Journal articles on the topic 'HIV, cardiovascular disease, interleukin-6'
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Zaaqoq, Akram M., Faisal A. Khasawneh, and Roger D. Smalligan. "Cardiovascular Complications of HIV-Associated Immune Dysfunction." Cardiology Research and Practice 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/302638.
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Prolonged survival in HIV infection is accompanied by an increased frequency of non-HIV-related comorbidities. It is suggested that cardiovascular diseases (CVD) occur earlier among HIV-positive patients compared with HIV-negative patients, and at a higher rate. Several factors have been proposed which can be categorized into traditional and nontraditional risk factors. Immune dysfunction is a nontraditional risk factor that contributes significantly to cardiovascular pathology. Markers of inflammation are elevated in HIV-infected patients, and elevations in markers such as high-sensitivity C-reactive protein, D-dimer, and interleukin-6 (IL-6) have been associated with increased risk for cardiovascular disease. However, the data currently suggest the most practical advice is to start antiretroviral therapy early and to manage traditional risk factors for CVD aggressively. A better understanding of the mechanisms of CVD in this population and further efforts to modify chronic inflammation remain an important research area.
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Funderburg, Nicholas T., Elizabeth Mayne, Scott F. Sieg, Robert Asaad, Wei Jiang, Magdalena Kalinowska, Angel A. Luciano, et al. "Increased tissue factor expression on circulating monocytes in chronic HIV infection: relationship to in vivo coagulation and immune activation." Blood 115, no. 2 (January 14, 2010): 161–67. http://dx.doi.org/10.1182/blood-2009-03-210179.
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Abstract HIV infection is associated with an increased risk of thrombosis; and as antiretroviral therapy has increased the lifespan of HIV-infected patients, their risk for cardiovascular events is expected to increase. A large clinical study found recently that all-cause mortality for HIV+ patients was related to plasma levels of interleukin-6 and to D-dimer products of fibrinolysis. We provide evidence that this elevated risk for coagulation may be related to increased proportions of monocytes expressing cell surface tissue factor (TF, thromboplastin) in persons with HIV infection. Monocyte TF expression could be induced in vitro by lipopolysaccharide and flagellin, but not by interleukin-6. Monocyte expression of TF was correlated with HIV levels in plasma, with indices of immune activation, and with plasma levels of soluble CD14, a marker of in vivo lipopolysaccharide exposure. TF levels also correlated with plasma levels of D-dimers, reflective of in vivo clot formation and fibrinolysis. Thus, drivers of immune activation in HIV disease, such as HIV replication, and potentially, microbial translocation, may activate clotting cascades and contribute to thrombus formation and cardiovascular morbidities in HIV infection.
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Kounatidis, Dimitris, Dimitra Rontogianni, Dimitrios Sampaziotis, Maria Vardaka, Chara Giatra, Christodoulos Dolapsakis, Evangelia Margellou, and Natalia G. Vallianou. "An HHV-8 Positive HIV Negative Multicentric Castleman’s Disease, who Responded well to Rituximab Alone." Cardiovascular & Hematological Disorders-Drug Targets 20, no. 1 (February 26, 2020): 84–86. http://dx.doi.org/10.2174/1871529x19666190227185318.
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Background: Multicentric Castleman Disease (MCD) presents with enlarged lymph nodes in multiple regions and systemic inflammatory symptoms, due to the dysregulation of cytokines, most commonly interleukin-6 (IL-6). Human herpes virus-8 (HHV-8) is strongly related to MCD (HHV-8-associated MCD) and is being implicated in cytokine dysregulation in patients, the majority of whom are HIV positive or immunosuppressed. Preferred treatment of HHV-8- associated MCD depends on the presence or not of concurrent Kaposi sarcoma and on whether the patient has life-threatening organ failure or poor performance status thought to be related to HHV- 8-associated MCD. Case Presentation: Herein, we describe a female patient with HHV-8 positive, HIV negative MCD, who responded well to the administration of rituximab once weekly for four weeks alone for three cycles. Conclusion: HHV-8 positive, HIV negative MCD treatment modalities are only anecdotal due to the rarity of this form of MCD. Administration of rituximab alone seems to be beneficial among patients with good performance status and the absence of life-threatening organ failure in cases of HHV-8 positive, HIV negative MCD.
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Triant, Virginia A. "Cardiovascular Disease and HIV Infection." Current HIV/AIDS Reports 10, no. 3 (June 25, 2013): 199–206. http://dx.doi.org/10.1007/s11904-013-0168-6.
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Arzhakova, M. A., T. A. Shekhovtsova, and D. V. Duplyakov. "Coronary Heart Disease in HIV-Infected Patients." Rational Pharmacotherapy in Cardiology 15, no. 6 (January 3, 2020): 900–905. http://dx.doi.org/10.20996/1819-6446-2019-15-6-900-905.
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Currently, there are methods of drug exposure to the infection caused by the human immunodeficiency viruses (HIV), that allow to suppress the active replication of the virus in the patient's body. The era of antiretroviral therapy, which has allowed HIV-infected people to live longer, has begun. This led to an increase in their cardiovascular diseases, which occur at an earlier age and are more severe than in people without HIV. Specific or “nontraditional” risk factors damaging vascular wall occur in HIV patients along with traditional risk factors. These factors include: the negative impact of HIV on endothelium, an imbalance of inflammatory mediators, pathological immune activation, a decrease in the level of CD4 cells, a change in the number and function of platelets. The question of the effect of antiretroviral therapy on the occurrence of atherosclerotic vascular lesions remains debatable. Acute coronary syndrome (ACS) is one of the most frequent and most severe cardiovascular events in HIV-infected patients. The risk of myocardial infarction is highest in patients with a viral load of HIV-1 ribonucleic acid (RNA)≥500 copies/ml and a CD4 cell count of <200/ml. The most common form of ACS in HIV patients is ACS with ST segment elevation. Treatment of ACS in HIV patients has some difficulties: a high frequency of stent thrombosis, the frequent occurrence of thrombocytopenia, drug interactions with antiretroviral therapy. The high risk of developing cardiovascular diseases in HIV patients necessitates the introduction of active measures of primary and secondary prevention, taking into account the specific interaction of all drugs taken by the patient.
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Jalbert, Emilie, Nisha Parikh, Todd Seto, Dominic Chow, Cecilia Shikuma, Lishomwa Ndhlovu, and Jason Barbour. "Elevated proinflammatory cytokine production by monocytes in HIV(+) individuals at risk for cardiovascular disease (P3033)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 55.17. http://dx.doi.org/10.4049/jimmunol.190.supp.55.17.
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Abstract Despite virologic suppression by HIV antiretroviral therapy, residual inflammation associated with chronic HIV infection increases the risk of developing cardiovascular disease. Monocytes have been shown to be major players in the development of atherosclerosis due to their proinflammatory responses to oxidized Low Density Lipoproteins. Our study sought to assess the functional properties of monocytes from peripheral blood of HIV-infected individuals. The cohort consisted of 33 HIV(+) subjects on HAART and 14 HIV(-) risk- and age- matched subjects. Our flow cytometry-based functional assay measured monocyte production of IL-1β, IL-8 and IL-6 in the absence of stimulation and in response to LPS or oxLDL. Without stimulation, HIV(+) subjects had a greater frequency of cells producing IL-1β and IL-8. In the presence of either oxLDL or LPS, both groups increased the frequency of responding cells compared to no stimulation, but HIV(+) subjects maintained a higher frequency of IL-1β(+) and IL-8(+) cells compared to HIV(-). There was no IL-6 production in either group in the absence of stimulation, but upon stimulation with either oxLDL or LPS, there was a higher frequency of IL-6 producing cells in the HIV(+) group. The higher level of inflammatory cytokine production in HIV(+) adults compared to HIV(-), both at rest and in the presence of stimulation, may in part account for increased risk of cardiovascular disease seen in the HIV(+) population.
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Abreu, R. Correia. "Characterization of cardiovascular risk factors and Framingham score in an HIV-1 population." Journal of Clinical Research and Reports 5, no. 5 (November 21, 2020): 01–04. http://dx.doi.org/10.31579/2690-1919/130.
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With the advent of high-potency antiretroviral treatment introduced in 1996, HIV infection ceased to be an acute and deadly disease to become chronic and controllable. However, the early aging of this population, which according to some authors and cohorts, is 10 years less than in the "normal" population, has been studied. Although the realities of these patients comorbidities are well known, the definition of time, when and how or with what to treat still seems to be a matter of debate. The aim of this study is to evaluate the incidence and prevalence according to the state of the art for the non-HIV population of cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus) and apply the adjusted Framingham Risk Score by recording analytical and clinical factors in an HIV-1 population with more than 50 years of age, followed in the Infectious Diseases Service for more than 6 months.
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Abreu, R. Correia. "Characterization of cardiovascular risk factors and Framingham score in an HIV-1 population." Journal of Clinical Research and Reports 5, no. 5 (November 21, 2020): 01–04. http://dx.doi.org/10.31579/2690-1919/0130.
