Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.68 (tissue plasminogen activator)
 11,311 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.
 ...
PMID:[Platelet activation in the early phases of acute myocardial infarction]. 980 73

The plasma fibrinolytic/proteolytic balance was assessed in 60 stable angina patients who underwent control coronary catheterization and the results were correlated with angiographic findings and control samples (n = 20). The concentrations of t-PA, PAI-1, collagenase (MMP-1), tissue inhibitor of MMP (TIMP-1), plasmin-antiplasmin (PAP) complexes and alpha2-macroglobulin (alpha2-M) were measured in plasma samples. The results showed a significant increase of PAP (p <0.001) and a reduction of alpha2-M (p <0.001) in the group of patients when compared to controls, indicating a degree of fibrinolysis/proteolysis activation. There was no correlation between the different parameters analyzed and the extent of angiographically proven atherosclerosis (one or more stenotic vessels), while the t-PA levels were significantly elevated (p <0.03) in patients with coronary stenosis > or =75% or occlusion. We conclude that there is a disturbance of the plasma fibrinolysis/proteolysis in patients with stable angina not related to the extent of atherosclerosis. The t-PA levels may be a good marker for coronary occlusion in these patients.
 ...
PMID:Fibrinolysis/proteolysis balance in stable angina pectoris in relation to angiographic findings. 1152 15


<< Previous 1 2 3