Cardiovascular Disease In HIV-infected Patients Research Articles

Potential Cardiovascular Disease Risk Markers Among HIV-Infected Women Initiating Antiretroviral Treatment

Inflammation and hemostasis perturbation may be involved in vascular complications of HIV infection. We examined atherogenic biomarkers and subclinical atherosclerosis in HIV-infected adults before and after beginning highly active antiretroviral therapy (HAART). In the Women's Interagency HIV Study, 127 HIV-infected women studied pre and post HAART were matched to HIV-uninfected controls. Six semiannual measurements of soluble CD14, tumor necrosis factor (TNF) alfa, soluble interleukin (IL) 2 receptor, IL-6, IL-10, monocyte chemoattractant protein 1, D-dimer, and fibrinogen were obtained. Carotid artery intima-media thickness was measured by B-mode ultrasound. Relative to HIV-uninfected controls, HAART-naive HIV-infected women had elevated levels of soluble CD14 (1945 vs 1662 ng/mL, Wilcoxon signed rank P < 0.0001), TNF-α (6.3 vs 3.4 pg/mL, P < 0.0001), soluble IL-2 receptor (1587 vs 949 pg/mL, P < 0.0001), IL-10 (3.3 vs 1.9 pg/mL, P < 0.0001), monocyte chemoattractant protein 1 (190 vs 163 pg/mL, P < 0.0001), and D-dimer (0.43 vs 0.31 μg/mL, P < 0.01). Elevated biomarker levels declined after HAART. Although most biomarkers normalized to HIV-uninfected levels, in women on effective HAART, TNF-α levels remained elevated compared with HIV-uninfected women (+0.8 pg/mL, P = 0.0002). Higher post-HAART levels of soluble IL-2 receptor (P = 0.02), IL-6 (P = 0.05), and D-dimer (P = 0.03) were associated with increased carotid artery intima-media thickness. Untreated HIV infection is associated with abnormal hemostasis (eg, D-dimer), proatherogenic (eg, TNF-α), and antiatherogenic (eg, IL-10) inflammatory markers. HAART reduces most inflammatory mediators to HIV-uninfected levels. Increased inflammation and hemostasis are associated with subclinical atherosclerosis in recently treated women. These findings have potential implications for long-term risk of cardiovascular disease in HIV-infected patients, even with effective therapy.

Metabolic and Cardiovascular Complications in HIV-Infected Patients: New Challenges for a New Age

Metabolic and Cardiovascular Complications in HIV-Infected Patients: New Challenges for a New Age

Cardiovascular Disease in Patients with HIV

The introduction of combination antiretroviral therapy (cART) has substantially decreased mortality among the HIV-infected population. In this setting, cardiovascular disease (CVD) has become a leading cause of morbidity and mortality. Compared with the general population, higher rates of myocardial infarction as well as a high prevalence of subclinical coronary atherosclerosis have been found in the HIV-infected population. It has been suggested that in HIV-infected patients, the atherosclerotic burden is not based solely on traditional cardiovascular risk factors. The interplay of other mechanisms such as chronic inflammation, effects of cART or immune activation after initiation of cART may predispose to accelerated and increased risk of CVD. Effective treatment are available today to reduce CVD in at-risk patients, and therefore early detection of subclinical coronary atherosclerosis is important. However, the mechanisms behind the development of CVD in HIV-infected patients may limit the usefulness of the traditional noninvasive screening tools for CVD used in the general population. This review will focus on the different plausible mechanisms behind the increased risk of CVD and the noninvasive methods by which atherosclerosis may be assessed in the HIV-infected population.

