Marine omega-3 fatty acids and atherosclerosis.
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Biomedical subjects
Publications and source records attributed to R C Becker.
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Post-infarction angina includes a syndrome of ischemic chest pain occurring either at rest or during minimal activity 24 hours or more following an acute MI. It develops in approximately 10 to 15 per cent of patients and is particularly common in non Q-wave infarcts involving the anterior myocardial wall. Post-infarction angina may result from ischemia either within the infarct zone or at a distance and frequently portends a poor long term prognosis. Platelet aggregation, coronary vasospasm, and thrombus formation at the site of a ruptured atherosclerotic plaque are each involved in its pathogenesis. The initial treatment of post-infarction angina includes identification and correction of factors that increase myocardial demand including congestive heart failure and arrhythmias. beta-Adrenergic blockers, calcium channel blockers, and nitrate preparations constitute the first line of medical therapy. The role of heparin is controversial, yet it continues to be used in clinical practice. Although thrombolytic agents are currently being investigated, early experience suggests that they may accelerate clinical stabilization and allow time for elective revascularization when required. Antiplatelet therapy with aspirin has proven benefit in the long term management of unstable angina. Patients unresponsive to medical therapy should be considered for intra-aortic balloon pump placement and early coronary angiography. Revascularization with either coronary angioplasty or coronary artery bypass grafting may then be performed as dictated by the overall clinical status, available facilities, and coronary anatomy.
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Over a 14-month period at the Cleveland Clinic Foundation, 424 strains of Clostridium were isolated; of these, 52 strains were Clostridium perfringens isolated from 41 patients. Eight strains of C. perfringens were isolated from the blood of six patients; five of these patients had neoplastic disease and three developed massive intravascular hemolysis with rapidly developing shock and death. Clinical details are given on three patients with fatal Clostridium perfringens sepsis, and the nature of presentation and pathophysiologic mechanisms are discussed.
Since infective endocarditis may affect individuals without pre-existing valvar heart disease, and Staphylococcus aureus is the organism most commonly involved, the binding characteristics of S aureus to several components of normal vascular endothelium and subendothelium were studied. S aureus adhered specifically to endothelial monolayers (6.08(1.10)%; p less than 0.005), fibronectin (5.43(0.81)%; p less than 0.001), fibrinogen (7.13(1.43)%; p less than 0.001), and acid soluble calf skin collagen (2.38(0.90)%; p less than 0.001). S aureus also adhered specifically to Von Willebrand factor (1.62(0.28)%, p less than 0.001). Protein A containing (Cowan I) and deficient (Wood) strains of S aureus adhered similarly to all surfaces and substrates (NS). Escherichia coli adhered poorly. Immunofluorescence microscopy of preconfluent endothelial cells identified an extensive pericellular fibronectin network at regions of cell to cell contact. Light microscopy showed S aureus binding solely within these regions. Therefore, the ability of S aureus to infect valvar endothelium may be dependent on the presence of a fibronectin receptor. The existence of specific receptor for S aureus on the endothelial cell surface itself remains undetermined.
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Primary cardiac tumors, while uncommon, are not rare neoplasms. They occur in individuals of all ages. A variety of benign and malignant tumors has been described. Presenting signs and symptoms mimic numerous systemic and cardiac disease states. Echocardiography, catheterization, and nuclear magnetic resonance techniques are diagnostic tools available to the physician. Early diagnosis and surgical intervention are curative measures for many benign cardiac tumors. Malignant variants are uniformly unresponsive to treatment.
Serum gamma-glutamyl transpeptidase was determined in 123 alcoholic patients and found elevated in all patients with liver disease but in only 52% of patients without significant liver disease. In patients without clinically obvious liver disease, the elevations were two to three times the upper limit of normal and decreased to normal in 80% of patients, eight weeks after abstinence. By contrast, in patients with liver disease, the elevations of serum gamma-glutamyl transpeptidase were of the order of eight to 10 times above normal and persisted at these high levels following eight weeks of abstinence. The degree of abnormality of the serum enzyme did not correlate with the daily amount of alcohol ingested or with the total length of time of alcohol consumption in these alcoholic patients. This study shows that serum gamma-glutamyl transpeptidase is persistently elevated in patients with clinically obvious liver injury, but only in 22% of chronic alcoholics without significant liver disease.
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