Triglyceride-Glucose Index, LDL and Cardiovascular Outcomes in Chronic Stable Cardiovascular Disease: Results from the ONTARGET and TRANSCEND trials.
Cardiovascular Disease
Mortality
Myocardial Infarction
Triglyceride Glucose Index
Journal
European journal of preventive cardiology
ISSN: 2047-4881
Titre abrégé: Eur J Prev Cardiol
Pays: England
ID NLM: 101564430
Informations de publication
Date de publication:
27 Oct 2023
27 Oct 2023
Historique:
received:
19
09
2023
revised:
22
09
2023
accepted:
25
10
2023
medline:
27
10
2023
pubmed:
27
10
2023
entrez:
27
10
2023
Statut:
aheadofprint
Résumé
The triglyceride-glucose (TyG) index has been proposed as an alternative to insulin resistance and as a predictor of cardiovascular outcomes. Little is known on its role in chronic stable cardiovascular disease and its predictive power at controlled low-density lipoprotein (LDL) levels. Our study population consisted of 29,960 participants in the ONTARGET and TRANSCEND trials that enrolled patients with known atherosclerotic disease. Triglycerides and glucose were measured at baseline. TyG was calculated as the logarithmized product of fasting triglycerides and glucose divided by 2. The primary endpoint of both trials was a composite of cardiovascular death, myocardial infarction, stroke or hospitalization for heart failure. The secondary endpoint was all-cause death and the components of the primary endpoint. Cox-proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) with extensive covariate adjustment for demographic, medical history and lifestyle factors. During a mean follow-up of 4.3 years, 4,895 primary endpoints and 3,571 all-cause deaths occurred. In fully adjusted models, individuals in the highest compared to the lowest quartile of the TyG index were at higher risk for the primary endpoint (HR 1.14; 95% CI 1.05-1.25) and for myocardial infarction (HR 1.30; 95% CI 1.11-1.53). A higher TyG index did not associate with the primary endpoint in individuals with LDL levels <100 mg/dl. A higher TyG index is associated with a modestly increased cardiovascular risk in chronic stable cardiovascular disease. This association is largely attenuated when LDL levels are controlled.Clinical Trial Registration Information - https://www.clinicaltrials.gov; Identifier: NCT00153101. The association of Triglyceride-glucose Index (TyG) with cardiovascular disease in chronic stable cardiovascular disease and its predictive power at controlled low-density lipoprotein (LDL) levels is unclear. Using a study population of 29,960 participants with chronic stable cardiovascular disease, we found that Higher TyG levels were associated with a modestly increased risk for incident cardiovascular events Low LDL levels largely attenuated the association of TyG with cardiovascular risk.
Sections du résumé
BACKGROUND
BACKGROUND
The triglyceride-glucose (TyG) index has been proposed as an alternative to insulin resistance and as a predictor of cardiovascular outcomes. Little is known on its role in chronic stable cardiovascular disease and its predictive power at controlled low-density lipoprotein (LDL) levels.
METHODS
METHODS
Our study population consisted of 29,960 participants in the ONTARGET and TRANSCEND trials that enrolled patients with known atherosclerotic disease. Triglycerides and glucose were measured at baseline. TyG was calculated as the logarithmized product of fasting triglycerides and glucose divided by 2. The primary endpoint of both trials was a composite of cardiovascular death, myocardial infarction, stroke or hospitalization for heart failure. The secondary endpoint was all-cause death and the components of the primary endpoint. Cox-proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) with extensive covariate adjustment for demographic, medical history and lifestyle factors.
RESULTS
RESULTS
During a mean follow-up of 4.3 years, 4,895 primary endpoints and 3,571 all-cause deaths occurred. In fully adjusted models, individuals in the highest compared to the lowest quartile of the TyG index were at higher risk for the primary endpoint (HR 1.14; 95% CI 1.05-1.25) and for myocardial infarction (HR 1.30; 95% CI 1.11-1.53). A higher TyG index did not associate with the primary endpoint in individuals with LDL levels <100 mg/dl.
CONCLUSION
CONCLUSIONS
A higher TyG index is associated with a modestly increased cardiovascular risk in chronic stable cardiovascular disease. This association is largely attenuated when LDL levels are controlled.Clinical Trial Registration Information - https://www.clinicaltrials.gov; Identifier: NCT00153101.
The association of Triglyceride-glucose Index (TyG) with cardiovascular disease in chronic stable cardiovascular disease and its predictive power at controlled low-density lipoprotein (LDL) levels is unclear. Using a study population of 29,960 participants with chronic stable cardiovascular disease, we found that Higher TyG levels were associated with a modestly increased risk for incident cardiovascular events Low LDL levels largely attenuated the association of TyG with cardiovascular risk.
Autres résumés
Type: plain-language-summary
(eng)
The association of Triglyceride-glucose Index (TyG) with cardiovascular disease in chronic stable cardiovascular disease and its predictive power at controlled low-density lipoprotein (LDL) levels is unclear. Using a study population of 29,960 participants with chronic stable cardiovascular disease, we found that Higher TyG levels were associated with a modestly increased risk for incident cardiovascular events Low LDL levels largely attenuated the association of TyG with cardiovascular risk.
Identifiants
pubmed: 37890035
pii: 7331252
doi: 10.1093/eurjpc/zwad340
pii:
doi:
Banques de données
ClinicalTrials.gov
['NCT00153101']
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.