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Biomedical subjects

S R Spielman

Publications and source records attributed to S R Spielman.

At least 37 records · Page 2Linked to original sources
PubMed1986

Prospective evaluation of ventricular arrhythmias using electrophysiologic techniques.

Electrophysiologic testing is known to be of value both diagnostically and in the evaluation of treatment modalities for patients with recurrent sustained ventricular tachycardia, out-of-hospital cardiac arrest, and syncope of unknown etiology. Attention is being focused on the possibility of identifying patients at high risk for such lethal ventricular arrhythmias in the hope that prophylactic therapy could prevent such arrhythmias from occurring. In this article, the authors discuss the potential role of electrophysiologic testing in this prospective identification and review the current data in the two groups of patients that have been studied extensively in this regard--post-myocardial infarction patients and patients with left ventricular dysfunction and congestive heart disease. The element of study artifact is also addressed.

Arrhythmias, Cardiac↗
PubMed1985

Electrophysiology of esmolol.

The electrophysiologic characteristics of esmolol were studied in 14 patients. Ten men and 4 women, mean age 57 years, were electrophysiologically evaluated at baseline, and also at 4 to 8 minutes after the administration of a maintenance infusion of esmolol. Plasma samples for esmolol blood levels were drawn at 10 minutes of the maintenance infusion, at the end of the maintenance infusion and 30 minutes after the maintenance infusion was discontinued. Results of this study showed that esmolol has typical beta-blocker electrophysiologic effects. Its major action was on sinus node function; it prolonged this basic sinus cycle length but had no significant effect on intrinsic automaticity as reflected by the corrected sinus node recovery time and sinoatrial conduction. Direct effects on atrioventricular (AV) nodal function were reflected by effects on AV nodal conduction and refractoriness. There was no direct effect on atrial function and, as expected, no effect on His-Purkinje or ventricular function. The intensity of esmolol's electrophysiologic effects on sinus node function, AV nodal conduction and AH interval is comparable to those of other beta blockers.

Adrenergic beta-Antagonists↗
PubMed1985

Efficacy of combination therapy with mexiletine and a type IA agent for inducible ventricular tachyarrhythmias secondary to coronary artery disease.

The efficacy of combination therapy using a type IA agent (quinidine or procainamide) and a type IB agent (mexiletine) in suppressing inducible sustained ventricular tachyarrhythmias was studied in 23 patients undergoing serial drug testing with programmed stimulation. All patients had coronary artery disease (CAD) with previous myocardial infarction and abnormal left ventricular function (mean ejection fraction 35%). Fifty-five percent of the patients presented with syncope or cardiac arrest. In 19 patients therapy had failed during empiric trials of 1 to 3 antiarrhythmic agents. All 23 patients had inducible sustained ventricular tachyarrhythmias (18 had uniform morphology sustained ventricular tachycardia (VT) and 5 had ventricular fibrillation [VF]) during control electrophysiologic study, and therapy had failed with a type IA agent and mexiletine alone. The combination therapy of mexiletine and the type IA agent prevented induction of any ventricular tachyarrhythmias in 8 of 23 patients. In 15 patients, the combination significantly prolonged the tachycardia cycle length and reduced the symptoms associated with the induced arrhythmia. Patients more likely to respond to the combination had shorter cycle lengths and polymorphic configuration of the control-induced arrhythmia. The increased efficacy of the combination therapy could not be attributed to higher plasma drug levels for the combination, as there was no significant difference in plasma levels for each drug when given alone or in combination. Thus, the increased efficacy most likely reflects a synergistic electropharmacologic effect of the 2 agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Antiarrhythmic drug efficacy for ventricular tachyarrhythmias associated with coronary artery disease as assessed by electrophysiologic studies.