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With the advent of high-potency antiretroviral treatment introduced in 1996, HIV infection ceased to be an acute and deadly disease to become chronic and controllable. However, the early aging of this population, which according to some authors and cohorts, is 10 years less than in the "normal" population, has been studied. Although the realities of these patients comorbidities are well known, the definition of time, when and how or with what to treat still seems to be a matter of debate. The aim of this study is to evaluate the incidence and prevalence according to the state of the art for the non-HIV population of cardiovascular risk factors (hypertension, dyslipidemia, diabetes mellitus) and apply the adjusted Framingham Risk Score by recording analytical and clinical factors in an HIV-1 population with more than 50 years of age, followed in the Infectious Diseases Service for more than 6 months.
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Polanka, Brittanny M., Suman Kundu, Kaku A. So-Armah, Matthew S. Freiberg, Samir K. Gupta, Tamika C. B. Zapolski, Adam T. Hirsh, et al. "Insomnia symptoms and biomarkers of monocyte activation, systemic inflammation, and coagulation in HIV: Veterans Aging Cohort Study." PLOS ONE 16, no. 2 (February 9, 2021): e0246073. http://dx.doi.org/10.1371/journal.pone.0246073.
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BackgroundInsomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated.MethodsWe examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, “Difficulty falling or staying asleep?,” with the following response options: “I do not have this symptom” or “I have this symptom and…” “it doesn’t bother me,” “it bothers me a little,” “it bothers me,” “it bothers me a lot.” Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95% confidence interval (CI).ResultsWe observed no significant associations between insomnia symptoms and sCD14 or IL-6. For D-dimer, veterans in the “Bothers a Lot” group had, on average, 17% higher D-dimer than veterans in the “No Difficulty Falling or Staying Asleep” group in the demographic-adjusted model (exp[b] = 1.17, 95%CI= 1.01–1.37,p= .04). This association was nonsignificant in the fully-adjusted model (exp[b] = 1.09, 95%CI= 0.94–1.26,p= .27).ConclusionWe observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia-CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted.
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Postorino, Maria Concetta, Filippo Luciani, Carmelo Mangano, Maria Stella Carpentieri, Paolo Scerbo, Armando Priamo, Giuseppina Berardelli, et al. "DEMOGRAPHICAL, VIRO-IMMUNOLOGICAL, CLINICAL AND THERAPEUTICAL CHARACTERISTICS OF HIV INFECTED PATIENTS IN A “EPIDEMIOLOGICALLY UNEXPLORED” REGION OF ITALY (CALABRIA REGION): THE CALABRHIV COHORT." Mediterranean Journal of Hematology and Infectious Diseases 7 (October 8, 2015): e2015054. http://dx.doi.org/10.4084/mjhid.2015.054.
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Background and Objectives HIV epidemics may differ among epidemiological contexts. We aimed at constructing an HIV clinical cohort whose main epidemiological, clinical and therapeutical characteristics are described (the CalabrHIV cohort, Calabria Region, Southern Italy). Methods The CalabrHIV cohort includes all HIV patients on active follow-up in all infectious disease centers in the Calabria Region as at October 2014. All information were recorded in a common electronic database. Not-infectious co-morbidities (such as cardiovascular diseases, bone fractures, diabetes, renal failure and hypertension) were also studied. Results 548 patients (68% males; 63% aged <50 years) were included in the CalabrHIV cohort. Major risk factors: sexual transmission (49%) and intravenous drug use (34%). 39% patients had HCV and/or HBV co-infection. An high percentage of late presenters was observed (68.4% patients with CD4+ nadir <350/mm3and 38.5% patients with AIDS at baseline). 83% patients on HAART had actually undetectable HIV-RNA. Hypertension was the most frequent co-morbidity (21.5%). Multi-morbidity was more frequent in >50 years-old patients than in <50 years-old ones (30% vs. 6%; p<0.0001). Co-morbidity was more frequent in HCV and/or HBV co-infected than in HIV mono-infected patients (46.6% vs. 31.7%: p=0.0006). Conclusion This cohort presentation study sheds light, for the first time, on HIV patients’ characteristics in the Calabria Region. Despite a small number of officially reported cases, the size of the cohort was substantial. We showed that HIV infected patients with chronic hepatites, were affected by concomitant not-infectious co-morbidities more than the HIV mono-infected individuals. New HCV treatments are eagerly awaited.
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Utay, Netanya Sandler, Anoma Somasunderam, John E. Hinkle, Bryon W. Petschow, Christopher J. Detzel, Ma Somsouk, Carl J. Fichtenbaum, Eric M. Weaver, Audrey L. Shaw, and David M. Asmuth. "Serum Bovine Immunoglobulins Improve Inflammation and Gut Barrier Function in Persons with HIV and Enteropathy on Suppressive ART." Pathogens and Immunity 4, no. 1 (May 3, 2019): 124. http://dx.doi.org/10.20411/pai.v4i1.276.
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Background: Systemic inflammation persists in chronic HIV infection and is associated with increased rates of non-AIDS events such as cardiovascular and liver disease. Increased gut permeability and systemic exposure to microbial products are key drivers of this inflammation. Serum-derived bovine immunoglobulin/protein isolate (SBI) supports gut healing in other conditions such as inflammatory bowel disease.Methods: In this randomized, double-blind study, participants receiving suppressive antiretroviral therapy (ART) with chronic diarrhea received placebo or SBI at 2.5 g BID or 5 g BID for 4 weeks, followed by a 20-week placebo-free extension phase with SBI at either 2.5 or 5 g BID. Intestinal fatty acid binding protein (I-FABP), zonulin, flagellin, lipopolysaccharide (LPS) and LPS-binding protein, and inflammatory markers were measured by ELISA or multiplex assays. Non-parametric tests were used for analysis.Results: One hundred three participants completed the study. By week 24 SBI significantly decreased circulating levels of I-FABP (-0.35 ng/mL, P = 0.002) and zonulin (-4.90 ng/mL, P = 0.003), suggesting improvement in gut damage, and interleukin-6 (IL-6) (-0.40 pg/mL, P = 0.002), reflecting improvement in systemic inflammation. In participants with the lowest quartile of CD4+ T-cell counts at baseline (189-418 cells/mL), CD4+ T-cell counts increased significantly (26 cells/mL; P = 0.002).Conclusions: Oral SBI may decrease inflammation and warrants further exploration as a potential strategy to improve gut integrity and decrease systemic inflammation among persons receiving prolonged suppressive ART.Keywords: HIV infection; CD4 T cell; Serum bovine immunoglobulin protein; Interleukin; Inflammation; Intestine; I-FABP
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Islam, Rahib K., Erinn Donnelly, and Kazi N. Islam. "Circulating Hydrogen Sulfide (H2S) and Nitric Oxide (NO) Levels Are Significantly Reduced in HIV Patients Concomitant with Increased Oxidative Stress Biomarkers." Journal of Clinical Medicine 10, no. 19 (September 28, 2021): 4460. http://dx.doi.org/10.3390/jcm10194460.
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Human immunodeficiency virus (HIV) attacks the immune system and weakens the ability to fight infections/disease. Furthermore, HIV infection confers approximately two-fold higher risk of cardiac events compared with the general population. The pathological mechanisms responsible for the increased incidence of cardiovascular disease in HIV patients are largely unknown. We hypothesized that increased oxidative stress and attenuated circulating levels of the cardioprotective gaseous signaling molecules, nitric oxide (NO), and hydrogen sulfide (H2S) were involved in the cardiovascular pathobiology observed in HIV patients. Plasma samples from both HIV patients and age–matched normal subjects were used for all assays. Oxidative stress was determined by analyzing the levels of advanced oxidation protein products (AOPP) and H2O2. Antioxidant levels were determined by measuring the levels of trolox equivalent capacity. ADMA, hs-CRP, and IL-6 were determined by using ELISA. The levels of H2S (free H2S and sulfane sulfur) and NO2 (nitrite) were determined in the plasma samples by using gas chromatography and HPLC, respectively. In the present study we observed a marked induction in the levels of oxidative stress and decreased antioxidant status in the plasma of HIV patients as compared with the controls. Circulating levels of the cardiovascular disease biomarkers: ADMA, hs-CRP (high-sensitivity C-reactive protein), and IL-6 were significantly increased in the circulatory system of HIV patients. The levels of both nitrite and H2S/sulfane sulfur were significantly reduced in the plasma of HIV patients as compared with normal subjects. Our data demonstrate significant increases in circulating biomarkers of oxidative stress and cardiovascular (CV) in conjunction with decreased bioavailability of H2S and NO in HIV patients. Diminished levels of these two cardioprotective gaseous signaling molecules may be involved in the pathogenesis of CV disease in the setting of HIV.
