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Cardiovascular Abnormalities in HIV-Infected Individuals
Additional content is available online at Elsevier eBooks for Practicing Clinicians
Approximately 37,900,000 people were living with human immunodeficiency virus (HIV) infection at the end of 2018, and 1,700,000 had become newly infected that year. An estimated 23,300,000 people living with HIV were accessing antiretroviral therapy (ART), up from 7,700,000 in 2010. The introduction of ART in 1996 and its increasingly widespread availability since then have dramatically reduced HIV-related mortality rates and has transformed HIV into a chronic disease for those receiving treatment. As a consequence, between 2010 and 2030 the proportion of people with HIV infection aged 50 years or older will increase from 28% to 73%, and the proportion with cardiovascular disease (CVD) from 19% to 78%. Over the same period the proportion taking a cardiovascular (CV) drug is projected to increase from 9% to 50%.
The types of CVD associated with HIV have changed from the pre-ART to the ART eras, ( Fig. 85.1 ) and will likely evolve further. In the pre-ART era, people with acquired immunodeficiency syndrome (AIDS) often had pericardial effusions and dilated cardiomyopathy; these complications still occur in persons without access to ART. Following the introduction of protease inhibitors (PIs) in the late 1990s, manifestations of atherosclerosis, specifically myocardial infarction (MI) and stroke, became prominent, and heart failure (HF), atrial fibrillation (AF), and sudden cardiac death have emerged.
Overview of changes in HIV treatment and HIV-associated cardiovascular diseases. The types of cardiovascular complications associated with HIV infection have changed in the pre-antiretroviral therapy (ART) and ART eras and are likely to continue evolving in the future as new medications and treatment approaches emerge. In the pre-ART era, dilated cardiomyopathy and pericardial effusions were the most commonly reported cardiovascular issues in patients living with HIV. After the introduction of protease inhibitors in the late 1990s, atherosclerotic complications including myocardial infarction were described. More recently, reports of heart failure and rhythm abnormalities are now emerging in the setting of HIV infection. In the future, among individuals with access to ART, HIV infection will be a chronic disease state with increased risk of coronary artery disease. CCR5, CC-chemokine receptor 5; NNRTI, non-nucleoside reverse-transcriptase inhibitor; NRTI, nucleoside reverse-transcriptase inhibitor.
Cardiovascular Risk Factors in People Living With Hiv
People living with HIV have elevated traditional coronary risk factors, particularly those receiving ART, compared with noninfected persons. Dyslipidemia, metabolic syndrome, hypertension, and cigarette smoking are all more prevalent among subjects with HIV, leading to higher calculated Framingham risk scores in this group than in noninfected individuals. In the North American AIDS Cohort Collaboration on Research and Design, smoking, hypercholesterolemia, and hypertension were calculated to account for 37%, 44%, and 42% of MIs, respectively. These risk factors also contributed to cancers and end-stage renal disease. Thus CV risk factors should merit aggressive treatment in people with HIV.
Dyslipidemia
The onset of HIV infection associates with a decrease in total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C), and an increase in triglyceride levels. The effect of ART on lipid levels varies among the classes of ART drugs and even varies among drugs within the same class. Two or three ART drugs are usually used in combination to block replication of the virus by more than one mechanism. As a consequence, the effect of single drugs can be difficult to ascertain. As a general rule, PIs, non-nucleoside reverse transcriptase inhibitors (NNRTIs), and nucleoside reverse transcriptase inhibitors (NRTIs) increase triglyceride levels and may increase LDL-C levels. The probability that each ART drug will adversely affect lipid levels is classified as low, intermediate, or high ( Table 85.1 ).
TABLE 85.1
Probability of Adverse Effects on Lipid Levels with HIV Drugs
| LIPID EFFECTS | PI | NRTI | NNRTI | INSTI | OTHER CLASSES |
|---|---|---|---|---|---|
| Low | Atazanavir | Tenofovir | Nevirapine | Raltegravir | Maraviroc |
| Atazanavir/Ritonavir | Abacavir | Etravirine | Elvitegravir | Enfuvirtide | |
| Lamivudine | Rilpivirine | Dolutegravir | Ibalizumab | ||
| Emtricitabine | Doravirine | Bictegravir | |||
| Intermediate | Saquinavir/Ritonavir | Zidovudine | Efavirenz | Cobicistat | |
| Darunavir/Ritonavir | Didanosine | ||||
| Fosamprenavir/Ritonavir | |||||
| High | Lopinavir/Ritonavir | Stavudine | |||
| Tipranavir/Ritonavir | |||||
| indinavir/ritonavir |
HIV, Human immunodeficiency virus; INSTI, integrase strand transfer inhibitors; NNRTI, non-nucleoside reverse transcriptase inhibitor; NRTI, nucleoside reverse transcriptase inhibitor; PI, protease inhibitor.
