HIV Cardiovascular Disease Research Articles

Inflammatory and Immune Mechanisms for Atherosclerotic Cardiovascular Disease in HIV.

Atherosclerotic vascular disease disproportionately affects persons living with HIV (PLWH) compared to those without. The reasons for the excess risk include dysregulated immune response and inflammation related to HIV infection itself, comorbid conditions, and co-infections. Here, we review an updated understanding of immune and inflammatory pathways underlying atherosclerosis in PLWH, including effects of viral products, soluble mediators and chemokines, innate and adaptive immune cells, and important co-infections. We also present potential therapeutic targets which may reduce cardiovascular risk in PLWH.

Unveiling Subclinical Cardiovascular Disease in HIV with Advanced Cardiovascular Imaging.

Unveiling Subclinical Cardiovascular Disease in HIV with Advanced Cardiovascular Imaging.

Abstract 15748: Association of Clonal Hematopoiesis in the Setting of Human Immunodeficiency Virus Infection With Subclinical Atherosclerosis and Vascular Inflammation

Background: Clonal hematopoiesis of indeterminate potential (CHIP) is associated with cardiovascular disease (CVD) and common in HIV, but whether CHIP contributes to atherosclerosis in HIV is unknown. We hypothesized CHIP is associated with atherosclerosis and arterial inflammation among people with HIV (PWH). Methods: We studied treated, suppressed PWH ages 35-70 years old with ≥1 CVD risk factor. CHIP mutations were detected with a validated targeted sequencing assay. We measured carotid intima-media thickness (IMT) longitudinally with ultrasound and aortic inflammation and lymph node activity using cross-sectional 18 F-FDG-PET. Inflammatory biomarkers were measured with a multiplex electrochemiluminescence assay. We used linear regression with adjustment for age, sex, nadir CD4 count, smoking, hypertension, diabetes, and hyperlipidemia. Results: We included 231 PWH (52±9 years, 7% female). 32 (14%) had CHIP with median variant allele fraction of 3.1%. Common mutations were in DNM3TA (n=21) and TET2 (n=6). Only age was associated with CHIP (OR 2.3 per decade older, 95%CI 1.2-3.9; p=0.003). Among N=165 (CHIP=22), mean IMT was 1.0 mm with and without CHIP (p=0.63), unchanged after adjustment (Figure). CHIP was not associated with prevalent or incident plaque. Over 3.2 years, IMT progression was faster among those with CHIP (0.033 mm/year; p=0.10), attenuated after adjustment (0.022 mm/year; p=0.27). Among 80 with FDG-PET, CHIP (n=12) was associated with higher lymph node activity (SUV p=0.04) that was attenuated in reference to background activity and adjusted for risk factors. CHIP was not associated with arterial inflammation (p=0.83), inflammatory markers, or viral persistence markers. Conclusions: Among PWH, CHIP mutations were not associated with subclinical atherosclerosis or arterial inflammation, proposed mechanisms of how CHIP could cause CVD. Clinical outcomes studies are needed to ascertain the impact of CHIP on CVD in HIV.

Impaired Endothelial Function and Enhanced Contractility of Microarterioles from Persons Living with Human Immunodeficiency Virus (HIV+) is Mediated by Inflamed Perivascular Adipose Tissue

This research investigates the mechanisms that contribute to the enhanced cardiovascular disease (CVD) in HIV+ persons. It tests the hypothesis that perivascular adipose tissue (PVAT) mediates the microvascular dysfunction. Subcutaneous microarterioles were dissected from gluteal skin biopsies from 11 HIV+ and 10 matched control women aged < 50 years who were free of CVD risk factors (except increased BMI). Arterioles were mounted on isometric myographs with or without PVAT. Nitric oxide (NO) and reactive oxygen species (ROS) were measured by fluorescence microscopy. PVAT significantly (P < 0.05) enhanced endothelium‐ dependent relaxation (EDR) and NO with acetylcholine and moderated contractions with thromboxane and endothelin 1 (ET1). But these effects of PVAT were significantly (P < 0.05) diminished in HIV+ vs control subjects. Although microarterioles from HIV+ had enhanced ROS with ET1. ROS was not affected by PVAT. Incubated PVAT from HIV+ persons released significantly (P < 0.05) more leptin (47 +/‐ 8 vs 22 +/‐ 3 ng · mg‐1) and less adiponectin (3.0 +/‐ 0.4 vs 4.6 +/‐ 0.5 µg · mg‐1) but more 8‐isoprostane F2α (2.5 +/‐ 0.4 vs 1.3 +/‐ 0.3 µmol · mg‐1) and inflammatory cytokines such as TNFα (11 +/‐ 1 vs 5 +/‐ 1 pg · mg‐1).ConclusionPVAT from young HIV+ women has enhanced oxidative stress and inflammation and impaired ability to enhance microarteriolar NO and moderated contractility. Thus, PVAT and adipokines should be novel foci for therapy to reduce CVD in HIV+ persons.

