Jerry L. Bauman

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.

Torsade de pointes due to quinidine: Observations in 31 patients

We performed a mail solicitation and obtained the records of 31 patients with documented torsade de pointes (TDP) due to quinidine. All 31 patients had heart disease: ischemic = 11 patients (36%), rheumatic = five patients (16%), hypertensive = four patients (13%), cardiomyopathic = four patients (13%), other = seven patients (22%). Quinidine was administered to these patients for the following reasons: atrial fibrillation or flutter = 22 patients (71%), ventricular premature beats = six patients (19%), ventricular or supraventricular tachycardia = three patients (10%). The 31 patients were receiving quinidine, 650 to 2400 (mean 1097) mg/day, and 14 patients had serum quinidine levels of 1.4 to 10.6 (mean 3.7) micrograms/ml. TDP occurred within 1 week of initiation of quinidine therapy in 23 (74%) of the patients. Twenty-eight (90%) of the 31 patients were receiving digoxin, and 5 (24%) of 21 patients had hypokalemia at the time of TDP. Off of quinidine therapy, corrected QT (QTc) intervals in 24 patients ranged from 390 to 580 (mean 470) msec and were prolonged in 17 patients (71%). On quinidine therapy, QTc intervals in 23 patients ranged from 390 to 630 (mean 510) msec and were prolonged in 21 patients (91%). In summary, patients with TDP due to quinidine usually had heart disease complicated by atrial fibrillation, were receiving digoxin, and were receiving moderate dosages of quinidine for less than 1 week prior to TDP. Approximately two thirds of patients with TDP due to quinidine had long QT intervals while off of quinidine.

Hemodynamic and electrophysiological actions of cocaine. Effects of sodium bicarbonate as an antidote in dogs.

BackgroundCocaine abuse has been implicated as a cause of death due to sudden cardiac arrest. Methods and ResultsWe examined the hemodynamic and electrophysiological effects of cocaine administered as a series of 5-mg/kg i.v. boluses coupled with a continuous infusion in anesthetized dogs. Sodium bicarbonate (50 meq i.v.) was administered as a potential antidote in 11 of 15 dogs, and intravenous 5% dextrose was given in the remaining four. In a dose-dependent fashion, cocaine significantly decreased blood pressure, coronary blood flow, and cardiac output; increased PR, QRS, QT, and QTc intervals and sinus cycle length; and increased ventricular effective refractory period and dispersion of ventricular refractoriness. No afterdepolarizations were noted in the monophasic action potential recording. Nonsustained monomorphic ventricular tachycardia occurred spontaneously in two dogs, and sustained ventricular tachycardia could be induced by programmed stimulation at the end of the dosing protocol in five of 11 animals. Sodium bicarbonate promptly decreased cocaine-induced QRS prolongation to nearly that measured at baseline but had no effect on the other electrocardiographic or hemodynamic variables. In one dog, sodium bicarbonate administration was associated with reversion of ventricular tachycardia to sinus rhythm. ConclusionsWe conclude that high-dose cocaine possesses negative inotropic and potent type I electrophysiological effects. Sodium bicarbonate selectively reversed cocaine-induced QRS prolongation and may be a useful treatment of ventricular arrhythmias associated with slowed ventricular conduction in the setting of cocaine overdose.

Effectiveness and costs of digoxin treatment for atrial fibrillation and flutter.

Clinical outcomes and costs associated with the use of digoxin in atrial fibrillation and flutter were evaluated in a prospective, observational study at 18 academic medical centers in the United States. Data were collected on 115 patients (aged > 18 years) with atrial fibrillation or flutter who were treated with digoxin for rapid ventricular rate (> or = 120 beats/min). The median time to ventricular rate control (i.e., resting ventricular rate < 100 beats/min, decrease in ventricular rate of > 20%, or sinus rhythm) was 11.6 hours from the first dose of digoxin for all evaluable patients (n = 105) and 9.5 hours for those only receiving digoxin (n = 64). Before ventricular rate control, the mean +/- SD dose of digoxin administered was 0.80 +/- 0.74 mg, and a mean of 1.4 +/- 1.8 serum digoxin concentrations were ordered per patient. Concomitant beta-blocker or calcium antagonist therapy was instituted in 47 patients (41%); in 19 of these, combination therapy was initiated within 2 hours. Adenosine was administered to 13 patients (11%). Patients spent a median of 4 days (range 1 to 25) in the hospital; 28% spent time in a coronary/intensive care unit and 79% in a telemetry bed. Loss of control (i.e., resting ventricular rate returned to > 120 beats/min) occurred at least once in 50% of patients and was associated with a longer hospital stay (p < 0.05). Based on 1991 data, the estimated mean hospital bed cost for patients with atrial fibrillation or flutter was

Cocaine-Related Sudden Cardiac Death: A Hypothesis Correlating Basic Science and Clinical Observations

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Impact of the cost of prescription drugs on clinical outcomes in indigent patients with heart disease

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Cocaine-Induced Channelopathies: Emerging Evidence on the Multiple Mechanisms of Sudden Death

Sudden, unexpected death due to cocaine in young otherwise healthy individuals occurs in an idiosyncratic manner and is commonly felt to be arrhythmogenic in nature, although the exact cause of death is rarely documented. In addition to indirect sympathomimetic actions, cocaine is a potent sodium channel blocking drug and, in this regard, most closely resembles agents such as flecainide. We suggest that sudden death due to cocaine is proarrhythmic in nature, occurring under similar circumstances as that due to specific antiarrhythmic drugs.

Racial and Gender Differences in Endothelin-1

Study Objective. To measure the impact that economic relief for prescription drugs to indigent patients with cardiovascular disease has on indicators of disease control.

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

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.

Comparison of Intravenous Diltiazem and Verapamil for the Acute Treatment of Atrial Fibrillation and Atrial Flutter

In summary, ET-1 levels were significantly increased in black men compared with white men. This racial difference could have important research implications if increased ET-1 levels are linked to left ventricular hypertrophy and other cardiovascular diseases, and it may serve as a foundation for future studies.