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Younas, Mehwish, Christina Psomas, Vikram Mehraj, Renaud Cezar, Pierre Portales, Edouard Tuaillon, Adeline Guigues, Jacques Reynes, Pierre Corbeau, and Jean-Pierre Routy. "Plasma Level of Soluble ST2 in Chronically Infected HIV-1 Patients with Suppressed Viremia." Open AIDS Journal 11, no. 1 (April 26, 2017): 32–35. http://dx.doi.org/10.2174/1874613601711010032.
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Introduction: Interleukin-33 (IL-33) is a cell damage-induced alarmin. The plasma concentration of suppression of tumorogenicity (sST2), a surrogate marker of IL-33 production, is a prognostic marker of cardiovascular disease. Observation: Recently, we reported that sST2 plasma levels were elevated in early HIV-1 infection and linked to markers of microbial translocation and of T cell activation. Results: Here we show that it is not the case in patients with suppressed viremia. Thus, IL-33 plays its alarmin role only during the early phase of the infection.
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Masupe, Tiny, Yohana Mashalla, Esther Seloilwe, Harun Jibril, and Heluf Medhin. "Integrated management of HIV/NCDs: knowledge, attitudes, and practices of health care workers in Gaborone, Botswana." African Health Sciences 19, no. 3 (November 4, 2019): 2312–23. http://dx.doi.org/10.4314/ahs.v19i3.3.
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Background: The epidemiologic transition and double disease burden from chronic infections and Non-communicable diseases (NCDs) worldwide requires re-engineering of healthcare delivery systems. Healthcare workers (HCWs) need to adapt to new integrated disease management approaches and change from current disease-specific management. Objectives: The study aimed to determine HCWs knowledge, capacity and skills for management of NCDs among HIV patients and their attitudes towards integrated HIV/NCDs disease management approaches for future clinical practice. Methods: Descriptive cross-sectional survey among HCWs attending to HIV patients at selected government facilities. Results: One hundred out of 105 responses were analysed. Only 6% could fully define NCDs. Awareness levels of NCDs were high: Diabetes and hypertension 98%; cancer 96%; cardiovascular diseases 86%. However, 11.8% and 58% classified HIV and malaria respectively as NCDs. Most respondents (88%) believe that integrating HIV/NCDs care would be good use of resources while 62% disagreed with current separate facility management of HIV patients with NCDs. Over 60% routinely screened HIV patients for NCDs risk factors: Smoking (87.2%), alcohol (90.8%), diet (84.9%) and physical activity (73.5%). Conclusion: There were gaps in detailed knowledge on NCDs, but positive attitude towards routine primary care integrated HIV/NCDs management, showing likely support for implementation of such policy.Keywords: Non-communicable diseases, knowledge, attitude, HIV, integration.
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Sharathkumar, Anjali, Brandy Trawinski, J. Michael Soucie, Anne Greist, Craig Haddix, and Amy D. Shapiro. "Cardiovascular Disease in Patients with Hemophilia: Single Centre Experience." Blood 112, no. 11 (November 16, 2008): 2272. http://dx.doi.org/10.1182/blood.v112.11.2272.2272.
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Abstract Background: Cardiovascular disease (CVD) is at epidemic levels (37%, Heart Disease and Stroke Statistics, 2008 Update) in the US and is also affecting hemophilia patients. Conflicting reports exist concerning the potential protective effect of hemophilia on the occurrence of CVD. Objective: To evaluate the prevalence and risk factors of CVD events in patients with hemophilia ≥40 years old. Methods: This cross sectional study included all patients with hemophilia followed at Indiana Hemophilia and Thrombosis Center (IHTC) from January 2004 to June 2008. The following data were obtained from patient medical records: demographics; hemophilia severity; inhibitor history; HIV/HCV infection; established CVD risk factors including body mass index (BMI), hypertension, diabetes, smoking, hypercholesterolemia, and lipid profiles; information on CVD events; and cause of death. CVD events were defined as documented ischemic heart disease, coronary artery disease, and stroke/transient ischemic attacks due to hypertension/atherosclerosis. Univariate and multivariate analyses were performed to identify risk factors for CVD in this population. Results: A total of 174 patients were identified; 17 (9.7%) were excluded due to incomplete medical records. Population characteristics are described in Table I. Compared to hemophilia A, hemophilia B patients were more frequently obese, hypertensive and prone to cardiac events (Table I). The life-time prevalence of CVD events for the entire cohort was 22.9% (36/157; 95% CI 16.7 to 29.7%). Mortality rate for the entire cohort was 10.8% (17/157); CVD contributed to 64.7% (11/17) of deaths. For hemophilia A, hypertension, high cholesterol, smoking, obesity/elevated BMI were associated with risk of CVD events while HCV infection and low HDL showed a trend towards significance. For hemophilia B, age, hypertension and presence of diabetes were associated with CVD events while smoking showed a trend towards significance. In multivariate analysis, older age, presence of hypertension, and smoking were predictors of CVD. Type and severity of hemophilia, presence of HIV/HCV infection, lipid profile abnormalities, HCV infection and inhibitor history did not influence the CVD risk. The loss of a considerable number of severe hemophilics due to HIV related deaths over the last two decades may have influenced the demographics of the study cohort. Conclusion: This single center study underscores the increasing burden of CVD in patients with hemophilia in the US, implying that the diagnosis of hemophilia regardless of severity does not confer a protective effect against CVD. Routine screening for CVD thus should be mandatory for hemophilia patients after the age of 40 years. Table I: Patient characteristics of hemophilia A and B Variable Hemophilia A (N=81) Hemophilia B (N=76) P value Severity Severe 21 (25.9%) 21 (27.63%) 0.001 Moderate 15 (18.5%) 32 (42.10%) Mild 45 (55.6%) 23 (30.26%) Age (decade) 40–50 35 (43.2%) 28 (36.8%) 0.757 51–60 24 (29.6%) 20 (26.3%) 61–70 16 (19.8%) 19 (25%) >70 6 (7.4%) 9 (11.9%) Mean Age (yrs) 54±11.32 57.35±13 0.092 Hypertension No 56 (69.1%) 42 (55.3%) 0.041 Yes 24 (29.6%) 34 (44.7%) Cholesterol (↑) No 50 (61.7%) 34 (44.7%) 0.103 Yes 21 (25.9%) 27 (35.5%) Missing data 10 (12.3%) 15 (19.75) Diabetes No 72 (88.9%) 63 (82.9%) 0.0359 Yes 9 (11.1%) 13 (17.1%) Obesity No 64 (79.0%) 35 (46.1%) 0.001 Yes 16 (19.8%) 40 (52.6%) HIV No 21 (25.9%) 73 (96.1%) 0.000 Yes 59 (72.8%) 3 (3.9%) HCV No 21 (25.9%) 29 (38.2%) 0.125 Yes 59 (72.8%) 47 (61.8%) Inhibitor No 75 (92.6%) 75 (98.7%) 0.059 Yes 5 (6.2%) 1 (2.3%) CVD events No 66 (81.5%) 55 (72.4%) 0.189 Yes 15 (18.5%) 21 (27.6%) CVD event type Cardiac 9/15 (60%) 18/21 (85.7%) 0.03 Stroke/TIA 8/15 (53.3%) 5/21 (23.8%) 0.563 Table II: Multivariate analysis showing association between variables and cardiovascular events for the entire cohort 95% Wald Confidence Limits Variable Odds ratio Lower limit Upper limit Hypertension 5.77 1.77 18.84 Smoking 5.99 1.92 18.72 Hemophilia B versus A 1.87 0.548 6.38 Age (51–60 years versus 40–50 years) 13.40 2.59 69.44 Age group (61–70 years versus 40–50 years) 4.14 0.78 21.871 Age group (>70 years versus 40–50 years) 44.46 5.72 345.75 Disease severity (Moderate versus Mild) 2.22 0.57 8.70 Disease severity (Severe versus Mild) 4.04 0.77 21.23 Diabetes 2.90 0.84 10.10 Obesity 0.491 0.149 1.615
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Michienzi, Sarah M., Thomas D. Chiampas, Amy Valkovec, Siria Arzuaga, Mahesh C. Patel, Scott Borgetti, and Melissa E. Badowski. "941. Incarcerated patients living with HIV: Atherosclerotic cardiovascular disease risk and management." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S503—S504. http://dx.doi.org/10.1093/ofid/ofaa439.1127.
