Copyright © 2008 American Heart Association. All rights reserved. Print ISSN: 0009-7322. Online
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2008;118;e54-e60; originally published online Jun 19, 2008;
Working Group 6
Robert C. Kaplan, Peter Kim, Janet Lo, Esteban Martinez, James M. Sosman and for
Feinberg, Nina Friis-Møller, Anuradha Ganesan, Marshall J. Glesby, David Hardy,
James H. Stein, Colleen M. Hadigan, Todd T. Brown, Ellen Chadwick, Judith
Prevention Strategies for Cardiovascular Disease in HIV-Infected Patients
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Prevention Strategies for Cardiovascular Disease
in HIV-Infected Patients
James H. Stein, MD, FAHA, Co-Chair; Colleen M. Hadigan, MD, MPH, Co-Chair;
Todd T. Brown, MD, PhD; Ellen Chadwick, MD; Judith Feinberg, MD; Nina Friis-Møller, MD, PhD;
Anuradha Ganesan, MD; Marshall J. Glesby, MD, PhD; David Hardy, MD; Robert C. Kaplan, PhD;
Peter Kim, MD; Janet Lo, MD; Esteban Martinez, MD, PhD;
James M. Sosman, MD; for Working Group 6
infection.1With increased life expectancy, HIV-infected patients
increasingly are experiencing complications of illnesses that are
not directly related to HIV infection.2Cardiovascular disease
(CVD), the leading cause of death in the United States,3recently
has been recognized as an important cause of morbidity and
mortality among patients with HIV (see Working Group 2,
Epidemiological Evidence for Cardiovascular Disease in HIV-
Infected Patients and Relationship to Highly Active Antiretro-
viral Therapy).2,4–6Among these patients, traditional CVD risk
factors predict CVD events; however, certain components of
the increased CVD risk observed in patients undergoing ART is
related primarily to the effects of ART on traditional CVD risk
factors; however, direct effects of ART on the vasculature and
other inflammatory, immune, and viral factors associated with
HIV infection may also contribute to increased CVD risk.5,7,8
A central tenet of preventing CVD is that the intensity of
risk-reducing interventions should be based on the level of
CVD risk.9Patients with established CVD are at the highest
risk and qualify for the most aggressive risk factor manage-
ment, with special focus on interventions that have been
proven to prevent cardiovascular death, myocardial infarc-
tion, and stroke. For patients without established CVD,
management is based on the presence of risk factors for
developing complications of CVD, such as death, myocardial
ffective antiretroviral therapy (ART) improves the survival
of patients with human immunodeficiency virus (HIV)
infarction, and stroke9–12(see Working Group 4, Screening
and Assessment of Coronary Heart Disease in HIV-Infected
Patients). The intensity of CVD risk-reducing therapy, how-
ever, must be modified by the context of the patient’s overall
health. This is an especially important consideration in
patients with HIV infection, who often have competing
morbidities that may be as likely to lead to death or disability
as CVD, such as complications of HIV, substance abuse, liver
disease, or malignancy.2Also, to achieve the aggressive goals
set forth in recent lipid and hypertension guidelines,10–12
multidrug therapy frequently is necessary, which places many
HIV-infected patients at risk for complications of polyphar-
macy. With these considerations, efforts to prevent CVD in
patients with HIV should focus on improving modifiable risk
factors such as cigarette smoking, hypertension, dyslipid-
emia, and disordered glucose metabolism. The initial choice
of ART regimen and subsequent ART modifications also may
be considered in planning CVD prevention strategies, with
the recognition that maintenance of viral suppression is the
primary concern, because the risks of inadequately treated
HIV infection outweigh any increase in CVD risk that may be
associated with ART, and with the understanding that uncon-
trolled viral infection may itself contribute to CVD risk.7,13,14
Cigarette smoking is highly prevalent among patients with
HIV (47% to 71%) and is more prevalent than in the general
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relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required
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The opinions expressed in this manuscript are those of the authors and should not be construed as necessarily representing an official position of the
US Department of Health and Human Services, the Centers for Disease Control and Prevention, the Agency for Healthcare Research and Quality, or the
US government. These opinions are not necessarily those of the editor or the American Heart Association.
