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Biomedical subjects

A E Epstein

Publications and source records attributed to A E Epstein.

At least 109 records · Page 6Linked to original sources
PubMed1988

Effect of catheter ablation of the atrioventricular junction on quality of life and exercise tolerance in paroxysmal atrial fibrillation.

The effect of catheter ablation of the atrioventricular junction (AV) and implantation of a rate-adaptive pacemaker on quality of life and exercise capacity was evaluated prospectively in 12 consecutive patients with paroxysmal atrial fibrillation (AF). All patients had been demonstrated to have paroxysmal AF that was refractory to medical therapy over a long period of time (mean 9 +/- 7 years). Patients performed a symptom-limited treadmill exercise test on the day before catheter ablation and 6 weeks after hospital discharge. Quality of life was measured using the physical dimension of the McMaster Health Index Questionnaire and the Psychological General Well-Being Index before and 6 weeks after ablation. There were no serious complications related to catheter ablation or permanent pacemaker implantation. All patients remain in complete AV block with a completely paced rhythm at a mean follow-up of 8 +/- 2 months. The McMaster Health Index scores increased from a mean of 0.69 +/- 0.20 before to 0.92 +/- 0.14 after ablation (p = 0.002). The mean Psychological General Well-Being score improved from 59.8 +/- 14.8 at baseline to 84.9 +/- 13.6 6 weeks after discharge (p = 0.001). Treadmill exercise duration increased from 6.4 +/- 4.6 to 9.9 +/- 2.6 minutes (p = 0.03) and correlated strongly with changes in functional capacity measured with the McMaster Health Index (r = 0.70, p = 0.03). These results suggest that catheter ablation of the AV junction and implantation of a rate-adaptive pace-maker significantly improve the quality of life and exercise capacity of patients with paroxysmal AF refractory to medical therapy.

Aged↗
PubMed1988

Intermediate-term results of the endocardial surgical approach for anomalous atrioventricular bypass tracts.

Between October 1974 and March 1, 1985, 26 patients with 29 anomalous AV bypass tracts underwent surgical treatment at the Medical Center of UAB, with follow-up from 1 to 14 years. Eleven of the patients underwent surgical correction of major associated cardiac anomalies. One patient had His bundle ablation, and 25 patients had direct surgical division of 28 bypass tracts with the use of an endocardial approach. Successful division was achieved in 27 (96%; confidence limits 88% to 99%) of 28 bypass tracts identified pre- and intraoperatively. There were no hospital deaths, but on formal follow-up there were three late deaths, all occurring in patients with major associated cardiac pathology. Neither preexcitation nor reciprocating tachycardia recurred, and functional status was excellent among patients without associated cardiac lesions. Because of the safety and, at least on intermediate-term follow-up, apparently curative nature of this operation (particularly for patients without other major cardiac pathology), surgical treatment is recommended for patients with bypass tracts having lethal potential, those with reciprocating tachycardia unresponsive to drugs, and to symptomatic patients facing many years of medications.

Adult↗
PubMed1988

Region of slow conduction in sustained ventricular tachycardia: direct endocardial recordings and functional characterization in humans.

Direct endocardial recording from a discrete region of slow conduction in the left ventricle was performed in a patient during sustained ventricular tachycardia. The tachycardia had a right bundle branch block and superior axis configuration with the earliest site of endocardial activation in the posterolateral left ventricle. At this site, the left ventricular electrogram during the tachycardia displayed two deflections with distinctly different responses to rapid pacing. During rapid pacing from the right ventricular apex, one deflection was transiently entrained, representing activation of the ventricle distal to a region of slow conduction in the reentrant circuit. However, the other deflection was not entrained and arose from activation proximal to this region. At a critically rapid pacing rate, interruption of the tachycardia was associated with conduction block in the region of slow conduction, as demonstrated by dissociation of the two deflections on the posterolateral left ventricular electrogram. At pacing rates that transiently entrained but did not terminate the tachycardia, decremental properties of conduction were demonstrated in the region of slow conduction, but not in the rest of the reentrant circuit. These responses of the posterolateral left ventricular electrogram to pacing during ventricular tachycardia strongly suggest that the recordings bracketed a discrete region of slow conduction in the left ventricle that was critical for the maintenance of ventricular tachycardia. Furthermore, these data demonstrate that this region of slow conduction in the left ventricle had decremental conduction properties and was the site of block during rapid pacing at rates sufficient to interrupt the tachycardia.

Bundle-Branch Block↗
PubMed1988

Incidence of reentry with an excitable gap in ventricular tachycardia: a prospective evaluation utilizing transient entrainment.

