Dataset Information

Association between the Plasma-Glycosylated Hemoglobin A1c/High-Density Lipoprotein Cholesterol Ratio and Carotid Atherosclerosis: A Retrospective Study.

ABSTRACT:

Background

Diabetes mellitus (DM) and dyslipidemia are the main risk factors for atherosclerosis. Elevated glycosylated hemoglobin A1c (HbA1c) and reduced high-density lipoprotein cholesterol (HDL-C) are associated with the progression of atherosclerosis. The aim of this study is at exploring the relationship between the HbA1c/HDL-C ratio and atherosclerosis evaluated using carotid artery intima-media thickness (cIMT) and carotid artery plaque.

Methods

In this retrospective study, we enrolled 1304 patients who had multiple cardiovascular risk factors or symptoms of suspected coronary artery disease. cIMT and carotid artery plaque were measured using ultrasonography. Logistic regression was used to explore the correlation between the HbA1c/HDL-C ratio and cIMT or carotid artery plaque. We used restricted cubic spline curves to assess nonlinear relationships between the HbA1c/HDL-C ratio and cIMT or carotid artery plaque.

Results

With increased quartiles of HbA1c/HDL-C, patients had higher cIMT and a greater carotid plaque burden. After adjusting for other relevant clinical covariates, patients with the highest HbA1c/HDL-C ratio (quartile 4 (Q4)) had a 2.88 times (95% confidence interval (CI): 2.02-4.10, P < 0.001) more abnormal mean cIMT, 3.72 times (95% CI: 2.55-5.44, P < 0.001) more abnormal maximum cIMT, and 2.58 times (95% CI: 1.70-3.91, P < 0.001) greater carotid artery plaque burden compared with patients who had the lowest HbA1c/HDL-C ratio (Q1). Moreover, the association of HbA1c/HDL-C with atherosclerosis remained significant in a subsample of patients with and without DM.

Conclusion

As a novel compound indicator for evaluating blood glucose homeostasis and dyslipidemia, the HbA1c/HDL-C ratio was positively correlated with carotid atherosclerosis evaluated using the mean and maximum cIMT as well as the carotid artery plaque burden.

SUBMITTER: Hu X

PROVIDER: S-EPMC8598339 | biostudies-literature |

REPOSITORIES: biostudies-literature

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