What do have arterial and venous disease in common?

Czech version

Authors: Jan Piťha ¹; Ondřej Auzký ¹; Karel Roztočil ²
Authors‘ workplace: Laboratoř pro výzkum aterosklerózy Centra experimentální medicíny IKEM Praha, přednosta prof. MUDr. Luděk Červenka, CSc., MBA ¹; Klinika transplantační chirurgie IKEM Praha, přednosta MUDr. Jiří Froněk, Ph. D., FRCS ²
Published in: Vnitř Lék 2014; 60(11): 985-989
Category: Reviews

Overview

Venous and arterial disease probably share a number of common risk factors. From the pathophysiological point of view a similar triggering mechanism was proposed for atherosclerosis and venous disease: subclinical inflammation. Life-threatening thrombotic events may also go through similar pathways in both entities and the culprit is probably dysfunctional endothelial cell in the vessel wall. In available clinical and population based studies, however, unequivocal data are presented regarding association between arterial and venous diseases and their risk factors. In our studies, we found a higher prevalence of lower ankle brachial index in women with chronic venous disease of the lower extremities At the same time, nevertheless we found no strong evidence of a direct link between preclinical atherosclerosis and the occurrence of venous thrombosis in patients with thrombophilias; in the latter group, however, we found a link between hypertension and thromboembolic events. Arterial and venous disease may thus be favorably managed by already well-established and available tools used in prevention of atherosclerotic cardiovascular disease. Evidence of a possible impact of pharmacotherapy on both arterial and venous disease stems from a large clinical study in which treatment with hypolipemic drug, rosuvastatin, significantly decreased not only incidence of cardiovascular events but also of venous thromboembolic events. Another promising drug for the treatment of both arterial and venous disease could be glycosaminoglycan sulodexide.

Key words:
atherosclerotic cardiovascular disease – chronic venous disease – risk factors – thromboembolic events

Sources

1. Libby P. Inflammation in atherosclerosis. Arterioscler Thromb Vasc Biol 2012; 32(9): 2045–2051.

2. Raffetto JD, Mannello F. Pathophysiology of chronic venous disease. Int Angiol 2014; 33(3): 212–221.

3. Vaya A, Mira Y, Ferrando F et al. Hyperlipidaemia and venous thromboembolism in patients lacking thrombophilic risk factors. Br J Haematol 2002; 118(1): 255–259.

4. Zdravotnická ročenka České republiky. UZIS ČR: Praha. ISSN 1210–9991. Dostupné z WWW: <http://www.uzis.cz/katalog/rocenky/zdravotnicka-rocenka-ceske-republiky>.

5. Lattimer CR. CVD: a condition of underestimated severity. Int Angiol 2014; 33(3): 222–228.

6. Eberhardt RT, Raffetto JD. Chronic venous insufficiency. Circulation 2014; 130(4): 333–346.

7. Rabe E, Guex JJ, Puskas A et al. Coordinators: Epidemiology of chronic venous disorders in geographically diverse populations: Results from the Vein Consult Program. Int Angiol 2012; 31(2): 105–115.

8. Auzky O, Lanska V, Pitha J et al. Association between symptoms of chronic venous disease in the lower extremities and cardiovascular risk factors in middle-aged women. Int Angiol 2011; 30(4): 335–341.

9. Erevnidou K, Launois R, Katsamouris A et al. Translation and validation of a quality of life questionnaire for chronic lower limb venous insufficiency into greek. Int Angiol 2004; 23(4): 394–399.

10. Musil D, Herman J. Příčina klinických projevů chronické žilní nedostatečnosti u pacientů s nadváhou a obezitou. Vnitř Lék 2005; 51(5): 523–528.

11. White RH, Zhou H, Romano PS. Incidence of idiopathic deep venous thrombosis and secondary thromboembolism among ethnic groups in California. Ann Intern Med 1998; 128(9): 737–740.

12. Nordstrom M, Lindblat B, Bergquist D et al. A prospective study of the incidence of deep-vein thrombosis within a defined urban population. J Intern Med 1992; 232(2): 155–160.

13. Cushman M, Tsai AW, White RH et al. Deep vein thrombosis and pulmonary embolism in two cohorts: the longitudinal investigation of thromboembolism etiology. Am J Med 2004; 117(1): 19–25.

