Dynamics of hemostatic indicators and endothelial dysfunction under the influence of statin therapy in patients with coronary heart disease

Dynamics of hemostatic indicators and endothelial dysfunction under the influence of statin therapy in patients with coronary heart disease

e106 Abstracts / Atherosclerosis 235 (2014) e84–e191 heterozygous FH lymphocytes, the SERMs produced similar effects on LDLR activity to those cause...

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e106

Abstracts / Atherosclerosis 235 (2014) e84–e191

heterozygous FH lymphocytes, the SERMs produced similar effects on LDLR activity to those caused in normolipidemic lymphocytes, although no synergism with lovastatin was expressed with any SERM. These drugs had no effect on DiI-LDL uptake by homozygous FH lymphocytes. Conclusion: The three SERMs increase, although with different efficiencies, LDLR activity in lymphocytes from normolipidemic and heterozygous FH subjects. This effect is independent of estrogen receptors, but it is preserved in the tamoxifen active metabolite endoxifen. We suggest that LDLR up-regulation contributes to the hypocholesterolemic action of these drugs. The synergism between SERMs and lovastatin on lymphocyte LDLR activity is mild, which may be due to the low cholesterol requirement of these cells.

Methods: The cross sectional, observational DYSIS study examined lipid goal attainment among 35362 statin treated patients. We present an analysis of 19 European countries and Israel. Results: 21094 patients were at very high cardiovascular risk. Of these, 17.7% had achieved the treatment target of <70mg/dl. 1912 patients were at high cardiovascular risk, of whom 29.4% had reached the <100mg/dl target. The median LDL-C gap for the very high and high risk groups combined ranged from 21 to 42mg/dl among the different countries.

LDL-C gap from target

09 - Hypolidaemic drugs present and future Country

n

EAS-0096. DYNAMICS OF HEMOSTATIC INDICATORS AND ENDOTHELIAL DYSFUNCTION UNDER THE INFLUENCE OF STATIN THERAPY IN PATIENTS WITH CORONARY HEART DISEASE

MEDIAN (mg/dl)

IQR (Q1-Q3, mg/dl)

total

23006

35

18

60

Austria

805

34

20

59

M. Kachkovskii, O. Rubanenko, V. Simerzin, N. Kirichenko

Belgium

668

27

14

47

Internal Medicine, Samara State Medical Institute, Samara, Russia

Baltics

1516

42

21

74

Germany

3847

39

22

62

Denmark

789

27

12

42

France

3172

38

20

62

Greece

514

40

22

65

Israel

675

22

10

39

Ireland

732

27

14

46

Italy

546

33

17

57

Netherlands

1115

27

12

43

Norway

806

31

15

50

Portugal

602

42

24

65

Russia

1442

38

19

65

Slovenia

697

40

19

69

Spain

2618

42

23

68

Sweden

865

27

15

46

UK

1597

21

11

38

Objectives: To study changes of the hemostatic system and endothelial dysfunction under the influence of 24 -week differentiated statin therapy in patients with coronary heart disease. Methods: The study included 162 patients with coronary heart disease and atherosclerosis of the brachiocephalic trunk, the average age was 54,73,5. Blood lipid indicators (low-density lipoprotein (LDL)) were studied in all patients. The level of fibrinogen, interval to the beginning of ADP induced platelet aggregation, D - dimer, von Willebrand factor (vWF) were determined. All patients were divided into 2 groups: one group consisted of 85 patients with moderately elevated LDL receiving atorvastatin 40 mg, second group - 77 patients with high level of LDL, receiving rosuvastatin 20 mg. Results: After treating patients for 24 weeks with atorvastatin and rosuvastatin the level of fibrinogen decreased by 19 % (p<0.001) and 20 % (p¼0.001), vWF decreased by 29,6% (p<0.001) and 33,6% (p<0.001), D dimer decreased by 29,8% (p¼0.005) and 22% (p¼0.03), interval to the beginning of ADP induced platelet aggregation increased by 12 % (p<0.001) and 17 %(p¼0.001) respectively. Conclusion: Decrease in fibrinogen levels in all groups during the treatment helps to reduce the viscosity of the blood plasma and the risk of thrombotic events. Reducing vWF reflects a decrease of endothelial dysfunction. Decrease in level D-dimer demonstrates reduction of intravascular coagulation and fibrinolysis activation. Increase interval to the beginning of ADP induced platelet aggregation in patients with coronary heart disease shows reduction of platelet activation hemostasis.

Mean LDL cholesterol was 10538mg/dl, total cholesterol 18646mg/dl, median HDL cholesterol 49mg/dl (IQR 40-58mg/ dl) and median triglycerides 131mg/dl (IQR 95-182mg/dl).

09 - Hypolidaemic drugs present and future EAS-0422. LDL-C TREATMENT GAPS IN STATIN-TREATED PATIENTS AT HIGH AND VERY HIGH CARDIOVASCULAR RISK IN EUROPE A.K. Gitta, B. Ambegaonkarb, P. Brudic, D. Lautschd a

Med. Klinik B Kardiologie, Herzzentrum Ludwigshafen, Ludwigshafen, Germany; b Outcomes Research, Merck&Co, Whitehouse Station, USA; c Medical Affairs, Merck&Co, Whitehouse Station, USA; d Medical Affairs, Merck Sharp & Dohme, Vienna, Austria Objectives: EAS/ESC guidelines for dyslipidemia define patients with coronary heart disease, diabetes, chronic kidney disease and periphery artery disease as patients at very high cardiovascular risk, and those with markedly elevated risk factors (total cholesterol >310mg/dl or severe hypertension) as patients at high risk. We analyzed in the DYSIS database how many patients in these categories achieved their LDL-C target and assessed the remaining gap.

Conclusion: Attainment of EAS/ESC guideline LDL-C targets in this population was generally poor. The observed remaining LDL-C gap to treatment targets varied among the countries, but was substantial in all. 09 - Hypolidaemic drugs present and future EAS-0288. NEW INSIGHTS INTO STATIN ACTION ON THE DYSLIPIDEMIA OF TYPE 2 DIABETES: NORMALISATION OF THE PLASMA LIPID PROFILE P.J. Meiklea, G. Wonga, R. Tana, B.A. Kingwellb, A. Orsonic, N. Hounslowd, P. Giralc, M.J. Chapmanc a

Metabolomics, Baker IDI Heart & Diabetes Institute, Melbourne, Australia; Metabolic & Vascular Physiology, Baker IDI Heart & Diabetes Institute, Melbourne, Australia; c INSERM UMR-S939, Pitie-Salpetriere University Hospital, Paris, France; d Kowa Research Europe, Kowa Company Ltd, Wokingham, United Kingdom b