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Platelet and plasminogen system activity in patients with different characteristics of acute coronary syndrome
Dotsenko cardiovascular diseases. In order to estimate LDL-chol, LDL-apo B and LDL-chol/LDL-apo B ratio from blood total chol, TG, HDL-chol and apo B values, we used a formula developed by Hattori et al (Atherosclerosis 1998;138:289 99). To investigate reliability of this calculation, the above values have been compared in diabetic patients and healthy persons. Methods: Research was performed in 59 healthy subjects (32 women and 27 man) and 72 patients with type 2 diabetes mellitus (18 NIDDM and 54 secondary IDDM; 48 women and 24 man) with mean LDL-chol (Friedewald formula) level 3.9 mmol/1, TG 1.83 mm01/1 and total chol level 5.8 mmol/I. Chol and TG were determine i by enzymatic method, HDL-chol according to standard Burstein precipitation method, and apoB serum concentrations were measured by RID (Immuno AG). Results: In comparison with values found in control group of healthy persons (LDL-chol 2.86±0.65 mmol/1; LDL-apo B 0.29±0.13 mmol/1; LDL-chol/LDLapo B 11.92±6.69), in patients group we found a significantly higher level of LDL-chol (4.19±1.35 mmol/1, p<0.001), LDLapo B (0.41±0.18 mmol/1, p<0.001) and LDL-chol/LDL-apo B ratio (13.76±15.97, p<0.001), respectively. Conclusions: Friedewald' s formula for LDL-chol includes IDL-chol, but the Hattori' s formula theoretically excludes IDL-chol. It suggests a better estimation for the correct LDL-chol. Also, as estimated LDL-apo B is useful for the detection of small dense LDL, without performing ultracentrifuge, additional information will be obtained for the qualitative and quantitative alteration of LDL. ~-~
EWA STUDY: EFFECTS OF H O R M O N E - R E P L A C E M E N T T H E R A P Y ON P L A S M A CONCENTRATIONS OF Lp(a) LIPOPROTEIN AND TGF-IM
S. Diurovic q, A. Westheim2, K. Berg q, I. Os 2. 1Department of Medical
Genetics, 2Department of Internal Medicine, Ulleu~l University Hospital, Oslo, Norway Background: High Lp(a) lipoprotein level has been shown to be an independent genetic risk factor for coronary heart disease (CHD). An inverse relationship between Lp(a) lipoprotein and TGF-~I has been demonstrated, and suggests that Lp(a) lipoprotein may interfere with the activation of TGF-~I resulting in attenuation of a dominant protective role of TGF-~I on coronary arteries. Methods and Results: In this study we examined the effects of HRT on Lp(a) lipoprotein and TGF-[31 in 99 postmenopausal women with angiographically documented CHD randomized to sequential transdermal 17~-estradiol for 14 weeks and then medroxyprogesterone (MPA) for 14 days (HRT) or to a control group (C). There was a significant reduction in Lp(a) lipoprotein serum levels after 3 months treatment in HRT group, but this difference disappeared after introduction of MPA. Levels of the active form of TGF-[31 were increased in HRT group compared to C group after 3 months treatment and the beneficial effects remained after 12 months as well. Additionally, negative association between TGF-~I and VCAM-1 was found (r--0.26, p-0.023). However, no associations were observed between TGF-[31 and ICAM-1, E-selectin or PAI-1 in the present study. Conclusion: Transdermal 17[3-estradiol in postmenopausal women lowers the concentration ofLp(a) lipoprotein and increases levels of active form of TGF-[31, what might represent mechanism for the cardioprotective effect of estrogen RT. However, combination therapy of estradiol and MPA negates the estradiol effects on Lp(a) lipoprotein. ~]
METABOLIC SYNDROME IN PATIENTS WITH P R E M A T U R E ISCHEMIC HEART DISEASE
L.M. Dobord~inidze, N.A. Gratsiansky, A.B. Dobrovolsky, V.P. Masenko, M.V. Konnov. Center for Atherosclerosis, IPCM, Moskow, Russia Aim: To assess frequency of metabolic syndrome (MS) as defined by ATP III Guidelines criteria in patients with premature coronary heart disease (C~D). Material: Eighty patients (49 men and 31 women, age 36 56 years) with overt CHD were selected for this analysis because their levels of high sensitivity C-reactive protein (CRP) were known. Except presence of premature CHD there was no other reason to measure CRP. Results: Number of patients satisfying criteria of MS was 17/49 (34.7%) among men and 25/31 (80.6%) among women (p<0.001). In women most frequent signs were low HDLCH (24/25), hypertension (22/25), abdominal obesity (21/25) while in men hypertension (16/17) and hypertriglyceridemia (14/17). Overall 42 patients had signs of MS and 38 had not. This was reflected by significantly higher average fasting insulin level in the former