14. Yusuf S, Hawken S, Ounpuu S et al. INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 2004; 364(9438): 937–952.

15. Mahmoodi BK, Gansevoort RT, Næss IA et al. Association of mild to moderate chronic kidney disease with venous thromboembolism: pooled analysis of five prospective general population cohorts. Circulation 2012; 126(16): 1964–1971.

16. Bova C, Marchiori A, Noto A et al. Incidence of arterial cardiovascular events in patients with idiopathic venous thromboembolism. A retrospective cohort study. Thromb Haemost 2006; 96(2): 132–136.

17. Prandoni P, Bilora F, Marchiori A et al. An association between atherosclerosis and venous thrombosis. N Engl J Med 2003; 348(15): 1435–1441.

18. Ageno W, Becattini C, Brighton T et al. Cardiovascular risk factors and venous thromboembolism: a meta-analysis. Circulation 2008; 117(1): 93–102.

19. Hong C, Zhu F, Du D et al. Coronary artery calcification and risk factors for atherosclerosis in patients with venous thromboembolism. Atherosclerosis 2005; 183(1): 169–174.

20. Migliacci R, Becattini C, Pesavento R et al. Endothelial dysfunction in patients with spontaneous venous thromboembolism. Haematologica 2007; 92(6): 812–818.

21. Bova C, Marchiori A, Noto A et al. Incidence of arterial cardiovascular events in patients with idiopathic venous thromboembolism. A retrospective cohort study. Thromb Haemost 2006; 96(2): 132–136.

22. van der Hagen PB, Folsom AR, Jenny NS et al. Subclinical atherosclerosis and the risk of future venous thrombosis in the Cardiovascular Health Study. J Thromb Haemost 2006; 4(9): 1903–1908.

23. Reich LM, Folsom AR, Key NS et al. Prospective study of subclinical atherosclerosis as a risk factor for venous thromboembolism. J Thromb Haemost 2006; 4(9): 1909–1913.

24. Bilora F, Boccioletti V, Petrobelli F et al. Atherosclerosis and secondary deep vein thrombosis: a difficult correlation. Clin Appl Thromb Hemost 2003; 9(2): 121–124.

25. Tsai AW, Cushman M, Rosamond WD et al. Cardiovascular risk factors and venous thromboembolism incidence: the longitudinal investigation of thromboembolism etiology. Arch Intern Med 2002; 162(10): 1182–1189.

26. Jezovnik MK, Poredos P, Stalc M. Impairment of the vasodilatation capability of the brachial artery in patients with idiopathic venous thrombosis. J Atheroscler Thromb 2010; 17(11): 1190–1198.

27. Jezovnik MK, Poredos P, Lusa L. Idiopathic venous thrombosis is associated with preclinical atherosclerosis. J Atheroscler Thromb 2010; 17(3): 304–311.

28. Auzký O, Pagáčová L, Sejda T et al. Preclinical atherosclerosis and other determinants of venous thromboembolism in patients with thrombophilias. Physiol Res 2010; 59(5): 721–728.

29. Auzký O, Dembovská R, Mrázková J. Relation between preclinical atherosclerosis and venous thromboembolism in patients with thrombophilias – longitudinal study. Physiol Res 2014; 63. Přijato do tisku 2014.

30. Glynn RJ, Danielson E, Fonseca FA et al. A randomized trial of rosuvastatin in the prevention of venous thromboembolism. N Engl J Med 2009; 360(18): 1851–1861.

31. Roztocil K, Antignani PL. Sulodexide: it is time for a program against chronic venous disease. Int Angiol 2014; 33(3): 209–211.

32. Coccheri S, Mannello F. Development and use of sulodexide in vascular diseases: implications for treatment. Drug Des Devel Ther 2013; 8: 49–65.

33. Lantis JC 2nd, Boone D, Lee L et al. The effect of percutaneous intervention on wound healing in patients with mixed arterial venous disease. Ann Vasc Surg 2011; 25(1): 79–86.

34. Steffen LM, Folsom AR, Cushman M et al. Greater fish, fruit, and vegetable intakes are related to lower incidence of venous thromboembolism: the Longitudinal Investigation of Thromboembolism Etiology. Circulation 2007; 115(2): 188–195.