American Journal of Cardiology
Volume 105, Issue 1 , Pages 17-24 , 1 January 2010

Comparison of Plasminogen Activator Inhibitor-1, Tissue Type Plasminogen Activator Antigen, Fibrinogen, and D-Dimer Levels in Various Age Decades in Patients With Type 2 Diabetes Mellitus and Stable Coronary Artery Disease (from the BARI 2D Trial)

  • Robert D. McBane II, MD

      Affiliations

    • Division of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota
    • Division of Hematology Research, Mayo Clinic, Rochester, Minnesota
    • Corresponding Author InformationCorresponding author: Tel: (507) 266-3964; fax: (507) 266-1617
  • ,
  • Regina M. Hardison, MS

      Affiliations

    • University of Pittsburgh, Pittsburgh, Pennsylvania
  • ,
  • Burton E. Sobel, MD

      Affiliations

    • Cardiovascular Research Institute, University of Vermont, Burlington, Vermont
  • ,
  • BARI 2D Study Group

      Affiliations

    • A list of BARI 2D participants has been previously published (“Baseline characteristics of patients with diabetes and coronary artery disease enrolled in the Bypass Angioplasty Revascularization Investigation 2 Diabetes [BARI 2D] trial.” Am Heart J 2008;156:528–536.e5).

Received 12 June 2009 ,Revised 23 August 2009 ,Accepted 23 August 2009.

References 

  1. Sobel BE, Frye R, Detre KM Bypass Angioplasty Revascularization Investigation 2 Diabetes trial. Burgeoning dilemmas in the management of diabetes and cardiovascular disease: rationale for the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial. Circulation. 2003;107:636–642
  2. Brooks MM, Frye RL, Genuth S, Detre KM, Nesto R, Sobel BE, et al. Hypotheses, design, and methods for the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial. Am J Cardiol. 2006;97:9G–19G
  3. Sobel E BARI 2D Trial investigators. Ancillary studies in the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial: synergies and opportunities. Am J Cardiol. 2006;97:53G–58G
  4. Kruszynska Y, Yu JG, Sobel BE, Olefsky JM. Effects of troglitazone on blood concentrations of plasminogen activator inhibitor 1 in patients with type 2 diabetes mellitus and in lean and obese normal subjects. Diabetes. 2000;49:633–639
  5. Yamamoto K, Takeshita K, Kojima T, Takamatsu J, Saito H. Aging and plasmiongen activator inhibitor-1 (PAI-1) regulation: implication in the pathogenesis of thrombotic disorders in the elderly. Cardiovasc Res. 2005;66:276–285
  6. Hamsten A, de Faire U, Walldius G, Dahlén G, Szamosi A, Landou C, et al. Plasminogen activator inhibitor in plasma: risk factor for recurrent myocardial infarction. Lancet. 1987;2:3–9
  7. Mannucci PM, Bernardinelli L, Foco L, Galli M, Ribichini F, Tubaro M, et al. Tissue plasminogen activator antigen is strongly associated with myocardial infarction in young women. J Thromb Haemost. 2005;3:280–286
  8. Thögersen AM, Jansson JH, Boman K, Nilsson TK, Weinehall L, Huhtasaari F, et al. High plasminogen activator inhibitor and tissue plasminogen activator levels in plasma precede a first acute myocardial infarction in both men and women: evidence for the fibrinolytic system as an independent primary risk factor. Circulation. 1998;98:2241–2247
  9. Festa A, Williams K, Tracy RP, Wagenknecht LE, Haffner SM. Progression of plasminogen activator inhibitor-1 and fibrinogen levels in relation to incident type 2 diabetes. Circulation. 2006;113:1753–1759
  10. Gurlek A, Bayraktar M, Kirazli S. Increased plasminogen activator inhibitor-1 activity in offspring of type 2 diabetic patients: lack of association with plasma insulin levels. Diabetes Care. 2000;23:88–92
  11. Tofler GH, Massaro J, Levy D, Mittleman M, Sutherland P, Lipinska I, et al. Relation of the prothrombotic state to increasing age (from the Framingham Offspring Study). Am J Cardiol. 2005;96:1280–1283
  12. Asselbergs FW, Williams SM, Hebert PR, Coffey CS, Hillege HL, Snieder H, et al. The effects of polymorphisms in genes from the renin-angiotensin, bradykinin, and fibrinolytic systems on plasma t-PA and PAI-1 levels are dependent on environmental context. Hum Genet. 2007;122:275–281
  13. Mansfield MW, Stickland MH, Grant PJ. Environmental and genetic factors in relation to elevated circulating levels of plasminogen activator inhibitor-1 in Caucasian patients with non-insulin-dependent diabetes mellitus. Thromb Haemost. 1995;74:842–847
  14. Folsom AR, Wu KK, Rosamond WD, Sharrett AR, Chambless LE. Prospective study of hemostatic factors and incidence of coronary heart disease: the Atherosclerosis Risk in Communities (ARIC) study. Circulation. 1997;96:1102–1108
  15. Bogaty P, Poirier P, Simard S, Boyer L, Solymoss S, Dagenais GR. Biological profiles in subjects with recurrent acute coronary events compared with subjects with long-standing stable angina. Circulation. 2001;103:3062–3068
  16. Gallistl S, Sudi KM, Borkenstein M, Troebinger M, Weinhandl G, Muntean W. Determinants of haemostatic risk factors for coronary heart disease in obese children and adolescents. Internation J Obes. 2000;24:1459–1464
  17. Van Guilder GP, Hoetzer GL, Smith DT, Irmiger HM, Greiner JJ, Stauffer BL, et al. Endothelial t-PA release is impaired in overweight and obese adults but can be improved with regular aerobic exercise. Am J Physiol-End Metab. 2005;289:E807–E813
  18. Rosito GA, D'Agostino RB, Massaro J, Lipinska I, Mittleman MA, Sutherland P, et al. Association between obesity and a prothrombotic state: the Framingham Offspring Study. Thromb Haemost. 2004;91:683–689
  19. Asselbergs FW, Williams SM, Hebert PR, Coffey CS, Hillege HL, Navis G, et al. Gender specific correlations of PAI-1 and t-PA levels with cardiovascular disease-related traits. J Thromb Haemost. 2007;5:313–320
  20. Asselbergs FW, Williams SM, Hebert PR, Coffey CS, Hillege HL, Navis G, et al. The gender-specific role of polymorphisms from the fibrinolytic, renin-angiotensin, and bradykinin systems in determining plasma t-PA and PAI-1 levels. Thromb Haemost. 2006;96:471–477
  21. Kalaria VG, Zareba W, Moss AJ, Pancio G, Marder VJ, Morrissey JH, et al. Gender-related differences in thrombogenic factors predicting recurrent cardiac events in patients after acute myocardial infarction. Am J Cardiol. 2000;85:1401–1408
  22. Perry A, Wang X, Goldberg R, Ross R, Jackson L. The relationship between cardiometabolic and hemostatic variables: influence of race. Metabolism. 2008;57:200–206
  23. Ajjan R, Carter AM, Somani R, Kain K, Grant PJ. Ethnic differences in cardiovascular risk factors in healthy Caucasian and south Asian individuals with the metabolic syndrome. J Thromb Haemost. 2007;5:754–760
  24. Greyling A, Pieters M, Hoekstra T, Oosthuizen W, Schutte AE. Differences in the association of PAI-1 activity with the metabolic syndrome between African and Caucasian women. Nutr Metab Cardiovasc Dis. 2007;17:499–507
  25. Wong TY, Islam FM, Klein R, Klein BE, Cotch MF, Castro C, et al. Retinal vascular caliber, cardiovascular risk factors, and inflammation: the multi-ethnic study of atherosclerosis (MESA). Invest Ophthalmol Vis Sci. 2006;47:2341–2350