The demonstration of transient entrainment has been proposed as evidence of reentry, with an excitable gap as the probable mechanism of tachycardia. A prospective series of 27 consecutive patients with sustained ventricular tachycardia induced by programmed electrical stimulation was studied to determine the frequency with which transient entrainment can be demonstrated and to define the optimal location of pacing and recording electrodes. In all patients, electrodes for pacing and recording were placed in both the left and right ventricles during electrophysiologic study. Among the 19 patients in whom the response to rapid pacing could be evaluated (25 episodes of ventricular tachycardia), transient entrainment was demonstrated in 79% (76% of episodes). Ten of 12 episodes of ventricular tachycardia with a left bundle branch block QRS configuration in lead V1 and 9 of 13 episodes with a right bundle branch block QRS configuration could be transiently entrained (p = NS). Transient entrainment was demonstrated for 8 of 11 episodes of ventricular tachycardia with a left bundle branch block configuration during pacing from the left ventricle, but for only 2 of 10 episodes during pacing from the right ventricular apex (p less than 0.05). Conversely, 9 of 13 episodes of ventricular tachycardia with a right bundle branch block configuration were transiently entrained during pacing from the right ventricular apex, but 0 of 10 episodes were transiently entrained by left ventricular pacing (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Comparison of unipolar and bipolar active fixation atrial pacing leads.

The purpose of this investigation was to compare the acute pacing and sensing characteristics of a new bipolar active fixation atrial pacing lead with those of a unipolar atrial lead of similar design. Pacing threshold voltage and current, lead impedance, and atrial electrogram amplitude and slew rate were measured at the time of surgery in 28 consecutive patients undergoing DDD pacing system implantation. Eleven patients received a Medtronic 6957J-58 unipolar active fixation atrial lead and 17 patients were given a Medtronic 4016-58 bipolar lead. Both leads are polyurethane-insulated with the distal electrode being a platinum alloy screw-helix with a surface area of 8.0 mm2. There were no significant differences in the threshold voltage (1.01 V unipolar versus 1.05 V bipolar) or current (1.93 mA unipolar versus 1.78 mA bipolar) of the two leads. The mean impedance of the bipolar active fixation lead was 618 ohms compared to 479 ohms for the unipolar lead (p = 0.02). The mean amplitude of the atrial electrogram was 4.64 mV for the bipolar lead and 3.11 mV for the unipolar lead (p = 0.02). The atrial electrogram exceeded 5 mV in 10 of 17 patients with the bipolar lead but zero of 11 with the unipolar lead. There was no significant difference in the mean slew rate of the leads (1.09 V/s bipolar versus 0.73 V/s unipolar; p = 0.18). Over a follow-up period of up to 10 months, all patients remained in either the DDD or DDI modes with no episodes of atrial sensing or pacing failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Failure of elective replacement indicator to predict end-of-life of the automatic implantable cardioverter-defibrillator.

A major limitation in the use of the automatic implantable cardioverter-defibrillator (AICD) is limited battery longevity and the absence of an accurate and precise end-of-life indicator. An elective replacement indicator, or ERI, was proposed by the manufacturer of the AICD in 1985. This ERI was evaluated in nine patients with AICDs. The ERI was exceeded at a mean of 10.9 +/- 3.0 months after implantation. Although 0.6 +/- 0.4 months of battery life were predicted to remain before battery failure, the devices were followed for 6.0 +/- 3.8 months (p = 0.002) during which time no device failed. Although 28.9 +/- 21.9 seconds of charging time were predicted to remain, 103.5 +/- 67.9 seconds were shown to be available by magnet charge time testing (p = 0.01). Thus, the ERI of the AICD, as originally proposed by its manufacturer, consistently underestimated both the predicted time to end-of-life as well as the cumulative charging time remaining before end-of-life for each AICD examined. We propose that this ERI not be used to predict end-of-life of the AICD. A "new" ERI has been recommended.

Adult↗
PubMed1987

Phenytoin in the treatment of inducible ventricular tachycardia: results of electrophysiologic testing and long-term follow-up.

