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Biomedical subjects

A M Greenspan

Publications and source records attributed to A M Greenspan.

At least 19 recordsLinked to original sources
PubMed2001

Evolving indications for permanent pacemakers.

New indications for permanent cardiac pacing have been developed in recent years, with numerous studies demonstrating improved clinical outcomes in a variety of disorders. Because hypertrophic obstructive cardiomyopathy, dilated cardiomyopathy, heart failure, neurocardiogenic syncope, and atrial fibrillation are common conditions, every clinician should be aware of evolving alternative therapies for them. Observational studies in patients with refractory, symptomatic hypertrophic obstructive cardiomyopathy and significant left ventricular outflow gradient at rest suggest that cardiac pacing may result in symptomatic and hemodynamic improvement. Clinical trials have not shown conclusive evidence regarding the long-term benefit from pacing in these patients, and it is unclear whether pacing will be a preferred treatment option. Preliminary data suggest that pacing is a viable adjunctive therapeutic approach for improving symptoms in patients with dilated cardiomyopathy and heart failure. Mortality benefit has yet to be established, but it is to be hoped that ongoing randomized clinical trials will provide definitive information on that issue. Patients with refractory neurocardiogenic syncope or those who are intolerant of medical treatment may benefit from pacing therapies, especially those that use rate-drop sensor algorithms. Biatrial pacing has emerged as a technique that resynchronizes atrial electrical activity and has been shown to prevent atrial fibrillation. Multisite atrial pacing for the prevention of atrial fibrillation is considered investigational but seems promising. Newer indications for pacing are expected to result in improved clinical outcomes for hypertrophic obstructive cardiomyopathy, dilated cardiomyopathy and heart failure, neurocardiogenic syncope, and the prevention of atrial fibrillation.

Atrial Fibrillation↗
PubMed1988

Relation of acute antiarrhythmic drug efficacy to left ventricular function in coronary artery disease.

This study assessed the relation between acute antiarrhythmic drug efficacy and left ventricular (LV) function in patients with sustained ventricular tachyarrhythmias, that is, sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Electrophysiologic studies (n = 560) were performed in 201 patients, separated for analysis into less than 30 and greater than or equal to 30% ejection fraction groups. Coronary artery disease was present in all patients. The 8 acute antiarrhythmic regimens were procainamide, quinidine, mexiletine, mexiletine + type 1A agent, flecainide or indecainide, amiodarone, amiodarone + type 1A and "miscellaneous" agents. At least 1 successful acute antiarrhythmic regimen was found in 47% of patients and in a significantly greater proportion of patients with ejection fraction greater than or equal to 30% (52 of 81 = 64%) than in those with ejection fraction less than 30% (43 of 120 = 36%, p less than 0.001). Drug trials were successful (initiation of less than 15 repetitive ventricular responses) in 32% of patients with ejection fraction greater than or equal to 30% versus 19% of those with ejection fraction less than 30% (p less than 0.001). There were no statistically significant differences between the 2 ejection fraction groups in type of heart disease, acute antiarrhythmic dosages or mean serum drug levels. A logistic regression analysis incorporating multiple clinically relevant factors found that ejection fraction was the only factor that correlated significantly with drug success or failure (p less than 0.002). Acute antiarrhythmic drug efficacy relates to LV function per se or to other pathophysiologic mechanisms of which ejection fraction may be a marker.

Administration, Oral↗
PubMed1988

Incidence of unwarranted implantation of permanent cardiac pacemakers in a large medical population.

Because of allegations that the implantation of many permanent cardiac pacemakers has been unjustified, we reviewed the indications for all new pacemakers implanted at 30 hospitals in Philadelphia County between January 1 and June 30, 1983, and paid for by Medicare. Complete chart data were evaluated for 382 implants. We determined whether the indications for implantation were appropriate and adequately documented on the basis of standard clinical practice. Implants were classified as possibly indicated primarily because of inadequate diagnostic evaluation (63 percent) or inadequate documentation of an accepted indication (36 percent). Implants were classified as not indicated primarily because a rhythm abnormality was incorrectly identified as a justifiable indication (84 percent). We found that 168 implants (44 percent) were definitely indicated, 137 (36 percent) possibly indicated, and 77 (20 percent) not indicated. Unwarranted implantation was both prevalent (73 percent of hospitals had an incidence of 10 percent or more) and independent of the type of hospital (university teaching, university-affiliated, and community hospitals). The additional tests most often required to clarify the need for a pacemaker in inadequately evaluated cases included electrophysiologic studies (37 percent) and ambulatory monitoring (31 percent). We conclude that in a large medical population in 1983, the indications for a considerable number of permanent pacemakers were inadequate or incompletely documented.

