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Biomedical subjects

E P Panchenko

Publications and source records attributed to E P Panchenko.

At least 37 records · Page 2Linked to original sources
PubMed1997

[The effect of long-term Fraxiparin treatment on hemostasis in patients with primary pulmonary hypertension].

The aim of the study was elucidation of hemostatic effects of low-molecular heparin Flaxiparin in patients with primary pulmonary hypertension (PPH). 10 PPH patients (mean age 39.0 (+)- 3.2 years, mean history of the disease 5.1 (+)- 0.9 years) were treated up to 6 months. For the first month Flaxiparin was injected in therapeutic doses 15,000 AXa ICU, twice a day. The next 5 months prophylactic doses were administered twice a day (7,500 AXa ICU). D-dimer, fragment 1 + 2, complex thrombin-antithrombin, beta-thromboglobulin, protein C, antithrombin III, antigen of tissue plasminogen activator and inhibitor of tissue plasminogen activator of type I, activity of the latter were measured before the treatment, after the therapeutic and prophylactic courses, 6 months after the treatment. Initially, the patients had procoagulative hemostatic disorders. i.e. activation of blood coagulation; fibrinolytic system was also affected. In the course of Flaxiparin therapy blood coagulation and fibrinolysis improved significantly. However, the effect was not persistent after the drug discontinuation. Flaxiparin can be recommended for treatment of PPH.

Adult↗
PubMed1996

[The indices of the fibrinolysis, blood coagulation and lipid transport systems in hypertension patients].

Lipid spectrum, basal insulin concentration, the activity of coagulation factor VII and inhibitor of plasminogen tissue activator, content of plasminogen tissue activator antigen were assessed in 54 hypertensive patients with left ventricular hypertrophy (mean age 48.9 +/- 0.9 years, mean duration of the disease 15.7 +/- 1.1 years) after discontinuation of hypotensive therapy. A correlation was found between a rise in thrombogenic, atherogenic and a fall in fibrinolytic potential of blood. These findings suggest an essential role of insulin in regulation of thrombogenesis and fibrinolysis in hypertensive patients.

Biological Transport↗
PubMed1992

[The anticoagulant properties of the endothelium studied by the standard venous occlusion test].

Venous occlusion (VO) during which thrombin (Th) is postulated to be generated is routinely used for evaluation of fibrinolytic potential of endothelium (E). This study was performed to find out whether VO can also be used for assessment of anticoagulant function of E. VO was performed in 98 male patients (pts) with ischemic heart disease. Levels of protein C (PrC) which is related to Th binding by thrombomodulin and fibrinopeptide A (FpA)--a marker of presence of free Th--were determined together with some other factors of coagulation and fibrinolysis. Differences between pre- and postVO PrC levels fluctuated from -54.8% to +57.3%. According to reaction of PrC to VO pts were divided into 2 groups: 13 pts with increase or no change and 17 pts with decrease (consumption) of PrC. In pts without PrC consumption there was a significant increase in FpA. In pts with PrC consumption FpA was unchanged. In pts with PrC consumption exceeding its median value for this group (14%) PAI-1 antigen level fell significantly (-8.4 + 4%) during VO. Thus PrC consumption after VO indicates that TH is effectively removed from blood stream by endothelial factors. Absence of consumption of PrC is a sign of ineffective anticoagulant function of E. Increase in PrC level during VO in some pts may be due to its escape from tissue depot.

Adult↗
PubMed1991

[Unstable angina: tissue plasminogen activator, tissue plasminogen activator inhibitors, protein C and other factors of the blood fibrinolytic system].

The authors examined the activities of plasminogen activator, its inhibitor, the levels of C protein, antithrombin III, alpha 2-antiplasmin, plasminogen, fibrinogen, fibrinogen/fibrin degradation products in 22 patients with unstable angina by using the vein occlusive test. No significant differences were found in the examined parameters while comparing the group of stable angina patients and healthy subjects. It was concluded that thrombogenesis disturbances in unstable angina were regional and the recording of peripheral blood fibrinolytic parameters failed to detect any changes characteristic of unstable angina.

Adult↗
PubMed1991

[Endogenous vasopressin and fibrinolysis in patients with angina pectoris].

A relationship was examined between blood vasopressin levels and the fibrinolytic system in 35 patients with angina pectoris (16 with vasospastic angina (VA) and 19 with exercise-induced angina) who had undergone vein occlusion testing. There was a positive correlation between the post-testing vasopressin levels and the activity of tissue plasminogen activator inhibitor (TPAI) (r = 0.54) which was more high in patients with VA (r = 0.61). Only did the patients with VA show a direct relationship between the vasopressin concentrations and the activity of tissue plasminogen activator (TPA) (r = 0.63), the concentration of fibrinogen-fibrin degradation products (FFDP) (r = 0.88). Thirteen patients having higher vasopressin levels (over 3.4 ng/ml) displayed a greater TPAI activity than did the patients with vasopressin levels of at least 3.4 ng/ml (26.2 +/- 4.9 and 15.0 +/- 1.42 IU/ml, respectively; p less than 0.05). There was a direct relationship between the vasopressin levels and the activity of TPA (r = 0.65), the concentration of FFDP (r = 0.78) in patients having a vasopressin level of above 3.4 ng/ml. The findings are in agreement with the concept that endogenous vasopressin is involved in the regulation of the blood fibrinolytic system.

Adult↗
PubMed1991

[Coronary sinus blood thromboxane and prostacyclin in spontaneous myocardial ischemia].