PIs increase triglyceride levels; in particular, ritonavir can cause extreme hypertriglyceridemia exceeding 1000 mg/dL. Ritonavir-saquinavir, ritonavir-lopinavir, and ritonavir-tipranavir combinations can also increase triglycerides. Atazanavir, either alone or in combination with ritonavir, associates less with an increase in triglycerides compared with these other PIs. Older PIs such as ritonavir also increase LDL-C, probably by increasing intestinal cholesterol absorption and not by increased synthesis. PIs have variable effects on HDL-C levels, which are often already low in persons with HIV due to smoking.
NNRTIs also increase LDL-C levels but do not depress HDL-C levels. Among NNRTIs, efavirenz associates with slightly more subjects developing hypercholesterolemia and hypertriglyceridemia in one study compared with nevirapine. Efavirenz can associate with greater increases in LDL-C but not total to HDL-C ratio compared with atazanavir-ritonavir. The newer NNRTI rilpivirine generally associates with lower total, HDL-C, LDL-C, and triglyceride levels than efavirenz. The NRTI tenofovir alafenamide, a newer formulation of tenofovir disoproxil fumarate (TDF), is associated with higher levels of LDL-C and HDL-C but similar total cholesterol to HDLC ratios compared with TDF.
The integrase strand transfer inhibitors (INSTIs), raltegravir, elvitegravir, and dolutegravir, and the C-C chemokine receptor type 5 coreceptor antagonist maraviroc have favorable effects on lipids, particularly compared with older forms of ART. Switching from a ritonavir-boosted PI regimen to darunavir/cobicistat can reduce triglyceride levels.
Most of the studies examining the effects of ART on lipid levels were of relatively short duration and were usually carried out in North American or European populations. However, ART is now initiated most often in people living in sub-Saharan Africa, where less data are available on the metabolic effects of treatment. In a recent meta-analysis of 14 trials of 21,023 individuals assessed between 2003 and 2014 from this region, ART associated with an increased risk of hypertriglyceridemia (RR 2.05, 95% CI, 1.51 to 2.77). No consistent associations were seen between ART and raised blood pressure, glucose, hemoglobin A 1c , and other lipids across these studies.
The use of newer ART with fewer adverse lipid consequences might lead to a reduction in CV risk among patients living with HIV. However, although not affecting lipids, integrase inhibitors cause weight gain, which may increase CV risk particularly after long-term use.
Lipodystrophy, the Metabolic Syndrome, and Obesity
Lipodystrophy is a syndrome characterized by fat accumulation in the dorsocervical region and an increase in or preservation of visceral fat, with subcutaneous and peripheral fat loss, resulting in relative central adiposity. Early PIs and the NRTIs stavudine and didanosine associated with lipodystrophy in at least 20% to 35% of persons taking these drugs long term, but newer PIs such as atazanavir do not appear to induce lipodystrophy.
Lipodystrophy in people with HIV commonly associates with features of the metabolic syndrome: insulin resistance, impaired glucose tolerance, hypertriglyceridemia, low HDL-C levels, and hypertension. The prevalence of the metabolic syndrome in subjects with HIV varies from 8.5% to 52% in published reports, with rates at the higher end of this range reported in Latin American countries and rates at the lower end in multicenter studies where patients had less exposure to ART. Development of the metabolic syndrome was common in the first 3 years after initiation of an ART regimen that included stavudine or lopinavir/ritonavir, but is less common with newer drugs. Most studies indicate that the metabolic syndrome predicts for CVD and death in persons with HIV.