Arrhythmias, Cardiac↗
PubMed1988

Proarrhythmic effects of antiarrhythmic drugs in patients with malignant ventricular arrhythmias evaluated by electrophysiologic testing.

The provocation or worsening of arrhythmias by antiarrhythmic regimens was evaluated in patients with malignant ventricular arrhythmias undergoing electrophysiologic studies. In 314 patients with sustained or nonsustained ventricular tachycardia or ventricular fibrillation, 801 drug studies were performed using a standard protocol of programmed electrical stimulation. The criteria for proarrhythmia were: 1) initiation of sustained ventricular tachyarrhythmia in a patient in whom only nonsustained tachycardia was induced at baseline; 2) conversion of a sustained tachycardia that could be terminated by programmed electrical stimulation at baseline to one that required cardioversion for termination during drug therapy; 3) initiation of a sustained tachyarrhythmia by a less aggressive mode of stimulation than was required at baseline; and 4) development of spontaneous or incessant ventricular tachycardia. Proarrhythmia criterion 1 occurred during 20 (18%) of 118 studies and at least once in 15 (28%) of 54 patients. Criterion 2 was met during 39 (7%) of 578 studies and at least once in 29 (13%) of 220 patients. Criterion 3 was achieved during 135 (20%) of 687 studies in patients with sustained ventricular tachyarrhythmias at baseline. Criterion 4 occurred during 9 (1%) of 801 drug studies. In 40 patients in whom well tolerated ventricular tachycardia was initiated with fewer extrastimuli during drug study than at baseline, the drug was continued and the patients were followed up. The recurrence rate of tachycardia was the same in these patients as in 73 patients followed up on regimens on which the number of extrastimuli required for initiation was not reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

The electrophysiologic properties of esmolol, a short acting beta-blocker.

Although beta-blockers have established efficacy in treating ventricular ectopy and PSVT, their applicability for acute antiarrhythmic interventions in patients with organic heart disease or COPD, is frequently limited by negative inotropic or bronchospastic side effects. The development of an ultrashort acting beta-blocker with rapid reversibility of its side effects would widen their applicability. Therefore, we tested the electrophysiologic properties of such a new short acting beta-blocker, esmolol, in 14 patients (10 with organic heart disease) with a mean EF of 47.6 +/- 17%, undergoing standard clinical electrophysiologic studies for various indications. Like most other beta-blockers, esmolol's major direct effects were on sinus node function and AV nodal conduction characteristics; significantly prolonging sinus cycle length, cycle length to Wenckebach and AH interval in sinus rhythm and at a paced cycle length of 600 ms. In contrast to most other beta-blockers, following termination of its infusion, esmolol shortened parameters of sinus node function and AV nodal refractoriness, with respect to the control values, suggesting a possible rebound phenomena. These effects occurred within 5 min of terminating the intravenous drug infusion. Esmolol had no significant effect on systolic blood pressure, electrocardiographic intervals and had rare adverse reactions. We conclude that esmolol is an ultra-short acting beta-blocker, with typical direct electrophysiologic effects on sinus node and AV nodal function, and a possible rebound phenomena following its discontinuation that may make it particularly suited to acute antiarrhythmic interventions in patients susceptible to adverse beta-blocker side effects.

Adrenergic beta-Antagonists↗
PubMed1987

Development of congestive heart failure and alterations in left ventricular function in patients with sustained ventricular tachyarrhythmias treated with amiodarone.