Coronary Vasculature and Myocardial Structure in HIV: Physiologic Insights From the Renin-Angiotensin-Aldosterone System.

The landscape of HIV medicine dramatically changed with the advent of contemporary antiretroviral therapies, which has allowed persons with HIV (PWH) to achieve good virologic control, essentially eliminating HIV-related complications and increasing life expectancy. As PWH are living longer, noncommunicable diseases, such as cardiovascular disease (CVD), have become a leading cause of morbidity and mortality in PWH with rates that are 50% to 100% higher than in well-matched persons without HIV. In this review, we focus on disease of the coronary microvasculature and myocardium in HIV. We highlight a key hormonal system important to cardiovascular endocrinology, the renin-angiotensin-aldosterone system (RAAS), as a potential mediator of inflammatory driven-vascular and myocardial injury and consider RAAS blockade as a physiologically targeted strategy to reduce CVD in HIV.

Apolipoprotein A-I mimetics attenuate macrophage activation in chronic treated HIV.

Despite antiretroviral therapy (ART), there is an unmet need for therapies to mitigate immune activation in HIV infection. The goal of this study is to determine whether the apoA-I mimetics 6F and 4F attenuate macrophage activation in chronic HIV. Preclinical assessment of the in-vivo impact of Tg6F and the ex-vivo impact of apoA-I mimetics on biomarkers of immune activation and gut barrier dysfunction in treated HIV. We used two humanized murine models of HIV infection to determine the impact of oral Tg6F with ART (HIV+ART+Tg6F+) on innate immune activation (plasma human sCD14, sCD163) and gut barrier dysfunction [murine I-FABP, endotoxin (LPS), LPS-binding protein (LBP), murine sCD14]. We also used gut explants from 10 uninfected and 10 HIV-infected men on potent ART and no morbidity, to determine the impact of ex-vivo treatment with 4F for 72 h on secretion of sCD14, sCD163, and I-FABP from gut explants. When compared with mice treated with ART alone (HIV+ART+), HIV+ART+Tg6F+ mice attenuated macrophage activation (h-sCD14, h-sCD163), gut barrier dysfunction (m-IFABP, LPS, LBP, and m-sCD14), plasma and gut tissue oxidized lipoproteins. The results were consistent with independent mouse models and ART regimens. Both 4F and 6F attenuated shedding of I-FABP and sCD14 from gut explants from HIV-infected and uninfected participants. Given that gut barrier dysfunction and macrophage activation are contributors to comorbidities like cardiovascular disease in HIV, apoA-I mimetics should be tested as therapy for morbidity in chronic treated HIV.

SUBCLINICAL CORONARY ATHEROSCLEROSIS AMONG INDIVIDUALS WITH HIV ON ANTIRETROVIRAL THERAPY - PRELIMINARY RESULTS FROM THE CANADIAN HIV AND AGING COHORT STUDY (CHACS)