The Executive Summary is available in the print issue of the journal (Circulation. 2008;118:198–210). The remaining writing group reports are
available online at http://circ.ahajournals.org (Circulation. 2008;118:e20–e28; e29–e35; e36–e40; e41–e47; and e48–e53).
These proceedings were approved by the American Heart Association Science Advisory and Coordinating Committee on February 29, 2008. A copy
of these proceedings is available at http://www.americanheart.org/presenter.jhtml?identifier?3003999 by selecting either the “topic list” link or the
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This article has been copublished in the Journal of Acquired Immune Deficiency Syndromes.
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© 2008 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.orgDOI: 10.1161/CIRCULATIONAHA.107.189628
AHA Conference Proceedings
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population.15,16Aside from having a history of CVD, current
cigarette smoking is the most powerful predictor of CVD
events among patients with HIV.5A reduction in CVD risk
and total mortality associated with smoking cessation has
been demonstrated in non–HIV-infected populations.17–20
Furthermore, smokers with HIV have higher total mortality
and are more likely to develop pneumonia, chronic obstruc-
tive pulmonary disease, cancers, and decreased quality of life
Preventing individuals with HIV from starting smoking is
critical, because stopping smoking remains a formidable
challenge. Efforts directed at educating teenagers about the
harmful effects of smoking and strategies to avoid use of
cigarettes are important, because smokers frequently begin
using cigarettes as teenagers or young adults.22A majority of
current smokers with HIV desire to quit smoking23; however,
physicians of patients with HIV are less likely than non-HIV
healthcare providers to ascertain smoking status.21A minority
of HIV care providers are confident that they can influence
smoking cessation.21Challenges to achieving successful
smoking cessation include lack of provider awareness, high
rates of relapse due to nicotine addiction, lack of social
network support, lack of access to proven smoking cessation
strategies, drug interactions, and fatalism.
Current guidelines recommend the “5A” approach: ask
about tobacco use, advise to quit, assess willingness to make
a quit attempt, assist with the quit attempt, and arrange for
follow-up.22Identification and successful treatment of smok-
ers can be improved by systems-based management tools,
such as incorporating smoking as a vital sign (so each patient
is “asked”) and assigning the physician responsibility for
advising the patient to quit smoking, for assessing their
willingness, and for assisting with pharmacotherapy. Pharma-
cotherapy is the preferred approach to smoking cessation now
that more effective medications are available, although their
long-term safety and efficacy remain to be established.24–26
Specific research needs related to smoking cessation as a
strategy to reduce CVD risk in patients with HIV infection
include pharmacokinetic and pharmacodynamic studies to
evaluate the effects of smoking cessation on ART and
interactions between ART and smoking cessation pharmaco-
therapies, because smoking cessation affects hepatic enzymes
involved in drug metabolism and may have other pharmaco-
dynamic effects that have not yet been studied (Table 1).
