Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents With HIV

Cardiovascular and Metabolic Complications in People With HIV

Cardiovascular Complications in People With HIV

Overview

Most people with HIV who are using continuous antiretroviral therapy (ART) and achieve viral suppression have a life expectancy that is approaching that of people without HIV.¹ However, a gap in mortality remains due to comorbidities such as atherosclerotic cardiovascular disease (ASCVD). As mortality from AIDS events among people with HIV has declined, the proportion of ASCVD-related deaths has increased. When compared to people without HIV, people with HIV have an approximately twofold higher risk of developing ASCVD, even after accounting for traditional cardiometabolic risk factors.² The age at incident ASCVD diagnosis among people with HIV is often younger than that of people without HIV. In this context, the 2018 Multisociety Cholesterol Guidelines identified HIV as an ASCVD risk enhancer.³ Factors influencing ASCVD risk among people with HIV include a higher prevalence of traditional cardiometabolic risk factors compared with the general population,⁴ ongoing systemic inflammation associated with HIV despite viral suppression,⁵ and cardiometabolic toxicity associated with certain ARV drugs.^6,7 Data also suggest that excess ASCVD risk relative to the general population is greater among women with HIV than among age-matched men with HIV.^8,9 In addition, differential access to screening and treatment of ASCVD risk factors also contributes to excess ASCVD risk among certain people with HIV in the United States.^10,11

While there has been extensive focus on the epidemiology and pathogenesis of ASCVD among people with HIV, there are also data demonstrating increased risk of other cardiac and vascular diseases. People with HIV have an increased risk of developing stroke (including ischemic and hemorrhagic), heart failure, arrhythmia or sudden cardiac death, and thrombosis.^12-15 Risk factors for these outcomes are thought to be similar to those for ASCVD, with an etiologic role for both traditional risk factors and HIV-related factors. Currently, this section of the guidelines is focused on primary prevention strategies for people with HIV, with an emphasis on ASCVD. As data emerge concerning primary and secondary prevention strategies for other cardiovascular outcomes specific to people with HIV, this section may be expanded.

HIV-Related Risk Factors for Atherosclerotic Cardiovascular Disease

Factors related to HIV and its treatment have been shown to be important contributors to excess cardiovascular disease (CVD) risk. Specifically, HIV-related inflammation has been associated with elevated CVD risk. This inflammation is increased in the presence of active viremia and decreases with ART, but still remains elevated when compared to those without HIV (see Introduction). Data from the SMART trial demonstrated that continuous ART not only improves HIV-related outcomes but also significantly reduces non-AIDS events, including CVD, an observation thought to be related to the beneficial effects of ART on inflammation.¹⁶ In the large Veterans Aging Cohort Study (VACS), myocardial infarction (MI) risk was independently associated with detectable or increased HIV RNA; compared to people without HIV, MI risk was increased by 39% in those with HIV RNA <500 copies/mL and by 75% in those with HIV RNA ≥500 copies/mL.¹⁷ In REPRIEVE, even low-level HIV viremia (median 62 copies/mL) was linked to increased rates of major adverse cardiac events (MACE), as viremic individuals had a higher risk than those with viral load below the limit of detection (adjusted hazard ratio 1.4; 95% confidence interval, 1.00–1.97)^4,18; however, another recent study did not show an association between HIV viremia and CVD.¹⁹ Based on these findings, continuous ART is recommended for all people with HIV to maintain viral suppression and reduce ASCVD risk (AII). Immunomodulatory therapy as an intervention to reduce HIV-associated ASCVD risk is not recommended except in a clinical trial (AII). See Immune Activation and Inflammation Among People With HIV Receiving Antiretroviral Therapy for additional details.

