Background Triglyceride glucose (TyG) index was recently reported to be associated with an increased risk of the development and recurrence of cardiovascular events, and atherosclerosis is a main speculative mechanism. However, data on the relationship between TyG index and atherosclerosis, especially in the setting of ischemic stroke, is rare. We aimed to explore the association between TyG index and carotid atherosclerosis in patients with ischemic stroke. Methods A total of 1523 ischemic stroke patients with TyG index and carotid artery imaging data were enrolled in this analysis. The TyG index was calculated as ln [fasting triglyceride (mg/dL) × fasting glucose (mg/dL)/2]. Carotid atherosclerosis was measured by common carotid artery intima-media thickness (cIMT), and abnormal cIMT was defined as a mean cIMT and maximum cIMT value ≥ 1 mm. Multivariable logistic regression models and restricted cubic spline models were used to assess the relationships between TyG index and abnormal cIMT. Risk reclassification and calibration of models with TyG index were analyzed. Results The multivariable-adjusted odds ratios (95% CIs) in quartile 4 versus quartile 1 of TyG index were 1.56 (1.06–2.28) for abnormal mean cIMT and 1.46 (1.02–2.08) for abnormal maximum cIMT, respectively. There were linear relationships between TyG index and abnormal mean cIMT (P for linearity = 0.005) and abnormal maximum cIMT (P for linearity = 0.027). In addition, the TyG index provided incremental predictive capacity beyond established risk factors, shown by an increase in net reclassification improvement and integrated discrimination improvement (all P < 0.05). Conclusions A higher TyG index was associated with carotid atherosclerosis measured by cIMT in patients with ischemic stroke, suggesting that TyG could be a promising atherosclerotic marker.
Background Choline and betaine have been suggested to play a pivotal role in neurotransmitter synthesis, cell membrane integrity, and methyl-group metabolism, exerting neuroprotective effects in patients with various neurological disorders. However, population-based evidence on choline and betaine with subsequent cardiovascular events after stroke is rare. Objectives We aimed to prospectively investigate the relationships of circulating choline and betaine with cardiovascular events and recurrent stroke in patients with ischemic stroke. Methods We performed a nested case-control study within the China Antihypertensive Trial in Acute Ischemic Stroke. A total of 323 cardiovascular events (including 264 recurrent strokes) and 323 controls (free of recurrent cardiovascular events) matched for age (±1 y), sex, and treatment group were included. The primary endpoint was a composite of cardiovascular events after ischemic stroke. Plasma choline and betaine were measured at baseline by ultra-high-performance LC-MS/MS. Conditional logistic regression models were applied, and discrimination, reclassification, and calibration of models with choline pathway metabolites were evaluated. Results Plasma choline and betaine were inversely associated with cardiovascular events and recurrent stroke after ischemic stroke. Specifically, in fully adjusted models, each additional SD of choline and betaine was associated with 35% (95% CI: 20%–48%) and 30% (95% CI: 14%–43%) decreased risks of subsequent cardiovascular events, respectively, and 34% (95% CI: 16%–48%) and 29% (95% CI: 12%–43%) decreased risks of recurrent stroke, respectively. In addition, both choline and betaine offered substantial risk discrimination and reclassification improvement for cardiovascular events and recurrent stroke beyond traditional risk factors, as evidenced by an increase in C statistics, the net reclassification index, and integrated discrimination improvement. Conclusions Plasma choline pathway metabolites, including choline and betaine, were associated with decreased risks of cardiovascular events and recurrent stroke and provided incremental value in risk discrimination and stratification in patients with ischemic stroke. This nested case-control study was based on the China Antihypertensive Trial in Acute Ischemic Stroke, which is registered at clinicaltrials.gov as NCT01840072.
Background Nonalcoholic fatty liver disease (NAFLD) patients are often prone to coronary artery disease (CAD), and CAD is found to be the main cause of death in NAFLD patients. The purpose of this study was to investigate the association between fatty acid desaturase 2 (FADS2) rs3834458 polymorphism and serum FADS2 level with NAFLD and CAD in Chinese Han population. Materials and Methods The serum level of FADS2 was detected by enzyme-linked immunosorbent assay (ELISA) in healthy people, NAFLD patients, and NAFLD patients combined with CAD (NAFLD+CAD). Polymerase chain reaction (PCR) was used to detect the genotypes of FADS2 rs3834458 in the three groups. Results Body mass index (BMI), glucose (GLU), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) of the NAFLD group and the NAFLD+CAD group were higher than those of the healthy control group (P < 0.05); the HDL-C of the NAFLD+CAD group was significantly lower than that of the healthy people and the NAFLD group (P < 0.05). The serum FADS2 concentration in the NAFLD+CAD group was significantly higher than that in the NAFLD group (P < 0.05) and the healthy people (P < 0.05). There was no significant difference in genotype distribution (χ2 = 5.347, P < 0.497) and allele frequency (χ2 = 3.322, P = 0.345) between the three groups. Logistic regression analysis showed that the T allele was not an independent risk factor for CAD with NAFLD (OR = 1.62, 95% CI: 0.422-6.180). Conclusions Serum FADS2 concentration was positively correlated with the susceptibility of NAFLD with CAD, while the polymorphism of rs3834458 was not associated with NAFLD with CAD.
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