Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 2.1
5-Year Impact Factor – 2.2
Scopus CiteScore – 3.4 (CiteScore Tracker 3.4)
Index Copernicus  – 161.11; MEiN – 140 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

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Advances in Clinical and Experimental Medicine

2006, vol. 15, nr 5, September-October, p. 911–916

Publication type: review article

Language: Polish

Zaburzenia gospodarki węglowodanowej a ryzyko chorób układu sercowo−naczyniowego

Glucose Metabolism Disturbances and the Risk of Cardiovascular Diseases

Roksolana Derzhko1,, Maria Witkowska1,

1 Katedra i Klinika Kardiologii AM we Wrocławiu

Streszczenie

Cukrzyca typu 2, a także nieprawidłowa tolerancja glukozy są czynnikami zwiększającymi zachorowalność oraz śmiertelność z powodu chorób układu sercowo−naczyniowego, zwłaszcza choroby niedokrwiennej serca (ch.n.s.). Duże prospektywne badania Framingham i Multiple Risk Factor Intervention Trial (MRFIT) wykazały, że chorzy na cukrzycę są zagrożeni 2−krotnie większym ryzykiem rozwoju ch.n.s. i niedokrwiennego udaru mózgu oraz 2–4−krotnie większą śmiertelnością z powodu ch.n.s. i udaru mózgu w porównaniu z osobami niechorującymi na cukrzycę. Po zawale serca u chorych na cukrzycę częściej dochodzi do powtórnego zawału oraz rozwoju zastoinowej niewydolności serca niż u pacjentów niechorujących na cukrzycę. Oporność na insulinę i towarzysząca kompensacyjna hiperinsulinemia są kluczowymi mechanizmami odpowiedzialnymi za przyspieszoną miażdżycę. Wpracy podkreślono istotne znaczenie wczesnego wykrywania zaburzeń gospodarki węglowodanowej w celu zapobiegania zdarzeniam sercowo−naczyniowym.

Abstract

Type 2 diabetes mellitus and impaired glucose tolerance (IGT), are associated with increased risk for morbidity and mortality from cardiovascular disease (CVD), particulary coronary heart disease (CHD). The large forward−looking Framingham study and Multiple Risk Factor Intervention Trial (MRFIT) have shown that persons with type 2 diabetes have twice the risk of incident CHD and ischaemic stroke and 2 to 4 times the risk of CHD and stroke mortality compared with their counterparts without diabetes. After myocardial infarction (MI), diabetic persons have a higher risk of recurrent MI and fatal CHD than do nondiabetic persons. Insulin resistance and compensatory hyperinsulinemia in prediabetes may be pathogenic mechanisms underlying risk for atherosclerosis. This article emphasises the importance of earlier detection the disturbances in glucose metabolism to prevent cardiovascular events.

Słowa kluczowe

choroba niedokrwienna serca, zaburzenia metabolizmu węglowodanów

Key words

coronary heart disease, disturbances of glucose metabolism

References (31)