The interaction between the efficacy and tolerance of amiodarone and the degree of left ventricular (LV) dysfunction was assessed in 126 patients with sustained ventricular tachyarrhythmias. In all patients radionuclide angiographic LV ejection fraction (EF) was measured before and after 8 to 12 months of amiodarone therapy. At baseline mean EF was 25 +/- 13% and 86 patients had an EF of 30% or less. In patients receiving amiodarone at steady state, there was a small but significant increase in EF (23 to 26%, p less than 0.05). Congestive heart failure (CHF) was present in 43 patients before amiodarone therapy. In 16 patients new (9 patients) or worsened (7 patients) CHF developed during the first year of amiodarone therapy. Development of CHF was not consistently related to a change in EF or heart rate. The clinical efficacy and tolerance of amiodarone were affected by the baseline EF and development of CHF. Efficacy and tolerance was 80% in patients with an EF of more than 30% and 60% in those with an EF of 30% or less. Among the 16 patients in whom new or worsened CHF developed, 6 (38%) died and 9 (56%) had recurrent ventricular tachyarrhythmias. Both baseline EF and development of CHF during amiodarone treatment significantly affect the prognosis in patients with ventricular tachyarrhythmias.

Adult↗
PubMed1987

Determinants of hospital cost and length of stay for patients undergoing electrophysiologic testing.

To assess the effects of various clinical factors in determining the cost and length of stay in patients undergoing electrophysiologic testing for cardiac arrhythmias, the hospital cost and length of stay data were reviewed in 222 consecutive inpatients who underwent electrophysiologic testing from January 1 to December 31, 1984. Admissions were classified as: primarily for treatment of arrhythmias (171 patients); primarily for treatment of arrhythmias but with serious concurrent illnesses that prolonged hospitalization (43 patients); or primarily for nonarrhythmic problems with electrophysiologic study an incidental part of hospitalization (8 patients). Based on allowable length of stay for the applicable DRGs, actual hospitalizations exceeded Medicare allowable length of stay by 50 to 500%. Retrospective review of hospital charts indicated that 3 clinical factors serve as effective markers in determining length of stay: need for amiodarone, induction of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF), and presence of serious other medical problems that require stabilization before electrophysiologic testing. Our data indicate that 3 classes of patients can be identified: I. DRG A (45%)--those who did not have sustained VT or VF induced, did not require amiodarone and had no serious concurrent illnesses. The mean length of stay was 7.1 days. II. DRG B patients (21%)--those who had sustained VT or VF induced, but did not require amiodarone and had no serious concurrent illnesses. The mean length of stay was 13.7 days. III. DRG C patients (34%)--those who either had a serious concurrent illness or required amiodarone. The mean length of stay was 19.7 days. This classification schema might allow a more appropriate system for determining reimbursement.

Amiodarone↗
PubMed1987

Proarrhythmic responses during electrophysiologic testing.

Antiarrhythmic drugs may worsen ventricular arrhythmias in certain patients. This effect, termed proarrhythmia, aggravation or provocation of arrhythmia, can be investigated with either noninvasive or invasive techniques. Using electrophysiologic study, 160 patients with ventricular tachycardia or ventricular fibrillation were evaluated during treatment with 432 different antiarrhythmic regimens. Proarrhythmic responses were noted in 68 drug trials (16%), and at least 1 event was observed in 51 patients (32%). Nonsustained ventricular tachycardia was converted to sustained ventricular tachycardia in 17% of these studies. Hemodynamically stable ventricular tachycardia was converted to an arrhythmia that required cardioversion for termination in 5% of the studies. Ventricular tachyrhythmia was more easily induced in 12% of trials. These proarrhythmic responses were not related to changes in QRS duration, QT interval or JT interval measured at baseline or to changes produced by antiarrhythmic drugs.

Anti-Arrhythmia Agents↗
PubMed1987

Influence of left ventricular dysfunction on flecainide therapy.

Seventy-six patients with ventricular tachyarrhythmias (40 sustained and 36 nonsustained) were treated with oral flecainide. Radionuclide left ventricular ejection fraction was 30% or less in 33 patients and greater than 30% in 43 patients. Before flecainide, compensated heart failure was present in 23 patients (ejection fraction less than or equal to 30% in 15 and greater than 30% in 8). Flecainide mean dose was 150 mg twice daily and mean plasma concentration was 720 ng/ml. New or worsened congestive heart failure occurred in seven patients on flecainide therapy, all with an ejection fraction of less than 30%; six had a previous history of compensated heart failure and of these, three died. Ejection fraction was the only independent variable that significantly influenced efficacy and tolerance of flecainide. After 1 year of therapy, efficacy and tolerance was 58% (25 of 43) in patients with an ejection fraction greater than 30% and 12% (4 of 33) in patients with an ejection fraction of 30% or less (p less than 0.001). Thus, congestive heart failure can occur during flecainide therapy, particularly in patients with a previous history of congestive heart failure and ejection fraction of less than 30%, and may particularly limit therapy in these patients. Clinical efficacy and tolerance were significantly lower in patients with an ejection fraction of less than 30%.