Novel Aspects of Nonfasting Lipemia in relation to Vascular Biology

Several cardiovascular risk factors have been described during the last decades. Postprandial hyperlipidemia has been recognized as an important factor contributing to atherogenesis; however chylomicron remnants have not been used widely in risk equations. One of the probable causes for this lack of consideration in clinical practice may be that the metabolism of chylomicrons and their remnants has been rather difficult to study and, more so, to modulate in vivo. The current issue of the International Journal of Vascular Medicine provides novel insight into the metabolic changes of chylomicrons and their remnants in relation to vascular damage. The paper by G. H. Tomkin and D. Owens “The chylomicron: relationship to atherosclerosis” provides an excellent overview of the molecular mechanisms involved in chylomicron synthesis and metabolism in humans. The paper by B. Klop et al. “Understanding postprandial inflammation and its relationship to lifestyle behaviour and metabolic diseases” describes novel aspects related to inflammation in different clinical conditions and under variable lifestyle situations. Following this line of inflammatory-dependent aspects of chylomicrons, the paper by M. Cao et al. “Dual AAV/IL-10 plus STAT3 anti-inflammatory gene delivery lowers atherosclerosis in LDLR KO mice, but without increased benefit” further explores aspects of cholesterol metabolism involving different molecular targets important for both hepatic and intestinal cholesterol metabolism. S. A. Lopez et al. proceed with a paper investigating the effects of oxidized chylomicron remnants on monocyte activation and the effects of the antioxidant drug probucol on this interaction “The oxidative state of chylomicron remnants influences their modulation of human monocyte activation.” L. D. Roche and et al. provide evidence suggesting that postprandial hypertriglyceridemia simulated by an infusion with artificial TG-rich lipoproteins (Lipofundin) induces oxidative stress and atherosclerotic lesions in an animal model prone to develop atherosclerosis “Lipofundin-induced hyperlipidemia promotes oxidative stress and atherosclerotic lesions in New Zealand white rabbits.” The paper by M. Napolitano et al. “Phospholipase A2 mediates apolipoprotein-independent uptake of chylomicron remnant-like particles by human macrophages” includes novel work showing that macrophage lipolytic enzymes mediate the internalization of postprandial TG-rich lipoproteins and that secretory phospholipase A2 (sPLA2) and cytosolic PLA2 play a more important role than extracellular lipoprotein lipase-mediated TG hydrolysis. M. M. Pallebage-Gamarallage et al. describe in the following investigation “A diet enriched in docosahexanoic acid exacerbates brain parenchymal extravasation of Apo B lipoproteins induced by chronic ingestion of saturated fats,” how dietary interventions can lead to modulation of cerebrovascular inflammation by oxidative stress. A. Van der Wiel provides a comprehensive update on the effects of alcohol ingestion on fasting and postprandial triglyceridemia “The effect of alcohol on postprandial and fasting triglycerides”, which is followed by a paper by B. Klop et al. “AT1 receptor gene polymorphisms in relation to postprandial lipemia” showing a novel relationship between polymorphisms of genes involved in the regulation of blood pressure with postprandial lipemia. J. P. H. van Wijk and M. Castro Cabezas contributed with an update on the effects of antiretroviral therapy in HIV-infected patients on TG metabolism “Hypertriglyceridemia, metabolic syndrome, and cardiovascular disease in HIV-infected patients: effects of antiretroviral therapy and adipose tissue distribution.” Finally, G. Charach et al. provided a review describing the effects of bile acid secretion and intestinal absorption on plasma lipoproteins and coronary atherosclerosis. M. Castro Cabezas Kathleen M. Botham John C. L. Mamo Spencer D. Proctor

Hypertriglyceridemia, Metabolic Syndrome, and Cardiovascular Disease in HIV-Infected Patients: Effects of Antiretroviral Therapy and Adipose Tissue Distribution

The use of combination antiretroviral therapy (CART) in HIV-infected patients has resulted in a dramatic decline in AIDS-related mortality. However, mortality due to non-AIDS conditions, particularly cardiovascular disease (CVD) seems to increase in this population. CART has been associated with several metabolic risk factors, including insulin resistance, low HDL-cholesterol, hypertriglyceridemia and postprandial hyperlipidemia. In addition, HIV itself, as well as specific antiretroviral agents, may further increase cardiovascular risk by interfering with endothelial function. As the HIV population is aging, CVD may become an increasingly growing health problem in the future. Therefore, early diagnosis and treatment of cardiovascular risk factors is warranted in this population. This paper reviews the contribution of both, HIV infection and CART, to insulin resistance, postprandial hyperlipidemia and cardiovascular risk in HIV-infected patients. Strategies to reduce cardiovascular risk are also discussed.