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Abstract Background The 2018 American Heart Association and American College of Cardiology (AHA/ACC) 2018 Guideline on the Management of Blood Cholesterol included human immunodeficiency virus (HIV) as an atherosclerotic cardiovascular disease (ASCVD) risk enhancer for the first time. Our study investigates if patients living with HIV in the Illinois Department of Corrections (IDOC) were prescribed appropriate HMG-CoA reductase inhibitor (statin) therapy following release of these guidelines based on risk. Methods This was a retrospective study of patients with > 1 visit in our multidisciplinary HIV IDOC Telemedicine Clinic from 1/1/19-6/1/19. Our prescriptive authority is limited to HIV and directly related conditions, and we provide recommendations to on-site providers for other comorbidities. Included patients were > 18 years of age, HIV positive, and incarcerated within IDOC. Excluded patients had existing ASCVD. Data from the first visit in the study period were extracted from the electronic medical record and analyzed utilizing descriptive statistics. Primary objectives were to quantify ASCVD risk and appropriate statin use in our population. Results Of the 158 patients included, average age was 42 years. The majority were male (89%), Black (73%), overweight/obese (117/148, 79%), on an integrase single-tablet regimen (78%), with CD4 >200 cells/µL (97%), and HIV RNA < 20 copies/mL (85%). Of the 18 females, 8 were transgender. Within the prior year, 65% had a lipid panel. For the 50 patients meeting criteria for 10-year ASCVD estimation, median (range) risk was 6.6% (0.8% - 31.9%). Only 12 patients were on statins. Of these, all were indicated per AHA/ACC guidelines with 10 prescribed appropriate intensity. An additional 45 patients had indications for statins but were untreated. In total, 47 patients (30%) were not receiving appropriate statin therapy. Conclusion Results of our study suggest ASCVD risk management is an area of improvement for inmates living with HIV, especially as we look towards caring for an aging HIV population. Future directions include comparing these data to data from a later time point to evaluate time for guideline uptake. Disclosures Thomas D. Chiampas, PharmD, BCPS, AAHIVP, Gilead (Employee)
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Ghazi, Lama, Jason V. Baker, Shweta Sharma, Mamta K. Jain, Adrian Palfreeman, Coca Necsoi, Daniel D. Murray, James D. Neaton, and Paul E. Drawz. "Role of Inflammatory Biomarkers in the Prevalence and Incidence of Hypertension Among HIV-Positive Participants in the START Trial." American Journal of Hypertension 33, no. 1 (September 6, 2019): 43–52. http://dx.doi.org/10.1093/ajh/hpz132.
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Abstract BACKGROUND The association between hypertension (HTN) and inflammatory biomarkers (interleukin-6 [IL-6] and high-sensitivity C-reactive protein [hsCRP]) in HIV-positive persons with CD4+ count >500 cells/mm3 is unknown. METHODS We studied HTN in participants of the Strategic Timing of AntiRetroviral Treatment (START) trial of immediate vs. deferred antiretroviral therapy (ART) in HIV-positive, ART naive adults with CD4+ count > 500 cells/mm3. HTN was defined as having a systolic blood pressure (BP) ≥140 mmHg, a diastolic BP ≥90 mmHg, or using BP-lowering therapy. Logistic and discrete Cox regression models were used to study the association between baseline biomarker levels with prevalent and incident HTN. RESULTS Among 4,249 participants with no history of cardiovascular disease, the median age was 36 years, 55% were nonwhite, and the prevalence of HTN at baseline was 18.9%. After adjustment for race, age, gender, body mass index (BMI), diabetes, smoking, HIV RNA and CD4+ levels, associations of IL-6 and hsCRP with HTN prevalence were not significant (OR per twofold higher:1.10, 95% confidence interval [CI]: 0.99, 1.20 for IL-6 and 1.05, 95% CI: 0.99, 1.10 for hsCRP). Overall incidence of HTN was 6.8 cases/100 person years. In similarly adjusted models, neither IL-6 (Hazard ratios [HR] per twofold higher IL-6 levels: 0.97, 95% CI: 0.88, 1.08) nor hsCRP (HR per twofold higher hsCRP levels: 0.97, 95% CI: 0.92, 1.02) were associated with risk of incident HTN. Associations did not differ by treatment group. Age, race, gender, and BMI were significantly associated with both the prevalence and incidence of HTN. CONCLUSIONS Traditional risk factors and not baseline levels of IL-6 or hsCRP were associated with the prevalence and incidence of HTN in START.
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Martin-Iguacel, R., J. M. Llibre, and N. Friis-Moller. "Risk of Cardiovascular Disease in an Aging HIV Population: Where Are We Now?" Current HIV/AIDS Reports 12, no. 4 (September 30, 2015): 375–87. http://dx.doi.org/10.1007/s11904-015-0284-6.
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Karanika, Styliani, Theodoros Karantanos, Herman Carneiro, and Sabrina A. Assoumou. "Development and Validation of the HIV-CARDIO-PREDICT Score to Estimate the Risk of Cardiovascular Events in HIV-Infected Patients." Cells 12, no. 4 (February 5, 2023): 523. http://dx.doi.org/10.3390/cells12040523.
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Importance: Commonly used risk assessment tools for cardiovascular disease might not be accurate for HIV-infected patients. Objective: We aimed to develop a model to accurately predict the 10-year cardiovascular disease (CV) risk of HIV-infected patients. Design: In this retrospective cohort study, adult HIV-infected patients seen at Boston Medical Center between March 2012 and January 2017 were divided into model development and validation cohorts. Setting: Boston Medical Center, a tertiary, academic medical center. Participants: Adult HIV-infected patients, seen in inpatient and outpatient setting. Main Outcomes and Measures: We used logistic regression to create a prediction risk model for cardiovascular events using data from the development cohort. Using a point-based risk-scoring system, we summarized the relationship between risk factors and cardiovascular disease (CVD) risk. We then used the area under the receiver operating characteristics curve (AUC) to evaluate model discrimination. Finally, we tested the model using a validation cohort. Results: 1914 individuals met the inclusion criteria. The model had excellent discrimination for CVD risk [AUC 0.989; (95% CI: 0.986–0.993)] and included the following 11 variables: male sex (95% CI: 2.53–3.99), African American race/ethnicity (95% CI: 1.50–3.13), current age (95% CI: 0.07–0.13), age at HIV diagnosis (95% CI: −0.10–(−0.02)), peak HIV viral load (95% CI: 9.89 × 10−7–3.00 × 10−6), nadir CD4 lymphocyte count (95% CI: −0.03–(−0.02)), hypertension (95% CI: 0.20–1.54), hyperlipidemia (95% CI: 3.03–4.60), diabetes (95% CI: 0.61–1.89), chronic kidney disease (95% CI: 1.26–2.62), and smoking (95% CI: 0.12–2.39). The eleven-parameter multiple logistic regression model had excellent discrimination [AUC 0.957; (95% CI: 0.938–0.975)] when applied to the validation cohort. Conclusions and Relevance: Our novel HIV-CARDIO-PREDICT Score may provide a rapid and accurate evaluation of CV disease risk among HIV-infected patients and inform prevention measures.
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Bellinati, Philipe Quagliato, Daniela Frizon Alfieri, Tamires Flauzino, Paulo Fernando Gasparetto Junior, Diogo Jorge Rossi, José Wander Breganó, Andrea Name Colado Simão, Elaine Regina Delicato de Almeida, Marcell Alysson Batisti Lozovoy, and Edna Maria Vissoci Reiche. "Association of Lower Adiponectin Plasma Levels, Increased Age and Smoking with Subclinical Atherosclerosis in Patients with HIV-1 Infection." Current HIV Research 18, no. 4 (September 8, 2020): 292–306. http://dx.doi.org/10.2174/1570162x18666200609114741.
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Background: The association between subclinical atherosclerosis and traditional cardiovascular disease (CVD) risk factors, inflammatory and metabolic biomarkers has been demonstrated around the world and specifically Brazilian human immunodeficiency virus type 1 (HIV-1)- infected individuals. However, the association between subclinical atherosclerosis and these aforementioned factors combined with anti-inflammatory biomarkers has not been examined in these populations. Objectives: To evaluate the association of the carotid intima-media thickness (cIMT) with CVD risk factors, inflammatory, metabolic and HIV-1 infection markers combined with adiponectin and interleukin (IL)-10 as anti-inflammatory variables. Methods: In this case-control study, 49 HIV-1-infected patients on combined antiretroviral therapy (cART) and 85 controls were compared for traditional CVD risk factors, inflammatory, metabolic, and anti-inflammatory variables. Further, we compared HIV-1-infected patients according to their cIMT (as continuous and categorized <0.9 or ≥0.9 mm variable) visualized by carotid ultrasonography doppler (USGD). Results: Twenty-four (48.9%) HIV-1-infected patients showed cIMT ≥0.9 mm. The patients had higher levels of C reactive protein on high sensitivity assay (hsCRP), tumor necrosis factor α, IL-6, IL-10, triglycerides, and insulin, and lower levels of adiponectin, total cholesterol and low-density lipoprotein cholesterol than controls (all p<0.05). Low levels of adiponectin were negatively associated with cIMT ≥0.9 mm (p=0.019), and explained 18.7% of the cIMT variance. Age (p=0.033) and current smoking (p=0.028) were positively associated with cIMT values, while adiponectin levels (p=0.008) were negatively associated with cIMT values; together, these three variables explained 27.3% of cIMT variance. Conclusion: Low adiponectin was associated with higher cIMT in HIV-1-infected patients on cART. Low adiponectin levels in combination with age and smoking could explain, in part, the increased subclinical atherosclerosis observed in these patients. Adiponectin may be a good candidate for predicting subclinical atherosclerosis in the management of HIV-1-infected patients in public health care, especially where USGD is not available.