Adult↗
PubMed1987

Reduction in sudden death and total mortality by antiarrhythmic therapy evaluated by electrophysiologic drug testing: criteria of efficacy in patients with sustained ventricular tachyarrhythmia.

Reports of the results of electrophysiologic testing of antiarrhythmic regimens have concentrated on inducibility of ventricular tachycardias during drug treatment. Many drug regimens, however, affect the tachycardia but fail to prevent its initiation. In this study, 258 patients who underwent serial electrophysiologic studies were followed up. The patients were divided into three groups on the basis of the results of electrophysiologic testing. Group 1 included patients in whom the initiation of ventricular tachycardia was prevented by the drug regimen. In groups 2 and 3 the ventricular tachycardia was still inducible with the discharge drug regimen. In group 2, the drug regimen demonstrated a beneficial response (that is, the tachycardia cycle length increased by greater than 100 ms and the tachycardia did not produce severe symptoms). In group 3, the regimen did not produce a beneficial response. During follow-up, recurrence of sustained ventricular tachycardia occurred in 7 (7%) of 103 group 1 patients but in 20 (39%) of 51 and 52 (50%) of 104 group 2 and 3 patients, respectively. However, the total mortality and sudden death mortality rates were substantially reduced in group 2 (12 and 4%, respectively) compared with group 3 (39 and 34%). In fact, the total mortality and sudden death mortality in groups 1 and 2 were not significantly different. Thus, under certain circumstances, a drug regimen that produces a beneficial response may be an acceptable clinical alternative, particularly when no regimen prevents induction of ventricular tachycardia.

Adolescent↗
PubMed1987

Risks and complications of clinical cardiac electrophysiologic studies: a prospective analysis of 1,000 consecutive patients.

The complications of clinical cardiac electrophysiologic studies were prospectively evaluated in 1,000 consecutive patients studied in one laboratory with an unaltered protocol to better assess the risks of this procedure. There were 728 men and the mean age of the entire group was 58 years (range 16 to 84). Coronary artery disease was the most common type of heart disease (56%) and 200 patients had no identifiable organic heart disease. The indication for study was a ventricular tachyarrhythmia or cardiac arrest in 582 patients. Each patient underwent an initial (baseline) study and 444 patients underwent serial drug studies (2.7/patient). There was one death during these studies. Other major complications included arterial injury (0.4%), thrombophlebitis (0.6%), systemic arterial embolism (0.1%), pulmonary embolism (0.3%) and cardiac perforation (0.2%). Significant arrhythmic complications included catheter-induced permanent complete atrioventricular (AV) block in 1 patient, nonclinical atrial fibrillation that required therapy in 10 patients and severe proarrhythmic events in 12 (3%) of 397 patients undergoing drug studies for ventricular tachyarrhythmias. Cardioversion was required for termination of ventricular tachyarrhythmias in 179 baseline studies (53% of patients with inducible arrhythmia), and in an additional 35 patients, cardioversion was required at least once during follow-up studies. Although clinical cardiac electrophysiologic studies are associated with complications, the risks are small and acceptable.

Arrhythmias, Cardiac↗
PubMed1987

Autonomic modulation of aminophylline influence on the electrophysiological effects of adenosine and adenosine triphosphate in the canine heart.

