Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial infarction and thrombolysis are proven to be associated with platelet activation. However, the time relationship of platelet activation with the onset of symptoms and with thrombolysis, and the response to aspirin are not well defined. In this study we measured platelet activity in the early phase of myocardial infarction treated with either streptokinase or recombinant tissue-type plasminogen activator (rt-PA) and evaluated whether and to what extent it may be counteracted by aspirin. Fourty-one patients (mean age 57 +/- 6 years) received thrombolytic therapy after coronary occlusion: 1.5 million units of streptokinase (Group 1; 21 patients) or 100 mg of rt-PA (Group 2; 20 patients). Ten randomly selected patients in either group were given 500 mg aspirin i.v. prior to infusion of the thrombolytic compound and, then, 325 mg/die of aspirin orally. Beta-thromboglobulin (BTG), a marker of platelet activity, was determined at admission, after thrombolysis and in the subsequent 48 hours. At admission, BTG plasma levels averaged 125 +/- 31 IU/ml in Group 1 and 134 +/- 35 IU/ml in Group 2 (NS). Thrombolysis produced a similar increase in platelet activity in both groups, and maximal values were reached at the third hour (196 +/- 43 IU/ml in Group 1 and 192 +/- 39 in Group 2, p < 0.001 vs baseline and NS between groups). Levels of BTG were higher in streptokinase-treated group starting from 24 hours (p < 0.05). Differences in BTG levels between aspirin-treated and aspirin-untreated patients became significant at 48 hours after thrombolysis in both groups. An inverse correlation was found between time elapsed from onset of symptoms and BTG value on admission (r = -0.86, p < 0.001); in patients admitted within 2 hours after the beginning of symptoms, and having the higher BTG levels, thrombolysis did not induce a significant increase in platelet activity; this, on the contrary, was observed in patients admitted later. Platelet activation is greater early after myocardial infarction and is differently influenced by thrombolytic treatment, depending on the delay of the patient's admission. Streptokinase and rt-PA induce a similar increase in platelet activity which is more persistent after streptokinase; cycloxygenase inhibition with aspirin seems to influence platelet activity only starting from the second day.
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PMID:[Platelet activation in the early phases of acute myocardial infarction]. 980 73

Mitral stenosis still remains a major problem in Southeast Asia including Thailand. It contributes to the morbidity and mortality related to thromboembolism which was associated with the left atrial thrombus. However, the pathogenesis of left atrial thrombus in these patients is not completely understood. Therefore, the objective of this study was to investigate the coagulation and platelet activity including the function of the endocardium in the left atrium and peripheral circulation in patients with mitral stenosis who were free of left atrial thrombus and to compare those hematologic markers activity in the peripheral venous blood between the patients with mitral stenosis and the control. Thirty-six patients with moderate to severe mitral stenosis were included in the study. Most of the patients were in functional class II and 50 per cent had atrial fibrillation. Blood was obtained from the femoral vein, femoral artery, pulmonary artery and left atrium of these patients before heparin was administered to determine the value of various hematologic markers. In the control group, blood for determining the hematologic markers was collected only from the antecubital vein. The results of this study demonstrated that the levels of prothrombin activation fragment 1+2 (F1+2), thrombin-antithrombin III complex (TAT) and Beta-thromboglobulin (beta-TG) in the left atrium of the patients with mitral stenosis were significantly higher than those in the femoral vein and femoral artery, whereas the level of thrombomodulin was significantly lower in the left atrium compared with the femoral artery and vein. When comparing with the control group, the levels of TAT, plasminogen activator inhibitors-1 (PAI-1) from the peripheral vein were significantly higher and the level of thrombomodulin was also significantly lower in the patients with mitral stenosis. In conclusion, the present study demonstrated an abnormal hypercoagulable state of the left atrium and systemic circulation related to the abnormalities of coagulation, platelets and the endocardium which may cause the formation of left atrial thrombus in patients with mitral stenosis.
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PMID:An abnormal systemic and regional hypercoagulable state in patients with mitral stenosis. 1506 Dec 99