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Biomedical subjects

D Tepper

Publications and source records attributed to D Tepper.

At least 37 records · Page 2Linked to original sources
PubMed1987

Evaluation of dosing interval and optimum dose of cibenzoline.

Fifteen patients with ventricular premature complexes (VPCs) were included in this open study designed to assess the relative efficacy of bid (two times daily) and tid (three times daily) dosing regimens for cibenzoline as compared with qid (four times daily) administration. Patients started therapy with qid administration; this was followed in sequence by tid and bid administration at the maximum effective total daily dose determined during the qid administration. Of the nine patients evaluated for efficacy for suppression of VPCs, eight demonstrated a 75% or greater suppression of VPCs with cibenzoline administered qid (total daily dose of 130-325 mg). This effectiveness was maintained in four patients with a bid regimen and in three with a tid regimen. All four patients who had ventricular tachycardia (VT) had a decrease in the number of VT episodes while receiving cibenzoline (only one of these patients had satisfactory suppression of VPCs at the same dosage regimen). Twelve patients continued to receive extended therapy with cibenzoline for up to two years, as this was considered to be the optimum antiarrhythmic treatment for these patients. Two patients had to be removed from the study and two had the dosage lowered because of adverse reactions (dry mouth, blurred vision, dizziness, congestive heart failure) although in one instance, the congestive heart failure was subsequently considered to be unrelated to cibenzoline. One patient was able to complete the short-term phase of the trial, but was not given extended treatment because of persistent dry mouth. Two patients had treatment discontinued during the extended therapy phase because of adverse reactions (fever, nausea, vomiting, asthenia).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Chronic flecainide therapy selected by electrophysiology testing of intravenous flecainide.

The utility of flecainide acetate was evaluated in 93 patients by means of electrophysiologic studies before and after intravenous flecainide administration to determine long-term efficacy. Twenty patients had a prior history of at least one cardiac arrest and 73 patients had sustained ventricular tachycardia (VT). The mean radionuclear ejection fraction was 32 +/- 5%. Flecainide was evaluated in 93 patients, with 44 patients no longer having VT following flecainide (47% efficacy). Procainamide was evaluated in 69 patients; 24 patients had an adverse reaction to reaction to procainamide and 28 of the 69 patients were protected on procainamide (40% efficacy). The mean serum concentration of flecainide achieved in the protected group was 298 +/- 36 ng/ml and 4.3 micrograms/ml for procainamide. Both flecainide and procainamide significantly prolonged refractoriness, lengthened QRS duration, while only procainamide increased the QT interval. All 93 patients were discharged on antiarrhythmic therapy, 42 on flecainide, 27 on other antiarrhythmic therapy guided by electrophysiologic testing, and 24 on amiodarone (when all other agents failed). Six of the 42 patients on flecainide complained of adverse side effects, but none were severe enough to warrant stopping therapy. Of the 42 patients on flecainide, four (9%) died suddenly over 18 +/- 4 months. Twenty-seven patients were on other therapy; eight of these have died, three suddenly (11%), four with myocardial infarctions, and one due to congestive heart failure. Twenty-four patients started amiodarone; 11 have died, five (21%) suddenly, four of congestive heart failure, one of pulmonary fibrosis, and one with myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Use of the Israeli Standardized Denver Developmental Screening Test in the maternal and child health services--assessment of its predictive value.

The translated version of the Denver Developmental Screening Test (DDST) for screening a total population of infants at 6 months of age was used in the Maternal and Child Health Services of the Department of Social Medicine. The failure rate was 18%. In subsequent birth cohorts, the Israeli Standardized Denver Developmental Screening Test (IDDST) was applied, and the failure rate was 3%. The results of 176 infants tested with the IDDST were transcribed on the DDST forms. Sensitivity and predictive values were appraised in relation to the developmental quotient (DQ) at age 2 as assessed by the Brunet-Lezine Developmental Test. Using a cutoff point of 2 SD below the mean DQ as the criterion, sensitivity and predictive value were 25 and 13%, respectively. The sensitivity and predictive value of the IDDST increased when the cutoff point was changed to -1 SD. The biserial correlation coefficient between the DDST at 6 months of age and the DQ score at 2 years was 0.37 and that between the IDDST and the DQ was 0.28. The predictive value of infant tests and the need for reevaluation of the IDDST for 6-month-old infants is discussed.