HIV and HAART-Associated Dyslipidemia

Effective highly active antiretroviral therapy (HAART) for human immunodeficiency virus-1 (HIV) infection has led to marked improvement in life-expectancy for those infected with HIV. Despite reductions in the incidence of AIDS with effective treatment, patients continue to experience considerable morbidity and mortality from non-AIDS illness such as premature cardiovascular disease, liver failure and renal failure. These morbidities, particularly premature cardiovascular disease, are thought to be related to a combination of the effects of an ageing HIV-infected population coupled with long-term effects of HIV infection and antiretroviral therapy (ART). One of the principle drivers behind the well documented increase in the risk of cardiovascular disease in HIV-infected patients is dyslipidemia.This review will focus on the clinical presentation of HIV and ART-associated dyslipidemia, what is known of its patho-physiology, including associations with use of specific antiretroviral medications, and suggest screening and management strategies.

Predicting the risk of cardiovascular disease in HIV-infected patients: the Data collection on Adverse Effects of Anti-HIV Drugs Study

HIV-infected patients receiving combination antiretroviral therapy may experience metabolic complications, potentially increasing their risk of cardiovascular diseases (CVDs). Furthermore, exposures to some antiretroviral drugs seem to be independently associated with increased CVD risk. We aimed to develop cardiovascular risk-assessment models tailored to HIV-infected patients. Prospective multinational cohort study. The data set included 22,625 HIV-infected patients from 20 countries in Europe and Australia who were free of CVD at entry into the Data collection on Adverse Effects of Anti-HIV Drugs Study. Using cross-validation methods, separate models were developed to predict the risk of myocardial infarction, coronary heart disease, and a composite CVD endpoint. Model performance was compared with the Framingham score. The models included age, sex, systolic blood pressure, smoking status, family history of CVD, diabetes, total cholesterol, HDL cholesterol and indinavir, lopinavir/r and abacavir exposure. The models performed well with area under the receiver operator curve statistics of 0.783 (range 0.642-0.820) for myocardial infarction, 0.776 (0.670-0.818) for coronary heart disease and 0.769 (0.695-0.824) for CVD. The models estimated more accurately the outcomes in the subgroups than the Framingham score. Risk equations developed from a population of HIV-infected patients, incorporating routinely collected cardiovascular risk parameters and exposure to individual antiretroviral therapy drugs, might be more useful in estimating CVD risks in HIV-infected persons than conventional risk prediction models.

Enfermedad cardiovascular en el paciente infectado por el virus de la inmunodeficiencia humana

With the introduction of effective antiretroviral therapy (ART), cardiovascular disease has gained importance as a cause of morbidity and mortality in HIV-infected persons. Herein, we will study the risk of cardiovascular disease in HIV-infected persons compared to the non-infected population. The relative contributions regarding the host, HIV infection and antiretroviral therapy will be presented in the light of current knowledge. The absolute risk of developing cardiovascular disease in HIV-infected patients receiving antiretroviral therapy is low. However, this risk is increasing compared to the risk in uninfected persons. This fact is substantially due to a higher prevalence of underlying traditional cardiovascular risk factors that are mostly host-dependent. HIV infection may contribute both directly through immune activation and inflammation and indirectly through immunodeficiency. The type of antiretroviral treatment, also to a lesser degree than HIV infection, may also contribute through its impact on metabolic effects and also because of the changes produced in body fat parameters. Prevention of cardiovascular disease in HIV-infected patients should be standard care. The traditional risk factors should be investigated and aggressively treated whenever possible, since they play a major role in the development of cardiovascular disease. Antiretroviral therapy should be initiated earlier in patients with high cardiovascular risk. From a purely cardiovascular perspective, the benefits of ART, regardless of the drugs used, clearly outweigh any potential risk.

Risk of cardiovascular disease in HIV-infected patients

The life expectancy of people living with HIV infection has improved dramatically since the use of highly active antiretroviral therapy (HAART). Now that patients with HIV infection are living longer, the focus of its treatment should shift to long-term management spanning decades. Diseases of ageing, including cardiovascular disease (CVD), have now become more important. The evidence of cardiovascular risk associated with HIV infection and antiretroviral therapy is explored and discussed in this article.