A growing body of recent evidence suggests that INSTIs cause weight gain and an increased prevalence of obesity. In some circumstances, weight gain might not be viewed as harmful; for example, someone with advanced HIV beginning treatment, where weight gain would be part of a return-to-health phenomenon, or weight gain after switching from a regimen that caused anorexia or nausea and vomiting. In a pooled analysis of weight gain in eight randomized, controlled trials of 5680 treatment-naïve subjects with HIV, INSTI use associated with more weight gain than were PIs or NNRTIs, with dolutegravir and bictegravir associated with more weight gain than elvitegravir/cobicistat. Among NNRTIs, rilpivirine was linked to more weight gain than efavirenz. Among NRTIs, tenofovir alafenamide associated with more weight gain than TDF, abacavir, or zidovudine. Weight gain was more common in women, African Americans, and those with lower CD4 cell counts. The long-term implications of weight gain in the setting of integrase inhibitors and HIV on CVD have not been well studied at this time.
Diabetes
Whether HIV infection itself associates with an increased risk of diabetes or whether the increased risk relates only to specific ART drugs has been controversial. The PIs indinavir and lopinavir/ritonavir and the thymidine analogue stavudine can cause insulin resistance ; however, these drugs are no longer recommended for initial treatment of HIV owing to their toxicity. In a large cohort study from Denmark, the risk of diabetes among patients with HIV infection was nearly triple that of the general population in 1996–1999, but this excess was absent in 1999–2010. The difference in risk in the two periods is likely due to a decreased use of drugs with adverse metabolic consequences.
In a meta-analysis of 39 studies of CV risk factors in 13,698 people with HIV, the prevalence of diabetes was 7.24% but ranged from 0.5% to 39.1%. Diabetes is more prevalent in persons with HIV compared with controls in some studies; for example, in an HIV cohort in Malawi where subjects had received ART for more than 10 years, the prevalence of diabetes was higher than in controls at all ages studied, and at age 60 or older was 13.2% in persons with HIV compared with 1.7% in controls.
Among people with HIV, physical inactivity associates strongly with CV risk factors, including diabetes. In a study of 11,719 individuals with HIV, only 13% reported high levels of physical activity. Compared with this group, those reporting very low levels of physical activity were more likely to have elevated triglycerides, obesity, hypertension, and diabetes. Other factors may play a role in the development of diabetes, including chronic inflammation, poor control of HIV disease, hepatitis C co-infection, along with demographic factors such as older age and male gender.
Hypertension and Chronic Kidney Disease
The prevalence of hypertension among persons with HIV averaged 19.8%, ranging from 4.8% to 63.3%, in the recent, large meta-analysis, mentioned earlier, where the prevalence of diabetes was 7.24%. In studies comparing subjects living with HIV to uninfected controls, hypertension is not consistently higher in the HIV groups; however, both hypertension and prehypertension increase the risk of MI in the presence of HIV, just as in uninfected persons.
In a meta-analysis comprising 61 studies and more than 200,000 subjects with HIV, with balanced geographic distribution, the prevalence of chronic kidney disease (CKD) varied from 6.4% with the MDRD equation, 4.8% with CKD-EPI, and 12.3% with Cockcroft-Gault. CKD was more prevalent in Africa and less prevalent in Europe compared with other regions. CKD associated with hypertension and diabetes but not sex, hepatitis B or C co-infection, CD4 count, or ART status.
When CKD is defined as either albuminuria or a decreased glomerular filtration rate, it associates with an increased risk of CV events in people with HIV. Among 35,357 subjects with HIV in the D:A:D cohort, lower glomerular filtration rate associated strongly with a higher risk of CVD. The development of CKD in persons with previously normal renal function has been reported with some forms of ART; specifically, TDF and the PIs atazanavir/ritonavir and lopinavir/ritonavir.
Smoking
Smoking rates are two to three times higher in HIV cohorts compared with the general population, in the range of 40% to 70% in most studies, and with a high average number of pack-years. Vaping is also prevalent among people with HIV but has as yet received little attention in the literature. Among 3251 subjects from the Danish HIV Cohort Study and 13,004 controls from the Copenhagen General Population Study, the population-attributable fraction of current or past smoking for MI was 72% (95% CI 55% to 82%) for HIV-infected individuals and 24% (95% CI, 3% to 40%) for controls. If all current smokers stopped smoking, 42% (95% CI 21% to 57%) and 21% (95% CI 12% to 28%) of all MIs could potentially be avoided in the HIV and control populations.