Additional factors related to HIV may further impact ASCVD risk. Lower CD4 T lymphocyte (CD4) cell count and nadir CD4 count have been shown to be associated with CVD events independent of traditional CVD risk factors or specific ART,^20,21 with VACS demonstrating CD4 <200 cells/mm³ as an independent predictor of MI with an increased risk of nearly 90%.^17,22 HIV-related CVD risk-enhancing factors include prolonged duration of HIV infection, delayed ART initiation, long periods of HIV viremia and/or treatment nonadherence, low current or nadir CD4 count (e.g., <350 cells/mm³), exposure to older antiretroviral (ARV) drugs associated with cardiometabolic toxicity, and coinfection with hepatitis C.²³

Women with HIV have also been shown to have a greater relative risk of ASCVD compared to men with HIV. Although data indicating the absolute risk of MI is similar between genders—12.71 versus 10.48 per 1,000 person-years for women and men with HIV, respectively—women with HIV have exhibited a nearly 3- to 4-fold increase in relative MI risk versus a 1.5- to 2-fold increase for men compared to sex-specific rates among people without HIV.^9,24-26 A substudy from REPRIEVE demonstrated the absence of an expected protective effect of female sex for the development of a MACE.⁴ The presence of HIV-related ASCVD risk-enhancing factors, including female sex, may strengthen the rationale for ASCVD prevention strategies, including statin initiation (see Statin Therapy in People With HIV), and may be used to inform decisions to avoid certain ARV medications that have been associated with increased ASCVD risk.

Antiretroviral Therapy and Cardiometabolic Complications

Specific ARV medications and classes have been associated with potential cardiometabolic toxicity, which has informed the U.S. Department of Health and Human Services Panel on Antiretroviral Guidelines for Adults and Adolescents (the Panel)’s recommendations on ART regimen selection to reduce risk for cardiometabolic complications. See Interactions Between ARV Drugs and Drugs for Treatment or Prevention of Cardiovascular Diseases below and Table 7 of What to Start for more information. Specifically, for individuals with elevated traditional ASCVD risk or known CVD, the selection of an ART regimen should consider options that minimize the introduction of new cardiometabolic adverse effects.

Antiretroviral Therapy and Atherosclerotic Cardiovascular Disease Risk

Individual ARV medications and classes have been linked to increased risk of CVD events. An association between abacavir (ABC) use and MI was first reported in the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study, with the increased risk noted only with recent/current ABC exposure (i.e., within 6 months) and particularly among participants with pre-existing cardiac risk factors.²⁷ Since the D:A:D report, multiple studies, systematic reviews, and meta-analyses have evaluated the relationship between ABC therapy and cardiovascular events, with some confirming the initially observed association and others failing to identify an association.^27-32 Retrospective analyses from the REPRIEVE study corroborated the D:A:D results, showing an increased hazard of a first MACE with ART regimens, including ABC versus tenofovir-containing regimens,³³ and an increased MACE hazard of 62% in participants with previous use and 41% with current use of ABC compared with participants who were never exposed.³⁴ An association between ABC and ASCVD risk reported in multiple large studies provides a rationale to consider underlying ASCVD risk when using ABC as a component of ART. Based on these data, the Panel recommends considering alternative ARV medications in place of ABC in people with HIV and higher underlying ASCVD risk or known CVD (AII).

An early study from the D:A:D cohort demonstrated a 16% increased risk of MI per year of cumulative protease inhibitor (PI) exposure,³⁵ specifically with older PIs (e.g., indinavir and ritonavir-boosted lopinavir [LPV/r]). A case-control study within the French HIV ANRS cohort CO4 also found a 33% increase in MI risk with LPV/r use.³⁶ A later study from the D:A:D cohort showed a 59% increased risk of CVD per 5 additional years of use with ritonavir-boosted darunavir (DRV/r) but not ritonavir-boosted atazanavir (ATV/r),³⁷ yet subsequent studies did not observe an association between boosted darunavir and increased CVD risk.^38-40 Based on these data, the Panel recommends considering alternative ARV medications in place of LPV/r in people with HIV and higher underlying ASCVD risk or known CVD (AII). If use of DRV/r is indicated, clinicians should weigh the potential benefits of therapy versus the potential cardiovascular risk.

