Biomedical subjects

M A Munger

Publications and source records attributed to M A Munger.

At least 19 recordsLinked to original sources

PubMed1999

Dose-related beneficial long-term hemodynamic and clinical efficacy of irbesartan in heart failure.

OBJECTIVES: The primary purpose of this study was to determine the acute and long-term hemodynamic and clinical effects of irbesartan in patients with heart failure. BACKGROUND: Inhibition of angiotensin II production by angiotensin-converting enzyme (ACE) inhibitors reduces morbidity and mortality in patients with heart failure. Irbesartan is an orally active antagonist of the angiotensin II AT1 receptor subtype with potential efficacy in heart failure. METHODS: Two hundred eighteen patients with symptomatic heart failure (New York Heart Association [NYHA] class II-IV) and left ventricular ejection fraction < or = 40% participated in the study. Serial hemodynamic measurements were made over 24 h following randomization to irbesartan 12.5 mg, 37.5 mg, 75 mg, 150 mg or placebo. After the first dose of study medication, patients receiving placebo were reallocated to one of the four irbesartan doses, treatment was continued for 12 weeks and hemodynamic measurements were repeated. RESULTS: Irbesartan induced significant dose-related decreases in pulmonary capillary wedge pressure (average change -5.9+/-0.9 mm Hg and -5.3+/-0.9 mm Hg for irbesartan 75 mg and 150 mg, respectively) after 12 weeks of therapy without causing reflex tachycardia and without increasing plasma norepinephrine. The neurohormonal effects of irbesartan were highly variable and none of the changes was statistically significant. There was a significant dose-related decrease in the percentage of patients discontinuing study medication because of worsening heart failure. Irbesartan was well tolerated without evidence of dose-related cough or azotemia. CONCLUSIONS: Irbesartan, at once-daily doses of 75 mg and 150 mg, induced sustained hemodynamic improvement and prevented worsening heart failure.

Adolescent↗

PubMed1997

ACE inhibitor effects on platelet function in stages I-II hypertension.

Angiotensin II enhances platelet aggregation through activation of the G protein-linked pathway present in platelets. Studies of several angiotensin-converting enzyme (ACE) inhibitors have demonstrated marked differences on platelets. Therefore this prospective, randomized, double-blind, crossover study compared the ex vivo effects of equivalent antihypertensive doses of captopril, enalapril, and fosinopril on platelet aggregation and thromboxane B2 (TxB2) formation in subjects with stage I-II essential hypertension. Nineteen male subjects with a baseline mean seated blood pressure of 141 +/- 3/100 +/- 1 mm Hg were enrolled. The decline in mean arterial pressure after 4 weeks of stable dosing was 10 +/- 1, 12 +/- 1, and 11 +/- 1 mm Hg for captopril, enalapril, and fosinopril, respectively (p = NS). There was no significant change in adenosine diphosphate (ADP)-, epinephrine-, or thrombin-stimulated platelet aggregation from baseline or between ACE inhibitors. Compared with baseline, fosinopril decreased TxB2 concentrations 27.5-67.6% with all stimuli after 1 and 5 min. Captopril also decreased TxB2 formation, but this effect was stimulus and time dependent. Enalapril consistently increased TxB2 concentrations, independent of stimuli or time. We conclude that different ACE inhibitors have distinct effects on platelet TxB2 formation without significant effects on platelet aggregation. Fosinopril may be a direct antagonist ofTxA2 synthase, suggesting benefit in syndromes of platelet activation or vascular occlusion.

Adult↗

PubMed1997

Evaluation of the indomethacin-nitroglycerin interaction with positron-emission tomography.

