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Biomedical subjects

W M Feinberg

Publications and source records attributed to W M Feinberg.

At least 37 records · Page 2Linked to original sources
PubMed1993

Effect of oral nimodipine on platelet function.

BACKGROUND AND PURPOSE: Nimodipine, a calcium antagonist, has been reported to have beneficial effects in acute ischemic infarction. Some calcium channel antagonists have antiplatelet effects. We investigated the effect of oral nimodipine on platelet function in healthy volunteers. METHODS: Twelve healthy volunteers (6 men and 6 women, mean age 32.9 +/- 5.6 years) took 30 mg nimodipine every 6 hours for 24 hours, followed by a week with no medication, followed by 60 mg every 6 hours for 24 hours. Ex vivo platelet function was measured at baseline, 1 hour after the first dose at each dosage strength, and 1 hour after the last dose at each dosage. Platelet studies included aggregation and adenosine triphosphate release in response to collagen, epinephrine, and adenosine diphosphate; maximal rate of primary aggregation; threshold adenosine diphosphate concentration for second-phase aggregation; and thromboxane B2 release at threshold aggregation. The bleeding time was measured at baseline and after the last 60-mg dose of nimodipine. RESULTS: No change in any platelet function study was seen with 30 mg nimodipine every 6 hours. Platelet function studies were also unchanged after 60 mg every 6 hours, except for a slight decrease in aggregation and adenosine triphosphate release in response to suprathreshold (10 microM) adenosine diphosphate (p = 0.001, Student's paired t test). There was no significant change in bleeding times. CONCLUSIONS: Oral nimodipine has minimal antiplatelet activity in young, healthy subjects.

Adenosine Triphosphate↗
PubMed1993

Ischemic stroke in patients with atrial fibrillation: effect of aspirin according to stroke mechanism. Stroke Prevention in Atrial Fibrillation Investigators.

Ischemic strokes occurring in patients with nonrheumatic atrial fibrillation are due to a variety of mechanisms, not exclusively to cardiogenic embolism. Without knowledge of antithrombotic therapy assignment, we categorized strokes in the Stroke Prevention in Atrial Fibrillation Study as presumed cardioembolic or noncardioembolic. We then compared patient clinical and echocardiographic variables, as well as the efficacy of aspirin prophylaxis, for each stroke type. Of 71 ischemic strokes, we categorized 46 (65%) as cardioembolic, 13 (18%) as noncardioembolic, and 12 (17%) as of uncertain cause. Patients developing noncardioembolic strokes, relative to cardioembolic strokes, were more commonly men (p = 0.005) and were more likely to have left ventricular wall motion abnormalities by two-dimensional echocardiography (p = 0.002). Aspirin reduced the occurrence of strokes categorized as noncardioembolic significantly more than it did those categorized as cardioembolic (p = 0.01). These results emphasize the value of considering stroke mechanisms in therapeutic trials of antithrombotic agents and suggest a differential effect of aspirin according to mechanism.

Aged↗
PubMed1990

Epidemiologic features of asymptomatic cerebral infarction in patients with nonvalvular atrial fibrillation.

We performed unenhanced computed tomographic scans on 141 asymptomatic patients with nonvalvular atrial fibrillation. Thirty-six patients (26%) had hypodense areas consistent with cerebral infarction. The majority of these were small deep infarcts, seen in 29 patients (21%), but 13 patients (9%) had cortical or large deep infarctions. Twelve patients had more than one infarct on computed tomographic scan. Increasing age and increased left atrial diameter were the only clinical features associated with asymptomatic infarction. Patients older than 65 years with a left atrial diameter greater than 5.0 cm (n = 23) had a 52% prevalence of asymptomatic infarction. Patients younger than 65 years with a left atrial diameter less than 5.0 cm (n = 38) had an 11% prevalence of silent infarction. Patients with only one of these risk factors (n = 72) had a 24% prevalence of silent infarction. Infarction was more common in those with chronic (34%) as opposed to intermittent (22%) nonvalvular atrial fibrillation, but this difference was not significant. Hypertension, diabetes, duration of atrial fibrillation, congestive heart failure, history of myocardial infarction, and echocardiographic evidence of left ventricular dysfunction were not associated with asymptomatic infarction. A history of hypertension was present in only 35% of our patients with small-deep asymptomatic infarction, similar to the percentage in patients without stroke. Asymptomatic cerebral infarction is common in nonvalvular atrial fibrillation. The association with enlarged left atria and the lack of correlation with major cerebrovascular risk factors suggests a cardioembolic mechanism. Further study is needed to determine the functional and prognostic significance of these strokes.

Aged↗
PubMed1989

Hemostatic markers in acute stroke.

