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Apolipoproteins, cardiovascular risk and statin response in type 2 diabetes: the Collaborative Atorvastatin Diabetes
V Charlton-Menys1, D J Betteridge, H Colhoun
1Cardiovascular Research Group, School of Clinical & Laboratory Sciences, Core Technology Facility (3rd Floor), University of Manchester, 46 Grafton Street, Manchester M13 9NT, UK.
Insights
The apolipoprotein B (ApoB) to apolipoprotein A-I (ApoA-I) ratio effectively predicts coronary heart disease (CHD) risk in type 2 diabetes patients. This ratio showed superiority over other lipid measures in predicting CHD events.
Area of Science:
- Cardiovascular Medicine
- Lipid Metabolism
- Diabetes Research
Background:
- Controversy exists regarding the optimal lipoprotein predictor of coronary heart disease (CHD) risk in non-diabetic populations.
- The predictive value of the apolipoprotein B (ApoB) to apolipoprotein A-I (ApoA-I) ratio in type 2 diabetes has not been previously investigated.
- Type 2 diabetes is associated with increased cardiovascular risk, necessitating precise risk assessment tools.
Purpose of the Study:
- To evaluate the apolipoprotein B (ApoB) to apolipoprotein A-I (ApoA-I) ratio as a discriminator of coronary heart disease (CHD) risk in individuals with type 2 diabetes.
- To compare the predictive performance of the ApoB:ApoA-I ratio against other lipid parameters, including LDL-cholesterol (LDLC):HDL-cholesterol (HDLC) and non-HDL-cholesterol (non-HDLC):HDLC ratios.
- To assess the impact of atorvastatin treatment on the ApoB:ApoA-I ratio and its association with CHD risk reduction.
Main Methods:
- A cohort of 2,627 participants without pre-existing vascular disease from the Collaborative Atorvastatin Diabetes Study were analyzed.
- Baseline levels of ApoB, ApoA-I, LDLC, and HDLC were measured.
- Coronary heart disease (CHD) and stroke events were tracked over a median follow-up of 3.9 years.
Main Results:
- The ApoB:ApoA-I ratio demonstrated the strongest association with CHD risk, outperforming other lipoprotein variables.
- The area under the receiver-operator curve for the ApoB:ApoA-I ratio was significantly greater than for the non-HDLC:HDLC ratio in predicting CHD.
- A 27% reduction in the ApoB:A-I ratio with atorvastatin therapy correlated with a 32% reduction in CHD risk.
- The ApoB:A-I ratio did not predict stroke outcomes.
Conclusions:
- The ApoB:ApoA-I ratio is a valuable predictor of CHD risk in type 2 diabetes, offering improvement over the non-HDLC:HDLC ratio.
- While superior to the non-HDLC:HDLC ratio, the ApoB:A-I ratio's advantage over the LDLC:HDLC ratio in predicting CHD may be marginal.
- The observed reduction in stroke risk with statin therapy may not be mediated by changes in lipoprotein levels or ratios.
Aims/Hypothesis:
Controversy surrounds whether the ratio of apolipoprotein B (ApoB) to apolipoprotein A-I (ApoA-I) is the best lipoprotein discriminator of CHD risk in non-diabetic populations, but the issue has never been investigated in type 2 diabetes.
Methods:
In 2,627 participants without known vascular disease in the Collaborative Atorvastatin Diabetes Study, ApoB, ApoA-I, LDL-cholesterol (LDLC) and HDL-cholesterol (HDLC) were assayed at baseline.
Results:
There were 108 CHD and 59 stroke endpoints over 3.9 years. The ApoB:A-I ratio at baseline was the lipoprotein variable most closely predicting CHD risk both by comparison of the hazard ratio for a 1 SD change or tertiles of frequency distribution. The areas under the receiver-operator curve for the ApoB:ApoA-I and the LDLC to HDLC [corrected] ratios, although not significantly different from each other, were greater (p = 0.0005 and p = 0.0125 respectively) than that of non-HDLC:HDLC. The 27% decrease in the ApoB:ApoA-I ratio on atorvastatin predicted a 32% (95% CI 5.4-51.2%) risk reduction in CHD, close to the 36% decrease observed. Neither the ApoB:ApoA-I nor any other lipoprotein concentration or ratio predicted the stroke outcome.
Conclusions/Interpretation:
Overall, the ApoB:ApoA-I ratio improved on the non-HDLC:HDLC ratio in predicting CHD, but, depending on the assessment chosen, its superiority over LDLC:HDLC may be marginal. The statin-induced decrease in stroke risk may not be lipoprotein mediated.
Trial Registration:
ClinicalTrials.gov NCT00327418.
Funding:
The study was supported by unrestricted grants from Diabetes UK, the Department of Health and Pfizer to the University of Manchester and to University College, London.
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