The hypothesis that local release of prostanoids may contribute to the pharmacologic effect of nitroglycerin (NTG) has long been debated. Results of prostanoid blockade by indomethacin on NTG-induced effects, to date, have been inconclusive. To quantitate the effects of intravenous indomethacin on NTG-induced myocardial blood flow by using positron-emission tomography, we conducted a prospective, controlled, parallel-design study comparing patients with coronary artery disease with healthy volunteers. Eight subjects, four Canadian Class II-III coronary artery disease (CAD) with luminal narrowing of > 80% in a minimum of two vessels, and four healthy volunteers were evaluated. Baseline global myocardial blood flow was equivalent between the groups. NTG produced a 49.3 +/- 4.7% increase in myocardial blood flow in healthy volunteers (p = 0.006) and an -0.5 +/- 19.8% decrease in the group with CAD (p = 0.62 between groups). After indomethacin, both groups had a 24% decline in myocardial blood flow (CAD, p = 0.25; healthy, p = 0.03). One patient with CAD had acute ischemia after indomethacin. The study demonstrated that short-term intravenous indomethacin decreases NTG-induced myocardial blood flow to the same degree in both subjects with CAD and healthy individuals. Impairment of myocardial blood flow from this pharmacologic combination may be most important in patients with severe fixed lesions.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1996

Circulating concentrations of proinflammatory cytokines in mild or moderate heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Proinflammatory cytokines are capable of modulating cardiovascular function by a variety of mechanisms. These cytokines are elevated in patients with severe heart failure, but changes in mild or moderate heart failure have not been reported. Therefore, simultaneous arterial and coronary sinus concentrations of interleukin-1alpha, soluble interleukin-2 receptor, interleukin-6, and tumor necrosis factor-alpha were measured in 78 patients with New York Heart Association functional class II to IV heart failure and compared with 17 healthy volunteers. Concentrations of interleukin-1alpha, soluble interleukin-2 receptor, and interleukin-6 were determined by a "sandwich" enzyme-linked immunosorbent assay and tumor necrosis factor-alpha by tissue culture technique. There were no statistical differences in interleukin-1alpha, soluble interleukin-2 receptor, or tumor necrosis factor-alpha concentrations in mild to moderate heart failure versus control subjects. Interleukin-6 was significantly elevated, 75 +/- 16 versus 0.4 +/- 0.4pg/ml (p = 0.002). Cytokine concentrations did not differ by heart failure etiology. Paired arterial and coronary sinus concentrations were not significantly different. Soluble interleukin-2 receptor concentrations were significantly correlated with New York Heart Association functional class (r = 0.59, p = 0.04) and negatively associated with exercise tolerance time (r = -0.59, p = 0.007). Thus, interleukin-6 is significantly elevated in mild or moderate heart failure.

Adrenergic alpha-Agonists↗

PubMed1994

Arterial oxygen saturation in chronic congestive heart failure.

Continuous, 24-hour, ambulatory pulse oximetry was used in 10 subjects with New York Heart Association functional class II to III heart failure and in 5 age-matched controls to test the prevailing view that arterial oxygen saturation is preserved during wakefulness in chronic mild to moderate heart failure. Subjects with heart failure were stabilized on digitalis and diuretics at the time of the study. All subjects maintained time-activity logs, with an emphasis on self-reported sleep and wakefulness. A desaturation event was defined as a decrease in arterial oxygen saturation > or = 4% from baseline lasting > 5 seconds. Variables assessed included total desaturation events, decrease in arterial oxygen saturation duration/event, nadir of arterial oxygen saturation/event, and desaturation index ([cumulative desaturation time/total monitoring time] x 100). The ratio of self-reported wakefulness:sleep desaturation time was 47:53% for subjects with heart failure versus 64:36% for controls (p = NS). Mean (+/- SEM) time of arterial oxygen saturation < 90% was 123 +/- 67 minutes for subjects with heart failure versus 22 +/- 25 minutes for controls (p < 0.01). Total desaturations were 220 +/- 63 and 76 +/- 35 (p = NS) for the heart failure and control groups, respectively. The heart failure group had a statistically, significantly greater decrease in arterial oxygen saturation, and a longer duration and deeper nadir of the desaturation event than did the age-matched control group. The desaturation index was 21 +/- 3% and 4 +/- 1% for the heart failure and control groups, respectively (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1994

Presence of azithromycin breast milk concentrations: a case report.

We describe a case of breast milk concentrations of azithromycin, an azalide antibiotic, in a woman with postpartum bilateral tubal ligation incisional cellulitis. Azithromycin appears to demonstrate a time-dependent versus time-accumulation profile in breast milk.

Adult↗

PubMed1993

Renal functional alterations induced by angiotensin-converting enzyme inhibitors in heart failure.