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Funderburg, Nicholas T., David A. Zidar, Carey Shive, Anthony Lioi, Joseph Mudd, Laura W. Musselwhite, Daniel I. Simon, et al. "Shared monocyte subset phenotypes in HIV-1 infection and in uninfected subjects with acute coronary syndrome." Blood 120, no. 23 (November 29, 2012): 4599–608. http://dx.doi.org/10.1182/blood-2012-05-433946.
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Abstract The mechanisms responsible for increased cardiovascular risk associated with HIV-1 infection are incompletely defined. Using flow cytometry, in the present study, we examined activation phenotypes of monocyte subpopulations in patients with HIV-1 infection or acute coronary syndrome to find common cellular profiles. Nonclassic (CD14+CD16++) and intermediate (CD14++CD16+) monocytes are proportionally increased and express high levels of tissue factor and CD62P in HIV-1 infection. These proportions are related to viremia, T-cell activation, and plasma levels of IL-6. In vitro exposure of whole blood samples from uninfected control donors to lipopolysaccharide increased surface tissue factor expression on all monocyte subsets, but exposure to HIV-1 resulted in activation only of nonclassic monocytes. Remarkably, the profile of monocyte activation in uncontrolled HIV-1 disease mirrors that of acute coronary syndrome in uninfected persons. Therefore, drivers of immune activation and inflammation in HIV-1 disease may alter monocyte subpopulations and activation phenotype, contributing to a pro-atherothrombotic state that may drive cardiovascular risk in HIV-1 infection.
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Toribio, Mabel, Evelynne S. Fulda, Sarah M. Chu, Zsofia D. Drobni, Magid Awadalla, Madeline Cetlin, Takara L. Stanley, et al. "Menopausal Symptoms and Cardiovascular Disease Risk Indices Among Women With HIV." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A293—A294. http://dx.doi.org/10.1210/jendso/bvab048.597.
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Abstract Background: Women with HIV (WWH) (vs. women without HIV) have an increased risk of cardiovascular disease (CVD) in relation to heightened systemic immune activation/inflammation. Moreover, WWH show evidence of advanced reproductive aging and unique patterns of hot flash symptomatology. General population studies have revealed that hot flashes may relate to surrogate markers of CVD risk. The relationship between hot flashes and immune activation as well as subclinical cardiac pathology among WWH has not been previously investigated. Methods: In a prospective, cross-sectional study, 23 WWH on anti-retroviral therapy and 19 women without HIV (ages 40–75), group-matched on age and BMI, were enrolled and completed reproductive health assessments, immune phenotyping and cardiovascular MRI. Women without prior CVD or diabetes were eligible. Results: Women were similar in age and BMI (WWH vs. women without HIV: 51 ± 5 vs. 52 ± 6 years, P=0.79 and 32 ± 8 vs. 31 ± 7 kg/m2, P=0.71). There was no significant between-group difference in the percentage of women without menses in the past year (p=0.52) or in the percentage of women with undetectable levels of anti-mullerian hormone (p=0.71). No women in either group were on estrogen and/or progesterone for treatment of menopausal symptoms. Hot flash frequency (days per week with hot flashes) was higher among WWH versus women without HIV (median [IQR], 7.0 [1.3, 7.0] vs. 0.8 [0.0, 2.1], p=0.01). In sensitivity analyses excluding either women with menses in the past year or with detectable AMH, WWH still reported a significantly higher number of days per week with hot flashes (7.0 [6.3, 7.0] vs. 0.4 [0.0, 2.3], p=0.007, and 7.0 [2.4, 7.0] vs. 0.8 [0.0, 2.1], p=0.01, respectively). Among WWH experiencing (vs. not experiencing) hot flashes in the past year, longer duration of ART use was noted (21.2 [16.0, 22.7] vs. 9.3 [3.3, 16.0] years, p=0.03). Among the entire cohort and among WWH, women with more than one hot flash per day had higher levels of soluble CD14, a marker of monocyte activation, compared to women with one or fewer hot flash per day (p=0.004 and p=0.02, respectively). Among WWH and a history of hot flashes, years since onset of hot flashes related to cardiovascular MRI-derived measures of subclinical pathology. Specifically, years since onset of hot flashes related directly to myocardial steatosis (intramyocardial triglyceride content; ρ=0.80, p=0.02) and inversely to diastolic function (left atrial passive ejection fraction; ρ=─0.70, p=0.03). Conclusions: WWH experienced a higher frequency of hot flashes compared to women without HIV. Among WWH, hot flash symptomatology related to systemic immune activation and to cardiovascular MRI-derived measures of CVD risk. Additional research is required to improve understanding of mechanisms underlying these relationships and determine if hot flashes are a sex-specific risk factor for CVD in WWH.
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Umeh, Obiamiwe C., and Judith S. Currier. "Lipids, metabolic syndrome, and risk factors for future cardiovascular disease among HIV-infected patients." Current HIV/AIDS Reports 2, no. 3 (September 2005): 132–39. http://dx.doi.org/10.1007/s11904-005-0006-6.
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Nozza, Silvia, Laura Timelli, Annalisa Saracino, Nicola Gianotti, Claudia Lazzaretti, Alessandro Tavelli, Massimo Puoti, et al. "Decrease in Incidence Rate of Hospitalizations Due to AIDS-Defining Conditions but Not to Non-AIDS Conditions in PLWHIV on cART in 2008–2018 in Italy." Journal of Clinical Medicine 10, no. 15 (July 30, 2021): 3391. http://dx.doi.org/10.3390/jcm10153391.
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Background: We aimed to describe the change in the incidence and causes of hospitalization between 2008 and 2018 among persons living with HIV (PLWHIV) who started antiretroviral therapy (ART) from 2008 onwards in Italy. Methods: We included participants in the ICONA (Italian Cohort Naïve Antiretrovirals) cohort who started ART in 2008. All the hospitalizations occurring during the first 30 days from the start of ART were excluded. Hospitalizations were classified as due to: AIDS-defining conditions (ADC), non-ADC infections and non-infections/non-ADC (i.e., cardiovascular, pulmonary, renal-genitourinary, cancers, gastrointestinal-liver, psychiatric and other diseases). Comparisons of rates across time were assessed using Poisson regression. The Poisson multivariable model evaluated risk factors for hospitalizations, including both demographic and clinical characteristics. Results: A total of 9524 PLWHIV were included; 6.8% were drug users, 48.9% men-who-have sex with men (MSM), 39.6% heterosexual contacts; 80.8% were males, 42.3% smokers, 16.6% coinfected with HCV and 6.8% with HBV (HBsAg-positive). During 36,157 person-years of follow-up (PYFU), there were 1058 hospitalizations in 747 (7.8%) persons; they had HIV-RNA >50 copies mL in 34.9% and CD4 < 200/mmc in 27%. Causes of hospitalization were 23% ADC, 22% non-ADC infections, 55% non-infections/non-ADC (11% cancers; 9% gastrointestinal-liver; 6% cardiovascular; 5% renal-genitourinary; 5% psychiatric; 4% pulmonary; 15% other). Over the study period, the incidence rate (IR) decreased significantly (from 5.8 per 100 PYFU in 2008–2011 to 2.21 per 100 PYFU in 2016–2018). Age > 50 years, intravenous drug use (IDU), family history of cardiovascular disease, HIV-RNA > 50, CD4 < 200, were associated with a higher hospitalization risk. Conclusions: In our population of PLWHIV, the rate of hospitalization decreased over time.
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Wiley, Brian, Kristin Erlandson, Katherine Tassiopoulos, Yizhe Song, Rachel Presti, Kelly L. Bolton, and Grant A. Challen. "Clonal Hematopoiesis Is Associated with Risk of Cardiovascular Disease in Individuals with Human Immunodeficiency Virus." Blood 138, Supplement 1 (November 5, 2021): 3277. http://dx.doi.org/10.1182/blood-2021-151843.
