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Biomedical subjects

J P Daubert

Publications and source records attributed to J P Daubert.

11 recordsLinked to original sources
PubMed1996

Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators.

BACKGROUND: Unsustained ventricular tachycardia in patients with previous myocardial infarction and left ventricular dysfunction is associated with a two-year mortality rate of about 30 percent. We studied whether prophylactic therapy with an implanted cardioverter-defibrillator, as compared with conventional medical therapy, would improve survival in this high-risk group of patients. METHODS: Over the course of five years, 196 patients in New York Heart Association functional class I, II, or III with prior myocardial infarction; a left ventricular ejection fraction < or = 0.35; a documented episode of asymptomatic unsustained ventricular tachycardia; and inducible, nonsuppressible ventricular tachyarrhythmia on electrophysiologic study were randomly assigned to receive an implanted defibrillator (n = 95) or conventional medical therapy (n=101). We used a two-sided sequential design with death from any cause as the end point. RESULTS: The base-line characteristics of the two treatment groups were similar. During an average follow-up of 27 months, there were 15 deaths in the defibrillator group (11 from cardiac causes) and 39 deaths in the conventional-therapy group (27 from cardiac causes) (hazard ratio for overall mortality, 0.46; 95 percent confidence interval, 0.26 to 0.82; P=0.009). There was no evidence that amiodarone, beta-blockers, or any other antiarrhythmic therapy had a significant influence on the observed hazard ratio. CONCLUSIONS: In patients with a prior myocardial infarction who are at high risk for ventricular tachyarrhythmia, prophylactic therapy with an implanted defibrillator leads to improved survival as compared with conventional medical therapy.

Adult↗
PubMed1996

Ventricular tachycardia induced cardiomyopathy: improvement with radiofrequency ablation.

Cardiomyopathy and congestive heart failure due to ventricular and supraventricular tachycardia is a well-recognized phenomenon. The mechanism of such cardiomyopathy is not clear. Ablation of the supraventricular tachycardia focus, either surgically or electrically, has been reported to result in the resolution of the left ventricular dysfunction. Similarly, the treatment of ventricular tachycardia with surgery or antitachycardia pacing has also been reported to result in improved ventricular systolic function. We present here a case of improvement in left ventricular systolic function after successful radiofrequency ablation of the ventricular tachycardia focus in the right ventricular outflow tract. We postulate that cardiomyopathy was due to the incessant or frequent ventricular tachycardia. To the best of our knowledge, this is the first such case being reported.

Aged↗
PubMed1994

Complete heart block complicating retrograde left ventricular catheterization: case report and review.

Complete heart block (CHB) following retrograde left ventricular catheterization is uncommon. We report a case of transient CHB in a patient with severe aortic stenosis and bifascicular block on the baseline surface electrocardiogram during retrograde left ventricular catheterization. The block resolved spontaneously without sequelae. A review of the literature using MedLine was performed and recommendations for temporary and permanent pacing are outlined.

Aged↗
PubMed1994

Strength-interval curves in canine myocardium at very short cycle lengths.

While ventricular electrophysiological properties have been intensively studied at normal heart rates, little is known about these properties at the very short cycle lengths (approximately 100 msec), which are present in ventricular fibrillation. We examined refractoriness in the right ventricles of six dogs at stimulation intervals of 80 to 300 msec. Starting at 300 msec, the basic (S1) cycle length was decremented by 10 msec each beat to 200, 150, or 125 msec. A 1-msec premature (S2) stimulus of 1, 5, 10, or 20 mA was then introduced. The S1-S2 interval was decremented until capture was lost. The refractory period was considered to be the shortest interval that captured the heart for each S2 strength. Only pacing episodes that did not induce fibrillation were included. Strength-interval curves maintained the same hyperbolic shape but shifted to very short refractory periods as the S1-S1 interval was decreased. At the shortest S1-S1 intervals, premature stimuli were capable of capturing the heart without inducing ventricular fibrillation for S1-S2 intervals as short as 83 +/- 3 msec. Thus, decremental rapid pacing can produce refractory periods shorter than the cycle length during ventricular fibrillation. This finding suggests that there is no need to postulate a discontinuous jump to new electrophysiological properties or relationships at the onset of fibrillation, but that the capability for fibrillation is an integral part of normal electrophysiological parameters when they are pushed to values that do not occur normally. The results of this study should be useful in the further development of active membrane models and cellular automata models of cellular electrical behavior.

Animals↗
PubMed1994

Antiarrhythmic agents in older patients. Current state of knowledge.