The efficacy and proarrhythmic potential of antiarrhythmic agents were evaluated. Programmed ventricular stimulation was performed in 160 consecutive patients with coronary artery disease during a baseline study and 432 subsequent drug studies. The tachyarrhythmias induced during baseline studies were sustained ventricular tachycardia (121 patients), ventricular fibrillation (16 patients), and symptomatic nonsustained ventricular tachycardia (23 patients). Regimens were completely successful if fewer than 6 repetitive ventricular responses were inducible during therapy and partially successful if no more than 15 repetitive ventricular responses were inducible. Procainamide and quinidine were the most successful single agents, with overall success rates of 24% and 35%, respectively. Either procainamide or quinidine combined with mexiletine was the most successful combination (overall success of 23%). Each anti-arrhythmic regimen showed a proarrhythmic potential. The incidence of proarrhythmic effects ranged from 4 to 13%, with no significant difference between regimens. In 13% of patients at least 1 regimen produced a proarrhythmic effect. Patients treated with an antiarrhythmic regimen that prevented induction of arrhythmia had significantly fewer arrhythmia recurrences than patients treated with a regimen that failed to prevent it. In conclusion, identification of an effective drug regimen is possible in 38% of patients with lethal ventricular arrhythmias, proarrhythmic effects occur in a significant number of patients during electrophysiologic testing of antiarrhythmic regimens, and the clinical outcome in patients in whom ventricular arrhythmias are not inducible with ventricular stimulation have a better prognosis than those in whom arrhythmias continue to be inducible on therapy.

Adult↗
PubMed1985

Ventricular activation in normal sinus rhythm: abnormalities with recurrent sustained tachycardia and a history of myocardial infarction.

Left ventricular activation was studied in 21 patients: 7 with normal electrocardiograms (group I), 7 with prior transmural myocardial infarction (group II) and 7 with prior transmural myocardial infarction (MI) and recurrent sustained ventricular tachycardia (VT) (group III). Fragmented electrograms were defined as those less than 3 mV in amplitude and longer than 60 ms in duration. Such electrograms were found in no group I patients, 6 of 7 group II patients and all 7 group III patients. An average of 2 of the 12 sites mapped in each patient displayed fragmented electrograms in group II; an average of 6 of the 12 sites displayed fragmented electrograms in group III (p less than 0.01). Twelve of the 84 total sites mapped in group II displayed fragmented electrograms, whereas 39 of the 84 sites mapped in group III patients did (p less than 0.01). The longest fragmented electrogram found in the 6 group II patients in whom such electrograms were found was shorter in duration than the longest electrogram found in each of the 7 group III patients with fragmented electrograms (76 ms vs 135 ms, p less than 0.005). The duration of endocardial activation was longer in group II patients (79 +/- 7 ms) than in group I patients (39 +/- 4 ms, p less than 0.001). Duration of activation was also longer in group III patients (151 +/- 12 ms) than in either of the other groups (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography↗
PubMed1985

Usefulness of electrophysiologic testing in evaluation of amiodarone therapy for sustained ventricular tachyarrhythmias associated with coronary heart disease.

The prognostic importance of electrophysiologic studies in patients with sustained ventricular tachyarrhythmias treated with amiodarone was prospectively studied in 100 consecutive patients. Sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) was inducible in all patients before amiodarone therapy. After amiodarone administration 2 groups of patients were identified. In group 1 patients the ventricular tachyarrhythmia was no longer inducible and in group 2 patients the arrhythmia remained inducible. In group 1, no recurrent arrhythmia occurred during a follow-up of 18 +/- 10 months. In group 2, 38 of 80 patients (48%) had arrhythmia recurrence during a follow-up of 12 +/- 9 months. The difference between group 1 and 2 could not be explained by clinical variables, amiodarone doses or plasma concentrations, or electrocardiographic variables. In patients in whom cardiovascular collapse or other severe symptoms where noted during electrophysiologic study after amiodarone treatment, recurrences caused sudden death (n = 12). However, in patients in whom the induced arrhythmia produced moderate symptoms, the recurrent arrhythmia was nonfatal VT (n = 26). Electrophysiologic testing provides clinical guidance and predicts prognosis in patients treated with amiodarone as it does for the evaluation of other antiarrhythmic agents.

Adult↗
PubMed1985

The clinical electrophysiology of intravenous indecainide.

