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Biomedical subjects

J L Halperin

Publications and source records attributed to J L Halperin.

At least 19 recordsLinked to original sources
PubMed1992

Antiarrhythmic drug therapy and cardiac mortality in atrial fibrillation. The Stroke Prevention in Atrial Fibrillation Investigators.

BACKGROUND AND OBJECTIVES: The relation between cardiac mortality and antiarrhythmic drug administration has not been fully determined. This relation was analyzed in 1,330 patients enrolled in the Stroke Prevention in Atrial Fibrillation Study, a randomized clinical trial comparing warfarin, aspirin and placebo for the prevention of ischemic stroke or systemic embolism in patients with nonvalvular atrial fibrillation. METHODS: Patients who received antiarrhythmic drug therapy for atrial fibrillation in this study were compared with patients not receiving antiarrhythmic agents. The relative risk of cardiac mortality, including arrhythmic death, in patients receiving antiarrhythmic drug therapy was determined and adjusted for other cardiac risk factors. RESULTS: In patients receiving antiarrhythmic drug therapy, cardiac mortality was increased 2.5-fold (p = 0.006, 95% confidence interval [CI] 1.3 to 4.9) and arrhythmic death was increased 2.6-fold (p = 0.02, 95% CI 1.2 to 5.6). Among patients with a history of congestive heart failure, those given antiarrhythmic medications had a relative risk of cardiac death of 4.7 (p less than 0.001, 95% CI 1.9 to 11.6) compared with that of patients not so treated; the relative risk of arrhythmic death in the treated group was 3.7 (p = 0.01, 95% CI 1.3 to 10.4). Patients without a history of congestive heart failure had no increased risk of cardiac mortality (relative risk 0.70, 95% CI 0.2 to 3.1) during antiarrhythmic drug therapy. After exclusion of 23 patients with documented ventricular arrhythmias and adjustment for other variables predictive of cardiac death, patients receiving antiarrhythmic drugs were not at increased risk of cardiac death or arrhythmic death. However, in patients with a history of heart failure who received antiarrhythmic drug therapy, the relative risk of cardiac death was 3.3 (p = 0.05, 95% CI 0.99 to 11.1) and that of arrhythmic death was 5.8 (p = 0.009, 95% CI 1.5 to 21.7) compared with the risk in patients not taking antiarrhythmic medications. CONCLUSIONS: Although antiarrhythmic drug therapy was not randomly determined in this trial, the data suggest that in patients with atrial fibrillation and a history of congestive heart failure, the risk of such therapy may outweigh the potential benefit of maintaining sinus rhythm.

Anti-Arrhythmia Agents↗
PubMed1992

Dextrocardia.

Explore the source record for details and available documents.

Adult↗
PubMed1990

Antithrombotic therapy in cardiac disease: an approach based on pathogenesis and risk stratification.

An approach to the management of thrombosis and embolism in various cardiovascular disorders is discussed. This approach is based on current knowledge of pathogenesis and risk of thromboembolism. Rational therapeutic guidelines are formulated along the lines of anatomic location (arterial circulation, cardiac chambers or prosthetic valves), pathophysiology (activation of platelets or the coagulation system, or both), and degree of thromboembolic risk. With clear understanding of these factors, it may be possible to determine the most suitable platelet inhibitor or anticoagulant regimen for the individual patient, and whether these agents should be given singly or in combination.

Anticoagulants↗
PubMed1989

Angiosarcoma of the left atrium mimicking myxoma: case report.

The case of a 65-year-old female patient with a pedunculated left atrial angiosarcoma is presented. Histologically, the tumor was composed of vascular spaces lined by atypical cells with similar cells in the solid portion of the tumor. Immunohistochemical stain for factor VIII-related antigen was positive in the cells forming vascular spaces. Immunoperoxidase stain for Ulex Europaeus I lectin was positive in cells lining vascular lumina and in individual cells in the solid portion of the tumor. Cardiac angiosarcomas characteristically occur in men, arise in the right atrium, are large mural masses that infiltrate widely at the time of presentation, and are usually rapidly fatal. Review of the literature reveals that this case of cardiac angiosarcoma is unusual by virtue of its occurrence in a female, left atrial location as a polypoid lesion, and prolonged symptom-free survival after surgical resection alone. Cardiac angiosarcoma may clinically and radiologically simulate myxoma.

Aged↗
PubMed1988

The prevalence and one-year outcome of limb arterial obstructive disease in a nursing home population.

To assess the utility of bedside diagnostic measures to detect prognostically significant peripheral vascular disease, we examined 60 nursing home residents by physical examination, Doppler sphygmomamometry and pneumatic oscillometry, and recorded the clinical history. Eighty-eight percent of the cases had tibial/brachial arterial systolic pressure indices below 0.95, the lower limit traditionally considered normal. Yet, no more than 5% of the patients carried a previous diagnosis of peripheral vascular disease or had intermittent claudication, leg ulcers or gangrene. Approximately half of the patients had tibial/brachial pressure indices less than 0.7, and one year later in these cases, there was significantly greater morbidity and nearly twice the mortality of patients with less severe disease. We conclude that simple bedside diagnostic tests of arterial disease used in this study discloses a high prevalence of disease in institutionalized elderly patients and identifies a group at particular risk for morbid complications.

