beta-Thromboglobulin in patients with acute myocardial infarction according to the treatment.

Many studies report on the increased activity of platelets in patients with heart disease, especially with acute myocardial infarction (MI). The aim of the present study was to evaluate dynamics of beta-thromboglobulin (beta-TG) concentration in patients with MI according to the disease duration and type of treatment. We investigated 29 patients, who were divided into two groups according to the type of treatment. beta-TG concentration was determined using the immunoenzymatic method (ELISA). Blood was taken 1st, 3rd, 5th, 8th and 11th day of infarction. Our results indicate that in the course of myocardial infarction there is a change in platelet activation. The treatment applied affects beta-TG concentration, and the thrombolytic therapy inhibits platelet activation.

Flow cytometric analysis of CD 62P expression in patients with acute myocardial infarction.

Much attention has been paid to the role of platelets in the pathogenesis of heart diseases, e.g. ischaemic disease and myocardial infarction. During platelet activation changes appear both in the internal structure and in the membrane. The release reaction is associated with the appearance of CD 62P (P-selectin). The aim of the present study was evaluate CD 62P expression in patients with acute myocardial infarction according to the disease duration and the type of treatment. We study 29 patients with acute myocardial infarction (MI). The patients were divided into two groups: group A--15 patients treated with heparin and aspirin and group B--14 patients treated with streptokinase, heparin and aspirin. The control group consisted of 21 healthy subjects. We indicated that P-selectin expression is influenced by infarction duration and type of treatment. Our study demonstrates that thrombolytic therapy inhibits platelet activation. Patients receiving streptokinase showed lower CD 62P expression than those treated only with heparin and aspirin, both before and after platelet activation with thrombin.

Platelet factor 4 as a marker of platelet activation in patients with acute myocardial infarction.

The aim of the present study was evaluate dynamics of platelet factor 4, as a marker of platelet activation, in patients with acute myocardial infarction according to the disease duration and type of treatment. In the recent years much attention has been paid to the role of platelets in the pathogenesis of ischaemic disease and myocardial infarction. Rupture or splitting of atheroma and increased platelet activation are a direct cause of acute thrombotic process in coronary vessels. During platelet activation alpha granules release proteins, e.g. platelet factor 4 (PF 4). We investigated 29 patients with acute myocardial infarction (MI); the patients were divided into two groups: group A--15 patients treated with heparin and aspirin; group B--14 patients treated with streptokinase, heparin and aspirin. Control group (C) consisted of 21 healthy subjects. PF 4 concentration was determined on the 1st, 3rd, 5th, 8th, 11th day of MI using the immunoenzymatic method. Our results indicate that in the course of myocardial infarction there is a change in the platelet factor 4 and that thrombolytic therapy inhibits platelet activation.

Phagocytic activity of platelets in patients with myocardial infarction.

The aim of our present study was to analyse the dynamics of changes in the phagocytic activity of platelets with myocardial infarction according to the treatment applied. Twenty patients with acute myocardial infarction and thirty healthy subjects were examined. Platelet count, phagocytic activity of platelets and the phagocytic index were determined. We observed reduced phagocytic activity of platelets in the first 24 hours of infarction, which may be due to exhaustion of most active platelets in a thrombus and microaggregates. A transitory increase in the phagocytosis activity of platelets observed on the third day of infarction may be caused by the release of large, more active platelets from splenic pool. On the eight day of infarction, the phagocytic activity of platelets became normalized in both experimental groups. Our study indicates that together with platelet activation the phagocytic activity gets reduced being a likely response to the thrombocytopenic factor. This can be confirmed by the increased number of platelets on the 8th day. Our results suggest a slightly attenuated phagocytic ability of platelets, irrespective of the treatment applied. The reduction seems to result from the effect of platelets exhaustion on the procoagulative activity in patients with myocardial infarction.

[Activation of the antibacterial properties and neutrophil myeloperoxidase and acid phosphatase in patients with unstable angina pectoris]. / Pobudzenie wlasciwosci bakteriobójczych oraz aktywacja mieloperoksydazy i kwasnej fosfatazy w granulocytach obojetnochlonnych u chorych na niestabilna dlawice piersiowa.

Neutrophils are very important in pathogenesis of ischemic disease. They take part in the biomorphology of thrombus and also in the damage of myocardium ischemia in a course of unstable angina pectoris. We evaluated the functional status of neutrophils in peripheral blood, by measurement of bactericidal activity and activity of granulocyte's enzymes: myeloperoxidase (MPO) and acid phosphatase in the patients with unstable angina pectoris. We studied a group of 43 people at the age from 34 to 74 years. The blood for investigation was obtained during the first five hours from the moment of hospitalization. The control group were 40 healthy people. The number of granulocytes was significantly higher in patients with unstable angina pectoris and granulocytes were metabolically activated which was shown in the bigger activity of granulocyte's enzymes like MPO and acid phosphatase than in the control group. The activation of neutrophils is developed by many factors in the course of unstable angina pectoris. They take part in the processes of thrombogenesis and thrombolysis and they are a very important origin for active oxygen metabolites, which are responsible for damage of myocardium ischemia.

[Peripheral blood neutrophil activation and the extent of myocardial infarction]. / Stan pobudzenia granulocytów obojetnochlonnych krwi obwodowej a rozleglosc zawalu serca.

The activation of polymorphonuclear granulocytes between 2 and 5 hours from the beginning of the pain was examined in patients with myocardial infarction. The efficient neutrophils activated in the first day of illness, take part in recanalization of coronary vessels, thus limiting the extent of myocardial infarction.