Further research also is needed on the costs and effectiveness
of systems-based approaches to smoking cessation.27
Hypertension is a powerful predictor of CVD events in the
general population.11,28The prevalence of hypertension
among patients with HIV infection has not been established
with certainty, but in 2 US cohorts, it was 12% to 20% among
individuals ?40 years old and 35% to 41% for individuals
?40 years old.29The best evidence suggests that ART may be
associated with a modest increase in blood pressure and the
prevalence of hypertension; however, these relationships may
be confounded by increases in body mass index and other risk
factors for the development of hypertension, so the effect of
ART on hypertension is unclear.29–31The prevalence of
hypertension is expected to increase as the age of patients
with HIV infection increases and the prevalence of HIV
increases among patients in ethnic subgroups at increased risk
of developing hypertension.29When hypertension is present,
the magnitude of increased CVD risk associated with this risk
factor probably is similar to that observed in the general
population.11,28In the general population, dietary interven-
tions are effective for reducing blood pressure.32,33In 1 study,
patients with HIV who completed an intensive lifestyle
intervention that included dietary and physical activity coun-
seling, modeled after the Diabetes Prevention Program, ex-
perienced a significant reduction in blood pressure.34,35Phar-
macotherapy for hypertension powerfully reduces CVD risk
in non–HIV-infected patients.11,28Guidelines for the effective
diagnosis and management of hypertension have been widely
adopted and should be applied to patients with HIV until
further data are available (Table 2).11,28
Specific research needs related to hypertension and CVD
risk in patients with HIV infection begin with the need to
obtain a better understanding of the prevalence of hyperten-
sion among patients undergoing ART, as well as the extent to
which it influences risk of coronary artery disease, stroke,
heart failure, and kidney disease. Pharmacokinetic and phar-
macodynamic studies that evaluate interactions between com-
monly used antihypertensive therapies and ART are needed,
given the overlap in metabolic pathways affected by ART and
certain antihypertensive medications.36
Untreated HIV infection is associated with decreased total
cholesterol and high-density lipoprotein cholesterol (HDL-C)
and with increased triglycerides and the presence of small
dense low-density lipoprotein (LDL) particles.37Atherogenic
lipoprotein changes, including increases in total cholesterol,
triglycerides, LDL cholesterol (LDL-C), small LDL, and
apolipoprotein B-100, are seen in patients taking ART;
however, HDL-C also increases with ART.12,38,39(See Work-
ing Group 1, Contribution of Metabolic and Anthropometric
Abnormalities to Cardiovascular Disease Risk Factors.) In
general, use of protease inhibitors is associated with more
adverse lipid changes than use of nonnucleoside reverse-
transcriptase inhibitors; however, the lipid effects of ART
vary within classes, and there is notable interindividual
variability in lipid responses to ART.40–47Lipids may worsen
dramatically in some patients, and dyslipidemia in HIV-
infected patients is associated with increased risk of
CVD.5,48–50Severe hypertriglyceridemia (?1000 mg/dL) is a
risk factor for pancreatitis, but the incidence of pancreatitis
among patients with HIV infection is not known. The
independent contribution of less severe degrees of hypertri-
glyceridemia to CVD risk in the HIV population is less clear,
because it is associated with other metabolic abnormalities
that also affect CVD risk, such as low HDL-C, hypertension,
and insulin resistance.
Adverse dietary habits are common in patients with HIV
and contribute to dyslipidemia51; therefore, a trial of dietary
modification may be appropriate before initiation of drug
therapy.12In patients with HIV, the only prospective cardio-
vascular outcomes data showing the benefits of lipid-
Stein et alCHD in HIV Conference: Prevention
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lowering therapy are studies showing that treatment with
statins improves endothelial function52,53; however, an obser-
vational study reported that among HIV-infected patients
with dyslipidemia, use of lipid-lowering therapy was associ-
ated with reduced CVD rates.50Pharmacotherapy for dyslip-
idemia powerfully reduces CVD risk in non–HIV-infected
patients.9,10Guidelines for the effective diagnosis and man-
agement of dyslipidemia have been widely adopted9,10and
are the basis of the general approach to the patient with HIV;
however, current pharmacological strategies for treating dys-
lipidemia in patients undergoing ART are limited by drug
interactions, relative lack of efficacy, and, potentially, pill
burden, as well as consideration of comorbidities (Table
2).12,54–58Therefore, separate guidelines for the management
of dyslipidemia in patients with HIV have been developed.12
These guidelines focus on the importance of reducing LDL-C
and non–HDL-C levels, given the proven CVD risk reduction
that is observed when these lipid markers are reduced in
patients without HIV.9,10,12
There are several research needs related to dyslipidemia
and CVD risk in patients with HIV infection (Table 1). Given
the reduced efficacy and safety issues with lipid-lowering
therapy in patients undergoing ART, confirmation of the
cardiovascular benefits of standard lipid-lowering strategies
in patients with HIV who are undergoing ART would be
ideal; however, cost and logistics may be prohibitive. Pro-
spective studies on progression of a surrogate marker, such as
carotid intima-media thickness or other markers of vascular
injury, would be useful. Current guidelines focus on LDL-C
and non–HDL-C; however, the additional predictive value of
apolipoprotein B-100 and other lipoprotein markers is not
known in patients with HIV. This is a matter of special
interest for patients with HIV, because many patients under-
going ART have combined dyslipidemia or hypertriglyceri-
demia, and some patients with increased triglycerides who
have achieved LDL-C and non–HDL-C targets may still have
an excess of atherogenic particles. More guidance is needed
regarding strategies for safely and effectively treating com-
bined dyslipidemia in patients with HIV. Finally, pharmaco-
kinetic and pharmacodynamic studies to evaluate interactions
between lipid-lowering therapies and newer ART agents are
needed. These studies also need to be performed with new
and selected older ART agents in children and teenagers.