To assess the time course of thrombosis and fibrinolysis after acute stroke, we measured concentrations of fibrinopeptide A (FpA), B-beta 1-42 peptide (B-beta 1-42), B-beta 15-42 peptide (B-beta 15-42), and crosslinked D-dimer (XDP) in 31 patients at varying times following acute ischemic stroke and in 13 neurologically stable patients with chronic strokes. FpA levels were markedly elevated during the first week after stroke and declined slowly during the first month. Mean FpA levels were not significantly elevated in chronic stroke patients. Mean XDP levels were slightly elevated during the first week and increased during the next 2 weeks after stroke. B-beta 1-42 and B-beta 15-42 levels were not elevated at any time following acute stroke. Our data suggest that fibrin formation greatly exceeds endogenous fibrinolysis during the acute phase of ischemic stroke. Endogenous fibrinolysis develops slowly following stroke. Prolonged elevation of FpA concentration suggests that thrombin activity and fibrin formation continue for up to 4 weeks in some patients with ischemic stroke.

Acute Disease↗
PubMed1989

'Peduncular hallucinosis' following paramedian thalamic infarction.

An 83-year-old man had the sudden onset of vivid formed hallucinations, agitation, and sleep disturbance suggesting "peduncular hallucinosis." A magnetic resonance scan revealed a right paramedian thalamic infarction with no abnormality of the cerebral peduncles or midbrain.

Aged↗
PubMed1988

Fibrin metabolism in patients with acute myocardial infarction during and after treatment with tissue-type plasminogen activator.

In order to define some of the determinants of successful thrombolysis and reocclusion during fibrinolytic therapy for acute myocardial infarction (AMI), specific molecular markers of fibrin metabolism were serially measured in 15 patients with AMI treated with tissue-type plasminogen activator (t-PA). Fibrin formation was assessed by measurement of fibrinopeptide A (FpA) and fibrinolysis by assay of B-beta peptides 1-42 and 15-42 and crosslinked fibrin degradation products (XDP). At baseline, FpA levels were high while markers of fibrinolysis were near normal. Following a 90-minute infusion of t-PA (0.5-1.1 mg kg-1 hr-1), all markers of fibrinolysis increased. Levels of FpA remained elevated despite heparin at the initiation of cardiac catheterization. None of these markers discriminated between patients with successful reperfusion from those without. At 4 hours, B-beta 15-42 peptide and XDP levels remained elevated suggesting persistence of fibrinolysis beyond the short circulatory half-life of t-PA. FpA levels at 4 hours were lower in patients who underwent acute coronary angioplasty compared to those who received additional low dose t-PA (12.3 +/- 4.5 vs. 30.4 +/- 5.5 ng/ml, p less than 0.05). By 48 hours, markers of fibrinolysis had returned toward normal except in 2 patients with persistently elevated B-beta 15-42 peptide levels who suffered reocclusion on days 5 and 6 (75 and 44 vs. 29 +/- 3 nM, p less than 0.005). In conclusion, molecular markers of fibrin metabolism during fibrinolytic therapy may provide clinically relevant data.

Angioplasty, Balloon↗
PubMed1988

Cerebrovascular complications of L-asparaginase therapy.

L-Asparaginase, commonly used in combination chemotherapy in the treatment of acute lymphoblastic leukemia, has been associated with hemorrhagic and thrombotic cerebrovascular events. Thrombosis of the cerebral veins or dural sinuses is common, and may be associated with either hemorrhage or infarction. This syndrome generally occurs after a few weeks of therapy, and may occur after L-asparaginase therapy is completed. Complications appear to result from depletion of plasma proteins involved in coagulation and fibrinolysis. We now report two additional cases of cerebrovascular complications associated with L-asparaginase therapy. We review the previously reported cases and discuss the clinical presentation, pathophysiology, and suggested treatment of this syndrome.

Acute Disease↗
PubMed1984

Epstein-Barr virus-associated myelopathy in an adult.

A 55-year-old man had a myelopathic syndrome and serologic evidence of Epstein-Barr virus infection. The patient's age and the neurologic and serologic findings suggested reactivation of a latent virus with direct invasion of the CNS. Epstein-Barr virus may exist in a latent state within the nervous system, and should be considered in myelopathic syndromes, even in older patients.

Antibodies, Viral↗
PubMed1984

Cysticercosis presenting as a subdural hematoma.

We describe a patient with a history of cerebral cysticercosis who presented with signs and symptoms of increased intracranial pressure; CT showed what seemed to be a subdural hematoma. At operation, the "hematoma" proved to be a subdural collection of multiple cysticercal cysts. This is the first report of this complication.

Adult↗
PubMedDate not supplied

Demonstration of acute post-viral myelitis with magnetic resonance imaging.

Post-infectious transverse myelitis is an important clinical entity in childhood, but the diagnosis is difficult to confirm by conventional radiologic investigations. We report a patient with acute, cervical, post-infectious transverse myelitis whose diagnosis had been established by the distribution and evolution of lesions on serial magnetic resonance imaging (MRI). Autopsy results confirmed the diagnosis of post-infectious transverse myelitis and the presence of MRI-identified lesions. To our knowledge, this patient is the first child reported with MRI findings in post-infectious transverse myelitis and suggests that MRI may be valuable in the diagnosis and management of children with this syndrome.

Acute Disease↗