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Biomedical subjects

J Morganroth

Publications and source records attributed to J Morganroth.

At least 73 records · Page 4Linked to original sources
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

Efficacy of oral and intravenous indecainide in ventricular arrhythmias.

To evaluate the efficacy of oral and intravenous indecainide, a new class IC antiarrhythmic agent, 3 separate protocols were performed in patients with benign or potentially lethal ventricular arrhythmias. An open-label intravenous trail in 10 patients was conducted using a dose of 1.7 mg/kg/min under constant monitoring. An oral short-term in-hospital trial in 20 patients (8 patients entered directly from the intravenous short-term trial) was conducted using a single-blind placebo dose titration protocol in which 50 mg of indecainide every 8 hours was increased at 3-day intervals to 75 mg, and then 100 mg every 8 hours depending on the observed change in ventricular arrhythmia frequency by Holter monitoring. Finally, an outpatient long-term oral trial was conducted in 17 of the 20 patients who completed the inpatient oral short-term trail. Two of the 10 patients from the inpatient intravenous trail did not enter the oral trial, because a proarrhythmic response developed in 1 and because of a lack of efficacy in the other. During the inpatient oral trial, 17 of 20 patients (85%) responded to indecainide and entered the long-term phase. Two of these patients were removed from the trial because of lack of efficacy at 3 and 10 months, respectively. In the oral therapy protocols, minor side effects of the central nervous system occurred in 4 of 17 patients (24%). Six of 20 patients (30%) each had more than a 25% increase in PR and QRS duration that was not associated with higher degrees of block.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

Risk factors for the development of proarrhythmic events.

Definitions of proarrhythmia, including clinical consequence, were applied to the flecainide and encainide data bases to determine risk factors for serious proarrhythmic events or deaths. Such outcomes with flecainide were far less common for patients with benign or potentially lethal ventricular arrhythmias compared to patients with predominantly lethal ventricular arrhythmias. No deaths from proarrhythmia during flecainide therapy occurred in patients without structural heart disease. Serious proarrhythmic events and deaths were more common in patients in whom therapy was initiated in hospital than in those in whom therapy was initiated out of hospital. When the flecainide dosage for patients with lethal ventricular arrhythmias was chosen using steady-state pharmacologic principles, the occurrence of all proarrhythmic events and deaths dropped from 26% and 13% to 10% and 0%, respectively. Structural heart disease, sustained ventricular tachycardia, inpatient initiation and large-dose escalation of class IC drugs are the primary risk factors for development of proarrhythmic events.

Anilides↗
PubMed1987

Application of a frequency definition of ventricular proarrhythmia.

To differentiate spontaneous variability from proarrhythmia in patients with benign or potentially lethal ventricular arrhythmias, 495 patients with 2 or more Holter tracings during placebo therapy were evaluated. The Holter session with the highest frequency of ventricular premature complexes (VPCs) and ventricular tachycardia was compared with the first placebo recording. Patients were segregated by their baseline frequency of VPCs. The percent of patients taking placebo in this trial who had the same increase in VPC frequency as has been ascribed to those with proarrhythmia varied from 0 of 470 patients with a baseline frequency of ventricular arrhythmia of 10 to 50 VPCs/hour, 3 of 44 (7%) with 51 to 100 VPCs/hour, 1 of 139 (0.7%) with 101 to 300 VPCs/hour and 1 of 265 (0.04%) with more than 300 VPCs/hour. Overall, 5 of 496 (1%) patients would have been classified as having proarrhythmia using the algorithm although only placebo was given. A 10-fold or greater increase in ventricular tachycardia beats in patients taking placebo occurred in 9 of 274 patients (3%). Thus, a simple algorithm to define proarrhythmia in patients with mixed cardiac disease and chronic ventricular arrhythmias can be defined and differentiated from spontaneous variability. This arbitrary algorithm defines proarrhythmia as an increase of more than 3 times when baseline VPC frequency is more than 100 VPCs/hour and more than 10 times when that frequency is less than 100 VPCs/hour with a false-positive rate of only 1%.

Algorithms↗
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

Differential utility of antiarrhythmic agents.