Disordered Glucose Metabolism
Use of ART is associated with increased visceral adiposity,
insulin resistance, and disordered glucose metabolism, which
increases future risk of type 2 diabetes mellitus and
CVD.43,59,60The prevalence of type 2 diabetes mellitus
among patients with HIV ranges from 6% to 18%, and for
men, it appears to be increased relative to noninfected
controls.61Impaired fasting glucose (defined as fasting blood
glucose ?100 mg/dL) or impaired glucose tolerance (defined
as a 2-hour glucose ?140 mg/dL after a 75-g glucose load) is
increased in patients with HIV60and is associated with ART
exposure.60,62–66In addition to ART exposure, risk factors for
insulin resistance and type 2 diabetes mellitus in patients with
HIV include male sex, increasing age, increasing body
weight, and increasing waist circumference, as well as eth-
nicity and hepatitis C coinfection.29,63,67Impaired fasting
glucose and impaired glucose tolerance are best treated
nonpharmacologically with lifestyle interventions such as
dietary changes and exercise, although medications can be
considered (Table 2).35,68,69In patients with HIV, regular
exercise and an intensive lifestyle intervention that includes
dietary and exercise counseling has salutary metabolic effects
and tends to reduce insulin resistance.34,70Metformin and
thiazolidinediones tend to improve insulin resistance in pa-
Controversial Issues, Gaps in Knowledge, and Future
1. Why are smoking rates higher in HIV-infected patients?
2. What are the optimal strategies for smoking cessation in HIV-infected
3. Do smoking cessation and the use of smoking cessation medications
affect the efficacy and safety of ART?
1. What is the prevalence of hypertension in HIV-infected patients?
2. What is the magnitude of increased CVD risk conveyed by
hypertension among patients with HIV?
3. Are there specific interactions between antihypertensive agents and
ART that should inform the sequence and dosing of antihypertensive
therapy in HIV-infected patients?
1. How much does the hypertriglyceridemia observed in patients
undergoing ART contribute to CVD risk?
2. Are the cardiovascular benefits of lipid-lowering therapy in patients
with HIV similar to those observed in the non–HIV-infected population?
3. What is the optimal sequence of lifestyle interventions and
pharmacological therapy in HIV-infected patients?
4. Are LDL-C and non-HDL-C the best targets of lipid therapy in patients
5. What is the utility of apolipoprotein B-100 and other lipoprotein
markers for CVD risk prediction in patients with HIV?
6. Given the potential for interaction between specific lipid-lowering
medications and ART, what are the optimal lifestyle and
pharmacological treatment strategies for managing dyslipidemia in
patients with HIV?
Disordered glucose metabolism
1. What are the mechanisms of insulin resistance in patients with HIV?
What is the role of viral infection, body composition, and ART?
2. What is the clinical significance of impaired glucose tolerance in the
patients with HIV? Should it be treated, and how?
3. What is the optimal treatment for diabetes mellitus? What are the
roles of lifestyle modification, insulin-sensitizing agents, and insulin?
