Prothrombotic status as part of metabolic syndrome

Česká verzia

Authors: A. Remková
Authors place of work: I. interná klinika Lekárskej fakulty UK, Bratislava, Slovenská republika, prednosta prof. MUDr. Anna Remková, Ph. D., DrSc.
Published in the journal: Vnitř Lék 2005; 51(10): 1120-1125
Category: Reviews

Summary

Metabolic syndrome is associated with prothrombotic status, which participates in the development of atherothrombotic complications. Nevertheless, dysregulation of haemostasis is of a complex nature and involves endothel activation, hyperactivity of thrombocytes, hypercoagulability and hypofibrinolysis. Increased expression of type 1 plasminogen activator inhibitor with subsequent hypofibrinolysis is the main haemostatic disorder in relation to insulin resistance and is currently considered as a part of a set of abnormalities within the scope of the metabolic syndrome. The mechanism which leads to prothrombotic status in metabolic syndrome is multifactorial. Recently, great significance has been attributed to cytokine-mediated low-degree inflammation which is closely linked to the metabolic syndrome and participates on dysregulation of haemostasis. Body weight reduction, physical activity and adequate pharmacological processes are effective means reducing the prothrombotic status impact in metabolic syndrome. Angiotensin converting enzyme inhibitors, which can favourably influence even haemostatic mechanisms according to recent data, serve as an example. The treatment of prothrombotic status in the metabolic syndrome could result in the decrease of atherothrombotic events, which are characteristic complications of metabolic syndrome.

Key words:
insulin resistance – hypertension – endothel – thrombocytes – fibrinolysis

Zdroje

1. Juhan-Vague I, Morange PE, Alessi MC. The insulin resistance syndrome: implications for thrombosis and cardivascular disease. Pathophysiol Haemost Thromb 2002; 32: 269-273.

2. Festa A, D´Agostino R, Tracy RP et al. Elevated levels of acute–phase proteins and plasminogen activator inhibitor-1 predict the development of type 2 diabetes. The Insulin Resistance Atherosclerosis Study. Diabetes 2002; 51: 1131-1137.

3. Engstrom G, Stavenow L, Hedblad B et al. Inflammation-sensitive plasma proteins, diabetes, and mortality and incidence of myocardial infarction and stroke: a population-based study. Diabetes 2003; 52: 442-447.

4. Stehouwer CDA, Lambert J, Donker AJM et al. Endothelial dysfunction and pathogenesis of diabetic angiopathy. Cardiovasc Res 1997; 34: 55-68.

5. Stehouwer CDA, Gall MA, Twisk JWR et al. Increased urinary albumin excretion, endothelial dysfunction, and chronic low-grade inflammation in type 2 diabetes: progressive, interrelated, and independently associated with risk of death. Diabetes 2002; 51: 1157-1165.

6. von Kanel R, Nelesen RA, Le Dzung T et al. Decrease in the plasma von Willebrand factor concentration following glucose ingestion: The role of insulin sensitivity. Metab Clin Exp 2001; 50: 1452-1456.

7. Mather K, Steinberg H, Baron A. Weight loss and endothelial function in obesity. Diabetes 2003; 26: 1927-1928.

8. Cominacini L, Fratta Pasini A, Garbin U et al. Elevated levels of soluble E-selectin in patients with IDDM a NIDDM: relation to metabolic control. Diabetologia 1995; 38: 1122-1124.

9. Ferri C, Desideri G, Valenti M et al. Early upregulation on endothelial adhesion molecules in obese hypertensive men. Hypertension 1999; 34: 568-573.

10. Ferri C, Desideri G, Baldoncini R et al. Early activation of vascular endothelium in nonobese, nondiabetic essential hypertensive patients with multiple metabolic abnormalities. Diabetes 1998; 47: 660-667.

11. Albertini JP, Valensi P, Lormeau B et al. Elevated concentrations of soluble E-selectin and vascular cell adhesion molecule-1 in NIDDM. Effect of intensive insulin treatment. Diabetes Care 1998; 21: 1008-1013.

