Relationship between high-sensitivity C-reactive protein and subclinical carotid atherosclerosis stratified by glucose metabolic status in Chinese adults.Clin Cardiol 2019; 42(1):39-46CC
Atherosclerosis is an inflammatory disease. Many studies demonstrated that hyperglycemia is not only increased inflammatory response, but also is a cause of atherosclerosis, implying that glucose metabolic status may be an important stratification factor when analyzing the relationship between inflammatory levels and subclinical carotid atherosclerosis. The aim of the present study is to assess the relationship between inflammatory levels and subclinical carotid atherosclerosis, stratified by different glucose metabolic status in a general population.
An assessment was performed in 7975 participants living in Tianjin, China. In the present study, we examined subclinical carotid atherosclerosis, as defined by increased carotid intima-media thickness [IMT] and plaques. Measurements were performed using a carotid artery B-mode ultrasound system. The glucose metabolic status was defined by the criteria of the American Diabetes Association, and high-sensitivity C-reactive protein (hs-CRP) as an inflammatory indicator, was measured by immunoturbidimetric assay. Multiple logistic models were used to assess a stratified relationship between hs-CRP levels and subclinical carotid atherosclerosis. Strata were defined according to glucose metabolic status.
The prevalence of increased IMT and plaques were 27.3% and 21.3%, respectively. The adjusted odds ratios (95% confidence interval) for IMT across hs-CRP quartiles were as follows: 1.00 (reference), 1.10(0.88-1.38), 1.08(0.86-1.35) and 1.32(1.06-1.66) in blood glucose-normal subjects; 1.00 (reference), 1.33(0.92-1.91), 1.33(0.93-1.91), and 1.59(1.10-2.30) in prediabetic subjects; 1.00 (reference), 0.94(0.54-1.62), 1.17(0.65-2.12) and 0.98(0.55-1.76) in diabetic subjects, respectively. Similar results were observed for plaques.
Our results suggest that inflammatory levels are differently related to subclinical carotid atherosclerosis by the different glucose metabolic status.