The treatment of ventricular arrhythmias in the elderly population is a challenging problem. Elderly patients are more predisposed to arrhythmias, are less responsive to antiarrhythmic agents and are more susceptible to the adverse effects of antiarrhythmic agents. Results from recent trial have altered the general approach to management of ventricular arrhythmias. The results of the Cardiac Arrhythmia Suppression Trials (CAST I and II) exemplified the disappointing results from numerous other studies, revealing the overall lack of efficacy of class I agents in reducing mortality in patients with coronary artery disease and asymptomatic premature ventricular complexes (PVCs). The results of CAST I and II also demonstrated the higher likelihood of older patients developing ventricular arrhythmias and toxicity to antiarrhythmic agents. Combined results of these studies have discouraged empirical antiarrhythmic therapy, especially in older patients with asymptomatic PVCs. In contrast, secondary prevention trials with beta-blockers in post-myocardial infarction patients have shown definitive survival benefit and reduction in ventricular arrhythmias, especially in the older patient population. Smaller trials with amiodarone have also shown survival benefit in post-myocardial infarction patients with or without PVCs. Management of ventricular tachycardia and fibrillation has become less empirical and more systematic with use of electrophysiologically guided and/or Holter monitor-guided therapy. Sotalol and amiodarone are especially effective agents. The efficacy of implantable cardioverter/defibrillators are also being compared with medical therapy systematically in multicentre trials. In general, empirical antiarrhythmic therapy is discouraged especially in the treatment of asymptomatic PVCs and should be reserved for systematic use in life-threatening arrhythmias.

Aged↗
PubMed1993

A fatal case of constrictive pericarditis due to a marked, selective pericardial accumulation of amyloid.

Distinguishing constrictive pericarditis from restrictive cardiomyopathy, usually due to amyloidosis, is a relatively frequent and difficult diagnostic problem. This report describes, for the first time, a patient with constrictive pericarditis caused by direct, extensive infiltration of the pericardium by amyloid, with only minimal amyloid in the myocardium, and a normal heart weight of 320 g. This patient demonstrates that amyloid may be predominantly deposited in the pericardium and actually cause constrictive pericarditis, as well as simulate its hemodynamic presentation by myocardial deposition. Given a clinical and hemodynamic presentation compatible with either constrictive or restrictive disease, an endomyocardial biopsy or other biopsy revealing amyloidosis does not necessarily rule out pericardial constriction that may be due to amyloid infiltration. The relationship between constrictive pericarditis, seen in this patient, and the other more common manifestations of amyloid heart disease, and the hemodynamic profiles of amyloid cardiomyopathy and constrictive pericarditis are reviewed.

Aged↗
PubMed1993

Epicardial mapping of ventricular defibrillation with monophasic and biphasic shocks in dogs.

To study the mechanism of defibrillation and the reason for the increased defibrillation efficacy of biphasic waveforms, the potential gradient in a 32 x 30-mm region of the right ventricle in 15 dogs was progressively lowered in four steps while a strong potential gradient field was maintained throughout the rest of the ventricular myocardium. The volume of right ventricle beneath the plaque was 10 +/- 2% of the total ventricular mass. A 10-msec monophasic (eight dogs) or 5/5-msec biphasic (seven dogs) truncated exponential shock 30% above the defibrillation threshold voltage was given via electrodes on the left ventricular apex and right atrium to create the strong potential gradient field. Simultaneously, a weaker shock with the same waveform but opposite polarity was given via mesh electrodes on either side of the small right ventricular region to cancel part of the potential difference in the region and to create one of the four levels of potential gradient fields. Shock potentials and activations were recorded from 117 epicardial electrodes in the small region, and in one dog global epicardial activations and potentials were recorded from a sock containing 72 electrodes. Each gradient field was tested 10 times for successful defibrillation after 10 seconds of electrically induced fibrillation. For both monophasic and biphasic shocks, the percentage of successful defibrillation attempts decreased (p < 0.05) as the potential gradient decreased in the small region. Defibrillation was successful approximately 80% of the time for a mean +/- SD potential gradient of 5.4 +/- 0.8 V/cm for monophasic shocks and 2.7 +/- 0.3 V/cm for biphasic shocks (p < 0.05). No postshock activation fronts arose from the small region for eight waveform when the gradient was more than 5 V/cm. For both waveforms, the postshock activation fronts after the shocks were markedly different from those just before the shock and exhibited either a focal origin or unidirectional conduction.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

High and low strength nonsynchronized shocks given during canine ventricular tachycardia.

