Abstract 311: CRP is Probably Not Causal in Atherosclerosis
Background: C-reactive protein (CRP) is thought to predict increased cardiovascular risk. However, the question of a causal relation to atherosclerosis is in doubt. We studied the relation of CRP to carotid total plaque area (TPA) and stenosis, and to plaque inflammation.
Methods: In 527 patients with measurement of cardiovascular risk factors and CRP, linear regression was used to assess the relation of CRP to total plaque area (TPA) and stenosis. In a subset of patients scheduled for carotid endarterectomy, preoperative PET/CT with 18F- FDG was used to assess plaque inflammation, validated in endarterectomy specimens.
Results: Mean age (SD) was 63.3 (12.27); 44.4% were female, 12.7% diabetic. 4.4% of patients had no plaque; in the rest it ranged from 1 to 788 mm2; median 102 mm2, interquartile range (IQR) 215 mm2. TPA > 361 mm2 was present in 10% of patients. Internal carotid (ICA) stenosis >= 60% was present in 38.3%; 34 had occlusion of one ICA; 1 had bilateral occlusion. Mean (SD) percent carotid stenosis (sum of right + left ICA) was 69.11 (56.0)%. Median hsCRP was 2.7; IQR 3.7. In stepwise linear multiple regression significant predictors of TPA (R2= 0.367, p< 0.00001) were age, smoking pack-years (pk-yrs), systolic blood pressure (SysBP), antihypertensive medication (BPMed), sex, lipid medication (LipMed) (in order of significance); CRP was excluded with p=0.35. Significant predictors of stenosis (R2 =0.226, p< 0.00001) were age, LipMed, pk-yrs, BPMed, SysBP. CRP was excluded with p=0.963. In 20 endarterectomy specimens, the direct burden of inflammation, as quantified by CD68 immunohistology, correlated with maximum 18FDG uptake (r=0.716, p<0.001). There was no evidence of a correlation between CRP and CD68 (r=0.159, p=0.50), nor with maximum 18FDG uptake (r=0.238, p=0.31). Furthermore, FDG was more strongly correlated with CD68 than CRP (p=0.02.CRP was inversely related to the extent of fibrous tissue (r=0.549, p=0.034).
Conclusion: CRP was not associated with plaque inflammation, TPA, or stenosis of the carotid arteries. CRP is probably not a causal factor in atherosclerosis.
Author Disclosures: J. Spence: None. M.S. Cocker: None. J. Tardif: None. R.S.B. Beanlands: None.
- © 2014 by American Heart Association, Inc.