OBJECTIVE: To review the effects of angiotensin-converting enzyme (ACE) inhibitors on renal pathophysiology and the compensatory mechanisms involved in heart failure. A clinical application of the use of these agents in the setting of concomitant heart failure and renal insufficiency also is presented. DATA SOURCES: A MEDLINE search was conducted using the terms heart failure, congestive; renal insufficiency; and angiotensin-converting enzyme inhibitors. STUDY SELECTION: All applicable animal and human trials were reviewed. DATA SYNTHESIS: Advances in the management of heart failure have led to new insights into the complex pathophysiology of this condition, particularly the favorable clinical effects noted with the ACE inhibitors. The net effect of ACE inhibitors on the renin-angiotensin system in patients with heart failure is to augment renal blood flow to a greater extent than cardiac output. Glomerular filtration rate is either unchanged or decreased by ACE inhibition. Sodium excretion is augmented primarily by alterations in glomerular hemodynamic parameters. ACE inhibitors may alter renal tubular function, both directly and indirectly, leading to increased diuresis and natriuresis. CONCLUSIONS: Although ACE inhibitors exert beneficial pharmacodynamic effects on the renal bed in patients with heart failure, clinical consideration of volume and neurohormonal status prior to institution of therapy is prudent.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1993

Pharmacy practice acts: a five-year follow-up.

OBJECTIVE: To rereview the status of state pharmacy practice acts since 1987. Additionally, this report discusses adoption of the 1992 National Association of Boards of Pharmacy Model State Pharmacy Practice Act as the standard state pharmacy practice statute. DATA SOURCES: State codes for 50 states and the District of Columbia, with attention focused on the pharmacy practice acts; Puerto Rico and the Virgin Islands were excluded. CASE LAW SELECTION: Case law utilizing state pharmacy statutes was selected to demonstrate pharmacists' liability. DATA EXTRACTION: The focus on each statute was the statutory definition of the "practice of pharmacy." DATA SYNTHESIS: Twelve pharmacy laws (24 percent) contain no definition of the practice of pharmacy. Compounding (92 percent), dispensing (100 percent), interpretation and evaluation of prescriptions (72 percent), consultation (85 percent), drug utilization review (69 percent), drug product selection (54 percent), drug administration (21 percent), pharmacokinetic consultation and patient assessment (13 percent) were noted in the laws for the remaining 38 states and the District of Columbia. Significant pharmacy activities codified since 1987 include consultation, drug administration, pharmacokinetic consultation, and patient assessment. Statutes defining pharmacy practice impact the profession by affecting liability and by mirroring society's view of the role of the profession. CONCLUSIONS: States have enacted new statutes principally in the areas of progressive pharmacy practice functions since 1987. Enactment of the definition of professional practice contained in the National Association of Boards of Pharmacy Model State Pharmacy Practice Act would serve the pharmacy profession by: (1) creating a uniform professional purpose; (2) creating legal responsibility that reflects contemporary practice; (3) allowing pharmacists to enlarge the scope of their practice as the profession's societal role evolves; and (4) conserving revenues normally consumed by lobbying for constant legislative revisions.

Data Collection↗

PubMed1993

Effect of angiotensin-converting enzyme inhibitors on ventricular remodeling and survival following myocardial infarction.

