Salmeterol and inhaled corticosteroids in patients with persistent asthma.
Explore the source record for details and available documents.
Adrenergic beta-Agonists↗
Biomedical subjects
M A Munger
Publications and source records attributed to M A Munger.
New recommendations from the 1999 American College of Cardiology/American Heart Association acute myocardial infarction guidelines.
OBJECTIVE: To review literature relating to significant changes in drug therapy recommendations in the 1999 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for treating patients with acute myocardial infarction (AMI). DATA SOURCES: 1999 ACC/AHA AMI guidelines, English-language clinical trials, reviews, and editorials researching the role of drug therapy and primary angioplasty for AMI that were referenced in the guidelines were included. Additional data published in 2000 or unpublished were also included if relevant to interpretation of the guidelines. STUDY SELECTION: The articles selected influence AMI treatment recommendations. DATA SYNTHESIS: Many clinicians and health systems use the ACC/AHA AMI guidelines to develop treatment plans for AMI patients. This review highlights important changes in AMI drug therapy recommendations by reviewing the results of recent clinical trials. Insights into evolving drug therapy strategies that may impact future guideline development are also described. CONCLUSIONS: Several changes in drug therapy recommendations were included in the 1999 AMI ACC/AHA guidelines. There is emphasis on administering fibrin-specific thrombolytics secondary to enhanced efficacy. Selection between fibrin-specific agents is unclear at this time. Low response rates to thrombolytics have been noted in the elderly, women, patients with heart failure, and those showing left bundle-branch block on the electrocardiogram. These patient groups should be targeted for improved utilization programs. The use of glycoprotein (GP) IIb/IIIa receptor inhibitors in non-ST-segment elevation MI was emphasized. Small trials combining reduced doses of thrombolytics with GP IIb/IIIa receptor inhibitors have shown promise by increasing reperfusion rates without increasing bleeding risk, but firm conclusions cannot be made until the results of larger trials are known. Primary percutaneous coronary intervention (PCI) trials suggest lower mortality rates for primary PCI when compared with thrombolysis alone. However, primary PCI, including coronary angioplasty, is only available at approximately 13% of US hospitals, making thrombolysis the preferred strategy for most patients. Clopidogrel has supplanted ticlopidine as the recommended antiplatelet agent for patients with aspirin allergy or intolerance following reports of a better safety profile. The recommended dose of unfractionated heparin is lower than previously recommended, necessitating a separate nomogram for patients with acute coronary syndromes. Routine use of warfarin, either alone or in combination with aspirin, is not supported by clinical trials; however, warfarin remains a choice for antithrombotic therapy in patients intolerant to aspirin. Beta-adrenergic receptor blockers continue to be recommended, and emphasis is placed on improving rates of early administration (during hospitalization), even in patients with moderate left ventricular dysfunction. New recommendations for drug treatment of post-AMI patients with low high-density lipoprotein cholesterol and/or elevated triglycerides are included, with either niacin or gemfibrozil recommended as an option. Supplementary antioxidants are not recommended for either primary or secondary prevention of AMI, with new data demonstrating lack of efficacy vitamin E in primary prevention. Estrogen replacement therapy or hormonal replacement therapy should not be initiated solely for prevention of cardiovascular disease, but can be continued in cardiovascular patients already taking long-term therapy for other reasons. Bupropion has been added as a new treatment option for smoking cessation. As drug therapy continues to evolve in treating AMI, more frequent updates of therapy guidelines will be necessary.
Adrenergic beta-Antagonists↗
Cardiopulmonary events during hemodialysis: effects of dialysis membranes and dialysate buffers.
Adverse cardiac and pulmonary events are frequently observed during hemodialysis and contribute to significant morbidity and mortality. The temporal relationship between these events during the intradialytic period has not been well defined. To examine the event rate and timing of silent ischemia, cardiac ectopy, and hypoxemia, we conducted a prospective, single-blind, randomized study of 10 subjects undergoing maintenance hemodialysis with four contiguous combinations of dialysis membranes (cuprammonium or polysulfone) and dialysates (acetate or bicarbonate). The frequency of oxygen desaturation events peaked during the first 2 hours, whereas silent myocardial ischemia and supraventricular ectopies occurred more often in the later hours. Ventricular ectopy occurred steadily throughout the intradialytic period. The combination of acetate dialysis and cuprammonium membrane is associated with the most frequent events. We conclude that cardiopulmonary events can occur frequently during hemodialysis, and the frequency is dependent on the type of dialysis membrane and dialysate buffer used.
Acetates↗
A chronobiologic approach to the pharmacotherapy of hypertension and angina.
OBJECTIVE: To review the chronobiology of hypertension and coronary artery disease and the application of chronotherapeutics to their treatment and prevention. DATA SOURCES: Clinical trials and review articles (English-language) on the topic of chronotherapy and cardiovascular disease were identified via a MEDLINE search from 1990 to March 2000, using the search terms chronotherapy, circadian rhythm, cardiovascular disease, hypertension, and angina. DATA EXTRACTION: Search and evaluation focused on published clinical trials and review articles of circadian variation associated with pharmacotherapy for cardiovascular disease. DATA SYNTHESIS: The existence of circadian rhythm in cardiovascular disease is well established. Heart rate and blood pressure peak during the morning hours and reach a nadir at bedtime. The incidence of myocardial infarction, stroke, sudden cardiac death, and myocardial ischemia also increases during the early-morning hours. Based on these relationships, researchers have begun to apply the science of chronotherapeutics, or timing of drug effect with biologic need, to improve cardiovascular outcomes. This includes administering traditional agents at specific times throughout the day and developing new agents--chronotherapeutic formulations with special release mechanisms--targeted at inducing the greatest effect during the morning surges. Chronotherapeutic agents are specifically designed to provide peak plasma concentrations during the early-morning hours, when effect appears most needed; lowest concentrations occur at night, when heart rate and blood pressure are lowest and, consequently, cardiovascular events are least likely to occur. CONCLUSIONS: Whether chronotherapy of cardiovascular disease offers an advantage in long-term outcomes over traditional therapy must be studied in clinical trials.
