Clinical Review

YOU HAVE A NEW JOB: Monitor the lipid profile

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References

TABLE 4

Lipid markers of remnant lipoproteins

Triglyceride (TG) >150–200 mg/dL
Very-low-density lipoprotein cholesterol >30 mg/dL
Unremarkable low-density lipoprotein cholesterol with elevated non-high-density lipoprotein cholesterol (HDL-C)
Low HDL-C in insulin-resistant patients
Elevated total cholesterol/HDL-C ratio and TG >150 mg/dL

A few words of advice

The driving forces of atherogenesis are increased numbers of apoB-containing lipoproteins and impaired endothelial integrity. ApoB and LDL-P are the available lab assays that most accurately quantify atherogenic particle number.

The lipid-concentration surrogates that you should be using to better predict apoB and CVD risk are:

  • TC (unless HDL-C is very high)
  • LDL-C
  • Non-HDL-C
  • TC/HDL-C ratio
  • TG/HDL-C ratio.

Because LDL is by far the most numerous of the apoB particles present in plasma, it is the primary agent of atherogenesis. However, apoB and LDL-P do not correlate with LDL-C when LDL particles are small, are TG-rich and cholesterol-poor, or simply cholesterol-poor (seen in some patients who have low LDL-C levels).7,15

Both NCEP ATP-III and AHA Women’s Guidelines use the TC/HDL ratio as a powerful risk predictor. However, as a goal of therapy, these guidelines recommend normalizing LDL-C and then non-HDL-C.8,11 In reality, normalization of non-HDL-C takes care of LDL-C as well. For example, say a patient has LDL-C <100 mg/dL, but non-HDL-C >130 mg/dL or TC/HDL-C ratio >4. These readings indicate residual risk and suggest that an elevated number of apoB particles is present. Therapy to normalize non-HDL-C or, better yet, apoB/LDL-P, is warranted. The clue that residual risk is present even when LDL-C is normal is the reduction of HDL-C and elevation of TG and non-HDL-C.

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