The
metabolic syndrome is a multiplex risk factor for atherosclerotic
cardiovascular disease. The core components of the
dyslipidemia of the
metabolic syndrome, which most likely initiate
atherosclerosis, are the "
lipid triad" of high plasma
triglycerides, low levels of
high-density lipoprotein cholesterol (HDL-C), and a preponderance of small, dense
low-density lipoprotein (
LDL) particles. Postprandial
lipemia is also recognized as an important component. Dysregulation of fat metabolism in the liver with overproduction of
very-low-density lipoprotein 1 (VLDL1) particles is considered the hallmark of the
dyslipidemia of the
metabolic syndrome. The cornerstone of
therapy is therapeutic lifestyle change. If this does not correct the
dyslipidemia,
drug therapy may be required.
LDL-C lowering with
statins is the first-line treatment; however, there is ongoing debate as to whether further aggressive
LDL-lowering
therapy with higher-dose
statins as opposed to comprehensive
lipid management is the optimal
therapy to reduce cardiovascular risk in subjects with the
metabolic syndrome. Combination of a
statin with a
fibrate and/or
nicotinic acid can improve all components of the
dyslipidemia. However, there are, as yet, no large cardiovascular outcome studies that show a reduction in cardiovascular morbidity or mortality using combination
therapy. The current
LDL-C goal in high-risk patients with the
metabolic syndrome is below 100 mg/dL, with a non-HDL goal of below 130 mg/dL. However, in very high-risk patients, such as those with established
cardiovascular disease, an
LDL-C goal of below 70 mg/dL is recommended.