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The data gained from clinical studies in the past years have indicated that the thrombolytic therapy (TL) has favourable effect on patients with acute myocardial infarction (AMI). It is aimed at reperfusion in the ischaemic area, a decrease in the extent of infarction site and a decrease in mortality. TL administered within the initial hours after the onset of AMI leads to better results than when administered after several hours. Currently, TL is not limited by age. The patients who were given streptokinase (SK) or anistreplase (APSAC) prior to more than 4 days, if necessary, urokinase or alteplase (rt-PA) should be given. There are differences in the opinions as to the optimal selection of thrombolytic drugs. However, all currently used drugs lead to a significant decrease in mortality due to AMI. The preferential use of accelerated administration of rt-PA in contrast to SK is justified in younger patients with extensive AMI of the anterior wall, in whom the therapy has begun within 4 hours since its onset. The occurence of severe bleeding indicates that TL should be halted and coagulation factors should be replaces by freshly frozen plasma or fibrinogen concentrate, if necessary, transfusion of full blood should take place. If the severe bleeding occurs shortly after the administration of SK, the persisting plasminaemia can be arranged by antifibrinolytic drugs. An improvement in TL results can be achieved by adjuvant antithrombotic therapy. At the same time, in addition to acetylsalicylic acid, the patient treated with rt-PA should be given heparin. Heparin administration is not necessary in patients treated with SK or APSAC. However, heparin is indicated in patients at risk due to systemic embolization in congestive heart disease, extensive infarction or atrial fibrillation. (Tab. 1, Ref. 28).

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The data gained from clinical studies in the past years have indicated that the thrombolytic therapy (TL) has favourable effect on patients with acute myocardial infarction (AMI). It is aimed at reperfusion in the ischaemic area, a decrease in the extent of infarction site and a decrease in mortality. TL administered within the initial hours after the onset of AMI leads to better results than when administered after several hours. Currently, TL is not limited by age. The patients who were given streptokinase (SK) or anistreplase (APSAC) prior to more than 4 days, if necessary, urokinase or alteplase (rt-PA) should be given. There are differences in the opinions as to the optimal selection of thrombolytic drugs. However, all currently used drugs lead to a significant decrease in mortality due to AMI. The preferential use of accelerated administration of rt-PA in contrast to SK is justified in younger patients with extensive AMI of the anterior wall, in whom the therapy has begun within 4 hours since its onset. The occurrence of severe bleeding indicates that TL should be halted and coagulation factors should be replaced by freshly frozen plasma or fibrinogen concentrate, if necessary, transfusion of full blood should take place. If the severe bleeding occurs shortly after the administration of SK, the persisting plasminaemia can be arranged by antifibrinolytic drugs. An improvement in TL results can be achieved by adjuvant antithrombotic therapy. At the same time, in addition to acetylsalicylic acid, the patient treated with rt-PA should be given heparin. Heparin administration is not necessary in patients treated with SK or APSAC. However, heparin is indicated in patients at risk due to systemic embolization in congestive heart disease, extensive infarction or atrial fibrillation. (Tab. 1, Ref. 28.)

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Endothelial damage and platelet hyperactivity may play a role in the vascular complications of essential hypertension. Restoration of endothelial function and reduction of increased platelet aggregation in essential hypertension are one of the aims of modern anti-hypertensive therapy. Therefore, the effect of angiotensin converting enzyme (ACE) inhibitors on endothelial and platelet functions is of interest. In the present study, 23 healthy normotensives and 23 age- and sex-matched patients with non-treated essential hypertension (1st and 2nd stage according to WHO) were investigated. Measurements of endothelial and platelet functions in hypertensives were carried out before therapy, after 1 week of placebo administration, after 1 week and after 1 month of perindopril therapy in a once daily dose of 4 mg. Plasma thrombomodulin (ELISA method) and beta-thromboglobulin (radio immunoassay method) were assayed and platelet aggregation (spontaneous and induced by adrenaline) was measured. The values of plasma thrombomodulin, a novel marker of endothelial function, were compared between age- and sex-matched normotensives and hypertensives. A significant decrease of adrenaline-induced platelet aggregation was observed after 1 month of perindopril therapy in comparison with the values before therapy or after 1 week of perindopril therapy ( P < 0.02 and P < 0.05 respectively). There were no significant changes in plasma thrombomodulin or beta-thromboglobulin following therapy. We failed to find significant changes of plasma thrombomodulin in patients in the early stages of hypertension, but its tendency to be higher than in normotensives does not rule out some vascular damage. The inhibitory effect of perindopril on platelet aggregation may be a further advantage of this drug. Since no changes were found after 1 week of therapy, the reduction of adrenaline-induced platelet aggregation after 1 month of therapy may be explained by an indirect effect of perindopril on platelet function, probably asa result of protective action on the arterial wall.