The Canadian HIV and Aging Cohort Study (CHACS) is a large, controlled, prospective cohort recruiting participants living with HIV, and participants unexposed to HIV. The CHACS focus on identifying the prevalence, type and determinants of premature cardiovascular disease in HIV+ individuals. The objective of the present cardiovascular imaging substudy nested in the CHACS is to compare subclinical coronary plaque burden and characteristics between HIV+ and HIV- individuals and to evaluate the association of coronary plaque with HIV-related factors. This cross-sectional study was approved by our ethics committee. Participants provided written consent. Consecutive HIV+ and HIV- participants were prospectively recruited for cardiac computed tomography (CT). Eligibility criteria were absence of known coronary artery disease and low/intermediate 10-yr Framingham risk score (FRS, 5-20%). CT was used for calcium scoring and plaque assessment. Assessors were blinded to HIV status. Multivariate regression models were used. A total of 265 participants (181 HIV+ (92% males), 84 HIV- (77 % males)) were included (mean 56 yo), with similar FRS. Smoking (p < 0.001) and dyslipidemias (p ≤ 0.02) were increased in HIV+ participants. All HIV+ participants were on antiretroviral therapy. After adjusting for cardiovascular risk factors, burden of calcium and overall plaque was similar between HIV+ and HIV- participants. However, HIV+ participants had an increased volume (25 and 5 mm3/participant, p=0.03) of noncalcified plaques compared to HIV- participants. Prevalence and volume of calcified (p= 0.12 and 0.29) and mixed (p= 0.18 and 0.17) plaques, as well as ≥ 70% stenosis (p=0.99) were similar between HIV+ and HIV- participants. In HIV participants, total plaque volume, noncalcified plaque volume and mixed plaque volume (p=0.01, 0.03 and 0.006) increased with the use of protease inhibitors; noncalcified plaque volume (p=0.02) increased with the use of nucleoside reverse transcriptase inhibitors. To our knowledge, this is the largest Canadian imaging study of HIV-associated coronary atherosclerosis. In line with previous studies, our results confirm that asymptomatic HIV+ individuals under antiretroviral therapy have increased noncalcified plaque in comparison to HIV- individuals, after adjustment for cardiovascular risk factors. Noncalcified plaques are usually considered vulnerable and this finding could suggest one anatomic substrate for the known increased risk of myocardial infarction in the HIV population. Additionally, our data are intended as a basis for novel correlative analyses (e.g. carotid wall biomechanics, advanced immunological factors, frailty) planned with other teams of the CHACS.

Insomnia as an Independent Predictor of Incident Cardiovascular Disease in HIV: Data From the Veterans Aging Cohort Study.

Insomnia is associated with increased cardiovascular disease (CVD) risk in the general population and is highly prevalent in people with HIV. The CVD risk conferred by insomnia in the HIV population is unknown. Using the Veterans Aging Cohort Study Survey Cohort, insomnia symptoms were measured and dummy coded with the item, "Difficulty falling or staying asleep?" (5-point scale from no difficulty to bothers a lot). Incident CVD event ICD-9 codes (acute myocardial infarction, stroke, or coronary artery revascularization) were identified with the Department of Veterans Affairs (VA) and Medicare administrative data and VA fee-for-service data. Those with baseline CVD were excluded. HIV-infected (N = 3108) veterans had a median follow-up time of 10.8 years, during which 267 CVD events occurred. Compared to HIV-infected veterans with no difficulty falling or staying asleep, HIV-infected veterans bothered a lot by insomnia symptoms had an increased risk of incident CVD after adjusting for demographics [hazard ratio (HR) = 1.64, 95% confidence interval (CI): 1.16 to 2.31, P = 0.005], CVD risk factors (HR = 1.62, 95% CI: 1.14 to 2.30, P = 0.007), additional potential confounders (hepatitis C infection, renal disease, anemia, alcohol use, and cocaine use; HR = 1.70, 95% CI: 1.19 to 2.43, P = 0.003), and HIV-specific factors (HIV-1 RNA, CD4 T-cell count, and antiretroviral therapy; HR = 1.66, 95% CI: 1.16 to 2.37, P = 0.005). Additional adjustment for nonbenzodiazepine sleep medication (HR = 1.62, 95% CI: 1.13 to 2.32, P = 0.009) did not attenuate the association; however, it fell short of significance at P < 0.01 after adjustment for depressive symptoms (HR = 1.51, 95% CI: 0.98 to 2.32, P = 0.060) or antidepressant medication (HR = 1.51, 95% CI: 1.04 to 2.19, P = 0.031). Highly bothersome insomnia symptoms were significantly associated with incident CVD in HIV-infected veterans, suggesting that insomnia may be a novel, modifiable risk factor for CVD in HIV.

Mild renal impairment is associated with calcified plaque parameters assessed by computed tomography angiography in people living with HIV.