12. Blann AD, Bushell D, Davies A et al. Von Willebrand factor, the endothelium and obesity. Int J Obes 1993; 17: 723-725.

13. Remková A. Sympatikový nervový systém a aterotrombogenéza. Cardiol 2003; 12: 72-77.

14. Jager A, van Hinsbergh VW, Kostense PJ et al. Von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects: the Hoorn Study. Arterioscler Thromb Vasc Biol 1999; 19: 3071-3078.

15. Meigs JB, Mittleman MA, Nathan D et al. Hyperinsulinemia, hyperglycemia, and impaired hemostasis. The Framingham Offspring Study. JAMA, 2000; 283: 221-228.

16. Chan NN, Fuller JH, Rubens M et al. Von Willebrand factor in type 1 diabetes: its relationship with endothelial nitric oxide production and coronary artery calcification. Med Sci Monit 2003; 9: 297-303.

17. Iwashima Y, Sato T, Watanabe K et al. Elevation of plasma thrombomodulin level in diabetic patients with early diabetic nephropathy. Diabetes 1990; 39: 983-988.

18. Remková A Hypertenzia a hemostáza. Bratislava: Slovak Academic Press 1998.

19. Remková A, Kováčová E, Príkazská M et al. Thrombomodulin as a marker of endothelium damage in some clinical conditions. Eur J Int Med 2000; 11: 79-84.

20. Galajda P. Diabetická endotelopatia. Interná Med 2003; 3: 85-89.

21. Mather KJ, Mirzamohammadi B, Lteif A et al. Endothelin contributes to basal vascular tone and endothelial dysfunction in human obesity and type 2 diabetes. Diabetes 2002; 51: 3517-3523.

22. Remková A. Fibrinolysis, platelet aggregation, and stroke. Progress in the Treatment of Stroke 2001; 2: 2-4.

23. Davi G, Catalano I, Averna M et al. Thromboxane biosynthesis and platelet function in type II diabetes mellitus. N Engl J Med 1990; 322: 1769-1774.

24. Davi G, Gresele P, Violi F et al. Diabetes mellitus, hypercholesterolemia, and hypertension but not vascular disease per se are associated with persistent platelet activation in vivo: evidence derived from the study of peripheral arterial disease. Circulation 1997; 96: 69-75.

25. Landin K, Tengborn L, Smith U. Elevated fibrinogen and plasminogen activator inhibitor (PAI-1) in hypertension are related to metabolic risk factors for cardiovascular disease. J Int Med 1990; 227: 273-278.

26. Lee AJ, Lowe GD, Woodward M et al. Fibrinogen in relation to personal history of prevalent hypertension, diabetes, stroke, intermittent claudication, coronary heart disease, and family history: the Scottish Heart Health Study. Brit Heart J 1993; 69: 338-342.

27. Kannel WB, Wolf PA, Castelli WP et al. Fibrinogen and risk of cardiovascular disease. The Framingham Study. JAMA 1987; 258: 1183-1186.

28. Aso Y, Matsumoto S, Fujiwara Y et al. Impaired fibrinolytic compensation for hypercoagulability in obese patients with type 2 diabetes: Association with increased plasminogen activator inhibitor-1. Metab Clin Exp 2002; 51: 471-476.

29. Agewall S, Wikstrand J, Fagerberg B. Prothrombin fragment 1+2 is a risk factor for myocardial infarction in treated hypertensive men. J Hypertens 1998; 16: 537-541.

30. Lemne C, De Faire U. Elevation of plasminogen activator inhibitor 1 in borderline hypertension is linked to concomitant metabolic disturbances. Eur J Clin Investig 1996; 26: 692-697.

31. Potter van Loon BJ, Kluft C, Radder JK et al. The cardiovascular risk factor plasminogen activator inhibitor type 1 is related to insulin resistance. Metab Clin Exp 1993; 42: 945-949.

