Increased Serum CRP-Albumin Ratio Is Independently Associated With Severity of Carotid Artery Stenosis.

Carotid artery stenosis (CAS), mainly caused by carotid atherosclerosis, is related to ischemic stroke. We investigated whether C-reactive protein (CRP) to albumin ratio (CAR) was associated with increased severity of carotid stenosis in patients undergoing carotid angiography. A total of 269 patients who were undergoing carotid angiography were included in this study. The patients were divided into 2 groups with respect to the severe CAS: group 1 (stenosis < 70%, n = 189) or group II (stenosis ≥ 70%, n = 80). C-reactive protein to albumin ratio was higher in group II compared to group I (0.56 ± 0.25 vs 0.14 ± 0.01, P < .001). The CAR (odds ratio [OR]: 1.051, 95%CI: 1.027-1.076, P < .001), neutrophil to lymphocyte ratio (NLR), and total cholesterol levels were independent predictors of severe CAS. The area under the receiver operating characteristic curve (area under the curve) for the CAR to predict severe CAS was 0.798 (95% CI: 0.741-0.854, P < .001). C-reactive to protein albumin ratio was an independent risk factor of severe CAS. Therefore, CAR might be considered a potential index in the severity of carotid artery disease.

The effects of iodixanol and iopamidol on adhesion molecule serum levels in patients with angina pectoris undergoing coronary angiography: a randomized study.

OBJECTIVE: To compare intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) serum levels between patients with stable (SAP) and unstable angina pectoris (USAP) undergoing coronary angiography (CAG), investigate effects of CAG on ICAM-1, VCAM-1 levels in SAP, USAP patients; probable different effects of non-ionic radiocontrast media (RCM), iso-osmotic iodixanol and low osmolar iopamidol, on these adhesion molecules (AM). METHODS: In this randomized, prospective study, 2 groups consisting of patients with SAP (n=22) and USAP (n=22) undergoing CAG were included. For halves of each group iopamidol, for the other halves iodixanol were used as RCM, in turn for randomization. The patients were divided into 4 subgroups according to clinical presentations and used RCM(SAP-iodixanol, SAP-iopamidol USAP-iodixanol, USAP-iopamidol). ICAM-1, VCAM-1 levels were measured just before and 12 hours after CAG. Repeated measurements were compared with two-way ANOVA test. RESULTS: Baseline VCAM-1 concentration was higher in USAP group than SAP group (p=0.001). ICAM-1, VCAM-1 concentrations increased significantly following CAG in SAP, USAP groups. ICAM-1, VCAM-1 concentration increments; didn't reach statistical significance in SAP-iodixanol subgroup, reached a borderline significance in SAP-iopamidol subgroup (p=0.06). In USAP-iodixanol subgroup; only VCAM-1 (p<0.001), in USAP-iopamidol subgroup; ICAM-1 (p=0.009), VCAM-1 (p=0.006) levels increased significantly following CAG. No complication was observed. CONCLUSION: To our knowledge, this is the first study indicating ICAM-1, VCAM-1 inducing effect of CAG in patients with SAP, USAP and differential effects of iodixanol and iopamidol on ICAM-1, VCAM-1 serum levels. Further studies are needed to clarify the effects of CAG and different RCM on vascular inflammation, vessel injury, serum AM levels and their clinical significance. This study should be taken as a pilot, hypothesis-generating study.