OBJECTIVE: To discuss the effects of angiotensin-converting enzyme (ACE) inhibitors on ventricular remodeling and survival after acute myocardial infarction (AMI). An overview is provided of the pathophysiologic changes produced by AMI and the ventricular remodeling process. ACE inhibitors have been studied for their use in the prevention of ventricular remodeling and reduction in postinfarction mortality. Trials in humans and animals are reviewed, including study methods, results, and limitations. DATA SOURCES: MEDLINE searches identified applicable literature, including experimental trials and review articles. STUDY SELECTION: All clinical trials of ACE inhibitors following AMI were reviewed. DATA EXTRACTION: Morbidity and mortality data evaluating the effect of postinfarction ventricular remodeling are rare. At the time of publication, all available clinical trials studying the effects of ACE inhibitors on postinfarction ventricular remodeling were included, regardless of whether morbidity and mortality were assessed. Data from the Survival and Ventricular Enlargement (SAVE) and Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II) trials include almost 10,000 patients. Data were extracted by two independent observers. Data quality and validity were assessed based on sample size, stratification of study population, and statistical power of the studies. DATA SYNTHESIS: ACE inhibitors may prevent the deleterious consequences of AMI, including ventricular remodeling and neurohumoral activation. Ventricular hypertrophy begins acutely following infarction, an early physiologic response to myocardial injury. Hemodynamic benefits from the initial phase of left ventricular hypertrophy include increased ventricular working capacity, normalized systolic wall stress, and maintenance of stroke volume. Although acute dilatation may delay hemodynamic deterioration for six to eight months, it also results in reduced coronary reserve, decreased ventricular compliance, and altered myocardial contractility. With chronic dilatation, the beneficial effects reach a plateau, stroke volume decreases, contractility is reduced, and cardiac failure may ensue. Ventricular hypertrophy is associated with worsened prognosis following infarction and may be the most important single determinant of late prognosis. Ventricular hypertrophy contributes to postinfarction heart failure, angina, and sudden death. Clinical trials show a beneficial effect of the ACE inhibitor captopril on the prevention of left ventricular dysfunction. Although captopril therapy significantly improved survival and myocardial function following AMI in the SAVE trial, these results cannot be generalized to all patient subpopulations. The CONSENSUS II trial demonstrated a decreased survival rate when enalapril was administered within 24 hours of AMI, indicating that timing of therapy may be an important consideration. Captopril therapy may positively affect outcome when initiated 3-16 days following infarction in patients with ejection fractions below 40 percent and who have no signs of ischemia or heart failure. Based on the CONSENSUS II results, enalapril therapy immediately following AMI cannot be recommended. CONCLUSIONS: Clinical trials have demonstrated that ACE inhibitors can limit ventricular hypertrophy following AMI, resulting in clinical benefit and improved survival. These effects may be secondary to modulation of neurohumoral activation or the antiischemic effect of ACE inhibitors, which may also reduce the incidence of reinfarction. Early intervention with ACE inhibitors (within 3-16 days of infarction) can slow the progression of cardiovascular disease and improve the survival rate.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1992

Evaluation of quinapril on regional blood flow and cardiac function in patients with congestive heart failure.

Quinapril, a nonsulfhydryl ACE inhibitor, was evaluated in ten New York Heart Association (NYHA) functional class (FC) II-III CHF patients to determine its effects on regional blood flow [effective renal plasma flow (ERPF), renal blood flow (RBF), renal vascular resistance (RVR), hepatic blood flow (HBF), hepatic vascular resistance (HVR), segmental limb pressure (SLP), creatinine clearance (CRCL)] and cardiac function [left ventricular ejection fraction (LVEF)]. Previous vasodilator therapy was withdrawn 2 weeks before baseline measurements. Stable regimens of digoxin and diuretics were continued throughout the study. ERPF was assessed using p-aminohippurate (PAH), HBF by indocyanine green (ICG) clearance, and LVEF by radionuclide scintography. Segmental limb pressures were measured by Doppler flow detection. Measurements were performed at baseline (B) and after 4 weeks of quinapril therapy (10 mg BID). Quinapril increased renal (P less than 0.05) and hepatic blood flow (P = 0.06) and significantly reduced renal and hepatic vascular resistance. Glomerular filtration rate and left ventricular ejection fraction were unchanged. Mean arterial pressure and brachial segmental pressures decreased without change in heart rate. Noninvasive cardiovascular assessments indicate that quinapril improves regional blood flow while exhibiting no change in left ventricular ejection fraction, in patients with NYHA FC II-III CHF.

Antihypertensive Agents↗

PubMed1992

Report of nitropatch explosions complicating defibrillation.

Reports of complications associated with the use of electrical defibrillators have been relatively rare. In two patients, defibrillation performed over a nitroglycerin skin patch resulted in electrical arcing with a resultant flash of light and thermal injuries. Skin burns as a complication of defibrillation over nitropatches has not been previously reported. Such burn injuries respond to standard therapeutic measures. Healthcare professionals who may perform defibrillation should be aware of this potential complication.

