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J A Reiffel

Publications and source records attributed to J A Reiffel.

At least 37 records · Page 2Linked to original sources
PubMed1998

Rhythm management in atrial fibrillation--with a primary emphasis on pharmacologic therapy: Part 3.

Atrial fibrillation (AF) is the most common, sustained, symptomatic tachyarrhythmia that clinicians are called upon to manage. Management strategies include ventricular rate control coupled with anticoagulation, versus restoration and maintenance of sinus rhythm. Rate control may be achieved pharmacologically, with agents that impair AV nodal conduction directly and/or by increasing parasympathetic/sympathetic balance, or by modifying or ablating the AV nodal region anatomically. Rhythm control may be achieved by electrical or pharmacologic conversion followed by maintenance of sinus rhythm by pharmacologic (or occasionally ablative) therapies. This article will present current approaches to rate and rhythm control issues in atrial fibrillation. Parts 1 and 2, published previously, dealt with rate control and with the restoration of sinus rhythm. Part 3, the current article, details the selection process of choosing a therapy to maintain sinus rhythm, including the likelihood of success, the risks of therapy, and individualization of therapy as dependent upon the nature of the structural heart disease present. It also discusses nonpharmacologic approaches that have been recently developed or are undergoing development. One suggested drug selection algorithm is provided.

Algorithms↗
PubMed1997

Prolonging survival by reducing arrhythmic death: pharmacologic therapy of ventricular tachycardia and fibrillation.

Antiarrhythmic drug therapy of sustained ventricular tachyarrhythmias is undertaken to reduce arrhythmic symptoms, recurrences, and mortality. Ideally, reduction of arrhythmic death will reduce total mortality as well, although this may not hold true in the presence of competing risk. Whether, in fact, antiarrhythmic therapy actually reduces arrhythmic death remains uncertain in the absence of any placebo-controlled trials. Nonetheless, the following conclusions can be drawn from the Electrophysiologic Study versus Electrocardiographic Monitoring (ESVEM) trial, the Cardiac Arrest Study Hamburg (CASH), and the Cardiac Arrest in Seattle: Conventional versus Amiodarone Drug Evaluation (CASCADE) study, as well as a beta blocker study by Steinbeck et al: (1) class I antiarrhythmics are less effective than amiodarone or sotalol for the prevention of recurrent sustained ventricular tachycardia/ventricular fibrillation; (2) sympathetic inhibition as a component of the antiarrhythmic regimen may strongly contribute to mortality reduction; and (3) the respective roles of antiarrhythmic drugs, implantable devices, and the concurrent use of both are in a state of flux, awaiting results of randomized controlled clinical trials.

Aged↗
PubMed1997

Sotalol for ventricular tachyarrhythmias: beta-blocking and class III contributions, and relative efficacy versus class I drugs after prior drug failure. ESVEM Investigators. Electrophysiologic Study Versus Electrocardiographic Monitoring.

In the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial, d,l-sotalol was associated with a lower arrhythmia recurrence and mortality than class I antiarrhythmic drugs. To further evaluate the relative efficacy of d,I-sotalol compared with class I drugs, and to assess the relative importance of its class II (beta-blocking) and class III effects, 6-year arrhythmia recurrence and mortality in patients receiving sotalol were compared with those in patients receiving class I drugs, subdivided according to whether they also received coadministered beta blockers. Relative efficacy was also determined for sotalol and for class I drugs as stratified by the presence/absence of prior drug failure. Arrhythmia recurrence was lower for the 84 patients receiving sotalol than for patients given class I agents with (n = 28) (p = 0.008) or without (n = 184) (p = 0.001) alpha beta blocker. Mortality was lower for patients taking sotalol than for those given a class I drug without alpha beta blocker (p = 0.034), but similar (p = 0.835) if alpha beta blocker was also administered. In contrast to class I drugs, which had lower efficacy rates when prior drug trials had failed, sotalol maintained its efficacy despite prior drug failures preceding or during the ESVEM trial. Both class II and III actions in the ESVEM trial were important to the clinical superiority of sotalol in the treatment of ventricular tachyarrhythmias.

Adrenergic beta-Antagonists↗
PubMed1997

Reproducibility of drug efficacy predictions by Holter monitoring in the electrophysiologic study versus electrocardiographic monitoring (ESVEM) trial. ESVEM Investigators.