In a previous study these investigators calculated that more life-years were lost from smoking than with HIV: 12.3 life-years (95% CI 8.1 to 16.4) compared with 5.1 life-years (95% CI 1.6 to 8.5). A 35-year-old living with HIV had a median life expectancy of 62.6 years if a smoker and 78.4 years if a non-smoker. These numbers illustrate the importance of stopping smoking in the context of HIV. Smoking cessation programs have the same modest success rates in people with HIV infection as in individuals without HIV. In a meta-analysis of eight trials including 1822 patients with HIV who were smokers, behavioral interventions increased abstinence rates by half. Intensive group therapy can double the rate of quitting, to 13% compared with 6.6% in controls in one study of subjects with HIV, but the difference had dissipated by 6 months. In another recent study of HIV subjects, the doubling of the quit rate persisted to 3 years, albeit at low levels, 10.3% versus 4.2% of controls.
Potential drug-drug interactions between ART and smoking cessation drugs have not been well studied. Reports of varenicline, bupropion, and nicotine-replacement therapy in people with HIV infection have generally been small, short, and uncontrolled but have shown similar safety and success rates to reports in individuals without HIV infection.
Smoking may contribute to worsening of HIV-related damage in the heart, kidney, and brain. Neurocognitive defects are common among older people living with HIV and are more prevalent and severe in smokers than in non-smokers. A quarter to half of persons living with HIV have deficits in multiple cognitive domains, including memory, verbal fluency, processing speed, and executive function, impairing their ability to accomplish many common tasks of daily living. Nicotine has antiinflammatory properties, and nicotine withdrawal may worsen neurocognitive defects. The presence of neurocognitive defects predicts failure of smoking cessation. Smoking thus impairs quality of life, as well as markedly shortening the duration of life in subjects with HIV. Smoking cessation reduces CV events in subjects living with HIV. The incidence of MI decreases within the first year and at 2 to 3 years was much reduced, although still double the rate of non-smokers with HIV. Thus, smoking cessation is a very desirable goal.
Mechanisms of Hiv-Related Atherogenesis
The pathogenesis of atherosclerosis in the setting of HIV infection is complicated and incompletely understood. Contributing mechanisms include the effects of the HIV proteins on immune and vascular cells, the immunodeficiency caused by the HIV infection, co-infection with cytomegalovirus (CMV), translocation of microbial products from the gut, chronic inflammation, and immune activation ( Fig. 85.2 ).
In individuals receiving ART with undetectable levels of the virus, the HIV infection is not cured and low-level transcription of HIV genes persists. HIV-encoded proteins such as transactivator of transcription (Tat) and negative factor (Nef) induce inflammation and endothelial dysfunction. In addition, the HIV envelope protein gp120 can stimulate endothelin-1 production.
CD4 + T cell depletion is the hallmark of HIV infection, and nadir CD4 + T cell count is a rough marker of the severity of immunodeficiency. Nadir CD4 + T cell count has been linked to increased carotid intima-media thickness (IMT), increased arterial stiffness, and incident MI. The CD4:CD8 ratio, a marker of immunosenescence, predicts CV events in some but not in other studies. Thus, markers of immune system damage and viral detectability relate to CV events in HIV. Immune abnormalities persist in individuals with HIV infection even after successful treatment with ART. The mechanisms linking immune system damage to atherosclerosis have not been elucidated. Although non–AIDS-related events, such as MI and stroke, are less common with complete viral suppression, such events still occur at rates higher than in an uninfected population.
Co-infection with CMV might play a part in HIV-associated atherosclerosis. Compared with uninfected individuals, subjects with HIV consistently have a higher proportion of CMV-specific CD8 + T cells, with the highest levels seen in those receiving long-term ART with HIV suppression. CMV co-infection links strongly to HIV viral persistence and may also have a role in chronic immune activation and inflammation by expansion of the HIV reservoir. These CMV-specific T cell responses also correlate with markers of atherosclerosis, such as coronary artery calcification (CAC) and carotid IMT. In the setting of HIV infection, high antibody titers to CMV, and to herpes simplex and varicella-zoster virus, associate with higher levels of biomarkers that accelerate inflammation and atherosclerosis.