Child Development↗
PubMed1986

Flecainide: a new antiarrhythmic agent.

PVCs (trigger mechanisms) and the vulnerability of the myocardium to sustain a life-threatening ventricular tachycardia (substrate) are two variables in the sudden death equation. Physicians treating patients at risk for sudden death should consider PVC frequency and vulnerability as interrelated variables. Risk assessment must take into consideration both variables. Antiarrhythmic drug efficacy can be assessed in terms of a reduction in trigger mechanisms (PVCs) as well as decreasing myocardial vulnerability (induction of VT at PES). Flecainide acetate, at a reduced dosage of 100 mg twice daily, is effective in both aspects, markedly decreasing PVC frequency and preventing VT induction at PES testing. Holter monitoring and electrophysiologic testing evaluate different aspects of the problem. With the addition of an agent as potent as flecainide, which is devoid of many of the bothersome side effects previously limiting antiarrhythmic therapy, an agent is now available that may be useful to treat both the trigger mechanism and the substrate in sudden death. We must be careful not to worsen the situation through the profound effects of flecainide on depolarization and refractoriness that in some patients cause life-threatening arrhythmias to be more frequent.

Animals↗
PubMed1986

QT prolongation and the antiarrhythmic efficacy of amiodarone.

Amiodarone is an antiarrhythmic agent known to cause prolongation of action potential duration which is reflected in the electrocardiogram as a prolongation of the QT interval. Prolongation of the QT interval in patients dying suddenly was compared with that in patients who remained alive to determine whether a difference existed between these two groups. The electrocardiogram and amiodarone levels were evaluated in 33 patients who presented with cardiac arrest and symptomatic ventricular tachycardia in whom no other antiarrhythmic agent was found effective in preventing induction of ventricular tachycardia during electrophysiologic studies. There were 30 men and 3 women (mean age 52 +/- 10 years). Twenty-three are alive after a mean follow-up period of 12 +/- 7 months. Ten died: six suddenly, three of non-cardiac causes and one of congestive heart failure. Using a two-way analysis of variance, the percent change in QT, QTc, JT and JTc intervals before and after amiodarone therapy was analyzed. Marked prolongation in the QT interval was present in patients who remained alive with amiodarone therapy. A significant difference in percent QT prolongation was seen between the latter patients and those who died suddenly (p less than 0.005). No difference was observed in the percent change in QRS interval between the two groups. The levels of amiodarone (2.5 versus 3.2 micrograms/ml) and its metabolite (desethylamiodarone) were not significantly different between the living patients and those who died suddenly. These findings suggest that a prolongation of the QT interval may be a marker for the therapeutic antiarrhythmic effect of amiodarone.

Aged↗
PubMed1986

Excitation-contraction coupling in rat myocardium: alterations with long term ethanol consumption.

The mechanical and electrical effects of chronic ethanol consumption were studied in rats maintained on 40% ethanol and water solution (40% of caloric intake) for a 30 week period and in controls. Left ventricular papillary muscles from male Wistar rats were studied by myography at 30 degrees C, 0.1 Hz stimulation, and external calcium concentration of 2.4 mmol X litre-1. No significant difference was found between alcoholic and control rats with regard to resting tension. Developed tension, time to peak tension, time to one half relaxation, and time to peak shortening were, however, significantly decreased in preparations from the study animals. Velocity of shortening and relengthening at all relative loads studied were depressed in alcoholic preparations. No significant difference was found in action potential between the two groups with regard to resting membrane potential, action potential amplitude, overshoot, or maximum rate of rise of the upstroke. In contrast, the duration at 50% (APD50) and 75% (APD75) of total repolarisation was significantly shorter for action potential in the alcoholic group than in the controls. Thus chronic ethanol ingestion results in an inability to develop normal levels of force, depressed force-velocity relation, and shortening of action potential duration.

