1/14. Fatal acute myocardial infarction during severe thrombocytopenia in a patient with idiopathic thrombocytopenic purpura.Because platelets play a major role in most thrombotic events, it is not surprising that all cases of myocardial infarctions in patients with idiopathic thrombocytopenic purpura (ITP) have been reported to occur only when platelets counts begin to rise. We report on a 69-year-old man with ITP who had acute myocardial infarction while he was severely thrombocytopenic (2000/microL). We hypothesize that the pathogenesis of myocardial infarction in thrombocytopenic patients with ITP may result from endothelial damage induced by autoantibodies directed against antigens present on both platelets and coronary endothelial cells.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/14. Plasminogen activator inhibitor-1, which is released from blood product transfusions, might be associated with (sub)acute thrombosis after coronary dilatation and stenting: a case report.We present the case of a 71-year-old man who suffered bleeding complications after coronary dilatation and stenting, necessitating a substantial number of platelet and whole blood transfusions in the following days. Postmortem analysis of plasma samples obtained after the transfusions revealed unexpectedly elevated levels of plasminogen activator inhibitor-1 (PAI-1) antigen and activity associated with a nonmeasurable euglobulin clot lysis time, disclosing extreme hypofibrinolysis, which might facilitate coronary thrombosis. The patient died suddenly on day 6, very likely due to coronary thrombosis. Our case suggests that PAI-1, which is released from platelets in blood product transfusions, might be under certain conditions a risk factor for (sub)acute thrombosis after coronary dilatation and stenting.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
3/14. Congenital protein c deficiency and myocardial infarction:concomitant factor vii hyperactivity may play a role in the onset of arterial thrombosis.A 29-year-old man with congenital protein c deficiency and acute myocardial infarction is reported. Four hours after the onset of chest pain, he was treated intravenously with tissue-type plasminogen activator. Subsequent coronary angiography revealed only slight stenosis of the left anterior descending coronary artery without any atherosclerosis. The propositus, his brother, and his mother, showed low levels of both protein C activity and antigen, while plasma thrombomodulin levels were normal. His grandfather had died from acute myocardial infarction at 38 years of age. We investigated several other risk factors for arterial thrombosis, including factor vii, fibrinogen, heparin cofactor ii, lipoprotein (a), and anticardiolipin antibodies. No other haemostatic abnormalities apart from factor vii hyperactivity were detected in this family. To study the effects of protein C and factor vii on procoagulant activity, prothrombin time was measured after the addition of activated protein C and factor vii to protein C-deficient plasma. The prothrombin time ratio decreased along with an increase in the factor vii level. It also decreased with a decrease in the activated protein C level. These findings indicated that the procoagulant activity of factor vii was enhanced by low protein C levels, suggesting that concomitant factor vii hyperactivity may cause acute myocardial infarction in patients with protein c deficiency.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
4/14. Acute myocardial infarction with normal coronary arteries in a case of polyarteritis nodosa: possible role of coronary artery spasm.A 20 year old man with no previous history of heart disease presented with acute left ventricular failure following extensive anterior wall myocardial infarction. Selective angiography revealed multiple aneurysms in the renal, mesenteric and hepatic arteries with an infarct in the lower pole of the right kidney. These findings, along with the presence of circulating hepatitis b surface antigen favoured the diagnosis of polyarteritis nodosa. In view of normal coronary angiogram and absence of myocardial vasculitis, coronary vasospasm was implicated as the cause of myocardial infarction. Such an occurrence, which could have different therapeutic and diagnostic implications, has not, to our knowledge, been previously described in polyarteritis nodosa.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
5/14. Thrombogenicity of intravenous 5-fluorouracil alone or in combination with cisplatin.Acute myocardial infarction was observed in two patients receiving standard intravenous doses of 5-fluorouracil (5-FU)-based chemotherapy. Therefore, the authors prospectively assessed the thrombogenicity of this agent by studying ten patients, six with head and neck cancer and four with gastrointestinal malignancies, receiving 5-FU (1 g/m2/day) as a constant intravenous infusion over a 4-day or 5-day period. The six patients with head and neck cancer also received a single dose of 100 mg/m2 of cisplatin on day 1. blood samples were obtained preinfusion, 24 hours into the infusion, and postinfusion. Samples were assayed for fibrinopeptide a (FpA) by enzyme-linked immunoassay, for protein C activity (PCa) using a chromogenic substrate (Spectrozyme PCa), and protein C (PCag) and free protein s antigen (PSag) by electroimmunoassay. No patient experienced a thrombotic event. A significant increase was observed in FpA levels during the infusion which returned toward baseline at the conclusion of the infusion. After infusion of 5-FU, the PCa value was significantly lower than the PCag (37 /- 17 versus 69 /- 24%; P less than 0.002). No effect on protein s was observed. The changes in the patients receiving 5-FU alone were comparable to those who also received CDDP. The authors conclude that during the infusion of 5-FU, the rise in FpA activation and reduction in PCa as compared to PCag are compatible with activation of coagulation.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
