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|Objective:||Non-fasting TRL-C contributes to cardiovascular risk; however, estimation of this parameter based on nonfasting lipid measures requires clarification. The aims of this study were therefore 1) to estimate TRL-C from non-fasting lipids; 2) to establish the performance of TRL-C and TRL-C/apolipoprotein (apo)A-I (vs. TG-based markers) to grade TRLs and atherogenic dyslipidaemia and 3) to relate TRL-C with non-fasting TG.|
|Study design:||Cohort study|
120 subjects with type 2 diabetes (86% white, 63% male, mean age 67 years, 58% with atherogenic dyslipidaemia and 92% on lipid-modifying therapy). Nonfasting lipid measures are summarised in Table 1.
Table 1. Baseline nonfasting lipid measures (mg/dL)
Discriminant Ratio (DR) methodology was used to compare the different lipid measures. Briefly, this methodology allows for comparison of different tests measuring the same underlying physiological variable by determining the ability of a test to discriminate between different subjects, discrimination between different tests, as well as the underlying correlation between pairs of tests adjusting for within-subject variation. Confidence limits were calculated for the DRs and for testing for equivalence of different DRs.
(1) TC - [(0.0106 * TC - 0.0036 * TG + 0.017 * apoB100 - 0.27) * 38.6] - HDL-C; and
(2) TC - [(0.0106 * TC -0.0036 * TG + 0.017 * [0.65 * (TC - HDL-C) + 6.3] - 0.27) * 38.6] - HDL-C.
Nonfasting TRL-C and log[TG] are as effective and interchangeable for assessing remnant atherogenic particles. For grading atherogenic dyslipidaemia, log[TG]/HDL-C is preferable.
Nonfasting TRLs, comprising chylomicrons remnants and very-low-density lipoprotein remnants, are an important contributor to lipid-related residual vascular risk. Measurement of TGs provides a surrogate measure for TRLs. However, it should be borne in mind that these lipoproteins are heterogeneous and metabolically dynamic, especially in the postprandial state. Moreover, it is the cholesterol content – not the TG content - of these lipoproteins that is atherogenic. Consequently, from the clinical perspective, measurement of the cholesterol content of these TG-rich particles would be preferable in assessment of the atherogenic load.
Some have proposed that remnant cholesterol may be an appropriate measure, supported by evidence from Mendelian randomization studies showing remnant cholesterol as causal for cardiovascular disease.1 Remnant cholesterol may be calculated as total C - (HDL-C + LDL-C).1,2 However, this equation does not hold in the nonfasting state, given that the Friedewald’s equation cannot be used to calculate LDL cholesterol. Access to direct lipoprotein measurement is also not feasible in routine clinical practice.3
The current study aimed to resolve these issues. The authors propose two equations which allow calculation of TRL-C based on routine nonfasting samples. Given that the need for fasting samples is being reconsidered, the use of these equations will offer the opportunity to monitor and manage TRL-C more effectively in routine practice.
1. Varbo A, Benn M, Tybjærg-Hansen A, Jørgensen AB et al. Remnant cholesterol as a causal risk factor for ischemic heart disease. J Am Coll Cardiol 2013, 61:427–36.
2. McPherson R. Remnant cholesterol: “Non-(HDL-C + LDL-C)” as a coronary artery disease risk factor. J Am Coll Cardiol 2013, 61:437–4.
3. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972, 18:499–502.
|Key words||triglyceride-rich lipoproteins; remnant cholesterol; residual vascular risk; atherogenic dyslipidaemia|