Aged↗
PubMed1987

Effect of nitroglycerin during hemodynamic estimation of valve orifice in patients with mitral stenosis.

In patients with mitral stenosis, valve orifice calculations using pulmonary capillary wedge pressure as a substitute for left atrial pressure may overestimate the severity of disease. Previous studies have shown that mitral valve area determined from transseptal left atrial pressure measurements exceeds that area derived from pulmonary wedge pressure measurements. This is probably due to pulmonary venoconstriction, which is reversed by nitroglycerin. Nitroglycerin, 0.4 mg, was administered sublingually to 20 patients with mitral valve disease during preoperative cardiac catheterization using the pulmonary capillary wedge pressure as the proximal hydraulic variable. At the time of a peak hypotensive effect, 3 to 5 minutes after nitroglycerin administration, the mean pulmonary capillary wedge pressure decreased from 23 +/- 2 (mean +/- SEM) to 19 +/- 2 mm Hg (p less than 0.005). The mean diastolic transmitral pressure gradient (12.6 +/- 1.2 mm Hg before and 11.5 +/- 1.0 mm Hg after nitroglycerin; p = NS) and cardiac output (4.0 +/- 0.3 to 4.1 +/- 0.3 liters/min; p = NS) did not change significantly. Nevertheless, the hemodynamic mitral orifice area, calculated using the Gorlin formula, increased from 0.8 +/- 0.1 to 1.1 +/- 0.2 cm2 (p less than 0.05). In 12 patients with isolated mitral stenosis, without regurgitation, the mitral valve orifice area after nitroglycerin was 0.4 +/- 0.2 cm2 larger than it was before drug administration (p less than 0.05). Administration of nitroglycerin during evaluation of mitral stenosis eliminates pulmonary venoconstriction, which raises the pulmonary capillary wedge pressure above the left atrial pressure in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Extraluminal compression of an aortic graft simulating recoarctation.

Restenosis rarely develops after surgical correction of coarctation of the aorta in adults. Late morbidity is usually related to residual hypertension or progressive aortic valve disease. A patient in whom symptoms and signs of recurrent coarctation developed 19 years after initial graft repair is described. Dehiscence of the original silk suture line was found at operation. Extensive thrombus had produced graft compression. Milder hypertension persisted in the postoperative period despite relief of the aortic obstruction.

Adult↗
PubMed1987

Peripheral vascular disease: medical evaluation and treatment.

Peripheral arterial obstructive disease with symptoms of ischemia in the limbs is a common cause of disability, morbidity, and even mortality in the elderly. The most important cause is atherosclerosis, which is ultimately a systemic problem, but the cardinal symptom in the limbs is intermittent claudication. Unfortunately, the elderly patient often displays severe ischemia with pain at rest, and ulceration or gangrene of the extremity, even where there was a paucity of prior claudication, perhaps due to associated illness which reduces mobility. The essential aspects of clinical diagnosis and assessment of severity of ischemia involve relatively simple bedside techniques, and noninvasive laboratory methodology is mainly of value in selection of patients for angiography and potential revascularization. While conventional therapy involves bypass surgery, an expanding array of drugs and the advent of interventional angiographic measures including angioplasty offer alternatives which were not available even a few years ago.

Aged↗
PubMed1986

Effect of labetalol on limb haemodynamics in patients following coronary artery bypass graft surgery.

Labetalol is a competitive inhibitor of alpha- and beta-adrenergic receptors and has an antihypertensive action. To determine limb haemodynamic effects, we measured calf blood flow and venous capacitance by venous occlusion plethysmography before and after oral labetalol in 10 patients 3-7 days following coronary bypass surgery. Vascular resistance was calculated as the ratio of mean arterial pressure to arterial flow. The peak effect of labetalol was taken as the point of maximum blood pressure decline, and this interval was selected for evaluation of the limb haemodynamic response. Ninety to 120 min after administration of 100-200 mg of labetalol the mean blood pressure fell from 88 +/- 3 to 79 +/- 3 mm Hg; (P less than 0.005). The mean arterial blood flow registered 5.1 +/- 1.0 ml 100 ml-1 limb tissue min-1 which was not significantly different from the control value of 4.4 +/- 0.8 ml 100 ml-1 limb tissue min-1. The calculated index of limb vascular resistance was not affected by labetalol administration, averaging 37 +/- 12 mm Hg 100-1 ml limb tissue min-1 before labetalol and 30 +/- 11 mm Hg ml-1 100 ml limb tissue min-1 at the time of peak hypotensive effect. There was a slight but statistically significant increment in limb venous volume to 1.9 +/- 0.3 from 1.5 +/- 0.3 ml 100 ml-1 limb tissue (P less than 0.025). Placebo administration produced no consistent changes in blood pressure, arterial blood flow, vascular resistance or venous capacitance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