No association non-fasting triglycerides with subclinical atherosclerosis
Association of fasting triglyceride concentration and postprandial triglyceride response with the carotid intima media thickness in the middle aged: the NEO studyChristen T, de Mutsert R, Gast KB, et al. - J Clin Lipidol, 2017, In press
High fasting and non-fasting plasma triglyceride concentrations (TGc) are well-known risk factors for cardiovascular disease. The recently updated consensus statement by the European Atherosclerosis Society indicate that measuring fasting TGc does not improve cardiovascular (CV) risk prediction compared to non-fasting TGc , which implies that fasting and non-fasting TGc may be exchangeable for clinical CVD prediction.
As most people in the Western world are predominantly in postprandial state during a day, which may lead to prolonged high plasma TGc, the population-based prospective Netherlands Epidemiology of Obesity (NEO) study (after exclusion n=5 574) investigated whether postprandial hypertriglyceridemia (over 150 minutes) was associated with larger carotid intima media thickness (IMT) as a measure of subclinical atherosclerosis and whether this association was stronger in strata of risk factors that are associated with deterioration of the vascular endothelium, such as smoking (16% of individuals).
- Mean fasting TGc was 1.21 mmol/L (SD 0.82) and mean TG response was 29.8 mmol/L*min (SD 24.0). Correlation coefficient of fasting TGc with TGc after 150 min was 0.92.
- Per SD of fasting TGc, the crude difference in IMT was 18.8 µm (95% CI 13.4-24.1) and after adjustment for age, sex and TGiAUC (TG incremental area under the curve) was 14.4 µm (95% CI 8.9-20.0). Further adjustment for all confounding factors attenuated this to 8.5 µm (95% CI 2.1-14.9).
- Per SD of TGiAUC, the crude difference in IMT was 13.2 µm (95% CI 7.0-19.4). Adjustment for age, sex and fasting TGc attenuated this to 2.7 µm (95% CI -3.6-9.0) and for all confounding factors resulted in loss of association (-1.7 µm, 95% CI -8.5-5.0).
- Association postprandial TG response and carotid IMT in high-risk subgroups; crude and after adjustment of all confounding factors were respectively for men 5.6 µm (95% CI -4.4-15.5) and -0.3 µm (95% CI -10.3-9.6), women 12.3 µm (95% CI 4.5-20.1) and -1.3 µm (95% CI -10.1-7.5), individuals with normal fasting glucose concentrations 12.0 µm (95% CI 5.0-19.0) and -2.3 µm (95% CI -10.0-6.5), impaired fasting glucose concentrations 8.1 µm (95% CI -4.2-20.5) and 3.2 µm (95% CI -8.9-15.3), never smokers 15.8 µm (95% CI 6.0-25.5) and 0.8 µm (95% CI -10.0-11.6), former smokers 8.3 µm (95% CI -0.1-16.7) and -6.6 µm (95% CI -15.5-2.2), current smoker 14.8 µm (95% CI -1.8-31.3) and 7.7 µm (95% CI -8.5-23.9).
There was a clear association between fasting TGc and IMT, which persisted after adjustment for postprandial TG response over 150 minutes. However, the association observed between crude TG response after a meal and IMT disappeared after adjusting for fasting TGc. These results imply that non-fasting and fasting TGc may not be exchangeable and that it may not be useful to perform a meal challenge in order to estimate a person’s risk of atherosclerosis. The association between TG response and IMT remained in smokers and pre-diabetics/diabetics after adjustment for fasting TGc, which may indicate that these conditions increase the susceptibility of the endothelial wall to either postprandial TG response or higher concentrations of remnant particles.