Impairment of the gut barrier is an early feature of HIV infection, leading to microbial translocation, a process whereby microbial products leak through the intestinal barrier and cause immune activation. , Plasma levels of markers of microbial translocation such as soluble CD14 and lipopolysaccharide independently predict HIV disease progression and mortality in individuals not receiving ART. Whether these markers predict adverse outcomes in ART-treated individuals is unsettled; however, gut damage and microbial translocation persist even when HIV infection is suppressed by ART. Plasma levels of the inflammatory markers interleukin-6 (IL-6) and tumor necrosis factor may be higher in individuals with higher levels of markers of microbial translocation. Although microbial translocation is thus another mechanism that might contribute to HIV-associated atherogenesis, interventions targeting this mechanism, specifically sevelamer, rifaximin, probiotics, and mesalamine, have not consistently lowered inflammatory markers or T cell activation.
The three mechanisms discussed earlier, latent HIV infection, co-infection with other viruses, and microbial translocation, all stimulate atherogenesis by increasing inflammation. HIV infection associates with high plasma levels of inflammatory and coagulation markers, specifically C-reactive protein (CRP), IL-6, and D-dimer, and these biomarkers strongly predict CV events and all-cause mortality in individuals with HIV infection. Subjects with HIV infection have higher arterial and lymph node inflammation as assessed by FDG-PET and CT imaging than uninfected individuals, and this marker of increased inflammation correlates with higher circulating levels of CRP, IL-6, and activated monocytes.
Inflammation is a therapeutic target to reduce CV events in individuals with or without HIV infection (see Fig. 85.2 ). Statin therapy reduces inflammation, but the effects of statins on inflammatory markers seem to be attenuated in the presence of HIV infection. Neither intensification of ART nor changing PI-based regimens to integrase inhibitors consistently reduces inflammatory markers. Short studies of aspirin treatment also had no effect on inflammatory markers in HIV infection. Taken together, these findings suggest that strategies beyond ART and treatment of traditional CV risk factors are needed to reduce inflammation with the aim of lowering the risk of atherosclerosis in the setting of HIV infection.
Canakinumab, a monoclonal antibody targeting IL-1β, reduces CV events in patients with previous MI and a high-sensitivity CRP level of ≥2 mg/L. In an on-treatment analysis, canakinumab-treated subjects who had a CRP reduction to <2 mg/L had significant reductions in CV endpoints, whereas no significant reduction in these outcomes was observed in patients who did not achieve a CRP reduction to this level. Similar success was reported for individuals who achieved on-treatment IL-6 levels less than the study median value but not for those who did not.
Would canakinumab reduce CV events in the setting of HIV? In a small study of subjects with HIV infection, canakinumab significantly reduced plasma IL-6 and CRP levels, with no effect on CD4, CD8, or RNA viral levels. Inflammation in the bone marrow and arterial inflammation fell after canakinumab administration. By contrast, in the general population with stable atherosclerosis, methotrexate did not reduce inflammatory markers or improve clinical outcomes. In a clinical trial in treated HIV, methotrexate lowered CD8 T cells and did not impact inflammation or endothelial function. These small preliminary studies with inflammatory biomarkers as surrogate endpoints will hopefully lead to larger clinical trials of antiinflammatory therapies with CV endpoints in the population living with HIV.
Markers of inflammation and coagulation predict CV and other adverse events in individuals with HIV infection ( Table 85.2 ). , The strong relationship between these markers and outcomes appears consistently across diverse HIV-infected populations including men, women, and different age groups. In combined data from three large cohorts of individuals with HIV infection, a 25% decrease in IL-6 or D-dimer levels in plasma associated independently with a 37% reduction in non-AIDS events or mortality.
TABLE 85.2
Biomarkers of Inflammation and Coagulation Are Associated with Adverse Events in HIV Infection
| STUDY (YEAR) | STUDY POPULATION | NUMBER OF PATIENTS | FOLLOW-UP | FINDINGS |
| SMART (2008) | Subjects with well-controlled HIV from 33 countries | 5472 | 3700 person-years | IL-6 and D-dimer levels in plasma were strongly associated with all-cause mortality IL-6, CRP, and D-dimer levels in plasma were associated with increased risk of CVD |
| FRAM (2010) | Subjects with HIV | 922 | 5 years | Fibrinogen and CRP levels were strong and independent predictors of mortality |
| ALLRT (2014) | Subjects with HIV and virologic suppression <1 yr after ART initiation |
143 | 48–64 weeks after ART initiation | High IL-6, sTNFRI, sTNFRII, and D-dimer plasma levels and KT ratio at 1 year were associated with increased risk of non-AIDS events |
| VACS (2016) | Subjects with HIV and uninfected controls | 2350 | 6.9 years | HIV infection was associated with elevated IL-6, sCD14, and D-dimer levels in plasma, which are associated with mortality |
| MACS (2016) | Subjects with well-controlled HIV | 670 | Up to 18 years | IL-6 and sCD14 levels in plasma were predictive of mortality |
| START (2017) | Subjects with HIV from 35 countries | 4299 | 3.2 years | Baseline IL-6 and D-dimer levels in plasma were associated with the risk of AIDS, serious non-AIDS events or death |
ART, Antiretroviral therapy; CRP, C-reactive protein; CVD, cardiovascular disease; HIV, human immunodeficiency virus; IL-6, interleukin-6; KT, kynurenine:tryptophan; sCD14, soluble CD14; sTNFRI, soluble tumor necrosis factor receptor type I; sTNFRII, soluble tumor necrosis factor receptor type II.