Selection of antiarrhythmic therapy may be based on suppression of spontaneous ventricular arrhythmias assessed by Holter monitoring, but the implications of discordant Holter results on repeat 24-hour monitoring has not been defined. This study examines the frequency and significance of reproducible Holter suppression on two 24-hour recordings in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial. Repeat 24-hour Holter monitoring was obtained in patients randomized to the Holter monitor limb of the ESVEM trial, during the same hospitalization, after a drug efficacy prediction. These Holters were not used to define drug efficacy but were subsequently analyzed to determine the reproducibility of drug efficacy predictions by Holter monitoring. A repeat 24-hour Holter monitor, following the one that predicted drug efficacy, was available in 119 patients. Ninety-nine patients (83%) also had suppression that met efficacy criteria on the second Holter monitor. There were no significant differences in arrhythmia recurrence (p = 0.612) or mortality (p = 0.638) in patients with concordant Holter results (n = 99; 1-year arrhythmia recurrence = 45%; 1-year mortality = 10%) compared with those with discordant Holter results (n = 20; 1-year arrhythmia recurrence = 45%; 1-year mortality = 16%). We conclude that (1) there is discordance between the first effective Holter monitor and a repeat Holter monitor in 17% of patients, and (2) suppression of ventricular ectopic activity on 2 separate 24-hour Holter monitors does not identify a group with a better outcome, nor does failure of suppression on the second Holter monitor identify a group with a worse prognosis.

Aged↗
PubMed1996

Implications of the Electrophysiologic Study versus Electrocardiographic Monitoring trial for controlling ventricular tachycardia and fibrillation.

The Electrophysiologic Study versus Electrocardiographic Monitoring (ESVEM) trial had 2 objectives. The first was to determine the accuracy of noninvasive versus invasive means of predicting the efficacy of drug treatment for ventricular tachycardia/ventricular fibrillation (VT/VF). A second objective was to determine the relative efficacies of 7 antiarrhythmic drugs used in the treatment of ventricular tachyarrhythmias. ESVEM was the first opportunity to compare prospectively the efficacy, safety, and tolerability of a variety of antiarrhythmic drugs in the same patient population. No significant difference was observed between suppression of spontaneous ventricular arrhythmias on Holter monitoring and suppression of inducible ventricular arrhythmias by electrophysiologic study (EPS) in terms of the ability to predict the success of drug therapy. There was also no difference in predictive accuracy if patients in the electrophysiologic limb showed suppression by Holter monitoring in addition to suppression by EPS. Sotalol was more effective than the other 6 antiarrhythmic drugs, all class I agents, in preventing death and recurrence of arrhythmia. Efficacy compared with placebo, however, was not evaluated. In the EPS limb, sotalol was also statistically more likely to achieve an efficacy prediction than any of the sodium channel blocking drugs. Amiodarone was not used in ESVEM. It has been suggested that these conclusions, which differ from those of other, less controlled, invasive and noninvasive studies, might be because of the particular efficacy criteria used in the ESVEM protocol. Retrospective analyses of the ESVEM data were performed using more rigid efficacy criteria than were used in the original ESVEM analysis: a greater degree of ectopy suppression was required for Holter monitoring, and more stringent efficacy definitions were required in the stimulation protocol of the EPS limb. Results from the retrospective analyses and other studies support the initial ESVEM conclusions. In patients with both spontaneous and inducible sustained ventricular tachyarrhythmias as well as frequent spontaneous premature ventricular contractions, therapy with sotalol (guided by either Holter monitoring or EPS) is a reasonable initial strategy because of its superior initial long-term efficacy and better acute and long-term tolerability compared with sodium channel blocking drugs.

Anti-Arrhythmia Agents↗
PubMed1996

Exploration of the precision of classifying sudden cardiac death. Implications for the interpretation of clinical trials.