The electrophysiologic effects of indecainide, a new class IC antiarrhythmic agent, were assessed in 10 patients with left ventricular dysfunction and inducible sustained ventricular tachycardia. Indecainide was administered intravenously in a dose of 60 to 90 mg/kg at a rate of 12.5 to 15 micrograms/kg/min. Indecainide had no effect on sinus node function or atrial and ventricular effective refractory periods. The AH (106 +/- 13 vs 130 +/- 24 msec, p less than 0.002) and HV (57 +/- 7 vs 73 +/- 19 msec, p less than 0.001) intervals were significantly increased. The QRS duration increased (102 +/- 9 vs 120 +/- 13 msec, p less than 0.001); however, the JT duration did not change. Induction of ventricular tachycardia was prevented in 1 of 10 patients. In the remaining nine patients, the ventricular tachycardia cycle length was significantly prolonged (248 +/- 47 vs 320 +/- 71 msec, p less than 0.001). Indecainide significantly depressed intracardiac conduction at several sites.

Adult↗
PubMed1985

Effect of long-term amiodarone therapy on thyroid hormone levels and thyroid function.

Both hyperthyroidism and hypothyroidism have been noted to occur in some patients treated with amiodarone for cardiac arrhythmias. To determine the frequency of the development of thyroidal abnormalities in patients receiving amiodarone, 45 euthyroid patients were prospectively evaluated. Serum samples were obtained for measurement of thyroxine, thyrotropin, triiodothyronine, and triiodothyronine resin uptake prior to initiation of amiodarone treatment and serially over a 12- to 27-month period during which amiodarone was administered. The patients were divided into four subgroups as follows: Group I (n = 22) had elevated thyroxine levels, Group IIA (n = 13) had normal thyroxine levels and normal thyrotropin levels, Group IIB (n = 7) had normal thyroxine levels and elevated thyrotropin levels, and Group III (n = 3) had subnormal thyroxine levels. Demographic factors (such as route of administration, cardiac diagnosis, sex of the patient, or indication for amiodarone therapy) and amiodarone levels had no significant effect on the thyroid hormone parameters. However, Group I patients were statistically older than the patients in the other groups. Linear regression analysis revealed a negative correlation for thyroxine levels and a positive correlation with thyrotropin levels with age for the whole group. The various groups were not statistically affected by duration of therapy, but a positive trend existed for increasing thyroxine levels. Although virtually all patients showed changes in their thyroid hormone levels, chemical hyperthyroidism (elevated thyroxine and triiodothyronine levels without symptoms) developed in only two patients (4 percent), and clinical hyperthyroidism (elevated thyroxine and triiodothyronine levels with symptoms) developed in no patients. Four patients (9 percent) became biochemically and clinically hypothyroid. Thus, amiodarone frequently influences thyroid hormonal parameters, but less commonly causes a change in actual thyroid function. However, hyperthyroidism and hypothyroidism do occur in a significant number of patients.

Age Factors↗
PubMed1985

Limitations of failure of procainamide during electrophysiologic testing to predict response to other medical therapy.

To determine whether failure of procainamide to prevent initiation of ventricular tachyarrhythmias during electrophysiologic testing predicted failure of other antiarrhythmic regimens, 81 consecutive patients with coronary artery disease whose ventricular tachyarrhythmias remained inducible during procainamide administration were studied. Overall, 26 (12%) of 216 subsequent drug studies were successful and at least one effective drug regimen was identified in 22 (27%) of the 81 patients. Drug success was significantly related to the arrhythmia induced at baseline study; 7% of drug studies were successful in patients with sustained ventricular tachycardia, 24% in patients with ventricular fibrillation, and 29% in patients with nonsustained ventricular tachycardia. An effective drug regimen was found in 11 (19%) of 59 patients with sustained ventricular tachycardia, 4 (50%) of 8 patients with ventricular fibrillation and 7 (50%) of 14 patients with nonsustained ventricular tachycardia. In patients with sustained ventricular tachycardia, failure of procainamide to suppress the arrhythmia correlated with failure of other agents used singly but not in combination. This study supports the view that when procainamide fails to prevent initiation of the arrhythmia in patients with inducible sustained ventricular tachycardia it is unlikely that other individual standard agents will be effective. However, combination regimens may suppress the arrhythmia and should be evaluated. In patients with nonsustained ventricular tachycardia, all agents should be evaluated because failure to respond to procainamide does not predict subsequent responses to other agents either alone or in combination.