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Abstract Introduction An estimated 1.2 million individuals in the United States are living with HIV (www.hiv.gov). Thanks to modern antiretroviral therapies (ART), the life expectancies of individuals living with HIV now approach those of people without HIV (Marcus 2020). But with this, an increase in the proportion of deaths due to non-infectious causes has occurred including, predominately, cardiovascular disease (CVD). Multiple studies have shown that HIV infection is an independent risk factor for cardiovascular disease. This increased risk is multifactorial due to an increased prevalence of traditional CVD risk factors and HIV-specific risk factors including ART, chronic inflammation and immune activation (Hsue 2010). Clonal Hematopoiesis, characterized by the expansion of blood cells stemming from a mutant hematopoietic stem/progenitor cell (HSPCs) is an emerging risk factor for cardiovascular disease. Mechanistically, this is thought to be driven, at least in part, by CH-induced proinflammatory circulating leukocytes (Jaiswal 2017, Bick 2020). Recent data suggest that inflammatory states may also promote the expansion of DNMT3A and TET2 CH mutant HSPCs suggesting a potential feedback loop (Zheng 2019, King 2019). CH has been recently reported to be increased among individuals living with HIV (Dharan 2021). Whether CH is a risk factor for HIV-associated CVD is not known. Given evidence of an increased prevalence of CH among those with HIV, we hypothesized that CH would predict risk of CVD. Methods We performed a nested case-control study drawn from the AIDS Clinical Trials Group Longitudinal Linked Randomized Trials (ALLRT) observational study which was a long-term study of individuals with newly diagnosed HIV receiving ART (N=4,371). Cases who developed a cardiovascular event were matched to controls with no event based on age at blood draw and sex. Peripheral blood mononuclear cells (PMBCs) were isolated from the blood draw closest to the time of CVD event or time of censoring, for cases and controls respectively. Extracted DNA was subjected to whole exome sequencing (WES) at a median depth of 500x. We also included WES data from 267 children sequenced using the same platform as a technical panel of normal (PON). Mutation calling was performed using Mutect2, VarDict and Varscan2. We retained variants that met the following criteria: 1) passed by at least two callers 2) showed statistically significant higher variant allele fraction (VAF) compared to our PON 3) had VAF between 2-35% 4) at least 6 reads supporting the variant 5) passed additional post-calling filters for germline variants and sequencing artifacts 6) were annotated as a putative driver of CH based on previously defined criteria. Results Over 13 years of follow-up we observed 83 cardiovascular events: 4 cases of ASC, 14 of stroke, 25 of cerebrovascular accident, 37 of myocardial infarction, 2 of peripheral artery disease, and 1 heart failure. The mean age of our participants was 51.6 years, 81% were male, 35% percent were African-American, 17% were Hispanic and 2% were Asian. Among 161 participants (83 cases and 78 controls) we observed at least one CH mutation in 14% of participants (18% of cases and 10% of controls). The median VAF was 3.5% with 23 individuals harboring a median of 1 mutation (range 1-2). In a conditional logistic regression model adjusted for race, Atherosclerotic Cardiovascular Disease (ASCVD) Risk Score and stratified by case-control matched pairs, CH was significantly associated with CVD (OR=3.70, 95% CI 1.03-13.23 p=0.045). Because of the possible confounding effects of classes of ART therapy on the CH-CVD association, we explored whether the prevalence of CH differed based on prior exposure to ART sub-class(es). We did not observe differences in the frequency of CH among individuals with prior exposure to different ART regimens (Non-Nucleoside Reverse Transcriptase Inhibitors 14%, Nucleoside reverse transcriptase inhibitors 17%, Protease inhibitors 20%, Integrase inhibitors 18%) Conclusions Among individuals with HIV, CH is associated with a nearly four-fold increased risk of CVD. These findings highlight the relevance of CH to HIV-associated CVD and provide support for interventions targeting potential CH-induced pro-inflammatory states among patients with HIV. Disclosures Erlandson: Gilead Sciences: Consultancy, Research Funding; Viiv Pharmaceuticals: Consultancy; Janssen Pharmaceuticals: Consultancy. Bolton: bristol myers squibb: Research Funding.
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Bang, Ajay, Deepti Deshmukh, and Sanjay Raut. "A STUDY OF CARDIAC MANIFESTATIONS IN PATIENTS WITH HIV/AIDS." International Journal of Advanced Research 9, no. 10 (October 31, 2021): 411–22. http://dx.doi.org/10.21474/ijar01/13560.
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Introduction:HIV/AIDS pandemic is evolving as a major public concern. Cardiovascular diseases are common in HIV-positive patients. Many patients without any symptoms or signs were found to have a cardiovascular disease on autopsy.It is expected that the risk of cardiovascular disease willrise in the following years due to the cardiovascular risk profile andincreased life expectancy of infected patients. Therefore,diagnosis andtherapy of HIV-associated cardiovascular diseases should be part of the evaluation and management of the HIV-positive patient. Objectives: To find out the frequency of cardiac manifestations on clinical examination, electrocardiography, chest X-ray, and echocardiographic examination. To assess the association of Cardiac abnormality with CD4 Count in patients with HIV/AIDS. Toevaluate the association between cardiac abnormalities with types and duration of antiretroviral therapy regimen (ART). Method:A total of 100 consecutive patients visiting ART OPD and admitted to our institute were examined for signs and symptoms of cardiovascular disease. All patients were evaluated with electrocardiography, chest X-ray, and 2 D echocardiography. CD4 count was measured for all patients using flowcytometry using a BD FACS Count system. Results:Out of 100 patients, 53% were male and 47% were female. Patients were divided into subgroups with CD4 count <200, 200-349, 350-499, and ≥500. The mean CD4 count was 403.62 ± 284.98. Prevalence of the cardiovascular abnormality on ECG, chest X-ray, and echocardiography were 74%, 10%, and 51% respectively. The left ventricular systolic dysfunction was the most common finding in our study with fractional shortening ≤25% in 34% of patients and LVEF <50% in 27% of patients followed by left ventricular diastolic function (26%), dilated cardiomyopathy (6%), pulmonary hypertension (4%), and regional wall motion abnormality (2%).Reduced LV ejection fraction (<50%) and left ventricular diastolic dysfunction were statistically significant in patients with CD4 count less than 200/mm3. Conclusion: In present study electrocardiographic, chest X-ray and echocardiographic abnormalities were present in 74%, 10% and 51% patients respectively. Cardiac abnormalities such as QTc prolongation, LBBB, reduced left ventricular ejection fraction, and left ventricular diastolic dysfunction were more significantly higher in patients with CD4 count less than 200/mm3. We could not find any statistically significant difference in cardiac abnormalities in patients on different ART regimens. Further studies are required with a higher sample size.
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Parameswaran, Rekha, Anne Greist, Lorrie Miller-Rice, Chris Roberson, Renee Murry, Matthew Sulkin, Henry Lynn, and Amy Shapiro. "Framingham Score in Congenital Hemophilia Patients (HP) with Cardiovascular Disease (CVD)." Blood 106, no. 11 (November 16, 2005): 320. http://dx.doi.org/10.1182/blood.v106.11.320.320.
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Abstract CVD risk factors of age, hypertension, high cholesterol (HC), smoking, diabetes are expressed in the Framingham coronary risk score. Previous data suggest that hemophilia may protect against CVD. However, CVD risk factors may place HP at risk as they age. HIV infected patients are a rapidly developing group with CVD. No data address the effect of established risk factors on CVD prevalence in HP. We report an extensive analysis of a single hemophilia treatment center (HTC) database for CVD risk factors and prevalence in HP. Framingham coronary risk scores were calculated for HP patients with documented CVD events, using age at time of event to calculate risk. HTC population ≥40 yrs, used as denominator, comprised 156 with FVIII deficiency (63 severe, 16 moderate, 77 mild);109 with FIX deficiency (24 severe, 53 moderate, 31 mild). Forty-eight HP had HIV infection, 113 had hepatitis C, and 25 had HIV/hepatitis C coinfection. Twenty-one HP, 10 with viral infection, ranging 49 to75 years, experienced 23 CVD events. They included 11 FVIII (0 severe, 1 moderate, 10 mild),10 FIX (2 severe,6 moderate, 2 mild). CVD events included 13 myocardial infarction (MI); 5 cerebrovascular accidents (CVA); 1 patient with carotid stenosis and 4 HP with coronary artery disease on catheterization. Two patients each had both MI and CVA. Four patients underwent coronary artery bypass graft surgery. Of 8 patients on antiplatelet therapy, 2 had major bleeds (CNS and GI bleed); one had a minor bleed (epistaxis). Of these 21 HP with CVD, one patient had HIV disease; 8 had hepatitis C, 1 had co-infection with HIV and hepatitis C. One patient was on Vioxx® at the time of his CVD event.Six are deceased, all due to CVD. Overall, CVD affected 7.9% of HP aged >40 years in this population. Of all HP with viral infection in this HTC population, 40% experienced CVD. Ten-year CVD risk per Framingham model at time of event ranged from 10% to 37% (mean 20.1%; median 16%). All HP patients with CVD met the definition of high coronary risk per AHA guidelines with 10-year risk of CVD>10%. Management of established CVD in HP is difficult due to need for invasive procedures and bleeding risk with antiplatelet therapy. Primary prevention of CVD is thus crucial. Aggressive risk factor modification is indicated in all HP with 10-year risk score >10% for primary prevention of CVD. To our knowledge, this is the first application of the well validated Framingham score in the HP population.We conclude that the easily calculable Framingham score should be assessed in all HP over age 40, especially those with viral infections, and incorporated into the comprehensive care model.