Phenytoin treatment of inducible ventricular tachyarrhythmias was assessed by serial electrophysiologic studies (EPS) in 64 patients with spontaneous ventricular tachycardia, cardiac arrest, or symptoms compatible with a ventricular tachyarrhythmia. Coronary artery disease was the primary cardiac disease in 75% of the patients. All subjects had either inducible ventricular tachycardia (greater than or equal to 10 repetitive beats) or ventricular fibrillation at electrophysiologic study. Phenytoin was administered intravenously in 38 studies and orally in 31 studies. The mean serum phenytoin level was 19.5 +/- 4.7 mcg/ml. Only seven patients (11%) had a negative electrophysiologic study (less than or equal to 10 repetitive beats) after the administration of phenytoin and were classified as phenytoin responders (group I). The remaining 54 patients (89%) were classified as nonresponders (group II). For the nonresponders, phenytoin increased the cycle length of identical monomorphic ventricular tachycardias from a mean of 31 ms to a mean of 327 ms (p less than 0.001). For the four patients tested receiving both intravenous and oral phenytoin, the intravenous response always predicted the oral response. For the seven patients in whom electrophysiologic study indicated phenytoin efficacy, two are alive and arrhythmia-event free, two had sudden death when the regimen was changed (one case, quinidine added; one case, subtherapeutic serum level), and three died from nonarrhythmic causes. For the 10 patients treated empirically with phenytoin, either alone (seven patients) or in combination with another antiarrhythmic agent (three patients), four died secondary to an arrhythmic event.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Demonstration of the presence of slow conduction during sustained ventricular tachycardia in man: use of transient entrainment of the tachycardia.

To test the hypothesis that an area of slow conduction is present during reentrant ventricular tachycardia in man, and that the earliest activation site during ventricular tachycardia is within or orthodromically just distal to the area of slow conduction in the reentry loop, we studied 12 episodes of ventricular tachycardia (mean rate 185 +/- 32 beats/min) that were induced in nine patients with ischemic heart disease. Rapid ventricular pacing was performed at selected sites during ventricular tachycardia while recording electrograms from an early activation site relative to the onset of the QRS complex (site A) and from a site close to the pacing site (site B). Rapid pacing from the right ventricular apex during ventricular tachycardia with a right bundle branch block pattern and from selected left ventricular sites during ventricular tachycardia with a left bundle branch block pattern (mean pacing rate 202 +/- 38 beats/min) resulted in constant ventricular fusion beats on the electrocardiogram except for the last captured beat (i.e., the ventricular tachycardia was entrained) in 11 of 12 episodes. During entrainment: sites A and B were activated at the pacing rate, conduction time from the last pacing impulse to the last captured ventricular electrogram at site A (St-A interval) was 359 +/- 69 msec and spanned the diastolic interval, while that at site B (St-B interval) was only 28 +/- 13 msec, site A had the same ventricular electrogram morphology as that during ventricular tachycardia, while site B had a different electrogram morphology, indicating that site A was activated in the same direction during entrainment as during ventricular tachycardia. Eight episodes of ventricular tachycardia were entrained at two or more different pacing rates. The St-A interval increased during pacing at the faster rate(s) in four of eight episodes, while the St-B interval remained unchanged. Rapid ventricular pacing performed from the same site during sinus rhythm (mean pacing rate 201 +/- 37 beats/min) resulted in an St-A interval of 103 +/- 37 msec (p less than .001 vs the value during entrainment) and an St-B interval of 31 +/- 15 msec (p = NS vs the value during entrainment). It is concluded that an area of slow conduction not demonstrable during sinus rhythm exists during ventricular tachycardia, and that the earliest activation site during ventricular tachycardia is at or orthodromically distal to this area of slow conduction.

Aged↗
PubMed1987

Symptomatic spinal epidural lipomatosis as a complication of steroid immunosuppression in cardiac transplant patients. Report of two cases.

Patients with Cushing's syndrome may develop spinal epidural lipomatosis, an abnormal accumulation of fat in the spinal epidural space. This accumulation of fat may cause compression of the spinal cord or cauda equina with resulting neurological deficit. Two cases of symptomatic spinal lipomatosis are reported in cardiac transplant patients receiving chronic corticosteroid treatment. The literature is reviewed, and diagnostic and therapeutic considerations are discussed.

Adrenal Cortex Hormones↗
PubMed1986

"Incessant" atrioventricular (AV) reciprocating tachycardia utilizing left lateral AV bypass pathway with a long retrograde conduction time.

Two patients with incessant or nearly incessant episodes of atrioventricular (AV) reciprocating tachycardia were studied and were found to be unique because of the location of a slowly conducting retrograde AV bypass pathway in the left lateral position. During the tachycardia in both patients, negative P waves were present not only in ECG leads II, III, and aVF, but also in leads I and aVL. The R-P'/P'-R ratios were 1.3 and 1.9, respectively. Cardiac electrophysiologic study revealed that in both tachycardias, retrograde ventriculoatrial conduction occurred utilizing a concealed left lateral AV bypass pathway with a long conduction time. Verapamil prolonged conduction over the AV bypass pathway in both patients. One patient was successfully treated with oral verapamil. The other patient underwent successful surgical interruption of the AV bypass pathway.

Adult↗
PubMed1985

Cellular characteristics of neoplastic angioendotheliosis. An immunohistological marker study of 6 cases.