The influence of aminophylline, a competitive antagonist of adenosine, on the chronotropic and dromotropic effects of adenosine and adenosine triphosphate was studied in pentobarbital anaesthetised dogs under various modifications of the autonomic nervous tone. Adenosine and adenosine triphosphate (3 mumol.kg-1 each) were rapidly (greater than or equal to 1 s) injected into the right atrium during both sinus rhythm and right atrial pacing (cycle length 300 ms) before and after infusion of aminophylline (5 mg.kg-1) (n = 21) as well as after increasing doses of aminophylline (n = 10). Some dogs underwent either muscarinic blockade with atropine (0.2 mg.kg-1) (n = 10), or beta adrenergic blockade with propranolol (1 mg.kg-1) (n = 10), or complete autonomic blockade with atropine and propranolol (n = 10). Aminophylline (5 mg.kg-1) antagonised the negative chronotropic and dromotropic effects of adenosine triphosphate and adenosine in dogs pretreated with atropine or atropine plus propranolol but did not affect them in autonomically intact dogs. In addition, the electrophysiological effects of adenosine were antagonised by only the highest doses of aminophylline in autonomically intact dogs and by aminophylline (5 mg X kg-1) in dogs pretreated with propranolol. It was concluded that (a) alteration of the electrophysiological effects of adenosine triphosphate and adenosine by aminophylline is appreciably influenced by the autonomic nervous tone and (b) autonomic blockade is required for the manifestation of the antagonism by aminophylline of the electrophysiological action of adenosine and adenosine triphosphate.

Adenosine↗
PubMed1986

Plasma norepinephrine in exercise-induced ventricular tachycardia.

The relation between plasma norepinephrine levels and the occurrence of ventricular tachycardia during exercise testing was prospectively evaluated in 17 patients. Ten patients had reproducible ventricular tachycardia exclusively during exercise or recovery, or both; 7 patients had ventricular tachycardia only during ambulatory electrocardiographic monitoring. The two groups did not differ in age, exercise duration, left ventricular ejection fraction at rest, heart rate throughout the exercise protocol, rest QTc interval, change in QTc interval during exercise, the presence of coronary artery disease or exercise-related myocardial ischemia. Furthermore, there was no difference between groups in plasma norepinephrine levels at rest, peak exercise or in the recovery period. Myocardial ischemia was detectable by thallium perfusion scan in only 2 of the 10 patients with exercise-induced ventricular tachycardia. The 10 patients with exercise-induced ventricular tachycardia underwent repeat exercise testing immediately after maximal intravenous beta-adrenergic blockade with propranolol. Although they had no change in exercise duration, ventricular tachycardia did not occur in 9 of these 10 patients. Plasma norepinephrine levels were significantly decreased compared with levels before beta-adrenergic blockade (p less than 0.0002). Thus, plasma norepinephrine levels do not distinguish patients with reproducible exercise-induced ventricular tachycardia from otherwise comparable patients. Propranolol is highly effective in abolishing this arrhythmia and this effect is associated with decreased norepinephrine levels.

Adult↗
PubMed1986

Flecainide: steady state electrophysiologic effects in patients with remote myocardial infarction and inducible sustained ventricular arrhythmia.

The effect of flecainide in 24 patients with inducible sustained ventricular arrhythmia and a history of remote myocardial infarction was determined. Flecainide was administered in oral doses individually adjusted to suppress all spontaneous ventricular tachycardia and 80% of ventricular premature complexes on 24 hour ambulatory (Holter) electrocardiography. Antiarrhythmic therapy, as assessed by Holter monitoring, was adequate in 20 (83%) of the study patients at a mean dose of 144 +/- 28 mg every 12 hours; the mean plasma flecainide level was 583 +/- 329 ng/ml. In 18 patients, the mean sinus cycle length, sinus node recovery time and atrial, atrioventricular nodal and ventricular refractory periods were unchanged. The AH interval increased by 15 +/- 15%, the HV interval by 35 +/- 32% and the QRS duration by 24 +/- 21%. Toxicity or failure to suppress ventricular premature complexes and ventricular tachycardia by Holter monitoring precluded electrophysiologic study with flecainide in four patients; two patients refused electrophysiologic study with flecainide for nonmedical reasons. Ventricular tachycardia was not inducible in 4 (22%) of 18 patients receiving flecainide. Sustained arrhythmia remained inducible in 14 patients (78%) despite evidence of antiarrhythmic efficacy on Holter monitoring, but the rate of the induced ventricular tachycardia was slower and symptoms were alleviated during ventricular tachycardia in 10 (56%) of 18 patients. The 4 patients who had no inducible ventricular tachycardia with flecainide, and the 10 patients who had inducible ventricular tachycardia with a longer cycle length and alleviation of their symptoms, have been followed up as outpatients for 16 +/- 7 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