Regional Gene Expression of LOX-1, VCAM-1, and ICAM-1 in Aorta of HIV-1 Transgenic Rats

BackgroundIncreased prevalence of atherosclerotic cardiovascular disease in HIV-infected patients has been observed. The cause of this accelerated atherosclerosis is a matter of controversy. As clinical studies are complicated by a multiplicity of risk-factors and a low incidence of hard endpoints, studies in animal models could be attractive alternatives.Methodology/Principal FindingsWe evaluated gene expression of lectin-like oxidized-low-density-lipoprotein receptor-1 (LOX-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in HIV-1 transgenic (HIV-1Tg) rats; these genes are all thought to play important roles in early atherogenesis. Furthermore, the plasma level of sICAM-1 was measured. We found that gene expressions of LOX-1 and VCAM-1 were higher in the aortic arch of HIV-1Tg rats compared to controls. Also, the level of sICAM-1 was elevated in the HIV-1Tg rats compared to controls, but the ICAM-1 gene expression profile did not show any differences between the groups.Conclusions/SignificanceHIV-1Tg rats have gene expression patterns indicating endothelial dysfunction and accelerated atherosclerosis in aorta, suggesting that HIV-infection per se may cause atherosclerosis. This transgenic rat model may be a very promising model for further studies of the pathophysiology behind HIV-associated cardiovascular disease.

Cardiovascular disease and HIV infection: host, virus, or drugs?

With effective antiretroviral therapy, cardiovascular disease has gained importance as a cause of morbidity and mortality in HIV-infected persons. We review the risk of cardiovascular disease in HIV-infected persons compared with that in uninfected persons and discuss the relative contributions of host, HIV, and antiretroviral therapy in the light of current knowledge. The incidence of cardiovascular disease in HIV-infected patients receiving antiretroviral therapy is low. However, the risk of cardiovascular disease increased compared with that in uninfected persons. This fact is substantially due to a higher prevalence of underlying traditional cardiovascular risk factors that are mostly host dependent. HIV may additionally contribute both directly through immune activation and inflammation, and indirectly through immunodeficiency. In a more modest way than that of HIV infection, the type of antiretroviral therapy may also contribute through its impact on metabolic and body fat parameters, and possibly through other factors that are currently unclear. Prevention of cardiovascular disease in HIV-infected patients should be standard of care. Traditional risk factors should be investigated and aggressively treated when possible. Antiretroviral therapy should be initiated earlier in patients with high cardiovascular risk. From a purely cardiovascular perspective, the benefits of antiretroviral therapy clearly outweigh any potential risk.

HIV and Antiretroviral Therapy: Lipid Abnormalities and Associated Cardiovascular Risk in HIV-Infected Patients

It has been demonstrated that patients on highly active antiretroviral therapy are at increased risk for developing metabolic abnormalities that include elevated levels of serum triglycerides and low-density lipoprotein cholesterol and reduced levels of high-density lipoprotein cholesterol. This dyslipidemia is similar to that seen in the metabolic syndrome, raising the concern that highly active antiretroviral therapy also potentially increases the risk for cardiovascular complications. This paper reviews the contribution of both HIV infection and the different components of highly active antiretroviral therapy to dyslipidemia and the role of these abnormalities toward increasing the risk of cardiovascular disease in HIV-infected patients; therapeutic strategies to manage these risks are also considered.

DISORDERS OF GLUCOSE METABOLISM IN HUMAN IMMUNODEFICIENCY VIRUS-INFECTED PATIENTS

Over the past 10 years, the development of highly active antiretroviral therapy (HAART) has dramatically improved morbidity and mortality in human immunodeficiency virus (HIV)-infected patients. Since the introduction of HAART however, unexpected metabolic abnormalities, including lipodystrophy, dyslipidaemia and dysregulation of glucose metabolism, are reported with increasing frequency in HIV-infected persons. Such metabolic disorders, if not treated, may be associated with an increased risk of cardiovascular disease in HIVinfected patients. In this paper, the prevalence, mechanisms and therapeutic strategies for the disorders of glucose metabolism in the context of HIV-infection are discussed.

State of the science conference: Initiative to decrease cardiovascular risk and increase quality of care for patients living with HIV/AIDS: executive summary.