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Thrombotic occlusion of coronary arteries is the reason of most acute coronary syndromes. A significant role in their prevention and therapy is taken by antiplatelet therapy. Acute coronary syndrome justifies also the use of anticoagulation therapy, name by heparin. The adjuvant therapy by means of heparin in thrombolysis seems to be necessary especially when alteplase (t-PA) is used. Peroral anticoagulants represent a further therapeutical procedure in patients with coronary ischaemia. Regarding the increased risk of bleeding, the cost and difficulties coinciding with therapy by cumarine derivates, the antiplatelet therapy is currently preferred. Cumarine derivates, however, should be used in patients with simultaneous atrial fibrillation, venous thromboembolism and it should be considered in patients with heart failure and pre-thrombotic states. Studies aimed at the assessment of the role of low-molecular heparin in acute coronary ischaemia currently take place. Encouraging results are gained from experience with high effective direct inhibitors of thrombin (e.g. hirudin) and antagonists of glycoprotein IIb/IIIa. It seems that they soon will find justification in the therapy of arterial thrombosis. Interesting field of the research is represented by the studies which compare low doses of acetylosalicylic acid with low doses of cumarine derivates. (Ref. 43.)

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Undesirable changes of haemostasis induced by some anti-hypertensive drugs can encourage the acceleration of atherogenesis. Therefore, the changes of haemostasis parameters in 22 patients with essential hypertension under long-term celiprolol therapy (> 2 months) were of interest. In the placebo group of 15 essentially hypertensive patients there were no significant changes in platelet activity. On the other hand, the therapeutic dose of celiprolol was shown to reduce total platelet aggregation, without any harmful effects on fibrinolytic activity and coagulation inhibitors such as protein C and antithrombin III. The metabolic neutrality of celiprolol accompanied by the proven platelet-inhibitory tendency is desirable in the new approach to hypertension treatment. Potentially anti-thrombotic or at least neutral prothrombotic properties of celiprolol may be important in terms of the favourable role of anti-hypertensive drugs in cardiovascular morbidity.

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The relationship between changes in blood coagulation, the occurrence and severity of risk factors of ischemic heart disease and the clinical condition of the patient was investigated. The at risk group of patients 42.2% had more than 3 pathological parameters. Intravascular blood coagulation was not activated in any of the patients. In patients with acute myocardial infarction (MI), 62.2% had more than 3 pathological parameters on the first day of MI development. Demonstrable activation of intravascular blood coagulation was found in 28.2% of these patients. On day 5 of MI, activation of intravascular blood coagulation was recorded in 57.7% of the patients treated by classical approach and in 15.4-30.8% of the patients on thrombolytic treatment. In the at risk group, primary hemostasis and the fibrinolytic system were more affected, in patients with MI the whole hemostatic mechanism was involved. On day 5 of MI, in patients with classical therapy pathological laboratory findings still persisted or were even more deteriorated, particularly increases in fibrinogen level. At that time, in patients on thrombolytic therapy no substantial changes of initial values were recorded. No correlation was found to exist between changes in hemostasis and the risk profile or between changes in hemostasis and the clinical severity of MI. The obtained results justify the administration of antithrombotic substances, especially in patients with unstable angina pectoris. On observing time constraints, administration of thrombolytics is justified in MI. (Fig. 9, Ref. 25.)

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The reduction of increased platelet aggregation in essential hypertension is one of the aims of modern antihypertensive therapy. Twenty-one hospitalized patients with non-treated essential hypertension were examined. The platelet function measurements were made before the therapy and after 1 week of celiprolol administration (300 mg/day). Fifteen essentially hypertensive patients were investigated before and after 1 week of placebo administration. Plasma beta-thromboglobulin was assayed, and the whole blood platelet aggregation (initial and total-induced by adrenaline and ADP) was measured. A significant decrease in adrenaline-induced (from 19 to 13%, p < 0.02) and ADP-induced aggregation (from 15 to 13%, p < 0.05) was observed after celiprolol administration. This reduction of adrenaline-induced platelet aggregation may be explained by the stimulation effect of celiprolol on platelet beta 2-receptors. Thus, some inhibitory effect of celiprolol on platelet aggregation is one of the further advantages of this drug in the therapy of essential hypertension.

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On the basis of the hemocoagulation and hemostasis parameters study the actual hemostasis state was evaluated in 30 patients treated for active deep venous thrombosis (DVT) in dependence on its extent. In comparison with 30 healthy persons there were found statistically significant changes in a majority of laboratory parameters that can indicate thrombophilic state. Platelet activation, increased coagulation system activity, decreased fibrinolytic activity as well as increased fibrinogen and fibrin degradation products were demonstrated. The positive correlation between the extent of DVT and the relevance of hemostasis changes was revealed which results to these conclusions: the more extensive DVT--the more intensive tendency to thrombophilia up to intravascular blood coagulation activation was observed. Although the adequate prolongation of the prothrombin time (during the coumarin therapy) or APTT (during the heparin therapy) was achieved, the laboratory parameters showed a therapy insufficiency. In the cases of laboratory signs of the activated intravascular blood coagulation we can recommended a fortification of the oral anticoagulant therapy by its combination with antiplatelet drugs or by its temporary replacement by the heparin therapy.