BACKGROUND: As cardiovascular clinical trials improve in sophistication and therapies target specific cardiac mechanisms of death, a more objective and precise system to identify specific cause of death is needed. Ideally, sudden cardiac death would describe patients dying of ventricular tachycardia and ventricular fibrillation. In this context, we explored the precision of current sudden death classification and implications for clinical trials. METHODS AND RESULTS: Deaths were analyzed in 834 patients who received an automatic implantable cardioverter-defibrillator (ICD). Three arrhythmia experts used a standard prospective classification system to classify deaths into accepted categories: sudden cardiac, nonsudden cardiac, and noncardiac. New aspects to this study included analysis of autopsy results and ICD interrogation for arrhythmias at the time of death. All of the patients receiving the ICD previously had documented sustained ventricular tachycardia/fibrillation or cardiac arrest. Of the 109 subsequent deaths in the 834-patient database, 17 (16%) were classified as sudden cardiac. Compared with the nonsudden cardiac and noncardiac categories, sudden cardiac death was more often identified in outpatients (59% versus 10%) and witnessed less often (41% versus 86%; both P < .001). The autopsy information contradicted and changed the clinical perception of a "sudden cardiac death" in 7 cases (myocardial infarction [n = 1], pulmonary embolism [n = 2], cerebral infarction [n = 1], ruptured thoracic [n = 1], and abdominal aortic aneurysms [n = 2]). Interpretable ICD interrogation was available in 53% of the deaths (47% unavailable: buried, programmed off, or other technical reasons). When evaluated, only 7 of 17 "sudden deaths" were associated with ICD discharges near the time of death. CONCLUSIONS: Even in a group of patients with an ICD, deaths classified as sudden cardiac frequently were not associated with ventricular tachycardia or ventricular fibrillation and were often noncardiac. It is possible to create a wide range of sudden cardiac death rates (more than fourfold) using the identical clinical database despite objective, prespecified criteria. Autopsy results frequently reveal noncardiac causes of clinical events simulating sudden cardiac death. ICD interrogation revealed that ICD discharges were often related to terminal arrhythmias incidental to the primary pathophysiological process leading to death.

Cause of Death↗
PubMed1995

How do physicians determine when to perform an "on-drug" electrophysiology study for efficacy determination in patients with sustained ventricular tachyarrhythmias: a previously unaddressed variable that may affect efficacy rates.

In patients with ventricular tachyarrhythmias, efficacy rates of antiarrhythmic agents, as judged by serial electrophysiological (EP) tests, have been variable. Factors underlying this variability have been reported to include: specific drug, type of arrhythmia, type of heart disease, left ventricular function, and number of prior drug failures. We hypothesized that variability in physician practice behavior as to when a drug assessment is performed might be another important factor affecting drug efficacy. Using a survey sent to 103 electrophysiology centers we determined from the 46 respondents that this is indeed the case. Twenty-six of the 46 respondents always, 9 of 46 sometimes, and 11 of 46 did not require ectopy reduction on continuous electrocardiographic monitoring before proceeding to an EP study. The ectopy reduction required, however, varies among physicians in percentage and type. Twenty-seven of the 35 respondents who utilize rhythm monitoring also require attainment of an acceptable blood level, a prespecified minimal target dose, and/or one or more ECG interval changes prior to proceeding to EP testing. Fifteen out of 46 do not require "therapeutic" drug levels. Of 11 who don't use rhythm monitoring, 5 also don't use blood levels. The lower value for "therapeutic ranges" varied by up to 3-fold and the upper value by up to 2 1/2-fold for individual drugs. The minimum time for testing varied from 1 half-life to over 10 half-lives. Similarly, the response to failure of a submaximal dose also varied: 9% always retested at a high dose, 2% never tested at a higher dose, and 91% were inconsistent. Moreover, what was considered the maximal dose for an individual drug varied by 3- to 6-fold for most agents queried. We believe these variations in dose, time, and coassessment factors must have an influence on efficacy rates of antiarrhythmic agents.

Anti-Arrhythmia Agents↗
PubMed1994

A consensus report on antiarrhythmic drug use.

During the past few years, a number of new antiarrhythmic agents have become available for use in the United States, encainide has been withdrawn from use, and others have had indications for use modified. Therefore, a meeting of arrhythmia specialists was convened in an attempt to develop guidelines for antiarrhythmic therapy. The resultant discussions and guidelines presented in this article address general issues such as the most important antiarrhythmic drug attributes, as well as therapy for particular arrhythmias such as premature ventricular contractions, ventricular tachycardia, ventricular fibrillation, ventricular ectopy, and supraventricular tachyarrhythmias.

Anti-Arrhythmia Agents↗
PubMed1994

Structural heart disease: its importance in association with antiarrhythmic drug therapy.