  1. Zimmet P: The burden of type 2 diabetes: are we doing enough? Diab Metab 2003, 29 (4 Pt 2), 609–618.
  2. Harris MJ, Flegal KM, Cowie CC: Prevalence of diabetes, impaired fasting glucose and impaired glucose tolerance US adults. The Third National Health and Nutrition Examination Survey, 1988–1994. Diab Care 1999, 21, 518–528.
  3. Tatoń J, Czech A, Berna M: Kardiodiabetologia, Via media, Gdańsk 2002.
  4. Adamiec R, Zdrojowy K, Sutkowska E: WET−Diab – badanie populacyjne mieszkańców Wrocławia w kontekście chorobowości z powodu cukrzycy – doniesienie wstępne. Diabetologia Praktyczna 2004, 5, 189–194.
  5. Haffner SM, Sehto S, Ronnemaa T: Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med 1998, 339, 229–234.
  6. Levitan EB, Song Y, Ford ES, Liu S: Is nondiabetic hyperglycemia a risk factor for cardiovascular disease? A meta−analysis of prospective studies. Arch Intern Med 2004, 164, 2147–2155.
  7. Kowalska I, Prokop JB, Bachórzewska−Gajewska H: Disturbances of glucose metabolism in men reffered for coronary arteriography. Post−load glycemia as predictor for coronary atherosclerosis. Diab Care 2001, 24, 897–901.
  8. Bartnik M, Rydel L, Ferrari R: The prevalence of abnormal glucose regulation in patients with coronary artery disease across Europe. The EuroHeart Survey on diabetes and the heart. Eur Heart J 2004, 25, 1880–1890.
  9. Brownlee M: Negative consequences of glycation. Metabolizm 2000, 49, 9–13.
  10. Rosja A, Morale MA: Advanced glycation and endothelial functions: a link towards vascular complications in diabetes, Life Science, 2004, 76, 715–730.
  11. Tan KCB, Chow WS, Ai VHG: Advanced glycation end products and endothelial dysfunction in type 2 diabetes. Diab Care 2002, 25, 1055–1059.
  12. Basta G, Schmidt AM, de Caterina R: Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes. Cardiovasc Res 2004, 63, 582–592.
  13. Stern DM, Van SD, Yan SF, Schmit AM: Receptor for advanced glycation endproducts (RAGE) and the complications of diabetes. Ageing Res Rev 2002, 1, 1–15.
  14. Chavakis T, Bierhaus A, Nawroth PP: RAGE (receptor for advanced glycation end products): a central plater in the inflammatory response. Microbes and Infections 2004, 6, 1219–1225.
  15. Inoguchi T, Li P, Umeda F: High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C−dependent activation of NAD(P)H oxidase in cultured vascular cells. Diabetes 2000, 49, 1939–1945.
  16. Hu FB, Stampfer MJ, Haffner SM: Elevated pisk of cardiovascular disease priori to clinical diagnosis of type 2 diabetes. Diab Care 2002, 25, 1129–1134.
  17. Norhammer A: Glucose metabolizm in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study. Lancet 2002, 359, 2140–2144.
  18. Rodriguez BL, Lau N, Burchfiel CM: Glucose intolerance and 23−year risk of coronary heart disease and total mortality. The Honolulu Heart Program. Diab Care 1999, 22, 1262–1265.
  19. DECODE Study Group: Glucose tolerance and mortality: comparison of WHO and American Diabetic Association diagnostic criteria. Lancet 1999, 354, 617–621.
  20. Hanefeld M, Fischer S, Julius U, Schyulze J, Schwanebeck U, Schmechel H, Ziegelasch HJ, Lindner J (The DIS Group): Risk factors for myocardial infarction and death in newly detected NIDDM: the Diabetes Intervention Study, 11−year follow−up. Diabetologia 1997, 39, 1577–1583.
  21. De Vegt F, Dekker JM, Ruhe HG, Stehouwer CD, Nijpels G, Bouter LM, Heine RJ: Hyperglycaemia is associated with all−cause and cardiovascular mortality in the Hoorn population: the Hoorn Study. Diabetologia 1999, 42, 926–931.
  22. Pyorala M, Miettinen H, Laakso M: Hiperinsulinemia predicts coronary heart disease risk in healthy middleaged men. The 22−year follow−up results of the Helsinki Policemen Study. Circulation 1998, 98, 398–404.
  23. Ginsberg HN: Insulin resistance and cardiovascular disease. J Clin Incest 2000, 106, 453–458.
  24. Stuehlinger M, Abbasi F, Chu JW: Close relationship between insulin resistance and an endogenous nitric oxide inhibitor. JAMA 2002, 287, 1420–1426.
  25. Marfella R: Effects of stress hyperglycemia on acute myocardial infarction. Diab Care 2003, 26, 3129–3133.
  26. Franklin K, Goldberg RJ, Spencer F: Implications of diabetes in patients with acute coronary syndromes. Arch Intern Med 2004, 164, 1457–1463.
  27. Pan XR, Li GW, Hu YH: Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diab Care 1997, 20, 537–544.
  28. Tuomilehto J, Lindstrom J, Eriksson JG: Prevention of type 2 diabetes mellitus by changes in lyfestyle among subjects with impaired glucose tolerance. N Engl J Med 2001, 344, 1343–1350.
  29. Katzmarzyk PT, Tremblay A, Petusse LI: The utility of international child and adolescent overweight guidelines for predicting coronary heart disease risk factors. J Clin Epidemiol 2003, 56, 456–462.
  30. Yusuf S: Effects of an angiotensin−converting−enzym inhibitor, ramipril, on cardiovascular events in high−risk patients. The Heart Outcomes Prevention Evaluation Study Investigation. N Engl J Med 2000, 342, 145–153.
  31. Freeman DJ: Pravastatin and the development of diabetes mellitus: evidence for a protective treatment effect in the West of Scotland Coronary Prevention Study. Circulation 2001, 103, 357–362.
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