The effect of integrase strand transfer inhibitors (INSTIs) on the risk of CVD is an area of active research, with recent studies showing inconsistent results. In a multicenter observational study of the international RESPOND consortium, INSTI exposure was associated with a nearly twofold greater incidence of a composite CVD endpoint within the first 6 months after exposure compared to no INSTI exposure,⁴¹ and the increased risk persisted throughout the first 24 months. Subsequently, two target trial emulation studies found no association between INSTI use and a composite CVD outcome that included MI, stroke, or invasive cardiovascular procedures, regardless of previous ART experience.^42,43 Based on current data, there is insufficient evidence to recommend modifying suppressive INSTI-based ART regimens in people with weight gain, higher underlying ASCVD risk, or known CVD.

Antiretroviral Therapy and Dyslipidemia

Higher levels of low-density lipoprotein cholesterol (LDL), high-density lipoprotein cholesterol (HDL), and triglycerides have been observed with tenofovir alafenamide (TAF), efavirenz (EFV), all boosted PIs, and elvitegravir/cobicistat (EVG/c).^44,45 Among the PIs, similar lipid changes have been shown in participants from a randomized trial of ATV/r- and DRV/r-based regimens.⁴⁶ Importantly, differences in lipid levels between two ART regimens can be due to a lipid-raising effect of a given medication and/or a lipid-lowering effect of the other medication. For example, levels of total cholesterol, LDL, HDL, and triglycerides are higher in participants who received TAF when compared with those who received tenofovir disoproxil fumarate (TDF) in multiple randomized controlled trials.^47,48 However, data from a placebo-controlled pre-exposure prophylaxis trial support that TDF exposure has an independent lipid-lowering effect (for total cholesterol, LDL, and HDL).⁴⁹ Further, data support that total cholesterol to HDL ratios did not differ between participants receiving TAF and those receiving TDF,^50,51 and the clinical significance of CVD risk from increases across all lipid indices without changes in total to HDL ratios is uncertain.

Antiretroviral Therapy and Diabetes/Insulin Resistance

Direct effects on diabetes mellitus (DM) and insulin resistance have been observed with older ARVs, including ZDV and LPV/r.⁵² Several studies have demonstrated an increased risk of DM with INSTI use,^53-55 an association that may be mediated in part by weight gain.⁵⁶ An association between ART and DM has not been consistently observed with other contemporary ARVs, including those recommended as initial therapy in the guidelines.

Antiretroviral Therapy and Other Cardiac Complications

EFV, as well as higher than recommended doses of fostemsavir and rilpivirine, have been associated with QTc (QT corrected for heart rate) prolongation.^57-59 These ARV drugs should be used with caution in people with pre-existing heart disease, QTc prolongation, or concomitant use of medications that may increase drug concentration or prolong the QTc interval. Both ATV/r and LPV/r have been associated with PR prolongation, particularly among people with risk factors, including pre-existing heart disease and concomitant use of medications that may cause PR prolongation.^60,61

Strategies for Atherosclerotic Cardiovascular Disease Risk Estimation and Screening For People With HIV

Cardiovascular risk assessment and prevention strategies developed for the general population do not reflect HIV-specific factors, such as inflammation and immune activation or potential contributions from certain ARV drugs, which are key mechanistic contributors to HIV-associated CVD. This section will address ASCVD risk estimation and lipid screening for people with HIV. ASCVD prevention strategies specific to people with HIV are further discussed in the Introduction and Statin Therapy in People With HIV sections.