Antiretroviral therapy (see also Working Group 2 on Epidemiological Evidence
1. How should the presence of metabolic abnormalities and potential for
treatment interactions affect the choice and sequence of ART initiation
2. How does a strategy of switching ART compare with managing CVD
risk factors in patients with ART-associated metabolic abnormalities?
3. What are the direct and indirect effects of ART on the vasculature?
4. Do the effects of ART on immune and inflammatory markers affect
CVD risk, and if so, how do these effects compare with traditional
CVD risk factors?
July 8, 2008
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tients with HIV; however, the long-term effectiveness of
these agents for the prevention and treatment of diabetes
mellitus in patients with HIV is not known.71–73Some studies
also suggest insulin resistance is increased among children
undergoing ART.74,75Patients initiating ART should be
screened for impaired fasting glucose and diabetes mellitus
by measurement of fasting glucose levels at baseline, annu-
ally, and after changes are made to ART regimens. Measure-
ments of insulin and hemoglobin A1C as screening tests are
not recommended by current guidelines.76Oral glucose tol-
erance testing may help to identify and distinguish between
patients with impaired glucose tolerance and those with
Specific research needs related to disordered glucose me-
tabolism and CVD risks include assessment of how well
recognition and management of diabetes mellitus are
achieved in patients with HIV (Table 1). Preliminary data
indicate that fewer than half of HIV-infected patients with
diabetes mellitus achieve hemoglobin A1C targets.77The
optimal treatment strategies for diabetes mellitus in patients
with HIV have not been determined. In this regard, potential
drug interactions and unique mechanisms of diabetes mellitus
need to be considered. In addition, further research to
characterize the CVD risk conveyed by disordered glucose
metabolism in patients with HIV infection relative to the
non-HIV population is needed, including research on the
extent to which disordered glucose metabolism and its asso-
ciated increase in CVD risk are reversed when ART is
Antiretroviral Drug Use and CVD Risk
Although control of HIV infection remains the overriding
priority when choosing an initial ART strategy or making
subsequent changes in ART, preexisting CVD and CVD risk
may also be given consideration. Observational studies have
suggested that increasing years of exposure to ART are
associated with increased CVD risk.5,43Several studies have
demonstrated improvements in CVD risk factors, particularly
improvements in lipid profile, through modification or selec-
tion of ART.41,42,78,79On the other hand, there are compelling
data to support an increase in total mortality and possibly
CVD risk when HIV is inadequately suppressed or ART is
withdrawn (see Working Group 2).13Indeed, 1 study demon-
strated that use of ART was associated with short-term
decreases in CVD risk and overall mortality.80Initiation of
ART currently is driven primarily by risk of HIV disease
progression and loss of immune function; however, the
metabolic profiles of drugs should be considered, especially
in patients with CVD or those who are at high or moderately
high cardiovascular risk (?10% risk of myocardial infarction
or coronary death over 10 years).10
Whether a strategy of switching ART is superior to
managing CVD risk factors in patients with ART-associated
metabolic abnormalities is not clear, and this decision must be
individualized on a per-patient basis. Treatment of HIV may
improve some CVD risk factors, while exacerbating others
(Table 1). Some of the excess CVD risk related to ART may
be attributed to alterations in lipids and disordered glucose
metabolism5; however, options for subsequent ART regimens
Table 2. Summary of Interventions to Reduce CVD Risk in Patients With HIV Infection
Risk Condition Treatment/Interventions Major FindingsLimitations
Cigarette smoking Interpersonal counseling Increased quit rates No studies of pharmacotherapy in
patients with HIV
Limited data from controlled studies
regarding safety and efficacy of
Hypertension Dietary and physical activity counseling*
Other antihypertensive agents
Dietary and physical activity counseling*
Statins, fibrates, fish oil, niacin
Reduced blood pressure
Drug interactions between CCBs and PIs
Dyslipidemia Modest improvement in lipids
Statins improve endothelial function
Multiple drug interactions with ART
Short duration; long-term efficacy for
CVD reduction not known
Effectiveness of newer lipid-lowering
agents not known
Interactions with newer ART regimens
need to be clarified
Lactic acidosis with metformin
CVD risks with TZDs not clear
Safety and efficacy of sulfonylureas not
Interactions with ART regimens need to
Small studies, often uncontrolled or used
older ART regimens
Dietary and physical activity counseling*
Metformin and TZDs
Improvement in glycemia
Metformin reduces insulin resistance and VAT
TZDs may improve SAT
Use of ART Modification of initial ART based on metabolic
profile and CVD risk
Modest effects on lipids and insulin resistance
Statins and fibrates may be more effective
Switching of ART to reduce metabolic side
Effects on CVD risk not known
Risk of viral relapse and resistance
Inadequately suppressed HIV increases
total and possibly CVD mortality
CCBs indicates calcium channel blockers; PI, protease inhibitor; TZDs, thiazolidinediones; VAT, visceral adipose tissue; and SAT, subcutaneous adipose tissue.
