Higher serum triglyceride-glucose index levels were independently associated with increased pericoronary adipose tissue attenuation (FAI40keV standardized regression coefficient 0.117) and high-risk plaque features in patients with chest pain.
Cross-Sectional (n=201)
No
The triglyceride-glucose (TyG) index, a marker of insulin resistance, correlates with pericoronary adipose tissue inflammation and high-risk plaque features on spectral CT, suggesting a mechanism for atherosclerosis progression.
Effect estimate: standardized regression coefficient 0.117
p-value: p=<0.001
Background and aims The triglyceride-glucose (TyG) index is a reliable alternative marker for insulin resistance (IR). Pericoronary adipose tissue (PCAT) can indirectly reflect coronary inflammation. IR and coronary inflammation play a key role in the development and progression of coronary atherosclerosis. Therefore, this study investigated the relationships between the TyG index, PCAT and atherosclerotic plaque characteristics to explore whether IR might lead to coronary artery atherosclerosis progression by inducing coronary inflammation. Methods We retrospectively collected data on patients with chest pain who underwent coronary computed tomography angiography using spectral detector computed tomography at our institution from June to December 2021. The patients were grouped based on their TyG index levels: T1 (low), T2 (medium), and T3 (high). Each patient was assessed for total plaque volume, plaque load, maximum stenosis, the plaque component volume proportion, high-risk plaques(HRPs), and plaque characteristics (including low attenuation plaques, positive remodeling, a napkin ring sign, and spot calcification). PCAT quantification was performed on the proximal right coronary artery using the fat attenuation index (FAI) measured from a conventional multicolor computed tomography image (FAI 120kVp ), a spectral virtual single-energy image (FAI 40keV ), and the slope of the spectral HU curve (λ HU ). Results We enrolled 201 patients. The proportion of patients with maximum plaque stenosis, positive remodeling, low-density plaques, and HRPs increased as the TyG index level increased. Moreover, the FAI 40keV and λ HU significantly differed among the three groups, and we identified good positive correlations between FAI 40keV and λ HU and the TyG index (r = 0.319, P 0.01 and r = 0.325, P 0.01, respectively). FAI 120kVp did not significantly differ among the groups. FAI 40keV had the highest area under the curve, with an optimal cutoff value of −130.5 HU for predicting a TyG index value of ≥9.13. The multivariate linear regression analysis demonstrated that FAI 40keV and λ HU were independently positively related to a high TyG index level (standardized regression coefficients: 0.117 P 0.001 and 0.134 P 0.001, respectively). Conclusions Patients with chest pain and a higher TyG index level were more likely to have severe stenosis and HRPs. Moreover, FAI 40keV and λ HU had good correlations with the serum TyG index, which may noninvasively reflect PCAT inflammation under insulin resistance. These results could help explain the mechanism of plaque progression and instability in patients with insulin resistance might be related to IR-induced coronary inflammation.
Ma et al. (Wed,) conducted a cross-sectional in Chest pain and suspected coronary artery disease (n=201). Serum triglyceride-glucose (TyG) index vs. Lower TyG index levels was evaluated on Independent association of FAI40keV with high TyG index level (standardized regression coefficient 0.117, p=<0.001). Higher serum triglyceride-glucose index levels were independently associated with increased pericoronary adipose tissue attenuation (FAI40keV standardized regression coefficient 0.117) and high-risk plaque features in patients with chest pain.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: