T. Does The Patient Have Elevated TG Level, or Low HDL-C Level, or Metabolic Syndrome?

objective

Identify other lipid abnormalities.

background

Elevated LDL-C level is considered the primary target of lipid-lowering therapy.  Epidemiologic and clinical studies have shown that a high blood TG level is an independent risk factor for CVD (Austin et al., 1998; Krauss, 1998).  However, when triglyceride levels are >200 mg/dL, the ATP-III cautions that the presence of increased quantities of atherogenic remnant lipoproteins can raise the risk of CHD far beyond what an LDL-C level alone can predict.  The atherogenic lipoproteins include small, dense LDL, very-low-density lipoprotein (VLDL), and intermediate-density lipoprotein (IDL), which are cholesterol-enriched particles that have many of the same properties as LDL-C.  The risk for CVD is higher in patients who have elevated levels of both, LDL-C and TG.

It is common to find low HDL-C levels in patients who have high levels of TG.  In addition, these low levels often accompany insulin resistance.  A low HDL-C level is considered an independent CHD risk factor and is clearly linked to increased CHD morbidity and mortality.  Various epidemiologic studies have shown that for every 1 percent decrease in HDL-C, there is a 2 to 3 percent increase in CHD risk.

Patients with high TG and low HDL-C often have several other CVD risk factors, including central obesity, impaired glucose tolerance, and HTN.  This constellation of findings is referred to as syndrome X, Reavan's syndrome, dysmetabolic syndrome, and, most recently defined by NCEP ATP-III as metabolic syndrome.

The goal of dyslipidemia management is ultimately to decrease CV risk, and the evidence is best at reducing such risk through LDL-C lowering therapies.  LDL-C remains the treatment priority, and should be addressed regardless of the TG level.  Once the LDL-C goal has been reached, treatment attention may shift to obtain optimal lipoprotein profiles.