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Jerry L Bauman

Publications and source records attributed to Jerry L Bauman.

11 recordsLinked to original sources
PubMed2006

Mechanisms, manifestations, and management of digoxin toxicity in the modern era.

Because of the common use of digoxin and because of its narrow therapeutic index, digoxin toxicity has been prevalent historically and, therefore, most clinicians are well aware of the classical dose/concentration-related signs and symptoms of toxicity. Yet, in the modern era the incidence of digoxin toxicity has been declining for a variety of reasons, including a new (lower) therapeutic range, the development of more effective drug therapies for heart failure, and more accurate dosing methods. In addition, digoxin toxicity, once commonly fatal, can now be quickly and effectively treated by the emergency administration of antidigoxin Fab fragments. Indeed, it may be possible to expand the use of Fab fragments to select patients with non-life-threatening digoxin toxicity, in order to save costs and improve patient comfort. Most cases of digoxin toxicity are caused by inappropriately high dosages, which are usually prescribed in the setting of renal dysfunction, while other cases can be attributed to system errors such as multiple prescriptions, poor patient counseling, or errors in transcribing. With modern computerized prescribing systems, such as direct physician order entry and prompts that alert the clinician to the potential for error, it is possible to decrease the incidence of digoxin toxicity even further. A realistic goal is to nearly eradicate once commonplace digoxin toxicity or at least make its occurrence a rare event.

Adverse Drug Reaction Reporting Systems↗
PubMed2004

Pharmacodynamics of beta-blockers in heart failure: lessons from the carvedilol or metoprolol European trial.

Heart failure is a growing public health problem in the United States, and the approach to the treatment of heart failure has undergone a radical transformation in the past decade. The use of beta-blocker therapy in heart failure patients is now widely recommended, based on evidence from large-scale clinical trials demonstrating that bisoprolol, carvedilol, and extended-release metoprolol succinate significantly reduce morbidity and mortality in patients with heart failure. Although these agents appear to provide similar benefits, the question remains whether pharmacologic differences among them could translate to differences in clinical outcomes. The Carvedilol Or Metoprolol European Trial (COMET) compared nonselective blockade of the beta1-/beta2-/alpha1-adrenergic receptors with carvedilol versus selective beta1-blockade with immediate-release metoprolol tartrate in patients with chronic heart failure. The trial found that carvedilol significantly reduced all-cause mortality compared with immediate-release metoprolol tartrate, although there were no differences in hospitalizations. Herein we review the pharmacokinetics and pharmacodynamics of metoprolol and carvedilol. In doing so, several issues regarding the design of COMET are identified that could alter the interpretation of the results of this trial. These include the choice of dose and dosage regimen of immediate-release metoprolol tartrate, a dosage form that has never been shown to reduce mortality in patients with heart failure. Additional studies are needed to fully understand whether there are any advantages of selective versus nonselective adrenergic blockade and whether there are any clinically meaningful differences in effectiveness between beta-blockers with proven benefit in the management of chronic heart failure. The results of COMET demonstrate that all beta-blockers and dosage forms are not interchangeable when prescribed for heart failure. Clinicians should choose only those agents (and dosage forms) that have been proven to reduce mortality in this patient population.

Adrenergic beta-Antagonists↗
PubMed2003

Evidence of the economic benefit of clinical pharmacy services: 1996-2000.

We sought to summarize and assess original evaluations of the economic impact of clinical pharmacy services published from 1996-2000, and to provide recommendations and methodologic considerations for future research. A systematic literature search was conducted to identify articles that were then blinded and randomly assigned to reviewers who confirmed inclusion and abstracted key information. Results were compared with those of a similar review of literature published from 1988-1995. In the 59 included articles, the studies were conducted across a variety of practice sites that consisted of hospitals (52%), community pharmacies and clinics (41%), health maintenance organizations (3%), and long-term or intermediate care facilities (3%). They focused on a broad range of clinical pharmacy services such as general pharmacotherapeutic monitoring (47%), target drug programs (20%), disease management programs (10%), and patient education or cognitive services (10%). Compared with the studies of the previous review, a greater proportion of evaluations were conducted in community pharmacies or clinics, and the types of services evaluated tended to be more comprehensive rather than specialized. Articles were categorized by type of evaluation: 36% were considered outcome analyses, 24% full economic analyses, 17% outcome descriptions, 15% cost and outcome descriptions, and 8% cost analyses. Compared with the studies of the previous review, a greater proportion of studies in the current review used more rigorous study designs. Most studies reported positive financial benefits of the clinical pharmacy service evaluated. In 16 studies, a benefit:cost ratio was reported by the authors or was able to be calculated by the reviewers (these ranged from 1.7:1-17.0:1, median 4.68:1). The body of literature from this 5-year period provides continued evidence of the economic benefit of clinical pharmacy services. Although the quality of study design has improved, whenever possible, future evaluations of this type should incorporate methodologies that will further enhance the strength of evidence of this literature and the conclusions that may be drawn from it.

Cost-Benefit Analysis↗
PubMed2002

Hawthorn.