The presence or absence of structural heart disease is an important factor to consider prior to initiating antiarrhythmic drug therapy with a class I or class III antiarrhythmic agent. An appropriate screen for structural heart disease and other associated proarrhythmic risk factors should include a complete history, physical examination, electrocardiogram (ECG), and echocardiogram in all patients; exercise test and Holter monitoring in many/most selected patients; and a signal-averaged ECG, chest x-ray, and invasive procedures only in selected/occasional patients. Whether and when to obtain the tests that are not indicated for all patients must be determined by each individual physician's practice strategy and philosophy, while keeping in mind the likelihood of finding an abnormality in a particular patient, the arrhythmia being treated, the nature of the drug to be used, and cost-effectiveness issues. Given the low incidence of proarrhythmia under most circumstances, screening for clinically unrecognized structural heart disease may appear difficult to justify in the current era of cost containment. However, due to the potential lethality of proarrhythmia, particularly in patients with structural heart disease, pre-drug assessment is prudent.

Anti-Arrhythmia Agents↗
PubMed1994

Electrophysiological testing of sinus node function: diagnostic and prognostic application-including updated information from sinus node electrograms.

Sinus node function, including automaticity, conduction, and refractoriness, can be studied in the human electrophysiology laboratory. This review details the current methods used for such studies and discusses their clinical value. Of special emphasis in this article is the role of sinus node electrography in the clinical laboratory. Included also is an update of the data relating the duration of sinus node depolarization as measure on sinus node electrograms to other parameters that assess sinus node function as well as data supporting the direct relationship between the duration of the sinus node depolarization as the severity of sinus node dysfunction.

Action Potentials↗
PubMed1991

Optimum duration of transtelephonic ECG monitoring when used for transient symptomatic event detection.

Transtelephonic electrocardiographic monitoring (TTM) has been used for postpacemaker follow-up study, postmyocardial infarction monitoring, and transient symptomatic event detection (TSED). For postpacemaker follow-up study, TTM is continued indefinitely. For postmyocardial infarction monitoring, TTM is continued for 1 year or more. For TSED, the appropriate duration for TTM has not yet been adequately assessed. Accordingly, the authors determined the yield, by week, of TTM for TSED. Five thousand fifty-two patients who made 20,590 calls were analyzed for this investigation. Ninety-five percent of patients making symptomatic calls or making a call in which an arrhythmia was documented did so within 5 weeks. Shorter periods would sacrifice yield, longer periods may not be cost-effective.

Arrhythmias, Cardiac↗
PubMed1989

Efficacy, safety, and tolerance of d-sotalol in patients with refractory supraventricular tachyarrhythmias.

The efficacy, safety, and electrophysiologic effects of intravenous and oral d-sotalol, an investigational class III antiarrhythmic agent, are not yet well characterized. We evaluated the electrophysiologic, antiarrhythmic, and hemodynamic effects of d-sotalol infusion (1.5 to 2.75 mg/kg) and of chronic oral therapy (200 to 400 mg bid) in 10 patients with chronic, paroxysmal supraventricular tachyarrhythmias refractory to 5 +/- 2 standard agents. Four patients had paroxysmal supraventricular tachycardia (PSVT), four had paroxysmal atrial fibrillation, two had atrial flutter, and one had nonparoxysmal reciprocating junctional tachycardia (NPRJT). PSVT was inducible or spontaneously present in 4 of 4 before d-sotalol. After intravenous d-sotalol PSVT was noninducible in three patients and slowed by 40% in one. Atrial fibrillation was inducible or spontaneously present in 4 of 4 before therapy. After intravenous d-sotalol, one became noninducible, and three achieved rate-slowing (the mean falling from 69 to 61 bpm). In one patient, atrial flutter became noninducible; in another, d-sotalol slowed the rate of atrial flutter by 28%. D-sotalol restored sinus rhythm in the patient with NPRJT. Intravenous d-sotalol increased the sinus cycle length; the QTc, PR, and AH intervals; and the AV nodal functional refractory period, the AV nodal effective refractory period; and the right ventricular effective refractory period significantly. The atrial effective refractory period, sinoatrial conduction time, and corrected sinus recovery time tended to increase, but did not reach statistical significance. The QRS, PA, and HV intervals did not change. Mean BP fell 13.4 +/- 9.2% after intravenous d-sotalol, but no adverse symptoms developed.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