Administration, Cutaneous↗

PubMed1991

Drug-induced supraventricular tachycardia: a case report of fluoxetine.

We report the occurrence of supraventricular tachycardia and hypotension in a 54-year-old woman after maintenance therapy with fluoxetine. Although cases of tachycardia and palpitations have been reported, supraventricular tachycardia and hypotension have not been directly attributed to fluoxetine.

Electrocardiography↗

PubMed1991

Medical versus pharmaceutical continuing education: are both appropriate for the pharmacist?

Continuing education (CE) courses in pharmacy and medicine often overlap with regard to their informational content. At the present time, however, it is feasible that two pharmacists could attend the same national meeting that has continuing medical education (CME) approval status and only one of them would receive CE credit from his state board of pharmacy. Therefore, a survey of 51 state board of pharmacy policies regarding acceptance of CME was conducted. Forty-five of the 51 boards of pharmacy require CE for relicensure. Twenty percent of state boards requiring CE accept CME credit without review, 24 percent do not accept CME credit, and the remaining 56 percent review submitted requests for CME credit. A general lack of uniformity exists among state boards regarding policies pertaining to CE credit. If CME credit was universally accepted, pharmacists would benefit from the increased availability of CE, the building of collegial relationships with other healthcare professionals, and the cost savings of combining courses that mutually benefit both pharmacists and physicians.

Accreditation↗

PubMed1990

Assessment of hemodynamic tolerance from a 24-hour intravenous infusion of fenoldopam mesylate in congestive heart failure.

To determine the maintenance of pharmacodynamic effects of fenoldopam mesylate, a dopamine-1 agonist, the invasive hemodynamic profiles of 33 patients with New York Heart Association functional class III to IV congestive heart failure were examined. Fenoldopam mesylate was initiated at 0.1 micrograms/kg/min and titrated to a cardiac index greater than or equal to 25% above baseline. Upon achievement of optimal hemodynamics, maintenance infusion was begun (mean dose 0.6 micrograms/kg/min). Fenoldopam mesylate (baseline vs maximal effect) decreased systemic vascular resistance by 37% (p less than 0.001), left ventricular filling pressure by 16% (p less than 0.05) and mean arterial pressure by 11% (p less than 0.05), with an associated augmentation in cardiac index and stroke volume index by 27% (p less than 0.001). Attenuation of hemodynamic effect (maximal effect vs time) was noted in cardiac index (14% p less than 0.001), systemic vascular resistance (13% p less than 0.05) and stroke volume index (13% p less than 0.05). None of the parameters exhibited complete attenuation to baseline values. Fenoldopam mesylate improves cardiac output and lowers systemic vascular resistance with relative attenuation of pharmacodynamic effect during a 24-hour intravenous infusion.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1990

Assessment of intravenous fenoldopam mesylate in the management of severe systemic hypertension.

To evaluate the acute BP response to iv fenoldopam mesylate (FNP), 14 patients with severe hypertension (diastolic BP 120 to 170 mm Hg) were studied in an open-label trial. Initial infusion rate of FNP was 0.1 microgram/kg.min. Titration to diastolic BP goal (95 to 110 mm Hg) was followed by a constant infusion phase (greater than or equal to 6 h), a detitration phase (2 h), and a postinfusion phase. FNP reduced BP by 27/29 mm Hg (p less than .001) with no significant effect on heart rate. Maintenance of the BP effect was noted through the 6 h of constant rate infusion. Mild, transient vasodilating-associated adverse effects were noted with FNP. We conclude that FNP is an effective, well-tolerated iv antihypertensive agent for acute BP reduction in a severely hypertensive population.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1990

Single-dose effects of ibopamine hydrochloride on renal function in patients with congestive heart failure.