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Tadayyon, Moh, and Stephen Cameron. "Key Data from the 10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV, 6–8 November 2008, London, UK." Antiviral Therapy 13, no. 8 (November 2008): 1115–27. http://dx.doi.org/10.1177/135965350801300809.
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Although the list of clinical complications associated with HIV therapy continues to grow, the underlying mechanisms remain incompletely understood. Metabolic abnormalities, such as dyslipidaemia, insulin resistance and cardiovascular disease continue to top the list, but there is an increasing appreciation of the effect of HIV and anti-retroviral therapy on body composition, bone metabolism, muscle function and autonomic nervous system control of lipid and glucose metabolism. The 10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV brought together physicians and researchers in the area of HIV management with world experts involved in adipose tissue metabolism and lipid regulation, bone and muscle metabolism and renin- angiotensin and blood pressure control to review and discuss recent findings in these areas. The data presented at the meeting highlight that studies of adipose tissue remain a major focus of attempts to unravel the pathophysiology that accompany lipodystrophy associated with HIV infection and/ or its therapy. There is also a growing appreciation and understanding of the direct role of HIV in the development of various comorbidities, including bone disease, cardiac dysfunction and neuropathologies, including peripheral neuropathy. Two key emerging themes were those of mitochondrial dysfunction and a heightened basal inflammatory state, exemplified by increased levels of proinflammatory cytokines, chemokines and markers such as C-reactive protein. These might prove to be the common denominators that link HIV-associated pathologies with diverse organ systems.
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Al-Kindi, Sadeer G., David A. Zidar, Grace A. McComsey, and Chris T. Longenecker. "Association of Anisocytosis with Markers of Immune Activation and Exhaustion in Treated HIV." Pathogens and Immunity 2, no. 1 (May 2, 2017): 138. http://dx.doi.org/10.20411/pai.v2i1.199.
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Background: Treated HIV infection is associated with heightened inflammation which can contribute to increased risk of cardiovascular disease (CVD). We have previously shown that anisocytosis, as measured by red cell distribution width (RDW), is independently associated with prevalent CVD in people living with HIV (PLHIV). In this study, we sought to identify immune correlates of RDW in PLHIV receiving antiretroviral therapy.Methods: We performed a cross-sectional and longitudinal analysis of 147 virally-suppressed PLHIV, who had LDL <130 mg/dL and evidence of heightened inflammation, in a randomized trial of statin therapy. A complete blood count and biomarkers of inflammation and immune activation/exhaustion were measured in peripheral blood at entry and after 24 and 48 weeks. Associations with RDW were estimated using linear regression and linear mixed models.Results: The median age (IQR) for the cohort at enrollment was 46 (40–53) years; 78% were male and 68% were African American. The median RDW for the cohort was 13.4% (12.9–14.0). Compared with the lowest RDW tertile, patients in the highest tertile were less likely to be male, and more likely to be African American, have lower hemoglobin, lower mean corpuscular volume, and higher platelet counts (all P<0.05). At baseline, RDW weakly correlated with C-reactive protein (r=0.196), d-dimer (r=0.214), fibrinogen (r=0.192), interleukin-6 (r=0.257), CD4+DR+38+ T cells (r=0.195), and CD4+PD1+ T cells (r=0.227), all P<0.05. Only IL-6, CD4+38+DR+ T cells, and CD4+PD1+ T_cells remained associated after adjustment for clinical factors known to affect RDW in the general population. Over 48 weeks, RDW did not change and there was no significant effect of statin (P=0.45). After adjustment for clinical parameters, RDW remained positively associated with CD4+38+DR+ and CD4+PD1+ T cells across all time points (P=0.05).Conclusion: In this population of treated HIV+ subjects, anisocytosis was associated with biomarkers of inflammation and T-cell activation/exhaustion over time and independent of clinical confounders. Therefore, RDW may be a useful prognostic biomarker of cardiovascular risk that partially reflects chronic inflammation and immune exhaustion in PLHIV receiving antiretroviral therapy.
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Spiff Eleazar, Emeka, Clara Idara Eleazar, Daniel Chukwu Nwachukwu, and Uchenna Ifeanyi Nwagha. "ECG abnormalities among HIV infected children placed on ART at Enugu, South East of Nigeria." African Health Sciences 20, no. 4 (December 16, 2020): 1742–8. http://dx.doi.org/10.4314/ahs.v20i4.26.
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Background: Cardiovascular abnormalities are not much reported among human immunodeficiency virus (HIV) infected children especially in Africa where there is high HIV disease. In addition, the use of highly active antiretroviral therapy (HAART) in such children may have a protective effect on the cardiovascular system.
Methods: Cross-sectional study of randomly selected eighty HIV infected and 80 aged matched non- HIV-infected chil- dren were used. HIV-infected children were on HAART for more than 5years and had steadily received the treatment for 6 months prior to the time of the tests. Heights and weights were measured and body mass index calculated. Cardiac indi- ces evaluated were heart rate (HR), PR interval, QRS duration, QT/QTC Interval, P/QRS/T Axis, RV5/SV1 voltage and RV5+SV1 voltage.
Results: The average heart rate was significantly higher among HIV infected children on HAART than their non-infected counterparts (P= 0.019). At 0.05 significance level, their PR interval was significantly higher than those in the control group (P=0.050). The average QRS duration result also showed a significant difference between that of test and control subjects (P = 0.022)
Conclusion: The HAART usage possibly improved the cardiovascular functioning in the infected children but the protective effects diminish with increase age and longer exposure.
Keywords: HIV; cardiovascular; children; HAART.
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Kuate Defo, Alvin, Mhd Diaa Chalati, Christopher Labos, Lesley K. Fellows, Nancy E. Mayo, and Stella S. Daskalopoulou. "Association of HIV Infection and Antiretroviral Therapy With Arterial Stiffness: A Systematic Review and Meta-Analysis." Hypertension 78, no. 2 (August 2021): 320–32. http://dx.doi.org/10.1161/hypertensionaha.121.17093.
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Incidence of cardiovascular disease in people living with HIV has increased as overall survival has improved because of combination antiretroviral therapy (cART). Arterial stiffness is a composite indicator of cardiovascular disease risk independent of traditional risk factors. We aimed to synthesize the evidence on the relation of HIV and of cART to arterial stiffness. Medline, Embase, CINAHL, PubMed, and Cochrane Libraries were systematically searched for studies relating HIV/cART to arterial stiffness until June 2019. A standardized extraction form was used to collect data from published reports. Random-effects meta-analyses were performed to produce standardized mean differences and 95% CIs from studies reporting carotid-femoral pulse wave velocity. We retrieved 995 citations. Seventy-four studies (N=18 711 participants/13 119 with HIV) were included: 59 cross-sectional, 9 cohort, and 6 randomized trials. In meta-analyses of 17 studies, arterial stiffness was found to be elevated overall in individuals with HIV relative to controls (standardized mean difference, 0.44 m/s [95% CI, 0.25–0.63]) and in cART-treated versus untreated individuals with HIV (standardized mean difference, 0.35 m/s [95% CI, 0.13–0.57]). Several studies suggested that cumulative exposure to cART is associated with a continual increase in arterial stiffness. However, early initiation of treatment might improve arterial stiffness later in life. The results highlight the need for monitoring of cardiovascular risk in this population. The cross-sectional nature of most studies (59/74) mainly allowed for the exploration of associations; large longitudinal studies are needed to confirm the observed associations and establish causality between HIV/cART and arterial stiffness.
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Morani, Zoya, Saumil Patel, Sudeshna Ghosh, Falah Abu Hassan, Shriya Doreswamy, Sandeep Singh, Venkata Neelima Kothapudi, and Rupak Desai. "COVID-19 in HIV: a Review of Published Case Reports." SN Comprehensive Clinical Medicine 2, no. 12 (November 2, 2020): 2647–57. http://dx.doi.org/10.1007/s42399-020-00593-6.
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AbstractPatients with COVID-19 present with a myriad of comorbidities. An immunocompromised state like HIV in patients with COVID-19 can be life-threatening. We searched PubMed/Medline, Scopus, and Web of Science for case reports and case series about COVID-19 in HIV patients. We finally reviewed 20 case reports including cases of 43 patients with HIV and COVID-19. The mean age of 43 adult patients was 51.56 ± 27.56 years (range 24–76 years). Of these, 30 were male (69.77%), 11 were female (25.58%), and 2 were transgender (4.65%). A total of 25 patients (58.14%) were above 50 years of age. The most common cardiovascular comorbidities were hypertension and hyperlipidemia (48.8%), diabetes (20.93%), and morbid obesity (11.63%). Out of 43 HIV patients with COVID-19, 6 resulted in death (13.95%). All the patients who died were elderly above 50 years and required mechanical ventilation. HIV patients infected with COVID-19 had a high mortality rate. A high burden of pre-existing comorbidities and an advanced age in these patients make them prone to disease progression and worse outcomes.