*Components and duration of lifestyle modification program in patients with HIV are not known.
Stein et al CHD in HIV Conference: Prevention
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may be constrained by HIV resistance, medication toxicity,
and tolerability. Newer drugs and emerging classes of ART
may provide better options with regard to CVD risk factors.
Specific research needs related to ART and CVD risk in
patients with HIV infection remain (Table 1). A better
understanding of how initiation, choice, and duration of ART
exposure affects CVD risk should be attained by prospec-
tively studying the affects of ART on traditional CVD risk
factors, emerging risk factors, vascular structure and function,
and well-validated CVD events such as cardiac death, myo-
cardial infarction, and stroke. In addition, a clearer under-
standing of the effects of ART on immune and inflammatory
markers that may play a role in CVD risk is needed. Studies
evaluating the time course and extent of the reversal of
adverse metabolic effects and excess CVD risk of ART when
ART is changed are needed. Finally, for children, research is
needed to more fully appreciate the influences of initiation,
selection, and duration of ART on cumulative CVD risk and
CVD risk assessment and risk reduction are essential com-
ponents of preventive medical care that are increasingly
important for patients with HIV infection. As the population
of HIV-infected patients ages and accumulates CVD risk that
is, at least in part, related to ART, efforts to appropriately
recognize and manage CVD risk will be necessary. Lifestyle
modification, including smoking cessation, increased physi-
cal activity, weight reduction for those who are overweight or
obese, and education on healthy dietary practices are the
cornerstones of CVD risk reduction. These strategies, com-
bined with appropriate management of dyslipidemia, disor-
dered glucose metabolism, and hypertension, will help max-
imize the long-term health of persons living with HIV.
Research is needed to identify the lifestyle modifications that
are most effective for reducing CVD risk in patients with
HIV, whether they differ by age, sex, ethnicity, and socio-
economic status, and what barriers exist to their implemen-
tation. It is especially important to develop simple and clear
messages to educate patients and HIV care providers about
the importance of CVD prevention in HIV patients, the
importance of identifying and treating CVD risk factors in
individuals at moderately high or high CVD risk, and how
smoking, adverse dietary habits, and physical inactivity
increase CVD risk.
Note Added in Proof
Recent data81suggest that use of a growth hormone–releasing factor
significantly reduces visceral fat in HIV-infected patients on
HAART with visceral fat accumulation. In addition, this strategy
improved lipids without aggravating glucose. These data raise the
important question as to whether strategies aimed at reducing
visceral fat, a known cardiovascular risk factor in non-HIV patients,
may improve CVD risk in HIV patients.
Potential conflicts of interest for members of the writing groups for
all sections of these conference proceedings are provided in a
disclosure table included with the Executive Summary, which is
available online at http://circ.ahajournals.org/cgi/content/full/
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KEY WORDS: AHA Conference Proceedings ? AIDS ? HIV ? infectious
diseases ? cardiovascular disease ? prevention
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