101
group (15.5+1.69 and 7.7+1.04 mcU/ml, respectively, p-0.0004). Patients with and without MS had similar age, levels of LDLCH (mean 159 mg/dl in both groups). Level of CRP (3.78+0.72 and 3.97+1.0 mg/1 also did not differ between groups. This probably reflected preponderance of men among patients without MS as men in this series had significantly higher CRP. Patients with MS compared with those without MS had higher levels of apoprotein B (157+8.8 and 125+6.75 mg/dl, respectively, p-0,0048) and activity of plasminogen activator inhibitor (18.3 and 11.7 IU/ml, p-0.0052) but lower lipoprotein (a) (13.2+4.59 and 28.4+5.99 mg/dl, p-0.0044). Conclusion: Contrary to men majority of women in a small randomly chosen group of patients with premature CHD satisfied ATP III criteria of MS. Low HDLCH, hypertension and abdominal obesity were most frequent components of MS in these women. [ 1 - ~ P L A S M A TFPI AND LP(a) LEVELS IN CORONARY ARTERY DISEASE N. Domanic 1, D. Bilgen2, H. Sonmez 2, C. Gurel 3, H. Ekmekci 2, Z. Ozturk 2, A.S. Demir 1, T. Ulutin3, V.A. Vural 1, E. Kokoglu2.
JDepartment of Cardiology, 2Department of Biochemistry, 3Department of Genetic and Teratology Research Center, School of Medicine, Istanbul University, Turkey Tissue factor pathway inhibitor (TFPI) is the main inhibitor of the factor VII a/Tissue factor pathway of blood coagulation A number of studies indicate that lipoprotein (a) levels correlate with the progression of atherosclerosis. Also, it was shown that TFPI is inactivated by binding to lp(a). The aim of the present study was to analyse and correlate plasma lp(a) and TFPI levels in patients with coronary artery disease confirmed by angiography. Enyzme linked immunsorbent assay (ELISA) procedure (Boehringer Mannheim,Asserachrom Stago)was used to determine the lp(a) and TFPI levels. The mean plasma total TFPI levels in patients with CAD and control group were 225,25±106,19 ng/ml (n:136), 166,86±53,2 ng/ml (n:34) respectively. Plasma TFPI levels in patients with CAD were found to the significantly higher than in the control group (p<0,0001). The mean plasma lp(a) levels in patients with CAD and control group were 62,04±48,79 Mg/ml (n:136) and 29,85±20,76 Mg/ml(n:31), with CAD were found to the significantly higher than in the control group. (p<0,0001). Also the low correlations were found between the plasma lp(a) and TFPI levels in patients with CAD. (r-0,18) (p<0,05). In conclusion, in this study high TFPI and lp(a) levels were found in patients with CAD. Thus elevated lp(a) levels may be causes increased plasma TFPI levels. [ i - ~ ] P L A T E L E T AND P L A S M I N O G E N SYSTEM ACTIVITY IN PATIENTS WITH DIFFERENT C H A R A C T E R I S T I C S OF ACUTE CORONARY SYNDROME O.R. Dotsenk0, V.Z. Netiazhenko, I.V. Melnik, T.V. Kozmyk. National
Medical University, Kyiu, Ukraine Objective: To compare platelet and plasminogen system activity in patients with non-ST-elevation myocardial infarction (MI), acceleration angina (AA), new-onset angina (NA) and postinfarction angina (PA). Methods: Study population consisted of 32 AA patients, 32 NA patients, 23 MI patients and 15 PA patients. On admission venous blood was analyzed for: platelet aggregation (spontaneous and inducted by ADP, serotonin and thrombin), antiheparin factor (F4), platelet fibrinolytic activity (FA), platelet-associated antithrombin (AT), fibrinogen (F), soluble fibrin (SF), fibrin degradation products (FDP), euglobulin lysis time (ELT), Hagemandependent lysis (CL), time (T) and velocity (V) of clot lysis by global turbodimetric test of endogenous fibrinolysis assessment. Results: No significant differences between patients with MI, AA and NA were found. In contrast, in patients with PA blood were more thrombogenic. In PA, MI, AA and NA patients F4 activity was 86,9 plus-minus 12,5%, 74,5 plus-minus 16,2%, 77,5 plus-minus 14,2%, 75,7 plus-minus 13,7%, respectively (p<0,05 for: P A v s MI, PA vs AA, P A v s NA). In PA, MI, AA and NA patients serotonin-dependent aggregation was 33,7 plus-minus 5,5%, 29,1 plus-minus 6,3%, 29,9 plus-minus 4,7%, 29,7 plus-minus 4,96%, respectively (p<0,05 for: P A v s MI, P A v s AA, P A v s NA). In PA, MI, AA and NA patients F was 6,09 plus-minus 0,7 g/l, 5,3 plus-minus 1,04 g/l, 5,6 plus-minus 0,7 g/l, 5,56 plus-minus 0,8 g/l, respectively (p<0,05 for: P A v s MI, PA vs AA, P A v s NA). Conclusions: Obtained data may stress the high endogenous thrombogenic potential in patients with acute coronary syndrome, developed in early post-MI period, which may be addressed during these patients follow-up.
