Copyright © 1998 by the European Society of Cardiology.
Progression of coronary artery disease in young male post-infarction patients is linked to disturbances of carbohydrate and lipoprotein metabolism and to impaired fibrinolytic function
a Departments of Emergency and Cardiovascular Medicine, Karolinska Hospital, Stockholm
b Department of Thoracic Radiology, Karolinska Hospital, Stockholm
c Department of Endocrinology, Karolinska Hospital, Stockholm
e Departments of Clinical Chemistry and Blood Coagulation, Karolinska Hospital, Stockholm
d Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Institute, Stockholm, Sweden
accepted July 26, 1997
Aims
To assess determinants of coronary artery disease progression in men with previous myocardial infarction.
Methods and Results
A total of 102 unselected non-diabetic Swedish men (age 40·4±3·6, range 2344 years) entered the study 36 months after a first myocardial infarction. The programme included metabolic and haemostatic investigations and routine coronary angiography at baseline, followed by re-angiography 5 years later. Of the original cohort, 76 patients underwent a second angiogram. Separate semiquantitative scoring systems were used for diffuse coronary atherosclerosis and distinct stenoses in 15 proximal coronary segments. Smoking, global severity of coronary atherosclerosis and presence of multi-vessel disease at baseline (P<0·001) characterized patients with severe progression of both diffuse and focal lesions. Higher plasma levels of low density lipoprotein cholesterol (P<0·01) and low density lipoprotein triglycerides (P<0·05), a lower plasma high density lipoprotein2cholesterol level (P<0·05) and higher plasma plasminogen activator inhibitor-1 activity (P<0·05), together with a high baseline stenosis score (P<0·001) characterized patients with severe progression of coronary atherosclerosis. On the other hand, more pronounced fasting and post-prandial glycaemia (P<0·05), together with higher plasma plasminogen activator inhibitor-1 activity (P<0·01) characterized severe progressors with respect to coronary stenosis. Multi-variate analysis identified the presence of multi-vessel disease as an independent predictor of progression of both coronary atherosclerosis (P=0·008) and stenoses (P=0·007), whereas a high low density lipoprotein tri-glyceride level (P<0·01) was independently related to progression of coronary atherosclerosis and a high fasting glucose level (P=0·02) to progression of coronary stenoses.
Conclusion
Disturbances in carbohydrate and lipoprotein metabolism and impaired fibrinolytic function are associated with progression of coronary artery disease in young male post-infarction patients.
Key Words: Lipoproteins plamsinogen activator inhibitor-1 glucose insulin myocardial infarction coronary angiography.
Correspondence: Dr Peter B
venholm, Division of Internal Medicine, Department of Emergency and Cardiovascular Medicine, Karolinska Hospital, S-171 76 Stockholm, Sweden.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
P.E. Morange, N. Saut, M.C. Alessi, J.S. Yudkin, M. Margaglione, G. Di Minno, A. Hamsten, S.E. Humphries, D.A. Tregouet, and I. Juhan-Vague Association of Plasminogen Activator Inhibitor (PAI)-1 (SERPINE1) SNPs With Myocardial Infarction, Plasma PAI-1, and Metabolic Parameters: The HIFMECH Study Arterioscler Thromb Vasc Biol, October 1, 2007; 27(10): 2250 - 2257. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Musaad and E. N. Haynes Biomarkers of Obesity and Subsequent Cardiovascular Events Epidemiol. Rev., May 10, 2007; (2007) mxm005v1. [Abstract] [Full Text] [PDF] |
||||
![]() |
M.-C. Alessi and I. Juhan-Vague PAI-1 and the Metabolic Syndrome: Links, Causes, and Consequences Arterioscler Thromb Vasc Biol, October 1, 2006; 26(10): 2200 - 2207. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. N Bavenholm and S. Efendic Postprandial hyperglycaemia and vascular damage - the benefits of acarbose Diabetes and Vascular Disease Research, September 1, 2006; 3(2): 72 - 79. [Abstract] [PDF] |
||||
![]() |
A M Smith, K M English, C J Malkin, R D Jones, T H Jones, and K S Channer Testosterone does not adversely affect fibrinogen or tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) levels in 46 men with chronic stable angina Eur. J. Endocrinol., February 1, 2005; 152(2): 285 - 291. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Sola, M. Q.S. Mir, F. A. Cheema, N. Khan-Merchant, R. G. Menon, S. Parthasarathy, and B. V. Khan Irbesartan and Lipoic Acid Improve Endothelial Function and Reduce Markers of Inflammation in the Metabolic Syndrome: Results of the Irbesartan and Lipoic Acid in Endothelial Dysfunction (ISLAND) Study Circulation, January 25, 2005; 111(3): 343 - 348. [Abstract] [Full Text] [PDF] |
||||
![]() |
C.J. Malkin, P.J. Pugh, T.H. Jones, and K.S. Channer Testosterone for secondary prevention in men with ischaemic heart disease? QJM, July 1, 2003; 96(7): 521 - 529. [Full Text] [PDF] |
||||
![]() |
C. J. Lyon, R. E. Law, and W. A. Hsueh Minireview: Adiposity, Inflammation, and Atherogenesis Endocrinology, June 1, 2003; 144(6): 2195 - 2200. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Kipnes, P. Dandona, D. Tripathy, J. G. Still, and G. Kosutic Control of Postprandial Plasma Glucose by an Oral Insulin Product (HIM2) in Patients With Type 2 Diabetes Diabetes Care, February 1, 2003; 26(2): 421 - 426. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. P. Kohler and P. J. Grant Plasminogen-Activator Inhibitor Type 1 and Coronary Artery Disease N. Engl. J. Med., June 15, 2000; 342(24): 1792 - 1801. [Full Text] [PDF] |
||||
![]() |
J. L. Anderson, J. B. Muhlestein, J. Habashi, J. F. Carlquist, T. L. Bair, S. P. Elmer, and B. P. Davis Lack of association of a common polymorphism of the plasminogen activator inhibitor-1 gene with coronary artery disease and myocardial infarction J. Am. Coll. Cardiol., November 15, 1999; 34(6): 1778 - 1783. [Abstract] [Full Text] [PDF] |
||||









