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Published on: January 28, 2020
C-reactive protein predicts progression of atherosclerosis measured at various sites in the arterial tree: the
Irene M Van Der Meer1, Moniek P M De Maat, A Elisabeth Hak
1Department of Epidemiology and Biostatistics, Erasmus Medical Center, Rotterdam, The Netherlands.
Insights
High levels of C-reactive protein (CRP) predict the progression of atherosclerosis in arteries. This inflammation marker is as significant as traditional risk factors like high cholesterol and hypertension.
Area of Science:
- Cardiovascular Medicine
- Inflammation Research
- Atherosclerosis Progression
Background:
- C-reactive protein (CRP) is a known predictor of myocardial infarction and stroke.
- The role of CRP in predicting the progression of subclinical atherosclerosis remains unclear.
Purpose of the Study:
- To investigate whether CRP predicts the progression of atherosclerosis at various arterial sites.
- To compare the predictive power of CRP with traditional cardiovascular risk factors.
Main Methods:
- CRP levels were measured in 773 subjects aged 55 years and older from the Rotterdam Study.
- Subclinical atherosclerosis was assessed at multiple arterial sites at baseline and after a mean of 6.5 years.
Main Results:
- Elevated CRP levels significantly predicted the progression of atherosclerosis in the carotid, aorta, iliac, and lower extremities.
- High CRP levels were associated with generalized atherosclerosis progression (OR, 4.5; 95% CI, 2.3 to 8.5).
- The predictive value of CRP for atherosclerosis progression was comparable to traditional risk factors like high cholesterol, hypertension, and smoking.
Conclusions:
- C-reactive protein is a significant predictor of atherosclerosis progression across multiple arterial locations.
- CRP's predictive ability for atherosclerosis progression is as potent as established cardiovascular risk factors.
Unlabelled:
Background and Purpose- C-reactive protein (CRP) predicts myocardial infarction and stroke. Its role as a predictor of the progression of subclinical atherosclerosis is not yet known. We investigated whether CRP predicts progression of atherosclerosis measured at various sites in the arterial tree.
Methods:
CRP levels were measured in a random sample of 773 subjects >/=55 years of age who were participating in the Rotterdam Study. Subclinical atherosclerosis was assessed at various sites at 2 points in time, with a mean duration between measurements of 6.5 years.
Results:
After adjustment for age, sex, and smoking habits, odds ratios (ORs) associated with CRP levels in the highest compared with the lowest quartile were increased for progression of carotid (OR, 1.9; 95% CI, 1.1 to 3.3), aortic (OR, 1.7; 95% CI, 1.0 to 3.0), iliac (OR, 2.0; 95% CI, 1.2 to 3.3), and lower extremity (OR, 1.9; 95% CI, 1.0 to 3.7) atherosclerosis. The OR for generalized progression of atherosclerosis as indicated by a composite progression score was 4.5 (95% CI, 2.3 to 8.5). Except for aortic atherosclerosis, these estimates hardly changed after additional adjustment for multiple cardiovascular risk factors. In addition, ORs for progression of atherosclerosis associated with high CRP levels were as high as those associated with the traditional cardiovascular risk factors high cholesterol, hypertension, and smoking. Geometric mean levels of CRP increased with the total number of sites showing progression of atherosclerosis (P=0.002 for trend).
Conclusions:
CRP predicts progression of atherosclerosis measured at various sites in the arterial tree.
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