title: Relationship of metabolic syndrome and fibrinolytic dysfunction to cardiovascular disease.
abstract: BACKGROUND
  The clustering of impaired glucose metabolism, elevated triglycerides, low HDL cholesterol, and abdominal obesity is known as the metabolic syndrome. Individuals with this syndrome suffer an excess of cardiovascular disease (CVD) for reasons that are unclear.
  
  
  RESULTS
  We randomly sampled 1276 adults of South Asian, Chinese, European, and Native Indian ancestry from 4 communities in Canada. Participants provided fasting blood samples for glucose, lipids, and fibrinolytic measurements; had an oral glucose tolerance test; and underwent a B-mode carotid ultrasound examination. CVD was determined by history and ECG. The prevalence of the metabolic syndrome was 25.8% (95% CI, 23.5 to 28.2) and varied substantially by ethnic group: 41.6% among Native Indians, 25.9% among South Asians, and 22.0% among Europeans, compared with 11.0% among the Chinese (overall, P=0.0001). People with the metabolic syndrome had more atherosclerosis (maximum intimal medial thickness, 0.78+/-0.18 versus 0.74+/-0.18 mm; P=0.0005), CVD (17.2% versus 7.0%; P=0.0001), and elevated plasminogen activator inhibitor-1 (24.2 versus 14.6 U/mL; P=0.001) compared with levels among people without the metabolic syndrome. For the same amount of atherosclerosis, people with the metabolic syndrome had a greater prevalence of CVD, even among nondiabetic individuals. This difference in CVD prevalence among the groups was attenuated after adjustment for plasminogen activator inhibitor-1 levels, suggesting that fibrinolytic dysfunction mediates the increased risk of CVD in individuals with the metabolic syndrome.
  
  
  CONCLUSIONS
  CVD among people with the metabolic syndrome is explained by their excess of atherosclerosis and impaired fibrinolysis. Interventions to prevent atherosclerosis progression and improve fibrinolytic function require evaluation in this high-risk group.
authors.affiliation: Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
authors.forename: Sonia S
authors.initials: SS
authors.lastname: Anand
authors.forename: Qilong
authors.initials: Q
authors.lastname: Yi
authors.forename: Hertzel
authors.initials: H
authors.lastname: Gerstein
authors.forename: Eva
authors.initials: E
authors.lastname: Lonn
authors.forename: Ruby
authors.initials: R
authors.lastname: Jacobs
authors.forename: Vlad
authors.initials: V
authors.lastname: Vuksan
authors.forename: Koon
authors.initials: K
authors.lastname: Teo
authors.forename: Bonnie
authors.initials: B
authors.lastname: Davis
authors.forename: Patty
authors.initials: P
authors.lastname: Montague
authors.forename: Salim
authors.initials: S
authors.lastname: Yusuf
mesh_terms: D000328:Adult; D001161:Arteriosclerosis / Q000175:diagnosis / Q000453:epidemiology; D001208:Asia / Q000208:ethnology; D044466:Asian People; D001786:Blood Glucose; D002170:Canada / Q000453:epidemiology / Q000208:ethnology; D002318:Cardiovascular Diseases / Q000175:diagnosis* / Q000453:epidemiology; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D015897:Comorbidity; D004562:Electrocardiography; D005060:Europe / Q000208:ethnology; D005260:Female; D005337:Fibrin / Q000378:metabolism; D005342:Fibrinolysis; D005951:Glucose Tolerance Test; D006801:Humans; D007198:Indians, North American; D008055:Lipids / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000175:diagnosis* / Q000453:epidemiology / Q000378:metabolism; D008875:Middle Aged; D015995:Prevalence; D018570:Risk Assessment; D012307:Risk Factors; D014463:Ultrasonography; D044465:White People
chemical_list: D001786:Blood Glucose; D008055:Lipids; D005337:Fibrin