed by antiarrhythmic drugs or surgery (or both) in 91 of 127 (72 percent). During a median follow-up period of 21 months, cardiac arrest recurred in 29 patients: 11 (12 percent) of the 91 in whom inducible arrhythmias had been suppressed (including 5 patients in whom treatment had been discontinued), 12 (33 percent) of the 36 in whom inducible arrhythmias persisted, and 6 (17 percent) of the 35 in whom arrhythmias could not be induced at the initial electrophysiologic study. Cox survival analysis identified the following three variables as significant independent predictors of recurrent cardiac arrest: persistence of inducible ventricular arrhythmias (relative risk, 3.97 [95 percent confidence interval, 1.80 to 8.75], P = 0.0006), a left ventricular ejection fraction of 30 percent or less (relative risk, 2.60 [1.21 to 5.53], P = 0.0138), and the absence of cardiac surgery (relative risk, 4.20 [0.99 to 17.77], P = 0.0512). We conclude that electrophysiologic testing is useful in quantifying the subsequent risk of cardiac arrest among survivors of out-of-hospital cardiac arrest.

Anti-Arrhythmia Agents↗
PubMed1987

Incidence and determinants of multiple morphologically distinct sustained ventricular tachycardias.

The incidence and determinants of multiple morphologically distinct ventricular tachycardias were examined prospectively in 71 consecutive patients with at least one documented spontaneous episode of sustained monomorphic ventricular tachycardia. Mean frontal and horizontal QRS axes were determined from the 12 lead electrocardiograms (ECGs) of 190 spontaneous and 352 induced tachycardias. Two or more morphologically distinct spontaneous tachycardias were observed in 19 (43%) of 44 patients who had at least two documented spontaneous episodes. In 43 (61%) of the 71 patients, multiple morphologically distinct tachycardias were induced by programmed ventricular stimulation. Overall, 57 (80%) of the 71 patients had at least two morphologically distinct tachycardias. Predictors of multiple tachycardia configurations were selected by multivariate analysis from clinical and angiographic variables and were similar for both spontaneous and induced ventricular tachycardia: presence of multiple previous myocardial infarctions (p = 0.032 spontaneous, p = 0.005 induced) and number of different antiarrhythmic drug treatments during which ventricular tachycardia was documented (p = 0.0089 spontaneous, p less than 0.0001 induced). These data demonstrate that a large majority of patients with sustained monomorphic ventricular tachycardia exhibit more than one distinct QRS configuration when adequate ECG documentation of multiple episodes is obtained during different antiarrhythmic drug treatments. In individual patients, caution should be used in attributing clinical significance to a single unique QRS configuration.

Anti-Arrhythmia Agents↗