 Supported in part by grant R01 HL61744–BARI 2D parent grant from the National Institutes of Health, Bethesda, Maryland; grant U01HL63804–BARI II Fibrinolysis and Coagulation Core (B.E. Sobel, primary investigator) from the National Institutes of Health; and grant R01 HL71306–Inflammation, Procoagulation, and Plaque Vulnerability (B.E. Sobel, primary investigator) from the National Institutes of Health. The Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trail was funded by grants U01 HL061744, U01 HL061746, U01 HL061748, and U01 HL063804 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland, and the National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. Significant supplemental funding has been provided by GlaxoSmithKline, Collegeville, Pennsylvania, Bristol-Myers Squibb Medical Imaging, Inc., North-Billerica, Massachusetts, Astellas Pharma US, Inc., Deerfield, Illinois, Merck & Co., Inc., Whitehouse Station, New Jersey, Abbott Laboratories, Inc., Abbott Park, Illinois, and Pfizer, Inc., New York, New York. Generous support was given by Abbott Laboratories, Inc., MediSense Products, Mississauga, Ontario, Canada, Bayer Diagnostics, Tarrytown, New York, Becton-Dickinson and Company, Franklin Lakes, New Jersey, JR Carlson Laboratories, Arlington Heights, Illinois, Centocor, Inc., Malvern, Pennsylvania, Eli Lilly and Company, Indianapolis, Indiana, LipoScience, Inc., Raleigh, North Carolina, Merck, Sante, Lyon, France, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey, and Novo Nordisk, Inc., Princeton, New Jersey.

PII: S0002-9149(09)02208-5

doi: 10.1016/j.amjcard.2009.08.643

American Journal of Cardiology
Volume 105, Issue 1 , Pages 17-24 , 1 January 2010