[Fermental (plasmin) blood system in patients with acute viral myocarditis].

For the first time it is established that patients with acute virus myocarditis (AVM) at all stages of severity of clinical course of the disease have changes in indicators of fibrinogens, soluble complexes of monomeric fibrin, products of its degradation, activated plasminogen, time recalcification of blood plasma to blood heparin, fibrinolytic activity of plasma, spontaneous fibrinolysis, time of lysis of euglobulin clot, blood heparin, antithrombin III, platelets. It testifies to suppression of fibrinolysis processes which expressiveness statistically reliably correlates with degree of severity of clinical course of AVM. Application of medicamentous correction is necessary for prevention of the development of disseminated intravascular blood coagulation syndrome.

[Enzymatic (plasmin) blood system in patients with acute virus myocarditis and its medical correction].

For the first time it is established that changes of parametres of coagulation hemostasis (fibrinogen Fg, soluble complexes of monomeasured fibrin -SCMF, products of fibrin degradation-PFD, 1st and 2nd waves of platelet aggregation), platelet hemostasis (platelets, a range index of platelet contact activation -RIPCA, activated partial platelet time--APPT, a total index thrombophilia TIT, platelet time--PT, prothrombin time (Prv), physiological anticoagulants (blood heparin-BH, antithrombin III--AT III, plasma tolerances to heparin--PTH), and fibrinolysis (lysis time of euglobulin clot--LTEC), enzyme condition of antiradical protection--superoxide scavenger (SOSC) which reduction in concentration leads to increase in concentration of malonic dialdehyde (MD) in erythrocytes (Er), thrombocytes (Tr), blood plasma (BP) in patients with acute virus myocarditis (AVM) of all severity groups and statistically correlate with the degree of severity of clinical course and demands medication correction.

[Coagulative hemostasis in patients with acute viral myocarditis].

For the first time it was established that changes of fibrinogen parameters, dissolved complexes of monomeric fibrinogen (DCMF), products of fibrinogen degradation (PDEF), first and second waves of platelet aggregation, activated partial platelet time (APPT), range index of contact platelet activation (RICPA), general index of thrombophilia (GIT), platelets, prothrombin time, heparin in blood, plasma tolerance to heparin (PTH), time lysis and euglobulin clot (TLEC), lipid peroxidation, antiradical defence ferment, superoxiddismutase (SOD) in patients with acute virus myocarditis of first, second and third group of severity correlate statistically reliably with grade of severity of clinical course of the disease and require correction with medications.

[State of physiological anticoagulant heparin, antithrombin III and their correction with medicines in patients with acute viral myocarditis].

For the first time, positive influence was shown of a complex blood heparin-antitrombin III on the state of the coagulant and fibrinolytic system of blood in patients with acute virus myocarditis that favours the normalization of clinical and laboratory indicators, improvement of the state of patients and reduction of average bed-day indicator (hospital stay) till 25 and 35 days in accordance with severity of clinical course of the disease and can be recommended as a choice of medicine.

[Total index of thrombocyte aggregation in patients with an acute viral myocarditis].

For the first time it is proved, that patients with an acute virus myocarditis have statistically confirmed authentic reduction in quantity of thrombocytes, extention of parameters of a activated partial thrombin time, reduction in concentration of a heparin-antithrombin III (AT-III) complex against suppressed enzyme of antiradical protection - superoxide dismutase and it has led to activization of a malonic dialdehyde in erythrocytes, thrombocytes and blood serum. In case of the development of an acute virus infection especially caused cardiotrophic strain Consaki, virus CVB 1-CVB 4, thrombocytes, according to P. Nemetchek-Gansler, acquire not pertaining to them ability for phagocytosis of viruses with following reduction in quantity of thrombocytes and increase in aggregation abilities of thrombocytes what influence the state of duration index of contact aggregation of thrombocytes with the tendency to shorten this duration, and also it may develop hypoxia, an ischemia and the subsequent necrosis of cardiomyocytes, that is to an acute virus myocarditis that demands corresponding correction with medications.