Biomarkers in HIV infection tend to group into clusters, with each cluster related to a cardiac phenotype. The inflammatory phenotype is characterized by higher levels of CRP, IL-6, and D-dimer, whereas the cardiac cluster comprises higher levels of protein ST2 (also known as IL-1 receptor-like 1), N-terminal pro-B-type natriuretic peptide and growth/differentiation factor 15. Diastolic dysfunction is common with the inflammatory cluster of biomarkers, and pulmonary hypertension (PH) is more common in the cardiac cluster. Both groups associate with a threefold increase in mortality over a 6.9-year follow-up after adjustment for other prognostic variables. These biomarker clusters in patients with HIV might be helpful for selecting patients for appropriate therapy to prevent CV events.
The most obvious mechanism by which ART increases atherosclerosis is by worsening blood lipid levels. Interestingly, even after adjustment for blood lipid levels in the large D:A:D study, cumulative exposure to the NRTIs abacavir or didanosine or to the PIs lopinavir-ritonavir or indinavir associated with an increased risk of MI.
ART might also increase the risk of CV events through other mechanisms. Insulin resistance, lipodystrophy, and other patterns of fat distribution can contribute to atherogenesis. The NRTI abacavir has been linked to an increased risk of MI in some but not all studies. This increased risk has been attributed to increased platelet reactivity and to endothelial dysfunction. In the D:A:D study, a difference in the risk of MI was noted between two widely used PIs, with atazanavir being associated with a lower risk than darunavir. This reduced risk of MI may result from a protective effect of atazanavir because it increases bilirubin levels and elevated bilirubin levels independently predict lower incident CVD in HIV. Overall, although current ART regimens appear to confer a much lower risk of CV events than older ART, longer-term data on newer regimens will be needed to ascertain this benefit.
Features of Atherosclerosis in People with HIV
Cardiac computed tomography (CCT) provides insight into the features of coronary disease in HIV patients. The prevalence of CAC by CCT was not higher in HIV-infected individuals compared with controls across seven studies. However, CT angiographic studies reveal that noncalcified plaques are much more common in persons living with HIV than in uninfected controls. In a meta-analysis of nine studies including 1229 HIV patients and 1029 controls, the prevalence of coronary stenosis greater than 30% or greater than 50%, or calcified plaques did not differ between HIV patients and controls. However, noncalcified plaques were more than three times more likely to be present in HIV patients, 58% compared with 17%. Noncalcified plaques are more likely to be lipid-laden and inflammatory and exhibit imaging features associated with plaque rupture. HIV subjects with higher levels of arterial inflammation as assessed by FDG-PET imaging were more likely than those with lower levels of inflammation to have plaques with high-risk features.
In non-HIV cohorts, carotid IMT associates with prevalent CVD and risk factors as well as increased risk of future stroke and MI. Many observational studies have compared carotid IMT in individuals with HIV and in controls. Across these studies, carotid IMT averaged 0.04 mm thicker (95% CI 0.02 to 0.06 mm, p < 0.001) in subjects with HIV than in uninfected controls. This conclusion should be viewed with caution due to differences among the studies in population characteristics, study designs, sample sizes, and ultrasound techniques. In some studies with serial measurements, carotid IMT progressed more rapidly in the HIV group than in controls. Carotid plaque also occurs more commonly in HIV patients compared with uninfected controls across six studies. Carotid IMT independently predicts mortality in HIV.
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