To investigate the association of mild renal impairment and coronary plaque in people living with HIV (PLHIV). PLHIV and non-HIV controls with serum creatinine less than 1.5 mg/dl were investigated. Estimated glomerular filtration rate (eGFR) (calculated by CKD-EPI formula) was related to coronary plaque indices obtained by CT angiography. One hundred and eighty-four PLHIV [HIV viral load, 49 (47,49) copies/ml, CD4+ cell count, median 536 (370, 770) cells/μl, duration HIV, 15 ± 7 years] and 72 HIV-negative controls without known cardiovascular disease (CVD) were studied. The two groups were well matched for traditional CVD risk factors. Serum creatinine (0.9 ± 0.2 vs. 0.9 ± 0.2 mg/dl, P = 0.96) and eGFR (96 ± 22 vs. 96 ± 24 ml/min per 1.73 m(2), P = 0.99) were similar between PLHIV and non-HIV, respectively. In PLHIV, eGFR inversely related to total severity of coronary plaque score (r = -0.27, P = 0.002), total coronary segments with plaque (r = -0.21, P = 0.005), calcified plaque segments (r = -0.15, P = 0.045), and Agatston score (r = -0.21, P = 0.006). Adjusting for total Framingham point score, BMI, and HIV parameters, eGFR remained significantly associated with calcified plaque and Agatston score in PLHIV. In HIV negative controls, eGFR did not correlate with calcified plaque (r = -0.20, P = 0.10) or Agatston score (r = -0.13, P = 0.29). Among PLHIV, those with eGFR less than 90 ml/min per 1.73 m(2) demonstrated increased total severity of coronary plaque score compared with those with eGFR greater than or equal to 90, P = 0.02). This relationship was stronger in PLHIV than the non-HIV group. Our data highlight a robust relationship between subclinical renal impairment and coronary artery disease among PLHIV. Further research is needed to understand the relationship between mild renal impairment and CVD in HIV.

Macrophage Inflammation and Cardiovascular Disease in HIV: Mechanistic Insights and Future Directions

Macrophage Inflammation and Cardiovascular Disease in HIV: Mechanistic Insights and Future Directions

Role of T-Cell Dysfunction, Inflammation, and Coagulation in Microvascular Disease in HIV.

BackgroundCompared to uninfected adults, HIV‐infected adults on antiretroviral therapy are at increased risk of cardiovascular disease. Given the increase in T‐cell dysfunction, inflammation, and coagulation in HIV infection, microvascular dysfunction is thought to contribute to this excess cardiovascular risk. However, the relationships between these variables remain undefined.Methods and ResultsThis was a cross‐sectional study of 358 HIV‐infected adults from the SCOPE cohort. Macrovascular endothelial function was assessed using flow‐mediated dilation of the brachial artery and microvascular function by reactive hyperemia. T‐cell phenotype was determined by flow cytometry. Plasma markers of inflammation (tumor necrosis factor‐α, interleukin‐6, high‐sensitivity C‐reactive protein, sCD14) and coagulation (fibrinogen, D‐dimer) were also measured. In all HIV+ subjects, markers of inflammation (tumor necrosis factor‐α, high‐sensitivity C‐reactive protein), coagulation (D‐dimer) and T‐cell activation (CD8+PD1+, CD4+interferon+cytomegalovirus‐specific) were associated with worse reactive hyperemia after adjusting for traditional cardiovascular risk factors and co‐infections. In treated and suppressed subjects, tumor necrosis factor‐α and CD8+PD1+ cells remained associated with worse reactive hyperemia after adjustment. Compared to the untreated subjects, CD8+PD1+ cells were increased in the virally suppressed group. Reactive hyperemia was predictive of flow‐mediated dilation.Conclusions CD8+PD1+ cells and tumor necrosis factor‐α were associated with microvascular dysfunction in all HIV+ subjects and the treated and suppressed group. Additionally, D‐dimer, high‐sensitivity C‐reactive protein, sCD‐14, and interleukin‐6 were associated with microvascular dysfunction in all HIV+ subjects. Although T‐cell dysfunction, inflammation, and microvascular dysfunction are thought to play a role in cardiovascular disease in HIV, this study is the first to look at which T‐cell and inflammatory markers are associated with microvascular dysfunction in HIV‐infected individuals.

Inflammation, immune activation, and cardiovascular disease in HIV.

