Homocysteine Facilitates the Formation of Carotid Atherosclerotic Plaque Through Inflammatory and Noninflammatory Mechanisms.

Background: Elevated homocysteine (Hcy) was considered a significant risk factor in the development and progression of carotid atherosclerosis (CAS), which involves a combination of inflammatory and noninflammatory mechanisms. However, epidemiological surveys have presented conflicting results. In this study, we aim to offer an epidemiological viewpoint on how elevated Hcy impacts CAS and its potential mechanisms. Methods: Levels of high-sensitivity C-reactive protein (hsCRP) were measured to assess the inflammatory status. The estimation of CAS events was performed by assessing carotid intima-media thickness using Doppler ultrasonography. Univariate analysis was conducted to investigate the variations in biochemical parameters among three groups: normal, carotid atherosclerotic thickening (CAT), and carotid atherosclerotic plaque (CAP) formation. Logistic regression analysis was conducted to identify the risk factors associated with the progression of CAT and CAP. In addition, multivariate linear regression analysis was conducted to identify the independent factors that correlated with hsCRP levels. Results: The study encompassed 3897 participants, with 2992 (76.8%) being males and 905 (23.2%) being females. The incidence of CAT and CAP rose with higher Hcy levels, with an overall odds ratio (OR) of 2.04 [95% confidence intervals (CI) 1.69-2.40] for CAT and 2.68 (95% CI 2.32-3.05) for CAP. After adjusting for gender, age, and blood markers, the OR for CAT and CAP decreased, with an overall OR of 1.05 (95% CI 0.81-1.28) and OR of 1.24 (95% CI 1.02-1.46), respectively. CAP risk independently increased when Hcy level exceeded 19.7 µmol/L (P = 0.030), but not CAT risk (P = 0.299). The impact of hsCRP on CAS events is similar to that of Hcy, and a multiple linear analysis found a significant independent correlation between hsCRP and Hcy (P = 0.001). Conclusions: Elevated Hcy levels can facilitate the formation of CAP through both inflammatory and noninflammatory processes, but it does not independently influence CAT.

Chronic Inflammation Plays a Role of a Bridge Between Cardiovascular Disease and Hyperglycemia.

Background: Chronic inflammation is believed to play a key role in managing cardiovascular disease (CVD) and glycometabolism, but the specific effects remain unclear. The subclinical features of CVD events and hyperglycemia linked to inflammatory status were evaluated in this study. In addition, independent factors associated with inflammatory status were identified. Methods: Inflammatory status was measured by high-sensitivity C-reactive protein (hs-CRP), CVD events estimated by carotid intima-media thickness (cIMT), and hyperglycemia determined by glycated hemoglobin (HbA1c). Univariate analysis was performed to identify the characteristics of HbA1c-defined normoglycemia, prediabetes, and diabetes, whereas multivariate linear regression analysis was conducted to identify independent factors that correlated with hs-CRP levels. Results: Compared with HbA1c-defined normoglycemia, individuals with prediabetes and diabetes had significantly higher risks of cIMT thickening [risk ratio (RR) was 2.21 and 2.40, respectively], carotid atherosclerosis (RR was 2.29 and 3.04, respectively), and carotid plaque (RR was 2.15 and 2.63, respectively). Diabetes had higher risks of carotid atherosclerosis (RR was 1.33) and carotid plaque (RR was 1.22) than prediabetes. Increasing prevalence of cIMT thickening, atherosclerosis, and plaque was correlated with hs-CRP levels rising. There was a notable linear relationship between HbA1c and hs-CRP levels (R2 = 0.8685). In addition, both men and women showed an independent correlation of hs-CRP levels with HbA1c and low-density lipoprotein cholesterol, whereas men also had thyroid-stimulating hormone and women had age as an independent factor. Conclusions: Chronic inflammation links hyperglycemia to CVD events, and the relevant risk factors would be potential targets for alleviating inflammation and delaying the progression of the atherogenic process.