6/14. Serum aminoterminal type III procollagen peptide reflects repair after acute myocardial infarction.In 16 patients with acute myocardial infarction and in 15 controls, procollagen type III aminoterminal peptide in serum (PIIINP) was measured consecutively. Serum PIIINP was increased on the second to third postinfarction day (p less than 0.01) and remained elevated for more than 4 months. Peak values were observed on the third to seventh postinfarction day. The individual peak changes were correlated to infarction size calculated from serum CK-MB and serum lactate dehydrogenase (p = 0.60, p = 0.02). The changes in distribution of PIIINP-related antigens in serum after gel chromatography were similar to changes observed during wound healing in humans. PIIINP is cleaved off procollagen type III during the biosynthesis of type III collagen, which characterizes the early stages of repair and inflammation. Our findings suggest that serum PIIINP reflects the repair processes and scar formation following acute myocardial infarction. The serum PIIINP alterations in acute myocardial infarction differ essentially from the changes in myocardial enzymes reflecting myocardial injury. Serum PIIINP may therefore provide new and clinically relevant information on the healing of myocardial infarction.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
7/14. serum sickness and acute renal failure after streptokinase therapy for myocardial infarction.A patient developed serum sickness and acute renal failure following therapy with streptokinase for myocardial ischaemia. There was a previous history of a cellulitic infection of the leg, and antibodies to streptokinase were measurable in a serum sample taken from the patient before therapy. A cryoglobulin was detected at the time of presentation with serum sickness. This contained polyclonal IgG (with anti-streptokinase activity), streptokinase, and C3. Circulating immune complexes were demonstrated by C1q-binding assay. Deposition of C3 was observed in skin and renal biopsies, and bound to erythrocytes. Renal histology, however, showed acute tubular necrosis, with no vasculitis or inflammatory cell infiltrate. This case provides an unusual example of the characterization of an immune complex comprising a specific antibody and an exogenous antigen, and has clinical implications for the use of streptokinase.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
8/14. The role of the fibrinolytic system in acute myocardial infarction after a normal exercise test.A 67-year-old man had an acute myocardial infarction with thrombosis in the left anterior descending artery shortly after normal exercise. We were able to measure the fibrinolytic components in this patient just prior to his developing acute myocardial infarction as well as during convalescence. In this case, marked increase in total plasminogen activator inhibitor-1 (PAI-1) antigen, mainly due to free PAI-1 antigen, was observed in basal conditions before the onset of acute myocardial infarction. On the appearance of ischaemia, plasminogen activator activity was suppressed, probably due to decreased tissue plasminogen activator antigen release and increased PAI activity, compared with that during convalescence. This suggests that some patients with coronary artery disease who have a high level of free PAI-1 antigen in basal conditions may have a strong tendency to develop acute myocardial infarction, due to further impaired fibrinolysis on the induction of ischaemia.- - - - - - - - - - ranking = 4keywords = antigen (Clic here for more details about this article) |
9/14. Myocardial infarct due to a unique atrial myxoma with epithelial-like cells and systemic metastases.A 73-year-old man had myocardial infarct and coronary emboli from a left atrial myxoma diagnosed at necropsy. The tumor was attached to the atrial roof and showed no local myocardial infiltration. Transmission electron microscopic (TEM), light microscopic, and immunoperoxidase (IPX) studies confirmed the neoplastic character of this lesion and pointed to undifferentiated mesenchymal cells as the origin of the atrial myxoma cells. This case emphasizes two aspects: (1) glandlike structures were also found in the myxoma, and their epithelial-like nature was supported by TEM and IPX studies, which showed positivity for carcinoembryonic antigen and H blood substance; (2) many systemic tumor masses were found, and their metastatic nature was evidenced by the markedly infiltrative and destructive character; the only cytologic marker that could discriminate this case from other usual, noninfiltrative cardiac myxomas was the epithelial-like cells.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
10/14. von willebrand factor fragment in type IIA von Willebrand's disease: demonstration of two different forms of fragments.A fast-migrating precipitin peak which showed a reaction of partial immunochemical identity with the major von willebrand factor (vWf) component was detected by crossed immunoelectrophoresis in agarose gel in plasma but not in platelets from a patient with type IIA von Willebrand's disease (vWD). Another patient undergoing urokinase therapy had a vWf fragment in plasma which was antigenically cross-reactive with the major vWf component. When plasma from both patients was mixed and electrophoresed together in the first dimension, two fast-moving precipitin arcs were demonstrated in the second dimension. These data indicate that two different kinds of vWf fragments can be generated in vivo.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
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