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C HAP TE R 36 / Lipid Management and Cardiovascular Disease 829

Hypoalphalipoproteinemia
Table 36-4 ■ CHARACTERISTICS OF THE METABOLIC
A familial HDL deficiency state, hypoalphalipoproteinemia, has
SYNDROME
been linked to premature CVD. Although high HDL levels may
Risk Factor Comments mobilize cholesterol from arterial luminal surfaces and return it to
the liver, low HDL usually reflects an enzymatic or apoprotein ab-
Abdominal obesity Men: 102 cm ( 40 in.)
(waist circumference) Women: 88 cm ( 35 in.) normality affecting the catabolism of LDL or VLDL. (See section
Triglycerides 150 mg/dL titled “Reverse Cholesterol Transport.”) Alterations of the human
HDL cholesterol Men: 40 mg/dL Women: 50 mg/dL apo A-I gene have been found in those with familial HDL defi-
Blood pressure 130/ 85 mm Hg ciency and premature CVD. 68 This suggests that low HDL may
Fasting glucose 110–125 mg/dL
represent a genetic marker for identifying those at risk for CVD.
The abnormalities related to VLDL catabolism explain the com-
Adapted from Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. (2001). Executive summary of the third report of the National mon coexistence of low HDL with elevated triglycerides. Further-
Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and more, when triglycerides are lowered, increases in HDL are ob-
Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA, served. In the absence of a genetic deficiency (i.e., A-I Milano,
285(19), 2486–2497.
Tangiers disease), lower HDL levels are related to environmental
factors such as cigarette smoking and physical inactivity (see Table
36-3 for causes of low HDL cholesterol).
Although raising HDL-C by delaying catabolism (e.g., CETP
VLDL. LDL cholesterol is more glycated in patients with dia- inhibition) may not enhance reverse cholesterol transport, elevat-
betes compared with nondiabetic subjects. Glycated LDL parti- ing HDL-C may have other cardioprotective benefits such as an-
65
cles have increased oxidative susceptibility. HDL is often low in tioxidant, anti-inflammatory, and anticoagulant effects that all
patients with diabetes as a result of increased HL triglyceride ac- may improve endothelial function. At present, niacin is the most
tivity. Additionally, hyperglycemia is associated with significantly effective HDL-raising therapy. Although the mechanism by which
increased mortality in patients with acute coronary syndrome. niacin raises HDL level is not well understood, the predominant
The Heart Protection Study (HPS) further confirmed the impor- hypothesis is that niacin inhibits the holoparticle uptake of HDL,
tance of lipid management in persons with type 2 diabetes. HPS resulting in delayed catabolism. 69
included 5,963 persons with diabetes (ages 40 to 80 years). Those
subjects receiving simvastatin 40 mg/day had significant reduc-
tions of 25% for major coronary events including stroke and Combined Dyslipidemias
revascularization. 12
High triglyceride levels are also related to high carbohydrate Combined dyslipidemias usually represent a combination of ge-
and alcohol intake. As a marker for CVD risk, the reduction of netic lipoprotein or apoprotein defects and environmental effects.
plasma triglyceride levels to less than 150 mg/dL is a desirable The specific lipid abnormalities observed provide clues to the ge-
goal. 2,3 Although not designated as an independent risk predictor netic disorders. Table 36-3 summarizes observed lipid abnormali-
by ATP III, the importance of elevated triglycerides is recognized ties and associated mechanisms. An understanding of these mech-
in a number of ways. In ATP III, triglyceride level is seen as a anisms guides the management of lipid abnormalities.
marker of elevated atherogenic remnant particle level thought to
increase risk of CAD and as an indication of lipid and nonlipid
risk factors in the metabolic syndrome. 2 THE MANAGEMENT OF HIGH
In addition, normal triglyceride level has been lowered to
2
150 mg/dL or less compared with 67 ATP II (see Table 36-5). A BLOOD CHOLESTEROL
new target for persons with elevated triglycerides is called “non-
HDL cholesterol.” Non-HDL cholesterol is the total cholesterol Since the late 1980s, a large and convincing body of evidence has
minus the HDL cholesterol. This number represents the sum of the associated elevated blood lipids with CVD. Furthermore, clinical
LDL and the VLDL cholesterol in determining a treatment goal for trials have demonstrated that reducing blood cholesterol is effec-
LDL cholesterol. The goal for LDL cholesterol is 30 mg/dL higher tive for both primary and secondary prevention of CVD. This re-
in persons with triglycerides of 200 mg/dL or more. This is based search has prompted groups such as the National Institutes of
on a normal VLDL value being 30 mg/dL. Health, American Heart Association, and the American College
of Cardiology to establish health policy guidelines for the detec-
tion and treatment of lipid disorders. 2,3,70–72

Table 36-5 ■ ATP III CLASSIFICATION OF TRIGLYCERIDES Recommendations for the Detection
(NCEP, 2001) of High Blood Cholesterol

Triglyceride (Tg) Level (mg/dL) Category Health policy recommendations for detection of high cholesterol
include the measurement of total cholesterol and HDL cholesterol
150 Normal
150–199 Borderline high in all adults aged 20 years and older, with repeat measurement
200–499 High within 5 years. Total cholesterol less than 200 mg/dL is considered
500 Very high desirable; levels between 200 and 239 mg/dL are classified as bor-
derline-high, and those more than 240 mg/dL are consideredhigh