Action Potentials↗
PubMed1986

Effects of hypothyroidism and hypoparathyroidism on rat myocardium: mechanical and electrical alterations.

The mechanical and electrical effects of hypoparathyroidism (Px), hypothyroidism (Tx), and hypothyroidism combined with hypoparathyroidism (TPx) were investigated by comparing simultaneously recorded transmembrane action potentials and isometric and isotonic contractions recorded from the myocardium. Left ventricular papillary muscles from male Wistar rats were studied electrically and mechanically in a muscle bath at 30 degree C, stimulated at 0.1 Hz and external calcium = 2.4 mM. No significant difference was found between control (C), Px, Tx, and TPx preparations with regard to resting tension and developed tension. However, time to peak tension, time to one half relaxation and time to peak shortening were significantly increased in preparations from animals that were Px, Tx, and TPx as compared with age-matched controls. Maximum velocities of shortening (Vs) and relengthening (Vr) at all relative loads studied were significantly depressed in Px preparations when compared with those of C muscles. A greater depression was found in the Tx muscle and still greater depression of these indices was noted in TPx muscles. No significant difference was found between C, Px, Tx, and TPx action potential with regard to resting membrane potential (RMP), action potential amplitude (AMP), overshoot (OS), or maximum rate of rise of the upstroke (Vmax).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1985

Prolonged repolarization: a historical perspective.

This symposium will more fully discuss QT prolongation--an area of controversy--prolonged QT syndromes, and new groups of agents that prolong repolarization and the QT interval (calcium blockers and antiarrhythmic agents). This is an important evolving field with old biases confronting a new and more thorough understanding of the phenomenon of prolonged repolarization.

Anti-Arrhythmia Agents↗
PubMed1985

Size and shape of enzymatically isolated ventricular myocytes from rats and cardiomyopathic hamsters.

Rod-shaped and branched ventricular myocytes from rats and cardiomyopathic hamsters (strain 53.58) were isolated enzymatically, and their widths and lengths were measured in physiological salt solutions containing normal levels of calcium (2.5 mmol). In rats of approximately 200 g body weight, the average myocyte width and length are 25 micron and 115 micron. The isolated cells are also classified according to shape with nearly 50% branched or otherwise irregular. Myocytes of the hearts of the 53.58 strain of cardiomyopathic hamsters at 7 months of age are significantly larger than control hamsters of the same age, indicating that cellular hypertrophy has occurred. Estimates of the number of cells in the ventricles indicate that there is a cell loss of nearly 13% in the myopathic heart. A consideration of the significance of wider and longer myocytes with undiminished myofibrillar mass lead to the conclusion that the decreased contractility displayed by the cardiomyopathic hamster heart must be due, at least in part, to functional defects in the myofibrillar apparatus, in the system of activation, or in cellular integration.

Age Factors↗
PubMed1985

Therapy for late post infarction ventricular tachycardia.

Non-sustained ventricular tachycardia (VT) in the late post myocardial infarction (MI) period (7-21 days) has been reported to be a predictor of sudden death. We suspected that patients with 3 beat VT on Holter monitoring in the late infarction period would demonstrate electrical instability at electrophysiologic studies. Forty-seven patients were identified as having at least 3 beat VT on Holter monitoring. Eighteen patients refused electrophysiologic studies or were not referred by their attending physician. The mean ejection fraction of this group was 43 +/- 16%. Eight patients have died, 3 sudden deaths in 13 +/- 5 months, a 17% incidence of sudden death. Twenty-nine patients underwent invasive electrophysiologic studies. Their mean ejection fraction was 37 +/- 7%, and 28 had inducible, 18 sustained ventricular tachycardia and 10 non-sustained VT. No complications were noted with electrophysiological testing in the post infarction patients. Using programmed electrical stimulation studies an effective antiarrhythmic agent preventing VT induction (usually experimental) could be found for each patient. After a mean follow-up of 12.5 +/- 4 months, the patient without inducible VT is alive and 26 of the 28 "inducible" patients are alive and well. Two patients died, one of stroke and one due to pump failure following a second MI. No sudden deaths were observed in this group. Two patients had breakthrough arrhythmias and were treated by alternative antiarrhythmic therapy that was also effective at the initial electrophysiologic studies. Thus, PES studies post MI are safe and may be an effective way to assess therapy for patients in the early post MI period, identified at high risk for sudden death.