Lipid Monitoring

Lipid screening should be performed in people with HIV (AIII), given the increased risk for ASCVD and the increased rate of dyslipidemia associated with certain ARV drugs. A fasting or random lipid profile should be obtained for all people with HIV at entry into care or at the time of ART initiation or modification. If a random profile is abnormal, a fasting lipid profile should be obtained. Lipid levels should be rechecked 3 to 6 months after starting ART or later if viral suppression is not achieved within 6 months. Lipid levels measured after initiation of ART should then be used to calculate an ASCVD risk score and determine indications for statin therapy (see Statin Therapy in People With HIV). Among people with HIV who are aged 40 years or older or who are any age and are receiving statin therapy, lipid monitoring should be performed annually to reassess ASCVD risk and inform decisions on statin management and/or other risk modification strategies. Further, specific to people on statin therapy, the approach to monitor lipids at least annually to assess adherence and the need for treatment intensification is consistent with recommendations by the 2018 American Heart Association (AHA)/American College of Cardiology (ACC)/Multisociety Guideline on the Management of Blood Cholesterol among people in the general population.⁶² For people with HIV who are under age 40 and not receiving statin therapy, lipid levels should be monitored every 1 to 3 years to reassess ASCVD risk. For all people with HIV, lipid monitoring may occur more frequently based on lifestyle factors or clinical scenarios, including changes in traditional ASCVD risk factors (e.g., weight gain, new diagnosis of hypertension, concomitant medications that affect lipids, or change to an ARV regimen with increased ASCVD risk).

Atherosclerotic Cardiovascular Disease Risk Scores

ASCVD risk prediction algorithms enable clinicians to quantify the risk of a future cardiovascular event and are used in clinical practice to stratify risk and to guide the intensity of ASCVD preventative measures and risk factor management, including statin use and antihypertensive therapy. Yet established ASCVD risk prediction scores validated in the general population typically do not include risk factors specific to HIV, and they have been shown to systematically underestimate risk among people with HIV. Data from multiple studies and a meta-analysis have shown that the ACC/AHA Pooled Cohort Equations (PCE) underpredict ASCVD risk in people with HIV in high-income countries.^63-68 Studies also suggest the accuracy of established ASCVD risk scores for people with HIV may vary by patient demographics and clinical characteristics, with underprediction of ASCVD risk demonstrated among women,^63,66,67 Black or African-American individuals,^63,67 and individuals with low or moderate predicted CVD risk versus high risk.^63,65,66 ASCVD risk score accuracy may also differ by region globally, with a study of REPRIEVE data showing underprediction of risk in high-income countries yet overprediction in low-income and middle-income countries.⁶⁷ Additional research is needed to better tailor ASCVD risk scores to people with HIV overall, as well as by geographic region and demographic and clinical characteristics.

In 2023, the AHA developed a new set of ASCVD risk equations for the general population. The Predicting Risk of CVD EVENTs (PREVENT) equations differ from the PCE on several levels, including the inclusion of a new derivation dataset of more than 6 million individuals, new variables reflecting a broader cardiovascular-kidney-metabolic framework, a new outcome including heart failure, and the removal of race from the models.⁶⁹ Because PREVENT was developed for the general population, this updated risk score does not incorporate risk factors specific to HIV or its treatment. Predicted ASCVD risk has been shown to be lower using PREVENT in the general population.⁷⁰ For people with HIV,⁷¹ 97% had a lower predicted risk, and 58% fewer would be strongly recommended for statins using the PREVENT (vs. PCE) risk score. Further study is needed to determine if and how the PREVENT risk estimates may inform the clinical management of people with HIV.

The PCE is recommended for predicting ASCVD risk among people with HIV, as it has been more extensively studied in this population and used in the REPRIEVE trial to inform recommendations on the use of statins in people with HIV (see Statin Therapy in People With HIV). For people with HIV aged 40 to 75 years, the 10-year ASCVD risk score should be calculated using the PCE at least annually, including whenever lipids are measured or in certain clinical scenarios that may affect ASCVD risk (e.g., changes in traditional CVD risk factors, such as weight gain, new diagnosis of hypertension, concomitant medications that affect lipids, or change to an ARV regimen with increased ASCVD risk) (BIII). Presently, there is insufficient evidence to recommend strategies to account for the underprediction of ASCVD risk by the PCE and other established ASCVD risk scores among people with HIV, including use of inflammatory biomarkers.

