Biomedical subjects

K F Adams

Publications and source records attributed to K F Adams.

58 records · Page 4Linked to original sources

PubMedDate not supplied

Oral torsemide in patients with chronic congestive heart failure: effects on body weight, edema, and electrolyte excretion. Torsemide Investigators Group.

STUDY OBJECTIVE: To assess the effects of torsemide on the primary end point of change in body weight from baseline, and the following secondary end points: urinary sodium, potassium, and chloride excretion, and urine volume after the first dose of drug. DESIGN: Randomized, parallel, double-blind, multicenter study in patients treated with torsemide 5 mg (n = 19), 10 mg (n = 18), or 20 mg (n = 14), or placebo (n = 15) for 7 days. PATIENTS: Sixty-six patients with New York Heart Association class II or III congestive heart failure and edema. RESULTS: At the end of the study, patients treated with torsemide 10 and 20 mg demonstrated a significant reduction in body weight compared with those receiving placebo (-1.62 and -1.30 kg, respectively), and those treated with torsemide 5 mg did not (-0.60 kg). The severity of edema decreased with increasing torsemide dose. Torsemide caused no greater frequency of adverse effects with increasing dose. CONCLUSION: Orally administered torsemide 5, 10, and 20 mg once/day for 7 days were well tolerated. Doses of 10 and 20 mg were effective in producing weight loss.

Administration, Oral↗

PubMedDate not supplied

Pathophysiology of heart failure.

Heart failure, a major contributor to cardiovascular disease morbidity and mortality, is newly diagnosed in approximately 400,000 patients each year, and is particularly prevalent in individuals over age 65 years. Average mortality rates 5 years after diagnosis are 45-60%, and may be as high as 50% after 1 year for those with New York Heart Association class IV heart disease. Heart failure occurs when myocardial muscle dysfunction prevents the heart from pumping enough blood at normal cardiac pressures to meet the metabolic needs of the body, especially during exercise, and compensatory hemodynamic and neurohormonal mechanisms are overwhelmed or maladaptive. Pathologic classifications are broadly based on the presence of systolic (dilated cardiomyopathy) or diastolic (hypertrophic or restrictive cardiomyopathies) dysfunction. The etiologies of heart failure may include inadequate coronary blood flow, pressure or volume overload, cardiomyopathy, or pericardial disease. Coronary artery disease, idiopathic dilated cardiomyopathy, and hypertension are the most frequent causes, and certain drugs may also worsen myocardial function. When contractility is reduced, stroke volume and cardiac output are decreased, and alterations in the kidneys may induce fluid retention to compensate for the perceived low output and reduced circulating blood volume. Fluid retention in turn causes preload or filling pressure to increase and symptoms of pulmonary congestion to emerge. Depressed contractility also results in a reduction in blood pressure, leading to compensatory neurohormonal activation and vasoconstriction, which significantly elevate afterload and further reduce stroke volume. The overall approach to heart failure includes defining the etiology, identifying precipitant factors, and assessing the severity of myocardial dysfunction and clinical symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMedDate not supplied

Pathophysiology of heart failure: changing perceptions.

Heart failure occurs when myocardial muscle dysfunction prevents the heart from pumping enough blood at normal cardiac pressures to meet the metabolic needs of the body, especially during exercise, and compensatory hemodynamic and neurohormonal mechanisms are overwhelmed or maladaptive. Pathologic classifications are broadly based on the presence of systolic dysfunction (dilated cardiomyopathy) and diastolic dysfunction (hypertrophic or restrictive cardiomyopathies). Coronary artery disease, idiopathic dilated cardiomyopathy, and hypertension are the most frequent causes, and myocardial function may be impaired by some drugs. When contractility is reduced, stroke volume and cardiac output are decreased, and alterations in the kidneys may induce fluid retention to compensate for the perceived low output and reduced circulating blood volume. Fluid retention, in turn, causes increased preload or filling pressure and symptoms of pulmonary congestion. Depressed contractility also results in a reduction in blood pressure, leading to compensatory neurohormonal activation and vasoconstriction, which significantly elevate afterload, further reduce stroke volume, and lead to deleterious cardiac remodeling. The overall clinical approach includes defining the etiology, identifying precipitant factors, and assessing the severity of myocardial dysfunction and clinical symptoms.

Cardiac Output, Low↗

PubMedDate not supplied

Current perspectives on beta-receptor antagonists in the treatment of symptomatic ventricular dysfunction.

Even though therapeutic advances have occurred, heart failure is still associated with significant morbidity and mortality. Digitalis, diuretics, and angiotensin-converting enzyme inhibitors have proven effective, but in many patients still do not prevent progressive and debilitating heart failure. Many hormonal factors are involved, but two, the renin-angiotensin-aldosterone (RAA) axis and the autonomic nervous system, apparently are critical in the pathophysiology of progressive ventricular dysfunction. Pharmacologic suppression of the RAA system is associated with significant clinical benefit, suggesting that antagonism of sympathetic nervous activity with beta-receptor-blocking agents might also be efficacious. Major alterations of the autonomic nervous system are characteristic of heart failure, with excessive sympathetic activity one of the earliest adaptations to the condition, and important in promoting the heart failure state and the progression of ventricular dysfunction. Certain beta-antagonists administered by careful and slow up-titration from small starting dosages proved effective in small trials. Large-scale, randomized, placebo-controlled studies continue to document that beta-blockers improve ventricular function and symptoms, and preliminary results suggests mortality and morbidity reductions as well. Although intolerance to beta-antagonism does occur, the majority of patients can be successfully treated with these agents.

Adrenergic beta-Antagonists↗