Cardiovascular disease is one of the leading causes of morbidity and mortality in people living with HIV. Several epidemiological studies have shown an increased risk of myocardial infarction and stroke compared to uninfected controls. Although traditional risk factors contribute to this increased risk of cardiovascular disease, HIV-specific mechanisms likely also play a role. Systemic inflammation has been linked to cardiovascular disease in several populations suffering from chronic inflammation, including people living with HIV. Although antiretroviral therapy reduces immune activation, levels of inflammatory markers remain elevated compared to uninfected controls. The causes of this sustained immune response are likely multifactorial and incompletely understood. In this review, we summarize the evidence describing the relationship between inflammation and cardiovascular disease and discuss potential anti-inflammatory treatment options for cardiometabolic disease in people living with HIV.

HIV-Derived ssRNA Binds to TLR8 to Induce Inflammation-Driven Macrophage Foam Cell Formation

Even though combined anti-retroviral therapy (cART) dramatically improves patient survival, they remain at a higher risk of being afflicted with non-infectious complications such as cardiovascular disease (CVD). This increased risk is linked to persistent inflammation and chronic immune activation. In this study, we assessed whether this complication is related to HIV-derived ssRNAs inducing in macrophages increases in TNFα release through TLR8 activation leading to foam cell formation. HIV ssRNAs induced foam cell formation in monocyte-derived macrophages (MDMs) in a dose-dependent manner. This response was reduced when either endocytosis or endosomal acidification was inhibited by dynasore or chloroquine, respectively. Using a flow cytometry FRET assay, we demonstrated that ssRNAs bind to TLR8 in HEK cells. In MDMs, ssRNAs triggered a TLR8-mediated inflammatory response that ultimately lead to foam cell formation. Targeted silencing of the TLR8 and MYD88 genes reduced foam cell formation. Furthermore, foam cell formation induced by these ssRNAs was blocked by an anti-TNFα neutralizing antibody. Taken together in MDMs, HIV ssRNAs are internalized; bind TLR8 in the endosome followed by endosomal acidification. TLR8 signaling then triggers TNFα release and ultimately leads to foam cell formation. As this response was inhibited by a blocking anti-TNFα antibody, drug targeting HIV ssRNA-driven TLR8 activation may serve as a potential therapeutic target to reduce chronic immune activation and inflammation leading to CVD in HIV+ patients.

Epicardial fat is associated with duration of antiretroviral therapy and coronary atherosclerosis.

Cytokines released by epicardial fat are implicated in the pathogenesis of atherosclerosis. HIV infection and antiretroviral therapy have been associated with changes in body fat distribution and coronary artery disease. We sought to determine whether HIV infection is associated with greater epicardial fat and whether epicardial fat is associated with subclinical coronary atherosclerosis. We studied 579 HIV-infected and 353 HIV-uninfected men aged 40-70 years with noncontrast computed tomography to measure epicardial adipose tissue (EAT) volume and coronary artery calcium (CAC). Total plaque score (TPS) and plaque subtypes (noncalcified, calcified, and mixed) were measured by coronary computed tomography angiography in 706 men. We evaluated the association between EAT and HIV serostatus, and the association of EAT with subclinical atherosclerosis, adjusting for age, race, and serostatus and with additional cardiovascular risk factors and tested for modifying effects of HIV serostatus. HIV-infected men had greater EAT than HIV-uninfected men (P=0.001). EAT was positively associated with duration of antiretroviral therapy (P=0.02), specifically azidothymidine (P<0.05). EAT was associated with presence of any coronary artery plaque (P=0.006) and noncalcified plaque (P=0.001), adjusting for age, race, serostatus, and cardiovascular risk factors. Among men with CAC, EAT was associated with CAC extent (P=0.006). HIV serostatus did not modify associations between EAT and either CAC extent or presence of plaque. Greater epicardial fat volume in HIV-infected men and its association with coronary plaque and antiretroviral therapy duration suggest potential mechanisms that might lead to increased risk for cardiovascular disease in HIV.

Reduced IgM levels and elevated IgG levels against oxidized low-density lipoproteins in HIV-1 infection.