Sudden cardiac death (SCD), which is recognized as the most common cause of death in adults, in 80% of cases results from a ventricular tachyarrhythmia that subsequently degenerates into ventricular fibrillation. Ventricular arrhythmias have been identified as a major factor in predicting a high risk of SCD and can be classified as benign, potentially lethal, or lethal. This system is based on the likelihood that the rhythm type predicts the occurrence of sudden death. Antiarrhythmic agents are employed to eliminate ventricular arrhythmias and their sequelae, particularly hemodynamic consequences. Many physicians use these drugs with the additional hope of preventing sudden death, although to date no data support such use. This article details the comparative utility of commonly available antiarrhythmic agents in terms of their safety and efficacy, and defines the bases for the recommendations of an algorithm that can be used to choose among the various drugs.

Anti-Arrhythmia Agents↗
PubMed1987

Antiarrhythmic agents for chronic ventricular arrhythmias.

A vast array of new antiarrhythmic agents have joined the old agents among the clinician's available resources. While treatment of ventricular arrhythmias is completely justifiable for patients with symptoms, their use to prevent sudden cardiac death has not yet been established. Because of their potential risks, the benefit/risk ratio must always be kept in mind. If we elect to treat patients who have benign or potentially lethal ventricular arrhythmias (usually to eliminate refractory symptoms) we typically begin with either a beta blocker or one of the new potent class IC antiarrhythmic agents such as flecainide or encainide. These drugs cause few side effects, no organ toxicity, and in the case of encainide or flecainide, have marked potency. Few important proarrhythmic effects are seen with these potent drugs in this group of patients. If these fail, one can try either a class IA or IB agent or a combination of a IA and IB agent. We always avoid amiodarone. In patients with lethal ventricular arrhythmias, one should choose a drug without negative inotropic potential such as quinidine or encainide as initial therapy. The combination of IA and IB agents should also be considered early in therapy. In patients with overt congestive heart failure with markedly depressed left ventricular function in the setting of lethal arrhythmias, disopyramide, beta blockers, and flecainide should be avoided. Amiodarone is used in this population only when the other available agents have proven to be ineffective or badly tolerated.

Amiodarone↗
PubMed1986

Bepridil hydrochloride for treatment of benign or potentially lethal ventricular arrhythmias.

To define the efficacy and safety of a new once-a-day calcium antagonist, bepridil, 21 patients with frequent ventricular premature complexes (VPCs) underwent a 14-day inpatient monitored trial. After Holter monitoring during placebo administration, patients underwent 2 days of a loading dose of bepridil followed by 12 days of bepridil, 400 mg/day. Holter monitoring during therapy showed that 10 patients (48%) had more than a 70% reduction in VPC frequency and 8 of 16 patients (50%) at least a 95% reduction in frequency of nonsustained ventricular tachycardia. Gastrointestinal and central nervous system side effects considered to be mild occurred in 13 patients (62%). One patient had an asymptomatic increase in VPC frequency and another had sustained ventricular tachycardia associated with a loading dose of 900 mg of bepridil. Thus, bepridil has moderate antiarrhythmic efficacy in patients with ventricular arrhythmias, but further definition of its potential for causing proarrhythmia must be determined.

Bepridil↗
PubMed1986

Intravenous atenolol for ventricular arrhythmias.

To determine the efficacy and safety of intravenous atenolol in patients with frequent and repetitive benign or potentially lethal ventricular arrhythmias, 40 patients received an open-label, single dose of 10 mg of intravenous atenolol, given in aliquots of 2.5 mg every 10 minutes. Twenty-four-hour Holter monitoring was performed on the day before, the day of, and the day after infusion of atenolol. A full 10-mg dose was given to 37 patients; asymptomatic bradycardia developed in 3 patients, and they were not included in the efficacy analysis. A single 10-mg dose of intravenous atenolol was effective rapidly in suppressing ventricular arrhythmias, with peak suppression occurring 1 to 2 hours after infusion and significant suppression lasting for 7 hours. Only 1 patient had symptoms (lightheadedness), plus hypotension lasting 45 minutes after the infusion was concluded. The mean plasma level of atenolol was 231 ng/ml 10 minutes after the infusion, with individual patient values of 148 to 457 ng/ml. Thus, a single intravenous dose of 10 mg of atenolol can significantly reduce the frequency of ventricular premature complexes and ventricular tachycardia within the first hour after infusion; suppression can last for 7 hours. Atenolol is well tolerated.

Adult↗
PubMed1986

Encainide for ventricular arrhythmias: placebo-controlled and standard comparison trials.