With successful antiretroviral therapy, patients infected with the human immunodeficiency virus (HIV) are living longer; however, recent reports suggest increased rates of coronary heart disease (CHD) among HIV-infected patients,1 and cardiovascular disease has become an important cause of morbidity and mortality in this population.2 Increased CHD rates in the HIV population may relate to traditional risk factors, including advancing age, higher smoking rates, dyslipidemia, insulin resistance, and impaired glucose tolerance. Cardiovascular disease may also be due to nontraditional factors, including changes in body composition with loss of subcutaneous fat and/or accumulation of visceral fat in some patients, inflammation, and direct effects of the virus on the vasculature, as well as to direct effects of specific antiretroviral drugs. Important questions remain as to the pathogenesis, detection, and treatment of cardiovascular disease and related risk factors in HIV-infected patients. These questions concern, among other things, the design of adequate trials to determine CHD incidence and the utility of existing CHD guidelines for screening, prevention, treatment, and risk stratification. To ascertain the state of the science with respect to these and related questions, a multidisciplinary conference with interested HIV specialists, cardiologists, endocrinologists, primary care physicians, National Institutes of Health representatives, and patient advocates was convened June 28–30, 2007, in Chicago, Ill, and chaired by Drs Steven Grinspoon and Robert Eckel. The discussions focused on 6 areas of interest, each with its own working group, including the following: (1) the contribution of metabolic and anthropometric abnormalities to cardiovascular disease risk factors (chaired by Drs Carl Grunfeld and Donald Kotler); (2) the epidemiological evidence for cardiovascular disease and its relationship to highly active antiretroviral therapy (HAART; chaired by Drs Judy Currier and Jens Lundgren); (3) the effects of HIV infection and antiretroviral therapy on the heart and vasculature (chaired by Drs Michael Dube …

Prevention Strategies for Cardiovascular Disease in HIV-Infected Patients

Effective antiretroviral therapy (ART) improves the survival of patients with human immunodeficiency virus (HIV) infection.1 With increased life expectancy, HIV-infected patients increasingly are experiencing complications of illnesses that are not directly related to HIV infection.2 Cardiovascular disease (CVD), the leading cause of death in the United States,3 recently 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 Antiretroviral Therapy).2,4–6 Among these patients, traditional CVD risk factors predict CVD events; however, certain components of ART appear to be associated with increased CVD risk.5 Much 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.9 Patients with established CVD are at the highest risk and qualify for the most aggressive risk factor management, with special focus on interventions that have been proven to prevent cardiovascular death, myocardial infarction, 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 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, however, 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 …

Epidemiological evidence for cardiovascular disease in HIV-infected patients and relationship to highly active antiretroviral therapy.

In the mid-1990s, case reports of myocardial infarction (MI) in young patients infected with human immunodeficiency virus (HIV) sparked interest in the relationship between HIV infection and cardiovascular disease (CVD).1,2 Although the initial focus was primarily on the relationship between dyslipidemia associated with antiretroviral therapy (ART) and cardiovascular risk, a broader appreciation of the complex interplay between traditional risk factors for CVD and HIV infection has emerged more recently. Several groups of investigators have designed studies to examine various aspects of the relationship between HIV infection, traditional cardiovascular risk factors, ART, and short- and longer-term cardiovascular risk3–11 (see also Working Group 1). Studies have included both clinical end points (MI, hospitalization for MI or angina, and revascularization) and surrogate markers of atherosclerosis (endothelial function or carotid intima-media thickness). Successive studies have generally improved in quality, with inclusion of data on traditional risk factors, longer follow-up, and more diverse patient populations. HIV and ART can contribute to an altered risk of CVD in 3 principal ways: (1) HIV may serve as a marker to identify a subgroup of the general population with an altered prevalence of traditional cardiovascular risk factors, unrelated to HIV or ART (eg, HIV-infected patients may have higher smoking rates); (2) HIV or ART may affect the risk of developing a traditional cardiovascular risk factor (eg, HIV or ART may worsen dyslipidemia); and (3) HIV or ART may affect the pathogenetic process that leads to CVD in ways other than via an effect on traditional risk factors (eg, through effects on inflammation or endothelial function). Importantly, there is substantial evidence to suggest that all 3 mechanisms are in operation and affect the risk of CVD in patients infected with HIV. All 3 factors should be considered in epidemiological studies assessing the relationship between CVD and HIV …