BackgroundChronic HIV infection is associated with increased risk of cardiovascular disease caused by atherosclerosis. Oxidized forms of low-density lipoprotein (LDL) are present in atherosclerotic lesions and constitute major epitopes for natural antibodies. IgM has been shown to be protective against atherosclerosis, whereas the role of corresponding IgG is less clear. The objective of this study was to determine if HIV + individuals have disturbed levels of IgM and IgG directed against oxidized forms of LDL as compared to HIV- individuals.MethodsNinety-one HIV + patients and 92 HIV- controls were included in this retrospective study. Circulating levels of IgG and IgM directed against two forms of oxidized LDL; copper oxidized (OxLDL) and malondialdehyde modified (MDA-LDL), total IgM and IgG, C-reactive protein (CRP), soluble CD14, and apolipoproteins A1 and B were determined.ResultsHIV + individuals had slightly lower levels of IgM against MDA-LDL and higher levels of IgG against MDA-LDL, OxLDL, and total IgG, than HIV- controls. Anti-MDA-LDL and Anti-OxLDL IgG displayed a positive correlation with viral load and a negative correlation with the CD4+ T-cell count. HIV + individuals also displayed elevated CRP and soluble CD14 levels compared to HIV- individuals, but there were no correlations between CRP or soluble CD14 and specific antibodies.ConclusionsHIV infection is associated with higher levels of IgG including specific IgG against oxidized forms of LDL, and lower IgM against the same epitope. In addition to dyslipidemia, immune activation, HIV-replication and an accumulation of risk factors for atherosclerosis, this adverse antibody profile may be of major importance for the increased risk of cardiovascular disease in HIV + individuals.

Protecting the heart after HAART; understanding the pathogenesis of cardiovascular disease in people living with HIV

Advances in themanagement of HIV and antiretroviral therapy (ART) have led to substantial improvements in diseasefree survival for patients with HIV. Life-expectancy is approaching that of the general population. Yet these gains have been tempered by increasing rates of non-AIDS-related co-morbidities. In fact the major burden of illness, health careutilisation andpremature death inHIVpositive patients is now due to diseases of ageing. Cardiovascular disease (CVD) occurs at two times the rate in the general population and is a cause of significant morbidity and mortality. Lifestyle factors such as cigarette smoking and underlying genetics are clearly important. Yet in HIV patients CVD is also promoted by complex interactions between HIV and ART driven coagulation, dyslipidaemia, inflammation and immune dysfunction. Understanding the pathogenesis of CVD in HIV will be of increasing importance as the HIV population ages. This will enable targeted prevention strategies andpersonalisedantiretroviral regimens tobeutilised. Some of the recent advances in the field are discussed in this review.

Risk of cardiovascular disease in HIV, hepatitis C, or HIV/hepatitis C patients compared to the general population

As a result of effective antiretroviral therapy HIV patients are living longer, and their risk of cardiovascular disease (CVD) is a growing concern. It remains unknown whether coinfection with hepatitis C (HCV) changes an HIV person's CVD risk, and how the risks compare to the general population. The objective of this study was to compare the Framingham Risk Score (FRS) and vascular age differences in persons with HIV, HCV or HIV/HCV disease to the general population. HIV, HCV, and HIV/HCV patients with clinic visits between 2004 and 2009 were sampled from medical clinics in Rochester, NY. Uninfected persons were randomly selected from the National Health and Nutrition Examination Survey (NHANES), and individually matched on gender, race, and age. We stratified by infection group and conducted separate multivariable linear regression analyses between each infection group and the gender, race, and age matched participants from NHANES. Rochester patients (HIV = 239, HCV = 167, HIV/HCV = 182) were compared 3 : 1 with the NHANES participants. After controlling for weight, marital status, current pharmacotherapies and the matching variables of gender, race, and age, HIV/HCV patients had a 2% higher general FRS compared with the general population (p = 0.03), and vascular age differences that were 4.1 years greater (p = .01). HCV patients had a 2.4% higher general FRS than the general population (p < .001), and vascular age differences that were 4.4 years greater (p < .001). CVD risk was elevated but not significantly different between HIV patients and the general population. Cardiovascular disease risk is elevated among HIV/HCV and HCV infected persons compared with the general population.

HIV and General Cardiovascular Risk

The incidence of cardiovascular disease (CVD) is increasing in HIV-infected people. Risk factors such as hyperlipidemia, impaired glucose tolerance, and insulin resistance have become common. CVD in HIV may also be related to nontraditional risk factors including accumulation of visceral fat, inflammation secondary to HIV, and effects of some antiretroviral drugs. This cross-sectional study described the CVD risk factors of 123 adults living with HIV and calculated the 10-year estimate for general cardiovascular risk score. Results showed that approximately 25% of the participants were considered to be at high risk for developing CVD in the next 10 years. Increased waist circumference and longer duration of smoking habit were associated with elevated general cardiovascular risk scores. Similar to the general population, most of the identified risks could be modified through lifestyle management.