Lipids & Cardiovascular Risk Labs

Divide apolipoprotein B by apolipoprotein A-1 for the single most informative number the two tests produce — atherogenic particles against protective ones, on a non-fasting sample, with sex-specific thresholds.

Convert apolipoprotein A-1 between g/L, mg/dL and mg/L. It is the HDL counterpart of apoB, and it reads the opposite way round: for apoA-1 it is a low result, not a high one, that carries the risk.

Convert apolipoprotein B between g/L, mg/dL and mg/L — and read the answer against the right number, because the apoB target and the apoB reference interval are nowhere near each other.

AIP is log₁₀ of triglycerides divided by HDL cholesterol, with both in mmol/L. Enter mg/dL instead and every answer is 0.36 too high — more than three times the width of the whole intermediate band.

Convert total, LDL and HDL cholesterol between mg/dL, mg/L, g/L and mmol/L — and see why the triglyceride on the same report needs a different factor entirely.

Estimate LDL cholesterol from total cholesterol, HDL and triglycerides using the Friedewald equation — and see the four situations in which the estimate should not be reported.

Estimate LDL cholesterol with the NIH equation 2 of Sampson and colleagues — derived against beta-quantification and usable up to a triglyceride of 800 mg/dL, where Friedewald stops at 400.

Work out the percentage LDL reduction between a current value and a target, and read it against the ACC/AHA statin intensity definitions to see which intensity is the sensible starting point.

Divide LDL cholesterol by HDL cholesterol for a unit-independent ratio — widely quoted, useful for explanation, and used by no major guideline as a treatment target.

Convert an Lp(a) in nmol/L to an approximate mg/dL — and see how far the answer moves across the range of conversion factors in use, because no exact conversion exists.

Subtract HDL from total cholesterol to get the cholesterol carried in every atherogenic particle — a measure that needs no fasting sample and no assumption about VLDL.

Subtract HDL and LDL from total cholesterol to get the cholesterol carried in triglyceride-rich lipoproteins and their remnants — free from any standard lipid panel, with thresholds that are conventional rather than guideline-based.

Divide total cholesterol by HDL cholesterol to get the Framingham risk ratio, read against sex-specific reference points — a risk marker rather than a treatment target.

Divide triglycerides by HDL cholesterol in mg/dL as a surrogate for insulin resistance and small dense LDL — and see why the same thresholds cannot be used in mmol/L.

Convert triglycerides between mg/dL, mmol/L, g/L and mg/L — and see why the molar value is a nominal unit conversion rather than a true molar concentration.

Estimate VLDL cholesterol as a fifth of the triglyceride concentration — the same assumption Friedewald rests on, with the same limits.