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Biomedical subjects

J H Patterson

Publications and source records attributed to J H Patterson.

81 records · Page 5Linked to original sources
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Is there an expanded role for digoxin in patients with heart failure and sinus rhythm? A protagonist viewpoint.

The evidence supporting the efficacy of digoxin in patients with heart failure who are in sinus rhythm is substantial. Digoxin improves hemodynamics, exercise capacity, symptoms, and quality of life and reduces hospitalizations. All of this is accomplished with a drug that is very inexpensive and can be given once daily. Its safety has been established through the DIG trial. Although digoxin does not decrease mortality beyond that of diuretics and ACE inhibitors, it does not increase mortality, unlike many positive inotropes. Furthermore, digoxin, in addition to ACE inhibitors and a diuretic, decreases the hospitalization rate due to worsening of heart failure. From a managed care perspective, as well as that of the patient, this is of enormous benefit. A pharmacoeconomic analysis estimated that continuation of digoxin in patients with stable congestive heart failure could save the healthcare system an estimated $ 400 million, based on costs from one hospital. The issue is not whether to use digoxin in these patients, but rather, how early to initiate therapy. From some of the recent data in patients with systolic dysfunction and mild heart failure, as well as knowledge of the neurohormonal activation that occurs early in these patients, it could be suggested that early use of neurohormonal modulators, including digoxin, would decrease the progression of heart failure. Thus, rather than waiting for symptoms despite optimal doses of an ACE inhibitor and diuretic, as suggested by the AHCPR practice guideline for heart failure, initiation of digoxin therapy in patients as early as NYHA class II at a dosage that will achieve a serum concentration of 1.0 ng/mL or less should occur. With the understanding of digoxin's effect on the neurohormonal systems, its role in patients with preserved systolic function needs to be reexplored. The debate can now focus on asymptomatic patients or those with preserved systolic function. Could these patients benefit from therapy with digoxin as well?

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Preservation of anterior ciliary vessels during strabismus surgery: a nonmicroscopic technique.

Preservation of anterior ciliary vessels (ACVs) during strabismus surgery using microscopic dissection techniques and the operating microscope has been previously described. We describe a technique using standard loupe magnification for vessel preservation, in 77 patients, ages 7 months to 69 years, who had surgery between January 1989 and September 1990. ACVs, with a small sheath of connective tissue, were dissected off the surface of the muscles and tendons using blunt and sharp dissection with Knapp iris hooks and Vannas scissors. Key elements of the dissection were sufficient separation of the vessel complex from the anterior tendon insertion and the use of blunt rather than sharp dissection. We successfully preserved 125 ACVs in 97 muscles. Ninety-five vessels were saved with 71 recessions, 14 with 13 resections, and 16 with adjustable sutures. The success rate of surgery was 85% in surgeries done either with or without anterior ciliary preservation. Vessel dissection time averaged 5 to 10 minutes per muscle. ACV preservation can be easily and successfully performed in routine strabismus cases. The procedure does not require the operating microscope and can be done under standard loupe (1.5 to 3.0 x) magnification. This procedure theoretically reduces the risk of anterior segment ischemia in situations where the patient is thought to be at significant risk for this complication.

Adolescent↗
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

A new class of antihypertensive therapy: angiotensin II receptor antagonists.

Despite the availability of safe and efficacious antihypertensive agents, hypertension continues to be a major source of morbidity and mortality in the United States. Losartan, the first of a new class of agents, the angiotensin II receptor antagonists, can be administered as monotherapy in the treatment of hypertension or to complement existing therapy. The angiotensin II receptor antagonists block the effects of angiotensin II through preferential binding to angiotensin II receptor subtype AT1 on the cell membrane. Compared with angiotensin-converting enzyme inhibitors, they may provide more complete blockade of the renin-angiotensin system and be associated with a lower frequency of cough as a side effect.

Angiotensin Receptor Antagonists↗