Adult↗
PubMed1985

Use of amiodarone in the treatment of persistent and paroxysmal atrial fibrillation resistant to quinidine therapy.

The efficacy of amiodarone was assessed in 38 patients with atrial fibrillation resistant to quinidine and an effort made to identify factors correlated with amiodarone response. The study group included 29 patients with and 9 without organic heart disease and either persistent (n = 11) or paroxysmal (n = 27) atrial fibrillation. All patients were treated with amiodarone and followed up in a research clinic. Efficacy was classified as excellent (no recurrent symptomatic atrial fibrillation) in 15 (55%) of 27 patients with paroxysmal and 5 (45%) of 11 patients with persistent atrial fibrillation. Efficacy was poor (no effect on atrial fibrillation) in 5 (19%) of 27 patients with paroxysmal and 6 (55%) of 11 patients with persistent atrial fibrillation. Efficacy was good (amelioration but not total suppression) in 7 (26%) of 27 patients with paroxysmal atrial fibrillation. Efficacy was related to echocardiographic left atrial dimension, left ventricular ejection fraction and, in patients with persistent atrial fibrillation, the duration of the arrhythmia. During the follow-up period of 15 months (range 1 to 36), overall efficacy (considering response and toxicity) was 67% in the 27 patients with paroxysmal and 45% in the 11 patients with persistent atrial fibrillation. It is concluded that amiodarone offers an additional therapeutic alternative in quinidine-resistant atrial fibrillation and that certain clinical factors are correlated with amiodarone response.

Adult↗
PubMed1985

Electrophysiologic testing in patients at high risk for sudden cardiac death. I. Nonsustained ventricular tachycardia and abnormal ventricular function.

Nonsustained ventricular tachycardia, although usually asymptomatic, is associated with a high risk of sudden cardiac death in patients with depressed left ventricular function. To test the vulnerability of such patients to symptomatic and potentially life-threatening arrhythmias, complete electrophysiologic studies were performed in 58 patients with clinically documented nonsustained ventricular tachycardia (greater than or equal to three complexes but less than 15 seconds of self-terminating ventricular tachycardia by 24 hour ambulatory electrocardiographic [Holter] or telemetric monitoring) and abnormal left ventricular function (ejection fraction less than 50% by radionuclide angiography). All patients had nonsustained ventricular tachycardia in the absence of antiarrhythmic drugs, acute ischemia, long QT syndrome, recent infarction or electrolyte abnormalities. The stimulation protocol for each patient included the introduction of single, double and triple ventricular extrastimuli at three cycle lengths (sinus, 600 and 450 ms) and two right ventricular sites (apex and outflow tract). A sustained ventricular tachyarrhythmia was induced in 23 patients (40%) and a nonsustained ventricular tachycardia in 14 patients (24%). Induction of sustained tachycardia correlated with the presence of akinesia or aneurysm, or both, by radionuclide angiography, but not with ejection fraction or presence or absence of coronary artery disease. These results indicate that: 1) patients with clinical nonsustained ventricular tachycardia and chronic left ventricular dysfunction have a high incidence of inducible sustained ventricular tachycardia or ventricular fibrillation; and 2) electrophysiologic testing may allow further substratification of risk of sudden cardiac death in high risk patients with nonsustained ventricular tachycardia.

Adult↗
PubMed1985

Improved method for evaluating ventriculoatrial conduction before implantation of atrial-sensing dual chamber pacemakers.