To examine the renal effects of ibopamine HCl we evaluated 15 patients with New York Heart Association Class II-III congestive heart failure and mild renal insufficiency (creatinine clearance [CLcr] = 45-85 ml min-1). Diuretics and vasodilators were withheld and a sodium (Na+)-restricted diet was initiated. All patients exhibited positive Na+ balance at the time of evaluation. Hourly urine volumes, urine chemistries, serum chemistries, PAH and inulin/iothalamate clearances were determined 2 h pre and 4 h post a single 200 mg oral dose of ibopamine. Effective renal plasma flow, creatinine clearance, filtration fraction, and the fractional excretion of sodium and potassium were not significantly altered postdose. A significant increase in urine output and decrease in urine osmolality were seen at all time points postdose. A significant reduction in serum potassium (2 and 3 h) and blood urea nitrogen (1, 3 and 4 h) concentrations occurred. Measurements of glomerular filtration rate by inulin or [125I]-iothalamate produced differing results in the patient groups studied. We conclude that a single dose of ibopamine does not produce significant improvements in renal function in patients with congestive heart failure, mild renal insufficiency and positive sodium balance.

Acute Kidney Injury↗

PubMed1990

Hyperventilation-induced reduction in cerebral blood flow: assessment by positron emission tomography.

The use of positron emission tomography (PET) has been well documented as a relatively noninvasive method of measuring cerebral blood flow (CBF), both globally and regionally. The utility of readily detecting alterations in CBF is apparent, particularly when applied to the evaluation of therapeutic interventions thought to influence CBF. We report the effects of hypocapnia, an experimental condition of known cerebral vasoconstriction, in ten normal volunteers. Subjects had brain blood flow evaluated utilizing H215O as the positron emitter before and after approximately five minutes of hyperventilation. Baseline CBF was measured as a mean +/- SD of 61.2 +/- 16.3 mL/min/100 g of tissue. Mean baseline arterial blood gas values were PaO2 107.4 +/- 14 mm Hg, PaCO2 37.7 +/- 0.89 mm Hg, and pH 7.39 (calculated from mean [H+]). Post hyperventilation, global CBF was measured as 31.1 +/- 10.8 mL/min/100 g. Mean arterial blood gas values were PaO2 141.7 +/- 21 mm Hg, PaCO2 19.7 +/- 5 mm Hg, and pH 7.63 (calculated from mean [H+]). CBF decreased by a mean of 49.5 +/- 11 percent. Data analysis using the Student's t-test showed a significant change over baseline in PaCO2 (p less than 0.001) and CBF (p less than 0.001), in the hyperventilated state. Correlations were noted between the decrease in CBF and change in PaCO2 (r = 0.81) as well as between hyperventilation PaCO2 and the change in CBF (r = 0.97). We conclude that, as measured by PET, CBF decreases significantly during a state of artificial hyperventilation to a degree consistent with results seen using other methods. PET appears to be a valuable tool in the assessment of interventions that could influence CBF.

Cerebrovascular Circulation↗

PubMed1990

Anistreplase: a new thrombolytic for the treatment of acute myocardial infarction.

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of anistreplase in the treatment of acute myocardial infarction (AMI) are reviewed. Anistreplase is an acylated form of the streptokinase-plasminogen complex. Acylation makes the complex temporarily inactive but protects it from neutralization by plasmin inhibitors. After deacylation, which begins immediately after injection, the streptokinase-plasminogen complex promotes thrombolysis by speeding the conversion of plasminogen to plasmin. Like other thrombolytic agents, anistreplase induces a systemic fibrinogenolytic state. The plasma half-life of anistreplase, 88-112 minutes, is longer than that of the other thrombolytic drugs marketed in the United States. Anistreplase lyses coronary artery thrombi when given by the intracoronary or i.v. route. I.V. anistreplase is comparable in efficacy to i.v. streptokinase but has not been directly compared with i.v. alteplase. Anistreplase therapy in patients with AMI may help preserve left ventricular function and prolong survival. Anistreplase is comparable in safety to other thrombolytic drugs. Although bleeding has occurred in 4-47% of patients treated with anistreplase, most episodes have been clinically unimportant and have occurred at a vascular puncture site; intracranial hemorrhage has occurred in less than 1% of patients. Cardiac arrhythmia and transient hypotension are common after anistreplase administration. Anistreplase is easy to administer and may be appropriate for use in patients with suspected AMI before hospital admission. The recommended dose is 30 units i.v. given over two to five minutes. Anistreplase is similar in efficacy and safety to other thrombolytic agents in the treatment of AMI. The drug's ease of administration may be an important clinical consideration.

Acute Disease↗