Cholesterol Management in the
Context of Risk Factor Profi le
Scott M. Grundy
10
Sources
LDL Cholesterol: the primary target of therapy
Risk assessment: fi rst step in risk management
Goals for cholesterol lowering therapy
Role of other risk factors in risk assessment
Secondary causes of lipid disorders
Therapeutic approaches to cholesterol-lowering
therapy
Therapeutic lifestyle changes
Drug therapy
Adherence to LDL-lowering therapy
Special and unresolved issues
Management of specifi c dyslipidemias
Very high LDL cholesterol (≥190 mg/dL)
Elevated serum triglycerides
Low HDL-C
Metabolic syndrome
Other unresolved issues
European guidelines for lipid management
Sources
The information contained in this chapter synthe-
sizes the evidence presented in the 2001 National
Cholesterol Education Program’s (NCEP’s) Third
Report of the Expert Panel on Detection, Evalua-
tion, and Treatment of High Blood Cholesterol in
Adults (Adult Treatment Panel III, or ATP III) [1],
the 2004 update of the ATP III report [2], and 2007
American Heart Association Secondary Prevention
Guidelines [3].
It should be noted that these guidelines are
intended to inform, not replace, the physician’s
clinical judgment, which must ultimately determine
the appropriate treatment for each individual.
LDL Cholesterol: the primary target of
therapy
Research from experimental animals, laboratory
investigations, epidemiology, and genetic forms of
hypercholesterolemia indicate that elevated LDL
cholesterol (LDL-C) is a major cause of coronary
heart disease (CHD) and cardiovascular disease
(CVD). In addition, recent clinical trials robustly
show that LDL-lowering therapy reduces risk for
CHD. Although ATP III [1] identifi ed prevention of
CHD as the major aim of cholesterol-lowering
therapy, in the light of recent clinical trials, there is
a trend to expand the endpoint to include all of
atherosclerotic CVD [4].
Based results of multiple lines of evidence, LDL-C
constitutes the primary target of cholesterol-lower-
ing therapy. As a result, the primary goals of therapy
and the cutpoints for initiating treatment are stated
in terms of LDL-C [1–3]. Clinical trial evidence that
LDL-lowering signifi cantly reduces risk for CVD is
very strong (summarized in refs 1–3). (Level of Evi-
dence: A)
Growing evidence indicates that very low density
lipoprotein (VLDL) approaches LDL in atherogenic
potential. Thus, in patients with higher triglyceride,
the sum of LDL + VLDL cholesterol (usually called
non-HDL-C) is a better predictor of atherosclerotic
risk than is LDL-C alone. Although some investiga-
tors contend that non-HDL-C is a preferred primary
target of therapy over LDL-C [5–7], this view has
not been universally accepted. For this reason, non-
HDL-C is designated a secondary target of choles-
The AHA Guidelines and Scientific Statements Handbook
Edited by Valentin Fuster © 2009 American Heart Association
ISBN: 978 -1-405-18463-2