73rd EAS Congress
EWA STUDY: EFFECTS OF H O R M O N E - R E P L A C E M E N T T H E R A P Y ON P L A S M A CONCENTRATIONS OF Lp(a) LIPOPROTEIN AND TGF-IM
S. Diurovic q, A. Westheim2, K. Berg q, I. Os 2. 1Department of Medical
Genetics, 2Department of Internal Medicine, Ulleu~l University Hospital, Oslo, Norway Background: High Lp(a) lipoprotein level has been shown to be an independent genetic risk factor for coronary heart disease (CHD). An inverse relationship between Lp(a) lipoprotein and TGF-~I has been demonstrated, and suggests that Lp(a) lipoprotein may interfere with the activation of TGF-~I resulting in attenuation of a dominant protective role of TGF-~I on coronary arteries. Methods and Results: In this study we examined the effects of HRT on Lp(a) lipoprotein and TGF-[31 in 99 postmenopausal women with angiographically documented CHD randomized to sequential transdermal 17~-estradiol for 14 weeks and then medroxyprogesterone (MPA) for 14 days (HRT) or to a control group (C). There was a significant reduction in Lp(a) lipoprotein serum levels after 3 months treatment in HRT group, but this difference disappeared after introduction of MPA. Levels of the active form of TGF-[31 were increased in HRT group compared to C group after 3 months treatment and the beneficial effects remained after 12 months as well. Additionally, negative association between TGF-~I and VCAM-1 was found (r--0.26, p-0.023). However, no associations were observed between TGF-[31 and ICAM-1, E-selectin or PAI-1 in the present study. Conclusion: Transdermal 17[3-estradiol in postmenopausal women lowers the concentration ofLp(a) lipoprotein and increases levels of active form of TGF-[31, what might represent mechanism for the cardioprotective effect of estrogen RT. However, combination therapy of estradiol and MPA negates the estradiol effects on Lp(a) lipoprotein. ~]
METABOLIC SYNDROME IN PATIENTS WITH P R E M A T U R E ISCHEMIC HEART DISEASE
L.M. Dobord~inidze, N.A. Gratsiansky, A.B. Dobrovolsky, V.P. Masenko, M.V. Konnov. Center for Atherosclerosis, IPCM, Moskow, Russia Aim: To assess frequency of metabolic syndrome (MS) as defined by ATP III Guidelines criteria in patients with premature coronary heart disease (C~D). Material: Eighty patients (49 men and 31 women, age 36 56 years) with overt CHD were selected for this analysis because their levels of high sensitivity C-reactive protein (CRP) were known. Except presence of premature CHD there was no other reason to measure CRP. Results: Number of patients satisfying criteria of MS was 17/49 (34.7%) among men and 25/31 (80.6%) among women (p<0.001). In women most frequent signs were low HDLCH (24/25), hypertension (22/25), abdominal obesity (21/25) while in men hypertension (16/17) and hypertriglyceridemia (14/17). Overall 42 patients had signs of MS and 38 had not. This was reflected by significantly higher average fasting insulin level in the former
101
group (15.5+1.69 and 7.7+1.04 mcU/ml, respectively, p-0.0004). Patients with and without MS had similar age, levels of LDLCH (mean 159 mg/dl in both groups). Level of CRP (3.78+0.72 and 3.97+1.0 mg/1 also did not differ between groups. This probably reflected preponderance of men among patients without MS as men in this series had significantly higher CRP. Patients with MS compared with those without MS had higher levels of apoprotein B (157+8.8 and 125+6.75 mg/dl, respectively, p-0,0048) and activity of plasminogen activator inhibitor (18.3 and 11.7 IU/ml, p-0.0052) but lower lipoprotein (a) (13.2+4.59 and 28.4+5.99 mg/dl, p-0.0044). Conclusion: Contrary to men majority of women in a small randomly chosen group of patients with premature CHD satisfied ATP III criteria of MS. Low HDLCH, hypertension and abdominal obesity were most frequent components of MS in these women. [ 1 - ~ P L A S M A TFPI AND LP(a) LEVELS IN CORONARY ARTERY DISEASE N. Domanic 1, D. Bilgen2, H. Sonmez 2, C. Gurel 3, H. Ekmekci 2, Z. Ozturk 2, A.S. Demir 1, T. Ulutin3, V.A. Vural 1, E. Kokoglu2.
