Chapter 10 Cholesterol Management in the Context of Risk Factor Profi lesmoking, very high carbohydrate intakes (>60% of
calories), and certain drugs (e.g., beta-blockers, ana-
bolic steroids, progestational agents). ATP III does not
specify a goal for HDL raising. Although clinical trial
results suggest that raising HDL will reduce risk, the
evidence is insuffi cient to specify a goal of therapy.
Further, currently available drugs do not robustly
raise HDL-C. Nonetheless, a low HDL should receive
clinical attention and management according to the
following sequence. In all persons with low HDL-C,
the primary target of therapy is LDL-C and non-
HDL-C a secondary goal. Since there are no drugs that
specifi cally raise HDL-C independently of lowering
apo B-containing lipoproteins, it has not been possi-
ble to test the hypothesis that HDL-raising therapy
will reduce risk for CHD. Therefore, any therapeutic
effort to raise HDL-C for the purpose of reducing
CHD is based on speculation based on epidemiology,
animal studies, and limited clinical studies.
Metabolic syndrome
The metabolic syndrome is a multiplex risk factor
for CVD [16,17]. ATP III identifi ed the metabolic
syndrome as a risk partner with LDL-C because of
its association with the increasing prevalence of
obesity in the United States and worldwide. To a
signifi cant extent the metabolic syndrome repre-
sents the metabolic consequence of obesity, although
other factors are involved in its pathogenesis. Not
only is the syndrome a multilayered risk factor for
CVD but it carries increased risk for type 2 diabetes
and is associated with other conditions including
nonalcoholic fatty liver disease, cholesterol gall-
stones, obstructive sleep apnea, and polycystic
ovarian syndrome. The syndrome is most strongly
associated with abdominal obesity but other factors
- physical inactivity, insulin resistance, endocrine
dysfunction, and racial/ethic predisposition – con-
tribute to its development. The syndrome is charac-
terized by fi ve components: atherogenic dyslipidemia
(elevated triglyceride, low HDL-C, small LDL parti-
cles, and commonly, elevated non-HDL-C), elevated
blood pressure, elevated glucose, a prothrombotic
state, and a proinfl ammatory state. The presence of
the metabolic syndrome essentially doubles the risk
for CVD. It can be identifi ed clinically by the pres-
ence of three or more of the following: abdominal
obesity, elevated triglyceride, reduced HDL-C, and
elevated blood pressure and glucose (see Table 10.7
Table 10.7 Diagnostic criteria for metabolic syndromeMeasure (any three
of the fi ve criteria
below constitute a
diagnosis of metabolic
syndrome) Categorical cutpointsElevated waist circumference*† ≥102 cm (≥40 inches) in men
≥88 cm (≥35 inches) in women
Elevated triglycerides ≥150 mg/dL (1.7 mmol/L)
or
On drug treatment for elevated
triglycerides‡
Reduced HDL cholesterol <40 mg/dL (0.9 mmol/L) in
males
<50 mg/dL (1.1 mmol/L) in
females
or
On drug treatment for reduced
HDL-C‡
Elevated blood pressure ≥130 mmHg systolic blood
pressure
or
≥85 mmHg diastolic blood
pressure
or
On drug treatment for
hypertension
Elevated fasting glucose ≥100 mg/dL
or
On drug treatment for elevated
glucose* To measure waist circumference, locate top of right iliac crest. Place a measuring
tape in a horizontal plane around abdomen at level of iliac crest. Before reading
tape measure, ensure that tape is snug but does not compress the skin and is
parallel to fl oor. Measurement is made at the end of a normal expiration.
† In the United States, some adults of non-Asian origin (e.g., White, Black,
Hispanic) with a marginally increased waist circumference (e.g. 94–101 cm
[37–39 in] in men and 80–87 cm [31–34 in] in women) may have a strong
genetic contribution to insulin resistance; they should benefi t from changes in
life habits, similarly to men with categorical increases in waist circumference.
A lower waist circumference cutpoint (e.g. ≥90 cm [35 in] in men and ≥80 cm
[31 in] in women) appears to be appropriate for persons of Asian origin.
‡ The most commonly used drugs for elevated TG and reduced HDL-C are
fi brates and nicotinic acid. A patient on one of these drugs can be presumed to
have high TG and low HDL.