Interactions Between Antiretroviral Drugs and Drugs for Treatment or Prevention of Cardiovascular Diseases

People with HIV may receive a statin to prevent ASCVD or medications for the treatment of CVD risk factors or underlying CVD. Some of these drugs may have clinically significant interactions with some ARV drugs. Before initiating or changing these medications, clinicians should carefully assess for potential interactions (AIII). Tables 24a to 24g and the Statin Therapy in People With HIV section of the guidelines, as well as the University of Liverpool HIV Drug Interaction site, provide guidance for managing these interactions. Major mechanisms of pharmacokinetic (PK) interaction between ARV drugs and cardiac drugs are noted in the sections below.

Cytochrome P450 Enzymes

Many cardiac drugs (such as certain antiarrhythmics, anticoagulants, beta-blockers, calcium channel blockers, statins, and others) are substrates of cytochrome P450 (CYP) enzymes and may interact with ARV drugs that are inhibitors or inducers of these enzymes. Concomitant use with:

• CYP inhibitors (such as the PK boosters ritonavir and cobicistat, and the capsid inhibitor lenacapavir) may—
  • Increase the systemic exposure and potentially toxicities of cardiac drugs that are CYP substrates
  • Decrease the efficacy of the antiplatelet drug clopidogrel (a prodrug) by inhibiting the formation of its active metabolite
• CYP inducers (such as EFV and etravirine) may—
  • Reduce concentrations and efficacy of the cardiac drugs that are CYP substrates

Drug Transporters

Interactions related to drug transporters may also play a role in drug disposition. For example, the INSTIs bictegravir, dolutegravir, and elvitegravir are inhibitors of organic cation transporter 2 (OCT2) and may reduce renal elimination of certain antiarrhythmics (such as dofetilide and disopyramide), thereby increasing concentrations of the cardiac drug and the risk for adverse events.

Because some interactions may result in serious toxicities or lack of efficacy, certain drug combinations are not recommended or are contraindicated. In these cases, clinicians should assess if alternative ARV drugs and/or alternative cardiac drugs can be used. In other cases, dosage modification and therapeutic drug monitoring of cardiac drugs may be needed to guide therapy, with close follow-up to assess efficacy and potential toxicity.

Management of Comorbidities and Traditional Cardiovascular Disease Risk Factors

Although HIV-specific factors influence CVD risk, traditional risk factors also play an important role among people with HIV. Although factors such as advancing age and other demographic characteristics cannot be changed, many CVD risk factors are modifiable with behavioral and pharmaceutical interventions. The AHA has outlined eight components of cardiovascular health for everyone: healthy diet; participation in physical activity; avoidance of nicotine; healthy sleep; healthy weight; and healthy levels of blood lipids, blood glucose, and blood pressure.⁷²

Traditional CVD risk factors predict incident CVD events and occur at higher rates among people with HIV compared with the general population.⁴ A 2025 global meta-analysis assessed common CVD risk factors among people with HIV and found higher odds of CVD incidence associated with DM, hypertension, dyslipidemia, smoking, and a prior history of CVD.⁷³ A U.S. population-based study among people with HIV found conventional risk factors, such as tobacco use, hypertension, and obesity, to be persistently associated with CVD incidence over follow-up periods for as long as 15 years.⁷⁴ Nontraditional risk factors for CVD that are not specific to HIV, including alcohol use disorders, depression, and hepatitis C virus coinfection, are also more common in people with HIV.

The aforementioned data highlight the importance of preventing and managing traditional risk factors among people with HIV. A longitudinal study comparing CVD risk factors among people with and without HIV found that associations between CVD and HIV status were attenuated when dyslipidemia and DM were well controlled.⁷⁵ Recommendations for screening and management of CVD risk factors are outlined in the HIVMA/IDSA 2024 update, Primary Care Guidance for Providers Who Care for Persons With Human Immunodeficiency Virus.⁷⁶ For women with HIV, ensuring optimal CVD risk factor modification regardless of CVD risk score and performing diagnostic evaluation for possible cardiac symptoms is critical given the greater relative risk of ASCVD.