Crataegus monogyna Jacq (Lindm), C. laevigata (Poir) DC, or related Crataegus species, collectively known as hawthorn, have been used in the treatment of cardiovascular diseases. Clinical studies have found that standardized extracts show promise as adjunctive agents for the treatment of left ventricular dysfunction. Other trials consistently demonstrate its ability to improve exercise tolerance and symptoms of mild to moderate heart failure. Preliminary evidence indicates that it improves left ventricular performance, as measured by ejection fraction. In order to properly use hawthorn in the treatment of heart failure, a large, controlled, multicenter trial in which mortality serves as the primary endpoint is needed.

Crataegus↗
PubMed2002

Cocaine-induced channelopathies: emerging evidence on the multiple mechanisms of sudden death.

Sudden death due to cocaine in the absence of myocardial infarction has been attributed to the precipitation of life-threatening arrhythmias not unlike that due to antiarrhythmic drugs. Cocaine is a slow on-off sodium blocker and a fast on-off potassium blocker. Effects on repolarization are biphasic: At low concentrations, cocaine delays ventricular recovery, whereas at higher levels, cocaine hastens it. Two distinct clinical profiles emerge from case reports of electrocardiographically documented life-threatening arrhythmias attributed to cocaine. The first is monomorphic slow ventricular tachycardia or idioventricular rhythm that occurs in overdose situations and appears to reflect excessive sodium channel block; it may respond to sodium bicarbonate. The second is torsade de pointes that occurs in recreational users who have underlying risks for this tachycardia (such as fully or partially expressed congenital long QT syndrome) and reflects potassium channel blockade. These clinical observations can be explained by recent findings regarding the electrophysiologic effects of cocaine. Other patterns of severe arrhythmias due to cocaine may yet emerge.

Adult↗
PubMed2002

Clinical observations with the amiodarone/warfarin interaction: dosing relationships with long-term therapy.

OBJECTIVES: The interaction between amiodarone and warfarin has only been described in patients being followed up for relatively short time periods. The objectives of this study were to characterize the interaction between these two agents in a clinical situation over a longer period of time in a larger cohort of patients, and to determine the relationship between the maintenance dose of amiodarone and the resultant need to adjust the dose of warfarin. DESIGN: This was an observational trial of a cohort of patients receiving a stable warfarin regimen in whom oral amiodarone was initiated. Patients received both amiodarone and warfarin for at least 1 year, and the dosage of warfarin was adjusted as clinically necessary to achieve an international normalized ratio of 2 to 3. Data from a total of 43 patients were analyzed. RESULTS: At baseline, prior to initiation of amiodarone, the warfarin dose was 5.2 +/- 2.6 mg/d. The magnitude of the interaction between these two agents peaked at 7 weeks, which resulted in a 44% mean maximum reduction in the warfarin dose. The warfarin dose inversely correlated with the maintenance dose of amiodarone (r(2) = 0.94, p < 0.005). Minor bleeding episodes occurred in five patients (12%). For patients receiving amiodarone maintenance doses of 400, 300, 200, or 100 mg/d, it is recommended that the daily warfarin dose be reduced by approximately 40%, 35%, 30%, or 25%, respectively. CONCLUSIONS: The magnitude of the amiodarone/warfarin interaction is highly dependent on the maintenance dose of amiodarone. This relationship can aid clinicians in adjusting the dose of warfarin patients receiving long-term amiodarone treatment.

Aged↗
PubMedDate not supplied

A method of determining the dose of digoxin for heart failure in the modern era.

BACKGROUND: The therapeutic range for digoxin in heart failure has recently changed to become lower and narrower, and the new range is associated with improved mortality. However, dosing methods have not been modified to reflect this change. In this study, we sought to develop a new method to determine the initial dose of digoxin in patients with heart failure. METHODS: Over a 6-month period, medical records were screened and reviewed for hospitalized adult patients who had a steady state digoxin concentration. A multiple linear regression was estimated relating digoxin concentration, digoxin dose, creatinine clearance, and ideal body weight to generate an equation relating the dose of digoxin with these variables and a specific target digoxin concentration of 0.7 ng/mL (0.9 nmol/L). This new method was then compared with 2 existing methods. RESULTS: Included in the study were 54 patients (mean [SD] age, 68 [15] years, with a mean (SD) creatinine clearance of 50 (25) mL/min (0.8 [0.4] mL/s) and mean (SD) ideal body weight of 62 (11) kg. Our proposed method and the Jusko and Koup method were more accurate than the Jelliffe method in predicting digoxin concentration. Root mean square errors were as follows: for the Jelliffe method (using ideal body weight), 0.810; for the Koup and Jusko method (with heart failure), 0.401; our proposed method, 0.375. The proposed method was then used to create a dosing nomogram. CONCLUSIONS: Because the new therapeutic window of digoxin is associated with improved outcomes, more intensive dosage refinement should be considered. To this end, we offer new dosing recommendations and a nomogram for determining the initial dose of digoxin in patients with heart failure.

Aged↗
PubMedDate not supplied

The COMET trial.

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Adrenergic beta-Antagonists↗