JDepartment of Cardiology, 2Department of Biochemistry, 3Department of Genetic and Teratology Research Center, School of Medicine, Istanbul University, Turkey Tissue factor pathway inhibitor (TFPI) is the main inhibitor of the factor VII a/Tissue factor pathway of blood coagulation A number of studies indicate that lipoprotein (a) levels correlate with the progression of atherosclerosis. Also, it was shown that TFPI is inactivated by binding to lp(a). The aim of the present study was to analyse and correlate plasma lp(a) and TFPI levels in patients with coronary artery disease confirmed by angiography. Enyzme linked immunsorbent assay (ELISA) procedure (Boehringer Mannheim,Asserachrom Stago)was used to determine the lp(a) and TFPI levels. The mean plasma total TFPI levels in patients with CAD and control group were 225,25±106,19 ng/ml (n:136), 166,86±53,2 ng/ml (n:34) respectively. Plasma TFPI levels in patients with CAD were found to the significantly higher than in the control group (p<0,0001). The mean plasma lp(a) levels in patients with CAD and control group were 62,04±48,79 Mg/ml (n:136) and 29,85±20,76 Mg/ml(n:31), with CAD were found to the significantly higher than in the control group. (p<0,0001). Also the low correlations were found between the plasma lp(a) and TFPI levels in patients with CAD. (r-0,18) (p<0,05). In conclusion, in this study high TFPI and lp(a) levels were found in patients with CAD. Thus elevated lp(a) levels may be causes increased plasma TFPI levels. [ i - ~ ] P L A T E L E T AND P L A S M I N O G E N SYSTEM ACTIVITY IN PATIENTS WITH DIFFERENT C H A R A C T E R I S T I C S OF ACUTE CORONARY SYNDROME O.R. Dotsenk0, V.Z. Netiazhenko, I.V. Melnik, T.V. Kozmyk. National
Medical University, Kyiu, Ukraine Objective: To compare platelet and plasminogen system activity in patients with non-ST-elevation myocardial infarction (MI), acceleration angina (AA), new-onset angina (NA) and postinfarction angina (PA). Methods: Study population consisted of 32 AA patients, 32 NA patients, 23 MI patients and 15 PA patients. On admission venous blood was analyzed for: platelet aggregation (spontaneous and inducted by ADP, serotonin and thrombin), antiheparin factor (F4), platelet fibrinolytic activity (FA), platelet-associated antithrombin (AT), fibrinogen (F), soluble fibrin (SF), fibrin degradation products (FDP), euglobulin lysis time (ELT), Hagemandependent lysis (CL), time (T) and velocity (V) of clot lysis by global turbodimetric test of endogenous fibrinolysis assessment. Results: No significant differences between patients with MI, AA and NA were found. In contrast, in patients with PA blood were more thrombogenic. In PA, MI, AA and NA patients F4 activity was 86,9 plus-minus 12,5%, 74,5 plus-minus 16,2%, 77,5 plus-minus 14,2%, 75,7 plus-minus 13,7%, respectively (p<0,05 for: P A v s MI, PA vs AA, P A v s NA). In PA, MI, AA and NA patients serotonin-dependent aggregation was 33,7 plus-minus 5,5%, 29,1 plus-minus 6,3%, 29,9 plus-minus 4,7%, 29,7 plus-minus 4,96%, respectively (p<0,05 for: P A v s MI, P A v s AA, P A v s NA). In PA, MI, AA and NA patients F was 6,09 plus-minus 0,7 g/l, 5,3 plus-minus 1,04 g/l, 5,6 plus-minus 0,7 g/l, 5,56 plus-minus 0,8 g/l, respectively (p<0,05 for: P A v s MI, PA vs AA, P A v s NA). Conclusions: Obtained data may stress the high endogenous thrombogenic potential in patients with acute coronary syndrome, developed in early post-MI period, which may be addressed during these patients follow-up.
73rd EAS Congress