Neoplastic angioendotheliosis (NAE) is a rare, mostly fatal disease characterized by proliferation of large blastoid cells in small vessels of various organs. The origin of neoplastic cells remain undetermined. In this study, cell markers were studied immunohistologically on paraffin sections of six cases of NAE, by applying avidin-biotin-peroxidase (ABC) method and five antibodies which can demonstrate marker antigens on formalin fixed and paraffin embedded specimens. It was shown that the neoplastic cells were heavily stained with an anti-B lymphocyte monoclonal antibody LN-1 (6/6), moderately stained with another anti-B lymphocyte antibody LN-2 (5/6) and heavily stained with a monoclonal antibody which reacts with all levels of leukocytes (Dako-LC) (6/6). The cells did not show positive reaction with an anti-myelomonocytic antibody anti-Leu M1. The reaction against anti-Factor VIII, which can depict endothelial cells, was mostly negative, and if positive, was faint and indefinite, leading to an assumption that the reaction was against antigens in serum and not against neoplastic cells. These results suggest that the neoplastic cells of NAE are in the B lymphocyte lineage.

Antibodies, Heterophile↗
PubMed1985

Further observations on transient entrainment: importance of pacing site and properties of the components of the reentry circuit.

Transient entrainment of circus-movement tachycardia utilizing an atrioventricular (AV) bypass pathway was studied in 13 patients (nine with the orthodromic form, two with the antidromic form, and two with both the orthodromic and antidromic forms). All patients had a left-sided AV bypass pathway. Pacing at selected rates faster than the spontaneous rate was performed during the tachycardia at a site proximal or distal to the AV node, an area of slow conduction within the reentry loop. Rapid pacing from a site proximal to the AV node (from the right atrium during the orthodromic form of the arrhythmia or the right ventricle during the antidromic form of the arrhythmia) always demonstrated at least one of the three entrainment criteria: constant fusion beats except for the last captured beat, which was entrained but not fused (first criterion); progressive fusion (second criterion); localized conduction block to a site(s) for 1 paced beat associated with interruption of the tachycardia followed by activation of that site(s) by the next paced beat from a different direction and with a shorter conduction time (third criterion). In contrast, rapid pacing from a site distal to the AV node (from the right ventricle during the orthodromic form of the arrhythmia, or the right atrium during the antidromic form of the arrhythmia) transiently entrained the tachycardia, but never demonstrated any entrainment criteria because the antidromic wave front from the pacing impulse always blocked in the AV node (concealed entrainment). We conclude that the location of the pacing site relative to the components of a reentry loop is critical to the demonstration of the criteria of transient entrainment; i.e., if it is proximal to an area of slow conduction and/or unidirectional block within a reentry loop, transient entrainment should be demonstrable, but if it is distal, it will not be demonstrable.

Adolescent↗
PubMed1985

Transient paradoxical renal vasoconstriction following cardiac operation. Treatment with volume depletion.

Following cardiac operation complicated by inferior myocardial injury, a patient developed normal cardiac output congestive heart failure associated with severe renal vasoconstriction, oliguria and azotemia. The patient's renal dysfunction responded to volume depletion with hemofiltration. These paradoxical renal responses to volume changes may be caused by transiently altered cardiac volume receptor thresholds or afferent signals resulting in cardiorenal dysfunction.

Constriction, Pathologic↗
PubMed1985

Significance of transient entrainment in pacing treatment of tachyarrythmias.

Rapid pacing techniques can be used to interrupt reentrant tachyarrhythmias whose reentry circuit includes an excitable gap. These rhythms include classic atrial flutter (Type I), ectopic atrial tachycardia, AV nodal reentrant tachycardia, AV junctional reentrant tachycardia involving an AV bypass pathway, ventricular tachycardia, and probably sinus node reentrant tachycardia. When utilizing rapid pacing techniques to interrupt any of these arrhythmias, it is necessary to pace at a critically rapid rate, and then for a critical duration of time at that rapid rate in order to interrupt the tachycardia. Pacing at rates short of the critically rapid rate, or short of the critical duration, will simply transiently entrain the tachycardia to the pacing rate without interrupting it. Therefore, when such pacing is terminated, the tachycardia will resume promptly at its previous spontaneous rate. Furthermore, for some arrhythmias, pacing may be achieved at an appropriately rapid rate to interrupt the tachycardia and the pacing may be maintained for an appropriate period of time. However, in the latter instances, the phenomenon of termination and reinitiation of the arrhythmia sometimes may occur, in which case cessation of pacing is not associated with interruption of the arrhythmia. Knowledge of this phenomenon is important when using either permanent or temporary pacing techniques to interrupt reentrant arrhythmias.

Atrial Flutter↗