The blood levels of 6-keto-PGE1 alpha and thromboxane B2 were measured in the coronary sinus of 15 males during and just after a spontaneous myocardial ischemic episode. The comparison was made in 30 males with coronary heart disease in the presence of exercise-induced angina in whom coronary sinus blood samples were taken during myocardial ischemia provoked by pacing and 6 males suffering from cardialgias without signs of coronary atherosclerosis. The patients with spontaneous anginal attacks had lower baseline 6-keto-PGE1 alpha (179.0 +/- 47.8 pkg/ml) than those with exercise-induced angina (336.0 +/- 65.7 pkg/ml; p less than 0.1). This difference became greater during ischemia (165.0 +/- 49.0 and 350.0 +/- 69.5 pkg/ml, respectively, p less than 0.05) and just after its elimination (166.0 +/- 48.7 and 413.0 +/- 76.0 pkg/ml, respectively, p less than 0.05). Coronary sinus blood thromboxane B2 levels were not substantially different in the presence or absence of myocardial ischemia. Thus, a decrease in the prostacyclin-forming function of the coronary endothelium plays a definite role in the genesis of spontaneous myocardial ischemic episodes.

Adult↗
PubMed1991

[Newly developed stenocardia: effect of intensive physical training on the indicators of the blood coagulation system and fibrinolysis].

The impact of 6-week strenuous exercise training (SET) on blood coagulative and fibrinolytic parameters (levels of fibrinogen, soluble fibrin, fibrinogen-fibrin degradation products, activities of plasminogen and plasmin) was studied in 28 patients with first angina pectoris, in 16 of whom in the first 3 months of onset of the disease, but angina pectoris lasting 3-4 prior to SET. The 6-week strenuous exercises in patients with first angina were found to cause a decrease in fibrinogen levels, exert no action on thrombin and fibrin formation. They did not diminish plasminogen activator release during exercise in patients with pre-exercise unstable angina.

Adult↗
PubMed1991

[Signs of thrombin formation in venous occlusion in patients with ischemic heart disease and the role of the protein C activation system in its utilization].

Elevated levels of fibrin peptide A were found in venous occlusion only in the patients unconsuming C protein, which indicates that there is a relationship between the thrombin production processes during venous occlusion and the C protein system functioning, the anticoagulant function of the endothelium in particular. Moreover, this makes it possible to employ the standard venous occlusion test to make an integral assessment of endothelial function.

Adult↗
PubMed1990

[Plasminogen activator inhibitor and protein C: their relation to plasma lipids and lipo- and apoproteins in ischemic heart disease of different duration].

The levels of plasminogen activator inhibitor (PAI), protein C (pC), total cholesterol (TC), high and low density lipoprotein cholesterols (HDLC and LDLC), apolipoproteins A1 (apoA1) and B (apoB) were measured in 45 patients with coronary heart disease angiographically documented and 10 healthy subjects without coronary heart disease and coronary atherosclerosis as evidenced by coronary angiography and provocative tests. Twenty three patients had primary angina (PA) with a duration of less than 3 months, twenty two patients presented with chronic coronary heart disease (CCHD) with a duration of more than 4 months. In general, a negative correlation between PAI and HDLC levels in the patients under study (r = -0.413; p = 0.02), it was higher in PA (r = -0.687; p = 0.02), but disappeared in CCHD (r = 0.027). The content of PAI correlated with the cholesterol index (r = 0.654; p less than 0.001 in the whole group), more greatly in PA (r = 0.865; p = 0.001) than in CCHD (r = 0.506, NS). There was a good correlation between the levels of pC and apoB in the whole group (r = 0.606; p less than 0.001) and in PA (r = 0.662; p = 0.001), but not in CCHD (r = 0.288, NS). The content of pC also correlated with a apoB/apoA1 ratio (r = 0.445; p = 0.002 in the whole group of patients). This correlation was significantly positive in PA (r = 0.455; p = 0.044), but not in CCHD (r = 0.022). Thus, higher levels of PAI coincided with atherogenic changes in those of HDLC, and an increase in the content of pC was in agreement with that of apoB. The interrelationships are particularly typical of early stages of CHD.

Adult↗
PubMed1988

[Newly developed stenocardia: functional activity of thrombocytes].

Platelet function (aggregation, circulating platelet aggregates, platelet factor 4, beta-thromboglobulin, thromboxane B2, 6-keto-PGF1 alpha, platelet count) was evaluated in patients with angina of new onset, as compared to individuals without coronary heart disease, and patients with angina of long standing (28 +/- 4.6 months). Some of the patients with angina of new onset were examined repeatedly 6 to 12 months after the onset of angina. Platelet activity was shown to be significantly higher in patients with stable angina of new onset, as compared to patients with lasting angina, where ADP and serotonin were used as inductors. Platelet aggregation, induced by platelet activation factor and collagen, was similar in all groups. Repeated investigation 6 to 12 months after the first anginal attacks demonstrated that most of platelet functional parameters declined or tended to decline.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

[Initial-onset stenocardia: characteristics of the blood coagulation system and fibrinolysis as reaction to physical exertion].

Blood coagulation and fibrinolysis were studied at rest and during bicycle ergometry in 45 patients with angina of new onset (ANO). Fourteen chronic coronary patients and 20 subjects, free of coronary heart disease or coronary atherosclerosis, were taken as controls. Fibrinolysis tended to be depressed in resting ANO patients. Potential fibrinolysis depended on the clinical pattern of the disease and was particularly depressed in patients with severe ANO. Stress did not activate fibrinolysis in patients with vasospastic angina and high basal plasminogen activator level at rest.

Adult↗