UNLABELLED: Cardioversion shocks given during ventricular tachycardia may cause ventricular fibrillation or acceleration of ventricular tachycardia, or arrest the tachycardia. A recently proposed theory may explain why the former two phenomena may occur. Briefly, this theory states that potential gradient shock fields of a critical strength delivered to tissue with a critical degree of refractoriness will cause circulating wave fronts of ventricular activation ("rotors") manifest as ventricular arrhythmia. We tested this theory by delivering nonsynchronized shocks 50% higher than defibrillation threshold or 50% lower than defibrillation threshold during 275 episodes of ventricular tachycardia in eight dogs with 5- to 7-day-old myocardial infarcts. Shocks stronger than the defibrillation threshold are likely to create shock fields in the ventricles everywhere stronger than this critical value, and therefore would not generate rotors. Shocks less strong than the defibrillation threshold may create shock fields within the ventricles that include the critical value, and therefore cause rotors if given when critically refractory tissue is present. Nonsynchronized shocks were used to increase the likelihood of encountering tissue with a critical degree of refractoriness. Ventricular fibrillation or acceleration of ventricular tachycardia occurred following 83 of 138 (60%) low strength shocks and following 20 of 137 (14.6%) high strength shocks. The pooled odds ratio for induction of ventricular fibrillation or accelerated ventricular tachycardia after low strength shocks as compared to high strength shocks was 8.9. CONCLUSION: when given during ventricular tachycardia, low strength shocks are much more likely to cause ventricular fibrillation or accelerated ventricular tachycardia than are high strength shocks (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Response of relatively refractory canine myocardium to monophasic and biphasic shocks.

BACKGROUND: Certain biphasic waveforms defibrillate at lower energies than monophasic waveforms, although the mechanism is unknown. METHODS AND RESULTS: The relative ability of monophasic and biphasic shocks to stimulate partially refractory myocardium was compared because defibrillation is thought to involve stimulating relatively refractory myocardial tissue. Shocks of 25-125 V were given during regularly paced rhythm in 11 open-chest dogs. Computerized recordings of shock potentials, and of activations before and after the shocks, were made at 117 epicardial sites. To quantify the shock field strength, the shock potential gradients were calculated at the electrode sites. Monophasic action potential (MAP) electrode recordings, obtained in five dogs, confirmed direct myocardial excitation by the shock, that is, activations beginning during the shock. Tissue was directly excited up to 4 cm from the shocking electrode, and the area directly excited increased as the shock was made stronger or given less prematurely. In six dogs, strength-interval curves for direct excitation were determined from plots of potential gradient versus refractoriness at each electrode site. The biphasic curves were located to the right of the monophasic curves by 8 +/- 4 msec, indicating a lesser ability to excite refractory myocardium. When the gradient at the directly excited border was at least 3.8 +/- 1 V/cm, conduction failed to propagate away from the directly excited zone after the shock, and MAP recordings made near the border showed a shock-induced graded response. This graded response, which prolonged repolarization, may have been responsible for the failure of conduction from the directly excited zone. Although better for defibrillating, the biphasic waveform was thus less effective than the monophasic one in exciting relatively refractory myocardium. CONCLUSIONS: These results indicated that waveform selection for defibrillation should not be guided solely by the ability of the waveform to stimulate tissue, as these two properties can be discordant.

Action Potentials↗
PubMed1990

Conduction disturbances caused by high current density electric fields.

During internal defibrillation, potential gradients greater than 100 V/cm occur near defibrillation electrodes. Such strong fields may cause deleterious effects, including arrhythmias. This study determined 1) the effects of such strong fields on the propagation of activation and 2) whether these effects were different for monophasic and biphasic shocks. Voltages and potential gradients during the shock, as well as activation sequences before and after the shock, were mapped from 117 epicardial electrodes placed over a 3 x 3-cm area on the right ventricle in six dogs. Pacing at a cycle length of 350 msec was given from a long narrow electrode on the right side of the mapped area to generate parallel activation isochrones. A monophasic shock, 10 msec in duration, or a biphasic shock with both phases 5 msec in duration was delivered 300 msec after the last paced stimulus via a mesh electrode on the left side of the mapped area as the cathode, with the anode on the right atrium. Shocks of 70-850 V were given, and the potential gradient and current density at each recording electrode were calculated from the measured potentials and fiber orientation by using a finite element method. Pacing was resumed 200 msec after the shock, and activation sequences were mapped for up to 5 minutes. Potential gradients ranged from 1 to 189 V/cm with high fields on the left side and low fields on the right side of the mapped area. Where the potential gradient was weak, the first activation sequence after the shock was similar to that before the shock, but activation blocked without conducting into areas where the gradient was greater than 64 +/- 4 (mean +/- SD) V/cm for monophasic and greater than 71 +/- 6 V/cm for biphasic shocks. These values are significantly different (p less than 0.003). The higher the potential gradient, the longer was the duration of block before conduction returned. Block duration, however, was generally shorter for biphasic than for monophasic waveforms of the same field strength. In conclusion, conduction block can follow either waveform, but biphasic waveforms cause less block than monophasic waveforms. This effect may partially explain the increased defibrillation efficacy of biphasic shocks.

Animals↗