32. Kvasnička J, Škrha J, Perušičová J et al. Koncentrace tkáňového aktivátoru plazminogenu (t-PA), jeho inhibitoru (PAI-1) a fibrinogenu v krevní plazmě pacientů s diabetes mellitus 1. a 2. typu. Čas Lék Čes 1996, 135: 174-177.

33. Kvasnička J, Škrha J, Perušičová J et al. The occurence of the cardiovascular risk factors - fibrinogen, t-PA, PAI-1 and inflammation in insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). Cor Vasa 1997, 39: 146-150.

34. Samad F, Uysal T, Wiesbrock S et al. Tumor necrosis factor  is a key component in the obesity-linked elevation of plasminogen activator inhibitor 1. Proc Natl Acad Sci USA 1999; 96: 6902-6907.

35. Juhan-Vague I, Alessi MC, Mavri A et al. Plasminogen activator inhibitor-1, inflammation, obesity, insulin resistance and vascular risk. J Thromb Haemost 2003; 1: 1575-1579.

36. Okrucká A, Pecháň J, Kratochvíľová H. Effects of the angiotensin-converting enzyme (ACE) inhibitor perindopril on endothelial and platelet functions in essential hypertension. Platelets 1998; 9: 63-67.

37. Remková A, Kratochvíľová H. Effect of the angiotensin-converting enzyme inhibitor perindopril on haemostasis in essential hypertension. Blood Coagul Fibrinolysis 2000; 11: 641-644.

38. Ferrari R, Arbustini E, Blann A et al. PERTINENT - PERindopril-Thrombosis, InflammatioN, Endothelial dysfunction and Neurohormonal activation Trial: a sub study of the EUROPA study. Cardiovasc Drugs Ther 2003; 17: 83-91.

39. Fogari R, Mugellini A, Zoppi A et al. Effect of losartan and perindopril on plasma PAI-1 and fibrinogen in hypertensive type 2 diabetic patients. J Hypertens 1999; 17 (Suppl 3): S58.

40. Fogari R, Zoppi A. Benefits of the bradykinins beyond blood pressure control: insulin sensitivity and thrombogenesis. Eur Heart J 2000; 2 (Suppl H): H7-H13.

41. Fogari R, Preti P, Banderali A et al. ACE-inhibition but not angiotensin II antagonism improves fibrinolysis and insulin sensitivity in hypertensive post-menopausal women. J Hypertens 1999; 17 (Suppl 3): S143.

42. Brown NJ, Agirbasli M, Vaughan DE. Comparative effect of angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor antagonism on plasma fibrinolytic balance in humans. Hypertension 1999; 34: 285-290.

43. Sakata K, Pawlak R, Urano T et al. Effects of a long-term pharmacological iterruption of the rennin-angiotensin system on the fibrinolytic system in essential hypertension. Pathophysiol Haemost Thromb 2002; 32: 67-75.

44. Krespi PG, Makris TK, Hatzizacharias AN et al. Moxonidine effect on microalbuminuria, thrombomodulin, and plasminogen activator inhibitor-1 levels in patients with essential hypertension. Cardiovasc Drugs Ther 1998; 12: 463-467.

45. Remková A, Kratochvíľová H. Effect of the new centrally acting antihypertensive agent rilmenidine on endothelial and platelet function in essential hypertension. J Hum Hypertens 2002; 16: 549-555.

46. De Luca N, Izzo R, Fontana D et al. Haemodynamic and metabolic effects of rilmenidine in hypertensive patients with metabolic syndrome X. A double-blind parallel study versus amlodipine. J Hypertens 2000; 18: 1515-1522.

47. Malý J, Malá H, Pecka M et al. Změny hemostázy u obézních při redukci hmotnosti. Vnitř Lék 2001, 47: 203-209.

48. Galajda P, Mokáň M. Poruchy hemostázy pri diabetes mellitus. Martin: Prokonzult 2001.