Indicators associated with coronary atherosclerosis in metabolic syndrome
Ting-Yu Chiu1, Ching-Yuan Chen, Shan-Yin Chen
1Cardiovascular Research Center, and School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC.
Insights
Metabolic syndrome (MetS) is linked to coronary atherosclerosis (CA) even after accounting for biomarkers. Specific glucose and cholesterol levels in MetS and non-MetS individuals independently predict CA.
Area of Science:
- Cardiovascular Medicine
- Metabolic Disorders
- Biomarkers
Background:
- Metabolic syndrome (MetS) is a cluster of conditions that increase the risk of heart disease, stroke, and type 2 diabetes.
- The specific metabolic factors contributing to coronary atherosclerosis (CA) within MetS are not fully understood.
- Investigating novel atherosclerotic biomarkers alongside traditional metabolic factors is crucial for a comprehensive understanding of CA risk.
Purpose of the Study:
- To determine the independent association of metabolic syndrome (MetS) with coronary atherosclerosis (CA).
- To identify specific metabolic factors and novel biomarkers that predict CA in subjects with and without MetS.
- To explore potential differences in the pathophysiology of CA based on MetS status.
Main Methods:
- Analysis of 550 subjects undergoing coronary computed tomography angiography.
- Definition of CA based on coronary artery calcification (CAC) scores or noncalcified plaques.
- Measurement of metabolic factors, high-sensitive C-reactive protein (hs-CRP), and adiponectin; MetS diagnosis per NCEP ATP III criteria.
Main Results:
- Metabolic syndrome (MetS) was significantly associated with coronary atherosclerosis (CA) after adjusting for novel biomarkers (OR, 2.88; P<0.001).
- In non-MetS subjects, fasting blood glucose ≥ 110 mg/dl or diabetes mellitus was an independent predictor of CA (OR, 1.40; P<0.05).
- In MetS subjects, a total cholesterol/HDL-C ratio ≥ 4.2 was an independent predictor of CA (OR, 4.44; P<0.001).
- Both predictors correlated with elevated hs-CRP and reduced adiponectin.
Conclusions:
- Metabolic syndrome (MetS) is an independent risk factor for coronary atherosclerosis (CA), even when accounting for advanced biomarkers.
- Specific thresholds for fasting blood glucose/diabetes and cholesterol/HDL-C ratio serve as independent indicators of CA in non-MetS and MetS populations, respectively.
- These findings suggest distinct pathophysiological pathways for CA in individuals with and without metabolic syndrome.
Background:
Metabolic factors associated with coronary atherosclerosis (CA) in metabolic syndrome (MetS) remain unclear.
Methods:
A total of 550 consecutive subjects without documented coronary artery disease who received contrast-enhanced coronary computed tomography angiography were analyzed. CA was defined as coronary artery calcification (CAC) scores >0 or, zero CAC score combining noncalcified plaques within the proximal third segment of major coronary arteries. Metabolic factors and novel atherosclerotic biomarkers including high-sensitive C-reactive protein (hs-CRP) and adiponectin were measured. MetS was recognized according to the ethnicity-specific National Cholesterol Educational Program Adult Treatment Panel III, 2001.
Results:
After adjusted with novel atherosclerotic biomarkers, MetS was significantly associated with CA Odds ratio [OR], 2.88; 95% confidence interval [CI], 1.88 to 4.42; p<0.001). Subgroup analysis revealed that fasting blood glucose ≥ 110 mg/dl/diabetes mellitus in non-MetS subjects (OR, 1.40; 95%CI, 1.08 to 1.82; p<0.05) and total cholesterol (TC)/high density lipoprotein-cholesterol (HDL-C) ≥ 4.2 in MetS subjects (OR, 4.44; 95%CI, 1.93 to 10.20; p<0.001) were independently associated with CA. Both indicators were significantly associated with increased serum hs-CRP and reduced adiponectin levels in all subjects.
Conclusions:
MetS is independently associated with CA after adjustment of atherosclerotic biomarkers. TC/HDL-C ≥ 4.2 in MetS and fasting blood glucose ≥ 110 mg/dl/diabetes mellitus in non-MetS subjects are independent indicators of CA, suggesting the potential difference in pathophysiology of CA.
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