Aged↗
PubMed1985

Long term lorcainide therapy guided by electrophysiology studies.

One hundred patients inducible at electrophysiologic studies underwent serial drug testing with procainamide, lidocaine and lorcainide to determine comparative efficacy. Acute intravenous administration was followed by repeat programmed electrical stimulation (PES) studies on separate days for each antiarrhythmic drug. Lorcainide prevented VT induction in 69% of the 100 patients studied, procainamide was effective in 50% of the 75 patients studied, and lidocaine prevented VT induction in 30% of 53 patients. Following PES and serial drug testing, 46 patients were started on lorcainide, 9 patients on procainamide, and 45 patients were started on other antiarrhythmic drug regimens. Seventy percent of the patients have remained on lorcainide therapy, while 47% have continued on other drug therapies started over a 20.5 +/- 3.2 month mean follow-up period. Despite sleep-wake disturbances and a need for sedation at night, lorcainide therapy was tolerated well in this population and remained an effective antiarrhythmic with prolonged administration.

Administration, Oral↗
PubMed1984

Lorcainide therapy for the high-risk patient post myocardial infarction.

Nonsustained ventricular tachycardia (VT) in the late period (7 to 21 days) after myocardial infarction (MI) is reported to be a predictor of sudden death. Patients with 3-beat VT on Holter monitoring in the late infarction period would be suspected to demonstrate electrical instability on electrophysiologic studies. Forty-seven patients were identified as having at least 3-beat VT on Holter monitoring. Eighteen patients refused electrophysiologic studies or were not referred. Eight patients died; 3 were sudden deaths in 13 +/- 5 months, a 17% incidence. Twenty-nine patients underwent invasive electrophysiologic studies and 28 had inducible VT, 18 sustained and 10 nonsustained. Lorcainide prevented VT induction in 21 of the 28 patients, whereas 12 of the 22 patients studied on procainamide were protected. Lidocaine, tested in 21 patients, prevented VT induction in only 5. Lorcainide and procainamide prolonged refractoriness in those patients protected at programmed electrical stimulation (PES), whereas the QT interval was prolonged in patients in whom VT could still be induced. Twenty-seven of the 28 patients were placed on drugs predicted to be effective by PES studies, 19 on lorcainide. After a mean follow-up of 12.5 +/- 4 months the patient with noninducible arrhythmia is alive and 26 of the 28 patients with inducible arrhythmia are alive and well. Two patients died, 1 of stroke and 1 of pump failure after a second MI. No sudden deaths were observed in this group. Two patients had breakthrough arrhythmias and were treated by alternative antiarrhythmic therapy that was also effective on initial electrophysiologic studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Comparison of noninvasive arrhythmia induction techniques with electrophysiologic studies and evaluation of lorcainide in patients with symptomatic ventricular tachycardia.

