Clinical Manual for Management of the HIV-Infected ... - myCME.com

Dyslipidemia
Background
In HIV-infected people treated with antiretroviral
therapy (ART), improved life expectancy and the aging
process are likely to increase morbidity and mortality
from coronary heart disease (CHD). Thus, identification
and reduction of modifiable risk factors for CHD are
important aspects of primary care for HIV-infected
patients. Several risk factors for CHD are common
among HIV-infected populations in the United
States and Europe. Dyslipidemia is a well-described
independent risk factor for CHD that occurs in a
high proportion of patients treated with antiretroviral
(ARV) medications. Other metabolic abnormalities
such as insulin resistance and diabetes may be caused
or compounded by ARVs. In addition, some traditional
CHD risk factors, including smoking, hypertension,
and inactivity, are prevalent in many HIV-infected
populations.
Before the widespread use of ARV medications,
increases in triglyceride (TG) levels and decreases
in total cholesterol (TC), high-density lipoprotein
(HDL) cholesterol, and low-density lipoprotein
(LDL) cholesterol were reported in individuals with
HIV disease. The introduction of combination ART,
particularly the use of protease inhibitors (PIs),
increased the prevalence of dyslipidemia in HIVinfected
patients. In fact, dyslipidemia is associated
with certain agents in each of the 3 major classes of
ARVs. In the PI class, ritonavir and ritonavir-boosted
PIs (with the exception of atazanavir) are particularly
likely to cause marked elevations of TG and LDL
levels. Nonnucleoside reverse transcriptase inhibitors
(NNRTIs) also may contribute to increases in TC,
LDL, and TG levels although the effects, particularly
with efavirenz, are more variable. Nucleoside analogue
reverse transcriptase inhibitors (NRTIs), specifically
stavudine, may increase TC and TG levels.
The pathogenesis of ARV-induced dyslipidemia is not
well understood. Current research suggests that the
dyslipidemia observed in patients taking ART is caused
by a combination of factors related to HIV disease,
ARV regimens, and individual patient characteristics.
Lipid abnormalities may appear or worsen within
Section 4—Complications of Antiretroviral Therapy | 4–5
a few weeks to months after starting ART. Not all
ARV-treated patients experience lipid abnormalities
to the same degree. Patients with a personal or family
history of dyslipidemia, glucose intolerance, diabetes,
obesity, or a combination of these health problems may
be genetically predisposed to lipid abnormalities that
become evident once ART is initiated.
Published research regarding the relationship between
ARVs and the risk of cardiovascular disease has not
been conclusive. The largest prospective study of CHD
events related to ARVs (the DAD study), showed a
small but significant increase in the risk of myocardial
infarction among HIV-infected patients treated with
ART; moreover, the effect increased with cumulative
years of ARV exposure. While awaiting definitive
results from this and other studies, it is important to
screen and treat patients for lipid abnormalities and for
other known CHD risk factors. For patients with CHD
or CHD risk equivalents (see below), ARV regimens
should, if possible, be selected to minimize the risk of
hyperlipidemia.
Guidelines for the evaluation and management of
dyslipidemia have been developed by the National
Cholesterol Education Program (NCEP). These
recommendations and follow-up reports are based on
studies of HIV-uninfected patients and may not be
entirely applicable to HIV-infected patients. Despite
this limitation, expert panels generally recommend
similar treatment goals when evaluating and managing
dyslipidemia in patients with HIV infection. (For
recommendations on screening, see chapter Initial and
Interim Laboratory and Other Tests.)
S: Subjective
The history should focus on factors indicating coronary
artery disease or cardiovascular risk. CHD risk factors
are conditions associated with a greater risk of serious
cardiac events. A CHD risk equivalent, such as diabetes,
is considered to be equal in risk to known CHD. Both
CHD risks and CHD equivalents should be the focus
of lifestyle modification strategies and lipid-normalizing
treatment.