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Updated: Jan 11, 2026
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Relationship of metabolic syndrome and fibrinolytic dysfunction to cardiovascular disease
Sonia S Anand1, Qilong Yi, Hertzel Gerstein
1Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Insights
Metabolic syndrome, characterized by obesity and abnormal lipids, significantly increases cardiovascular disease (CVD) risk. Impaired fibrinolysis and atherosclerosis explain this heightened CVD risk in affected individuals.
Area of Science:
- Cardiology
- Endocrinology
- Public Health
Background:
- Metabolic syndrome is a cluster of conditions including impaired glucose metabolism, high triglycerides, low HDL cholesterol, and abdominal obesity.
- Individuals with metabolic syndrome face an elevated risk of cardiovascular disease (CVD), but the underlying reasons are not fully understood.
Purpose of the Study:
- To investigate the prevalence of metabolic syndrome across different ethnic groups in Canada.
- To determine the association between metabolic syndrome, atherosclerosis, and CVD.
- To explore the role of fibrinolytic dysfunction in mediating CVD risk in metabolic syndrome.
Main Methods:
- A random sample of 1276 adults from South Asian, Chinese, European, and Native Indian ancestries in Canada.
- Assessment of metabolic syndrome components, including fasting blood samples for glucose, lipids, and fibrinolysis.
- Oral glucose tolerance tests and B-mode carotid ultrasound for atherosclerosis measurement.
- CVD determination through medical history and ECG.
Main Results:
- The overall prevalence of metabolic syndrome was 25.8%, with significant ethnic variations (Native Indians 41.6%, South Asians 25.9%, Europeans 22.0%, Chinese 11.0%).
- Individuals with metabolic syndrome exhibited higher prevalence of atherosclerosis (P=0.0005) and CVD (P=0.0001) compared to those without.
- Elevated plasminogen activator inhibitor-1 levels were observed in individuals with metabolic syndrome (P=0.001), and this factor partially explained the increased CVD prevalence.
Conclusions:
- Cardiovascular disease in metabolic syndrome is attributed to increased atherosclerosis and impaired fibrinolysis.
- Fibrinolytic dysfunction appears to be a key mediator of heightened CVD risk in individuals with metabolic syndrome.
- Further research and interventions targeting atherosclerosis progression and fibrinolytic function are crucial for this high-risk population.
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.
Methods And 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.
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