Other Management Considerations and Unanswered Questions

Estrogen, Progestins, or Testosterone Therapy and Cardiovascular Risk

Studies have produced conflicting results on associations between estrogen, progestins, or testosterone therapy and CVD risk, varying by study design, study population, duration and timing of therapy, and other clinical factors.^77-80 Research on relationships between these drugs and CVD among people with HIV is even more limited.^81-84 Data on testosterone use among people with HIV have been limited to the treatment of testosterone deficiency and lack longitudinal information on CVD-related outcomes.^85,86 Studies of estrogen use suggest a potential increase in CVD risk; however, this association may vary by dose, mode of delivery, and underlying physiological stress.^79-‍81,87 A longitudinal study of combined estrogen and progestin use for oral contraception among people with HIV suggested increased CVD risk, though the association was not statistically significant.⁸⁸

As the population with HIV ages, a growing number of women with HIV are entering menopause. CVD is the leading cause of morbidity and mortality in menopausal women, and this risk is increased in women with HIV.^89,90 Studies of the cardiovascular risk associated with menopausal hormone therapy have led to changes in guidelines over the years.⁹⁰ Systemic hormone therapy is not currently recommended for CVD prevention or treatment.⁹¹ However, hormone therapy remains the most effective treatment for vasomotor symptoms.⁹² Some research suggests that women with HIV are undertreated for menopausal symptoms.⁹³ However, data are lacking on menopause and hormone therapy in women with HIV, including whether menopause amplifies the effects of HIV on CVD risk.⁹⁴ Current HIV primary care guidelines recommend that menopause-related hormone therapy for women with HIV should not differ from the care of women without HIV.⁷⁶

Cardiovascular Risks of Adults Who Acquired HIV Perinatally or During Adolescence

An increasing number of adults acquired HIV perinatally or during adolescence, but the cardiovascular effects of perinatal or adolescent HIV acquisition and long-term ART use are unclear. For individuals who acquired HIV perinatally, it is hypothesized that exposure to HIV and ART in utero while the cardiovascular system is developing, use of older ART drugs with cardiometabolic and mitochondrial toxicity, lifelong duration of infection, and a longer period of chronic inflammation may further exacerbate the already heightened CVD risk observed in people with HIV. Investigation of the cardiovascular complications of perinatal HIV infection has largely focused on youth and adolescents. Abnormalities in cardiac structure and function have been well documented and include systolic and diastolic dysfunction, left ventricular hypertrophy and dilatation, and myocardial fibrosis.^95-99 Studies of perinatally acquired HIV have also demonstrated elevated rates of surrogate markers of atherosclerosis (including carotid intima-media thickness, arterial stiffness, and endothelial dysfunction),^100,101 impaired glucose metabolism and insulin resistance,¹⁰² lipodystrophy and metabolic syndrome,¹⁰³ and increased Pathobiological Determinants of Atherosclerosis in Youth (or PDAY) cardiovascular risk scores.^104,105 Adults with perinatally acquired HIV also appear to be at risk for cardiometabolic comorbidities, with a large North American study of young adults aged 18 to 30 years demonstrating a high incidence of DM, hypercholesterolemia, hypertriglyceridemia, hypertension, and chronic kidney disease.¹⁰⁶ Current gaps in knowledge regarding CVD risk among those who acquired HIV perinatally or during adolescence include (1) the clinical significance of cardiac structural and functional abnormalities and surrogate markers of atherosclerosis with respect to coronary plaque and cardiac endpoints; (2) whether the epidemiology and pathophysiology of CVD differ for people with similar durations of perinatally versus horizontally acquired HIV, including HIV acquired during adolescence; (3) whether the epidemiology and pathophysiology of CVD differ for people in low- and middle-income versus high-income countries; (4) the optimal approach to estimate ASCVD risk and frequency of monitoring in adults who acquired HIV perinatally or during adolescence; and (5) whether primary prevention approaches (e.g., statins) for adults with HIV aged 40 and older apply to younger adults who acquired HIV perinatally or during adolescence.

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