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The circadian variation in platelet function may play a role in the morning increase of coronary thrombotic complications. The circadian variation of plasma beta-thromboglobulin levels--as an indicator of in vivo platelet activation--was investigated in seven healthy volunteers using a commercial radioimmunoassay kit. There was a statistically significant rhythm culminating with an amplitude of 30 micrograms/l (95% tolerance interval/15-45 micrograms/l) at 10.00 hours (95% tolerance interval/07.00-13.00 hours). The morning increase of plasma beta-thromboglobulin indicates an increased in vivo platelet activation at this time of day. This finding could correlate with the morning peak in the onset of myocardial infarction. It might also help in timing therapy of diseases which are associated with platelet hyperactivation.

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Plasma beta-thromboglobulin, initial (spontaneous) and total platelet aggregation, induced by adrenaline or ADP, were determined in 15 patients with essential hypertension before and after 1 week of diltiazem therapy. Diltiazem significantly decreased the spontaneous platelet aggregation in a therapeutic dose of 3 x 60 mg/day. This antiaggregatory effect is the further advantage of the antihypertensive therapy with diltiazem that may be of importance for the inhibition of atherosclerotic and thrombotic complications in essential hypertension.

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1. Plasma levels of beta-thromboglobulin, initial and total platelet aggregation (induced by adrenaline or adenosine diphosphate [ADP]) were determined in 26 normotensive subjects and 26 patients with untreated essential hypertension. Groups of 18 essential hypertensive patients and 18 age- and sex-matched normotensives were compared. 2. After 7 days of treatment with prazosin in a dose of 2-8 mg daily the above measures were repeated in 18 essential hypertensive patients. A significant increase in plasma levels of beta-thromboglobulin, initial and total adrenaline-induced as well as ADP-induced platelet aggregation was found in hypertensives. Prazosin restored the mean arterial blood pressure in hypertensives to normal, but it had no significant influence either on increased beta-thromboglobulin levels or on initial and total aggregability. 3. The results confirm increased platelet aggregation and in vivo platelet activation in patients with essential hypertension; however there is a discrepancy with previous reports about those results obtained after prazosin therapy. The results suggest that increased platelet aggregation and in vivo activation need not be restored to normal after effective antihypertensive therapy alone. They give reason for the combination of antihypertensive together with anti-aggregatory therapy in essential hypertension.

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Derangements of hemostasis and hemocoagulation in patients with malignancies are known as paraneoplastic syndrome. Their origin, however, has not been unequivocally established and explained, and data on their occurrence are controversial. Examination of 157 patients with different malignant tumor diseases yielded pathological laboratory findings in 94.2%. The most frequent finding was the state of hypercoagulation in 41.0%; hypercompensated syndrome of disseminated intravascular blood clotting (DIC) was found in 10.9%, compensated DIC syndrome in 18.0%, consumptive coagulopathy in 3.8%, and in 19.2% hypocoagulation state caused by other abnormalities. The laboratory finding was normal only in 5.8% of the patients. In the light of the high occurrence rate of hemostatic and hemocoagulation changes in malignant diseases, established by laboratory analysis, the use of anticoagulants and antiaggregation substances appears to be justified in the majority of cases, both to prevent the development of these changes which may complicate the course of the malignant condition, and in preoperative care to reduce the rate of postoperative thromboses in patients with tumors.

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Plasma levels of beta-thromboglobulin, initial and total platelet aggregation (induced by adrenaline or ADP) were determined in twenty-eight normotensive subjects and thirty patients with untreated essential hypertension. After 7 days of treatment with prazosin in a dose of 2-8 mg daily the above measurements were repeated in eighteen essential hypertensive patients. A significant increase in plasma levels of beta-thromboglobulin, initial and total adrenaline- and ADP-induced platelet aggregation was found in hypertensives. Prazosin restored the mean arterial blood pressure in hypertensives to normal, but it had no significant influence either on increased beta-thromboglobulin levels or on platelet aggregation. The results show that increased in vivo activation as well as increased platelet aggregation need not be restored to normal after effective decrease of blood pressure. The results suggest that a combination of drugs with an antihypertensive and antiplatelet (antiaggregating) effect (or use of a drug with both an antihypertensive and antiaggregating effect) can further decrease the development of severe complications of essential hypertension.

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