Twenty-six patients (19 men and 7 women) with symptomatic ventricular tachycardia (VT) were studied using invasive and noninvasive techniques to induce VT. Of the study population, 12% had syncope and VT on Holter monitoring, 30% had cardiac arrest and 58% had symptomatic VT. All patients had antiarrhythmic agents stopped 5 half-lives before evaluation and then had autonomic profile (upright tilt, cold pressor test, exercise testing and hand grip) as well as programmed electrical stimulation studies performed. Autonomic profile testing induced VT in 5 of 26 patients (19%) and in only 1 patient was the arrhythmia reproducibly induced. All 26 patients had VT induced on electrophysiologic testing; 9 patients had nonsustained and 17 had sustained VT. Lorcainide administered intravenously prevented VT induction in 20 of 26 patients tested, whereas procainamide was effective in 11 of 24 patients. Ten of the 13 not protected by procainamide were protected by lorcainide. Twenty patients were started on long-term lorcainide therapy and followed up for 29 +/- 3.4 months. Five patients have discontinued therapy, 2 because of breakthrough arrhythmias, 2 because of severe sleep-wake disturbances and 1 because of private physician preference. An additional 3 patients died during therapy because of myocardial infarction in 1, progressive myopathy in 1 and sudden death in 1. Sixty percent of patients started on lorcainide therapy have continued. In this patient population, noninvasive induction of VT is not a sensitive or reproducible technique in assessing antiarrhythmic therapy. Furthermore, when selected on the basis of electrophysiologic testing, lorcainide is a well-tolerated and effective antiarrhythmic agent.

Aged↗
PubMed1984

Antiarrhythmic action of bethanidine.

Studies were performed in 20 patients with symptomatic ventricular tachycardia (VT) to determine the efficacy of bethanidine compared with procainamide in preventing VT induced by programmed electrical stimulation. Before administering bethanidine, 5 to 10 mg/kg, the patients received 15 mg of protriptyline orally 24 and 2 hours before electrophysiologic studies to prevent the orthostatic hypotensive effects of bethanidine. Sustained VT (VT not spontaneously stopping) was induced in 8 and nonsustained VT (10 beats or more, terminating spontaneously) was induced in 4 patients. Bethanidine, 5 mg/kg, protected in 7 patients, and 10 mg/kg protected 1 additional patient. Procainamide, 1,000 and 1,500 mg intravenously, protected 8 of 16 patients. Bethanidine prevented VT induction in 50% of the patients not protected by procainamide. Bethanidine facilitated VT induction in 3 patients, while procainamide facilitated VT induction in 1 patient. Four patients with symptomatic VT have received bethanidine therapy for an average of 11 +/- 1.3 months, without clinical recurrence of their VT. Concomitant administration of protriptyline attenuated the acute hemodynamic changes caused by bethanidine and chronic combined therapy of protriptyline and bethanidine abolished the severe orthostatic changes in blood pressure caused by bethanidine. These studies show that bethanidine is effective in preventing VT induction and, thus, its use may not be restricted only to cases of primary ventricular fibrillation.

Bethanidine↗
PubMed1984

The efficacy of cibenzoline in preventing PES induction of ventricular tachycardia in the dog.

The electrophysiologic effects of cibenzoline were studied using programmed electrical stimulation (PES) techniques and were compared to those of quinidine. Cibenzoline, like the conventional class 1 agent quinidine, was effective in preventing arrhythmia induction. Twelve dogs were given 0.02 mg/kg digoxin intravenously for seven days to achieve a steady-state digoxin level. On the eighth day, cibenzoline was administered in incremental doses (0.5 to 10.5 mg/kg) and PES was performed at 30-minute intervals. A mean dose of 2.6 +/- 0.8 mg/kg cibenzoline prevented ventricular tachycardia induction. At this dose, cibenzoline had no significant effect on mean arterial blood pressure, but PR interval increased by 17 +/- 9 per cent, QRS duration by 27 +/- 14 per cent, and the ventricular refractory period (ERP) for the first extra stimulus increased by 35 +/- 9 per cent. A gradual decrease in heart rate and an increase in PR interval and QRS duration was caused by incremental doses of cibenzoline. In six additional animals, quinidine was administered in incremental doses (1 to 30 mg/kg) and PES performed at 30-minute intervals. A mean of 15 +/- 5 mg/kg prevented induction of ventricular tachycardia in five animals. No significant change in heart rate, PR, QRS, and ERP was found at the effective dose.

Animals↗