Efficacy data obtained from the use of encainide in the treatment of patients with benign or potentially lethal ventricular arrhythmias are reviewed. These include an oral dose multicenter titration study involving 111 patients in whom encainide was given from 25 to 75 mg, 4 times/day, which was followed by a 3-center, reduced dose study in which 35 patients received a forced escalation of encainide from 10 to 30 mg, 4 times/day. Frequent Holter monitoring was used to judge efficacy. An 8-center, double-blind, parallel, placebo-controlled outpatient trial was conducted using encainide from 10 to 50 mg, 3 times/day, in 125 patients. This trial defined the lower end of the dose response curve for encainide to be 25 mg, 3 times/day. The data from all these trials show that when properly titrated, encainide is effective in decreasing ventricular premature complex frequency by at least 75% in about 80% of patients. A similar percentage will have abolition of ventricular tachycardia. When encainide was compared with quinidine in a 9-center placebo-controlled crossover study, encainide demonstrated more efficacy at 25 mg, 4 times/day, compared with quinidine at 200 mg, 4 times/day, in all arrhythmia parameters. Encainide was also better tolerated than quinidine and there was no statistically significant difference in the prevalence of asymptomatic proarrhythmia as detected by Holter monitoring between these 2 drugs. Long-term data in 220 patients over 36-month follow-up show continued encainide efficacy. Thus, encainide is a potent, effective class 1C antiarrhythmic agent and it has minimal negative inotropic effects and is well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Effectiveness of low-dose nadolol for ventricular arrhythmias.

To determine the minimal effective dose of nadolol to suppress frequent ventricular premature complexes (VPCs), 23 patients with at least 30 VPCs/hour on 2 baseline 24-hour Holter recordings were studied. The initial dose of nadolol was 10 mg/day orally, and this dose was doubled at weekly intervals until arrhythmia suppression was achieved, adverse effects appeared, or a maximal dose of 160 mg/day was reached. After each dose level a 24-hour ambulatory Holter monitor was recorded. A pharmacokinetic trial was conducted in patients who responded to nadolol treatment. Frequent VPCs were suppressed at least 75% by nadolol in 11 of 23 patients (48%) and the minimal effective dose was 10 mg/day in 3 patients, 20 mg/day in 4, 40 mg/day in 3 and 80 mg/day in 1 patient. At these doses, minimal steady-state levels of nadolol in serum (Cmin) ranged from 3.9 to 47.0 ng/ml, and these serum concentrations were proportional to the oral dose of nadolol (r = 0.753, p less than 0.001). No relation, however, was observed between Cmin levels and percent reduction of VPCs. Cmin and heart rate changes were comparable between responders and nonresponders, suggesting that the degree of beta blockade was similar between these 2 groups. Adverse reactions were noted in 6 patients, and 2 had an asymptomatic increase in the frequency of VPCs and 1 patient an increase in beats of ventricular tachycardia. This study details the importance of selecting an individualized dose for nadolol for control of ventricular arrhythmias; in more than half of the patients doses of 20 mg/day or less were effective.

Adolescent↗
PubMed1986

Dose-response range of encainide for benign and potentially lethal ventricular arrhythmias.

A multicenter, 2-week, double-blind, placebo-controlled, parallel group study was performed to determine the dose-response relation of encainide administered 3 times daily and to determine its onset of action. To be included in the study, patients with benign or potentially lethal ventricular arrhythmias were required to have an average of at least 30 ventricular premature complexes (VPCs) per hour on 48-hour Holter monitoring after a 48-hour washout period without antiarrhythmic drug treatment. Patients were randomly assigned to receive either placebo or 10, 25 or 50 mg of encainide 3 times daily (tid) for 2 weeks. Of the 125 patients who entered the study, 122 were available for efficacy analysis. Efficacy was determined using 24-hour Holter monitoring on days 1, 7 and 14. There was no difference in frequency of VPCs or of ventricular tachycardia events in the placebo and 10-mg-tid encainide arms. At doses of 25 and 50 mg of tid, encainide was effective in suppressing VPCs and in reducing the number of episodes of ventricular tachycardia. A positive dose-response relation was identified. The onset of effect of encainide was apparent at 3 hours and lasted for 24 hours with tid dosing. No difference in on-therapy conditions were found among the 4 study arms. No patients were discontinued from the study because of electrocardiographic changes. There was no statistically significant change in vital signs or physical examination data. In 1 patient an elevated serum glucose level developed. No symptomatic proarrhythmic events occurred and none required discontinuation of study medication.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