Angina Pectoris↗
Growth hormone: a promising treatment for the failing heart?
Many pathologic processes that accelerate the progression of heart failure, such as cardiac remodeling and impaired contractility, may be modulated by administration of recombinant growth hormone. The agent improves structural and functional aspects of the failing heart both in the short term and after several months of therapy. However, conflicting clinical results cast doubt on whether it has a clear benefit in all of these patients. In addition, growth hormone therapy may be associated with cardiac and noncardiac adverse effects. Many questions must be addressed before its place in heart failure therapy is established. Optimal patient population, dosing regimen, duration of therapy, and effect on patient survival are unknown. Until larger, blinded studies are completed, growth hormone therapy remains an investigational approach to managing refractory heart failure.
Animals↗
beta-blocker therapy: a standard of care for heart failure.
beta-Adrenergic-blocking agents underwent extensive research over the past 2 decades and emerged as a proven state-of-art therapy for the failing human heart. Through blockade of chronically elevated cardiac adrenergic stimulation, selective and nonselective agents with vasodilating properties prevent progression of myocardial dysfunction and cardiac remodeling. Most important, beta-adrenergic blockers added to conventional therapy of vasodilators and diuretics significantly increase survival to a 5-year rate similar to that of cardiac transplantation. The agents also significantly reduce hospitalizations, improve quality of life, and are well tolerated in clinical trials. The challenge in treating heart failure is to ensure that every eligible patient receives these life-saving drugs.
Adrenergic beta-Antagonists↗
Candesartan cilexetil: comparison of once-daily versus twice-daily administration for systemic hypertension. Candesartan Cilexetil Study Investigators.
This randomized, double-masked, placebo-controlled, forced-titration, parallel-arm study was designed to compare the blood pressure (BP)-lowering effect of candesartan cilexetil, a potent antagonist of the angiotensin II receptor subtype AT1, administered once daily with that of the same agent administered twice daily at the same total daily dose of 16 mg. After a 4- to 5-week placebo run-in period, 277 patients with a sitting diastolic BP of 95 to 109 mm Hg were randomly allocated to receive placebo (n = 92) or candesartan cilexetil 8 mg once daily for 4 weeks, followed by forced titration to either 16 mg once daily (n = 91) or 8 mg twice daily (n = 94) for 4 weeks. At 8 weeks, mean reductions in trough sitting diastolic BP were similar for the once- and twice-daily treatment groups (9.4 and 10.3 mm Hg, respectively). After 8 weeks of treatment, no statistically significant differences were observed in diastolic or systolic BP, peak or trough BP, or sitting or standing BP between the 2 active-treatment groups. The rates of positive responses (defined as a trough sitting diastolic BP of <90 mm Hg or a decrease in BP of > or =10 mm Hg) were also similar (approximately 60%) in the once- and twice-daily candesartan cilexetil groups. Furthermore, placebo-corrected trough-to-peak ratios for sitting diastolic BP exceeded 75% for both candesartan cilexetil regimens, indicating a persistent 24-hour duration of drug effect. Ambulatory BP monitoring performed in a subset of patients (n = 44) confirmed the consistent 24-hour BP-lowering effect and preservation of diurnal variation with once-daily dosing. No significant between-group differences were observed in the incidence or severity of clinical or laboratory adverse events. The results of this study suggest that identical daily doses of candesartan cilexetil administered once or twice daily have comparable efficacy and tolerability and that no additional clinical benefit is derived from twice-daily administration.
Adult↗
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↗
Pharmacy practice acts: a decade of progress.
OBJECTIVE: This 10-year follow-up study of previously published surveys of pharmacy practice acts examines 50 state and the District of Columbia pharmacy practice acts to assess the range of statutory definitions and determine the direction and magnitude of statutory changes since 1988. 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. DATA EXTRACTION: The focus on each statute was the statutory definition of the "practice of pharmacy." DATA SYNTHESIS: Comparing 1998 with 1988, codification of interpreting and evaluating prescriptions increased 22% (1998; 39/47, four states contain no definition of the practice of pharmacy), compounding 8% (47/47), consultation 19% (41/47), dispensing 2.5% (47/47), drug administration threefold (24/47), drug product selection twofold (45/47), drug utilization review 70% (35/47), patient assessment 6.5-fold (6/47), pharmacokinetic services threefold (3/47), pharmacist prescribing 4.6-fold (15/47), and participation in drug research 10.5-fold (10/47). CONCLUSIONS: Since 1988, state pharmacy practice acts have increased the codification of pharmaceutical care services as integral pharmacy functions. Although substantial progress has been made over the past decade, a number of states have not incorporated definitions of pharmaceutical care functions into their state statutes. Enactment of the National Association Boards of Pharmacy Model State Pharmacy Act is one way for pharmacists' practice to expand with the evolution of the practice of pharmacy.
Humans↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