Screening and Assessment of Coronary Heart Disease in HIV-Infected Patients

Human immunodeficiency virus (HIV)–infected individuals are living longer in the era of antiretroviral therapy. As a result, they are increasingly prone to the development of concomitant chronic disease. Coronary heart disease (CHD) is the leading cause of death in the United States and Europe. Recent studies suggest that CHD rates may be increasing among HIV-infected patients (see Epidemiological Evidence for Cardiovascular Disease in HIV-Infected Patients and Relationship to Highly Active Antiretroviral Therapy, Working Group 2), and thus appropriate screening strategies for CHD in this population are needed. Recently, approaches to screening and assessment of cardiovascular disease (CVD) in HIV-infected individuals were discussed at a State of the Science Conference. Although insufficient evidence now exists to recommend a screening strategy for CHD in HIV that differs from that recommended in the non-HIV population, emerging risk factors and surrogate markers for atherosclerosis unique to the HIV population suggest specific strategies that may be useful in this population. Two broad screening categories are discussed here. The first screening strategy seeks to define the pretest likelihood of disease by identifying the presence of predisposing risk factors such as hypertension, elevated serum cholesterol, cigarette smoking, and physical inactivity. The second screening strategy aims at the detection of established CHD, even in its earliest stages. The currently available recommendations and guidelines for screening for the presence of cardiovascular risk factors in the general, non–HIV-infected population are detailed in Table 1.1–7 View this table: Table 1. Recommendations and Guidelines for Screening for Cardiovascular Risk Factors in the General Population The currently available recommendations and guidelines for screening for the presence of CVD risk factors in persons with HIV infection are detailed in Table 2. These recommendations take into account the evidence for dyslipidemia, insulin resistance, and changes in body fat distribution that have been shown to occur …

Effectiveness of lipid-lowering therapy in HIV patients

The aim of this article is to analyse the effectiveness of lipid-lowering therapy in HIV-infected patients. Although data on prevention of cardiovascular disease in HIV-infected patients are limited, available evidence suggests that intervention guidelines should be similar to those that are recommended for the general population. The main target of lipid-lowering therapy is LDL cholesterol; therefore statins are the drugs of choice. The efficacy of statins in HIV-infected persons appears to be lower than expected, although adherence to statin therapy has not been well assessed. Statins combining high potency and little clinically meaningful interactions with antiretroviral therapy (pravastatin, fluvastatin, atorvastatin and rosuvastatin) should be preferred as initial therapy, though comparative studies in HIV-infected persons are scarce. A combination of a statin at medium doses with either ezetimibe or a fibrate other than gemfibrozil may result in more satisfactory results than higher doses of statin monotherapy when LDL cholesterol goals are difficult to achieve or there persist elevated triglycerides and low HDL cholesterol, respectively. Adequate choice and dosing of lipid-lowering drugs, given as isolated agents or in combination therapy, and care for good drug compliance in HIV-infected patients at moderate or high cardiovascular risk should help maximize their long-term health.

Cardiovascular disease in HIV-infected patients: does HIV infection in and of itself increase cardiovascular risk?

Cardiovascular disease is increasingly recognized to be a significant cause of morbidity and mortality among patients with chronic HIV infection in the current era of effective antiretroviral therapy. HIV-infected patients treated with antiretroviral therapy have increased traditional cardiovascular risk factors, but whether HIV infection in and of itself confers a significant increase in cardiovascular risk is largely unknown. This review summarizes recent data investigating cardiovascular risk in HIV patients and the evidence for an effect of HIV per se. The potential physiological mechanisms by which HIV might contribute to coronary artery disease are reviewed. Several interesting studies in the last year have evaluated cardiovascular endpoints and surrogate measures such as carotid intima-media thickness and endothelial function in HIV-infected patients compared with uninfected control groups. Several studies to date using surrogate measurements such as carotid intima-media thickness and endothelial dysfunction suggest a possible independent HIV effect on cardiovascular risk, but some studies have yielded conflicting results. Numerous potential mechanisms by which HIV might contribute to coronary artery disease exist. These mechanisms include effects of HIV proteins to attract monocytes to the intimal wall, and impair cholesterol efflux, and effects of activated monocytes to induce an inflammatory response. More definitive prospective studies are needed to fully answer whether HIV infection per se promotes cardiovascular disease, but ample evidence suggests that HIV and related inflammatory responses could contribute to increased cardiovascular disease.

Carotid intima media thickness with no cardiovascular disease in HIV-infected patients correlates with a hyperactivated/pro-apoptotic T-cell phenotype

Background HIV-infected patients may be at increased risk of cardiovascular disease (CVD), and present higher carotid intima media thickness (IMT) compared with healthy controls. Besides clinical and metabolic factors, atherosclerosis in HIV is influenced by immune and inflammatory parameters. Given that T-cell activation correlates with CVD and HIV accounts for heightened T-cell hyperactivation, we hypothesized that early IMT increases associate to T-cell hyperactivation.