Pacemaker-mediated tachycardia may occur when a spontaneous ventricular premature depolarization is retrogradely conducted to the atrium with a ventriculoatrial (VA) interval that exceeds the atrial refractory period of an atrial-sensing dual chamber pacemaker. Previous methods for evaluating VA conduction have failed to predict clinical occurrences of pacemaker-mediated tachycardia. In this study, maximal VA intervals after ventricular extrastimuli during atrial or atrioventricular (AV) sequential pacing were compared with intervals measured by the standard method of ventricular pacing. VA intervals were 201 +/- 53 ms during ventricular pacing and 224 +/- 52 ms after ventricular extrastimuli during atrial pacing (p = NS). VA intervals were 305 +/- 77 ms after ventricular extrastimuli during AV sequential pacing and were longer than VA intervals during ventricular pacing (p less than 0.001) or after ventricular extrastimuli during atrial pacing (p less than 0.01). Thus, the ventricular extrastimulus technique during AV sequential pacing reveals substantially longer VA intervals than does ventricular pacing and explains why pacemaker-mediated tachycardia might occur when pacemaker atrial refractory periods are designed or programmed according to VA intervals measured only during ventricular pacing.

Adult↗
PubMed1985

Conversion from intravenous to oral mexiletine in the acute management of repetitive ventricular arrhythmia.

We evaluated the safety and efficacy of intravenous mexiletine and a method for converting from intravenous to oral mexiletine therapy. Fifteen patients with repetitive ventricular ectopy (13 had ventricular tachycardia) received intravenous mexiletine at a rate of 10 mg/min for 30 to 60 minutes. Ventricular ectopy was suppressed with minimal side effects in 10 of 15 subjects. Oral mexiletine was begun immediately after completion of the intravenous infusion at a dose of 10 mg/kg/24 hr in the 10 responders to intravenous therapy. In eight, the oral dose was effective in suppressing the arrhythmia, but it induced side effects in three of them. In one of these three, dose reduction resulted in adequate arrhythmia control with acceptable toxicity. In the two who did not respond to the original dose, a larger dose (15 mg/kg/24 hr) induced arrhythmia control with acceptable side effects in one subject. Thus rapid control of nonsustained repetitive ventricular arrhythmia can be achieved with intravenous mexiletine in about two thirds of patients, and conversion to oral therapy can often be achieved smoothly without significant arrhythmia recurrence.

Administration, Oral↗
PubMed1985

Pacemakers: normal function.

AV sequential pacemakers are particularly useful in patients who have developed "pacemaker syndrome" with single-chambered ventricular demand units, since the normal atrioventricular relationship is then restored. Fully automatic pacemakers are indicated for patients with AV block, with or without sinus node dysfunction, or with moderate sick sinus syndrome and AV nodal or His-Purkinje disease, with at least some ability to increase atrial rate with exercise.

Electrocardiography↗
PubMed1985

Pacemakers: abnormal function.

Although intermittent or total loss of capture may occur at any time following pacemaker implantation, the peak incidence is either very early (less than 4 weeks) or very late (more than 3 years) in the life of the device. Oversensing may be a cause of recurrent syncope in patients who, during routine office visit testing, appear to have normally functioning pacemakers.

Aged↗
PubMed1984

Early experience with an implantable cardioverter.

We tested the efficacy and safety of a fully programmable cardioverter weighing 95 g, in terminating sustained ventricular tachycardia. The device was implanted tranvenously under local anesthesia in seven patients. On command from a programmer or automatically, the cardioverter delivered shocks through a lead inserted to the apex of the right ventricle. It also served as a demand ventricular pacemaker and could perform programmed ventricular stimulation or overdrive pacing. Cardioversion of ventricular tachycardia required less than 0.5 J (mean) and was well tolerated by the patients, who were awake and not sedated. In one patient, a shock terminated ventricular tachycardia with the device in the automatic mode but produced atrial fibrillation with a rapid ventricular response that was intermittently recognized as ventricular tachycardia, triggering additional shocks. One such shock in the ST segment produced ventricular fibrillation that was terminated transthoracically in the emergency room, without residual impairment. We conclude from these preliminary observations that cardioversion of sustained ventricular tachycardia by means of an implantable catheter device is feasible, but for the present its use in the automatic mode must be cautious and selective. The unit's small size, ease of implantation, usefulness for noninvasive electrophysiologic studies, programmability, and bradycardia pacing functions are advantages. The next-generation device must be able to defibrillate and provide better differentiation of arrhythmias.

Adult↗