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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Human plasma complement C3 is independently associated with coronary heart disease, but only in heavy smokers (the
Marleen M J van Greevenbroek1, Marjon Jacobs, Carla J H van der Kallen
1Laboratory of Metabolism and Vascular Medicine, Cardiovascular Research Institute Maastricht and Department of Internal Medicine, Maastricht University, The Netherlands. m.vangreevenbroek@intmed.unimaas.nl
Insights
Plasma complement C3 is linked to coronary heart disease (CHD) risk, but only in heavy smokers. This association persists even after accounting for other metabolic risk factors.
Area of Science:
- Cardiovascular Science
- Immunology
- Metabolic Syndrome Research
Background:
- Complement C3 is an emerging risk factor for coronary heart disease (CHD).
- Elevated C3 levels are observed in metabolic syndrome.
- Smoking may directly impact complement C3 structure and function.
Purpose of the Study:
- To investigate the association between plasma C3 and prevalent CHD.
- To examine if smoking behavior modifies the cardiovascular risk associated with plasma C3.
Main Methods:
- The CODAM study population (n=562) was analyzed.
- The association between plasma C3 and CHD was assessed.
- Effect modification by smoking status was examined.
Main Results:
- Higher plasma C3 levels correlated with increased CHD prevalence.
- A significant interaction between C3 and heavy smoking was found (p=0.01).
- In heavy smokers, C3 remained a significant independent predictor of CHD after adjusting for traditional and metabolic risk factors.
Conclusions:
- Plasma complement C3 is associated with prevalent CHD.
- This association is specific to heavy smokers.
- The link between C3 and CHD in heavy smokers is independent of key metabolic risk factors.
Background:
Complement C3 is an emerging risk factor for coronary heart disease (CHD) and is particularly increased in the metabolic syndrome. A direct effect of smoking on structure and function of complement C3 has been suggested.
Hypothesis:
Smoking behavior may affect the cardiovascular risk that is associated with plasma complement C3.
Methods:
The association between plasma C3 and CHD was studied in the CODAM (Cohort on Diabetes and Atherosclerosis Maastricht) study population (n=562, 61% male) with examination of effect modification by smoking.
Results:
The overall prevalence of CHD was 23.3%. Higher plasma C3 levels were associated with a higher CHD prevalence, and there was a significant interaction with heavy smoking (p=0.01). In never & light smokers, the univariate OR for CHD per 1s.d. (0.33 g/L) increase in C3 was 1.09 [95% confidence interval (CI) 0.85-1.41] (p=0.505) whereas in heavy smokers it was 2.05 [1.43-2.93] (p<0.001). The association in the group of heavy smokers remained significant (OR 2.38 [1.54-3.68], p<0.001) after adjustment for traditional risk factors for cardiovascular disease and also after further adjustment for other cardiometabolic risk factors, i.e. the metabolic syndrome, CRP and insulin resistance (HOMA2IR) (OR C3 between 2.16 and 2.29, all p ≤ 0.001).
Conclusion:
Human plasma complement C3 is associated with prevalent CHD, but only in heavy smokers, and this association is independent of important metabolic cardiovascular risk factors.
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