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Espejo Ortiz, Cristian E., Yamile G. Serrano Pinto, Juan G. Sierra Madero, Alvaro Lopez Iñiguez, and Brenda Crabtree-Ramírez. "381. HIV Patients with COVID-19 Hospitalized in a Tertiary Care Center in Mexico City." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S260. http://dx.doi.org/10.1093/ofid/ofaa439.576.
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Abstract Background The main risk factors for severe COVID-19 described are diabetes, hypertension, cardiovascular disease, obesity, chronic lung and renal disease. HIV infection has not been found to be an independent factor for severe COVID-19, however, only small case series of HIV and COVID-19 have been reported. The aim of this study is to describe clinical characteristics and outcomes of HIV positive patients with COVID-19 hospitalized in a tertiary care hospital in Mexico City. Methods A single-center review of HIV-infected patients diagnosed with COVID-19 was performed using medical records from March 1st, 2020 to May 20th, 2020. We describe the clinical characteristics and outcomes Results A total of 11 PLWH were diagnosed with COVID-19, only 9 were hospitalized and are described here. One died, 6 were discharged and 2 remain hospitalized (table 1). Overall, the median age was 46 years, all males and most (7/9) were on INSTI based ART regimen and undetectable HIV viral load (9/9), with a median of CD4 counts of 581 cell/mm3. The median days since onset of COVID19 symptoms was 7 days. 6/9 had at least one comorbidity: hypertension (3/9) and chronic kidney disease (3/9). 7/9 had body max index >25. 7/9 had moderate to severe lung disease, evidenced by computed tomography. 4/9 required invasive mechanical ventilation, and all were successfully extubated. Table 1. Characteristics and outcomes * Conclusion Most of the HIV patients who required hospitalization due to COVID19 had comorbidities. In spite of severe and critical presentations, most patients have recovered. Outcomes appear no different from those seen for non-HIV infected patients, however larger studies to determine the risk that HIV infection confers to COVID19 outcomes are needed. Disclosures All Authors: No reported disclosures
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Pourcher, Valérie, Julie Gourmelen, Isabelle Bureau, and Stéphane Bouee. "Comorbidities in people living with HIV: An epidemiologic and economic analysis using a claims database in France." PLOS ONE 15, no. 12 (December 17, 2020): e0243529. http://dx.doi.org/10.1371/journal.pone.0243529.
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Objectives As people living with HIV (PLHIV) age, the burden of non-HIV related comorbidities increases resulting in additional healthcare costs. The present study aimed to describe the profile, the prevalence and the incremental costs of non-HIV related comorbidities in PLHIV compared to non-HIV matched controls (1:2 ratio) in France. Methods The French permanent sample of health beneficiaries (Echantillon généraliste de bénéficiaires [EGB]), a claims database representative of the national population, was used to assess comorbidities in PLHIV which were identified by the ICD-10 diagnosis codes of hospitalization, full healthcare coverage, and drug reimbursements between 2011 and 2014. The control group was matched by year of birth, gender, region of residence, and economic status. Total costs of outpatient care and hospitalizations were analysed from a societal perspective. A general linear model was used to assess the incremental cost per patient in PLHIV. Results A total of 1,091 PLHIV and 2,181 matched controls were identified with a mean ± standard deviation age of 46.7 ± 11.5 years. The prevalence of alcohol abuse (5.8% vs 3.1%; p<0.001), chronic renal disease (1.2% vs 0.3%; p = 0.003), cardiovascular disease (7.4% vs 5.1%; p = 0.009), dyslipidaemia (22% vs 15.9%; p<0.001), hepatitis B (3.8% vs 0.1%; p<0.001) and hepatitis C (12.5% vs 0.6%; p<0.001) was significantly higher in PLHIV compared with non-HIV controls. Other comorbidities such as anaemia, malnutrition, psychiatric diseases, and neoplasms were also more prevalent in PLHIV. Hospitalizations were significantly increased in PLHIV compared to controls (33.2% vs 16%; p<0.001). Mean total cost was 6 times higher for PLHIV compared to controls and 4 times higher after excluding antiretroviral drugs (9,952€ vs. 2,593€; p<0.001). Higher costs per person in PLHIV were significantly associated to aging (42€ per patient/year), chronic cardiovascular disease (3,003€), hepatitis C (6,705€), metastatic carcinoma (6,880€) and moderate or severe liver disease (6,299€). Conclusion Our results demonstrated an increase in non-HIV related comorbidities among PLHIV compared to matched controls. This study contributes to raise awareness on the burden of chronic comorbidities.
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Vogt, Paul R., Gennadiy Grigorevich Khubulava, and Sergey Pavlovich Marchenko. "EurAsia Heart - international cooperation in cardiovascular surgery." Pediatrician (St. Petersburg) 5, no. 4 (December 15, 2014): 127–31. http://dx.doi.org/10.17816/ped54127-131.
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Cardiovascular diseases are the major cause of death in neonates, children, adolescents and adults. Untreated congenital heart disease is the major cause of death worldwide in children younger than five years of age, exceeding the combined death rate caused, e.g. by malaria, tuberculosis or HIV [6]. In many developing countries, life expectancy is limited to an average of 58 to 64 years of age [1, 2]. In addition quality of life is markedly reduced while the number of disabled patients and patients depending from social welfare is steadily increasing. The major cause is undiagnosed and untreated cardiovascular diseases. Eighty percent of all cardiovascular deaths worldwide occur in developing countries [3]. Cardiology and cardiovascular surgery are powerful tools to increase the life expectancy, to improve and normalize the quality of life, to preserve patients able to work and to reduce the overall health care costs as well as costs for social welfare for those otherwise disabled by chronic cardiovascular diseases. Developing countries invest in cardiology and cardiovascular surgery. However, the establishment of a cardiovascular centre is a challenging task. The problem is that several specialties have to be developed simultaneously: cardiology, cardiac surgery, perfusion techniques, anaesthesia, intensive care as well as postoperative medical treatment - for adults and for children. The attractiveness of EurAsia Heart Foundation allowed establishing numerous international co-operations with excellent institutions, interested and engaged in teaching and education abroad.
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Castelli, Roberto, Riccardo Schiavon, Carlo Preti, and Laurenzia Ferraris. "HIV-Related Lymphoproliferative Diseases in the Era of Combination Antiretroviral Therapy." Cardiovascular & Hematological Disorders-Drug Targets 20, no. 3 (November 26, 2020): 175–80. http://dx.doi.org/10.2174/1871529x20666200415121009.
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HIV-positive patients have a 60- to 200-fold increased incidence of Non-Hodgkin Lymphomas (NHL) because of their impaired cellular immunity. Some NHL are considered Acquired Immunodeficiency Syndrome (AIDS) defining conditions. Diffuse large B-cell Lymphoma (DLBC) and Burkitt Lymphoma (BL) are the most commonly observed, whereas Primary Effusion Lymphoma (PEL), Central Nervous System Lymphomas (PCNSL), Plasmablastic Lymphoma (PBL) and classic Hodgkin Lymphoma (HL) are far less frequent. Multicentric Castleman disease (MCD) is an aggressive lymphoproliferative disorder highly prevalent in HIV-positive patients and strongly associated with HHV-8 virus infection. In the pre-Combination Antiretroviral Therapy (CART) era, patients with HIV-associated lymphoma had poor outcomes with median survival of 5 to 6 months. By improving the immunological status, CART extended the therapeutic options for HIV positive patients with lymphomas, allowing them to tolerate standard chemotherapies regimen with similar outcomes to those of the general population. The combination of CART and chemotherapy/ immuno-chemotherapy treatment has resulted in a remarkable prolongation of survival among HIVinfected patients with lymphomas. In this short communication, we briefly review the problems linked with the treatment of lymphoproliferative diseases in HIV patients. Combination Antiretroviral Therapy (CART) not only reduces HIV replication and restores the immunological status improving immune function of the HIV-related lymphomas patients but allows patients to deal with standard doses of chemotherapies. The association of CART and chemotherapy allowed to obtain better results in terms of overall survival and complete responses. In the setting of HIVassociated lymphomas, many issues remain open and their treatment is complicated by the patient’s immunocompromised status and the need to treat HIV concurrently.
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Knudsen, Andreas D., Lisanne Krebs-Demmer, Natascha I. D. Bjørge, Marie B. Elming, Marco Gelpi, Per E. Sigvardsen, Anne-Mette Lebech, et al. "Pericardial Adipose Tissue Volume Is Independently Associated With Human Immunodeficiency Virus Status and Prior Use of Stavudine, Didanosine, or Indinavir." Journal of Infectious Diseases 222, no. 1 (February 6, 2020): 54–61. http://dx.doi.org/10.1093/infdis/jiaa057.
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Abstract Background Increased pericardial adipose tissue is associated with higher risk of cardiovascular disease. We aimed to determine whether human immunodeficiency virus (HIV) status was independently associated with larger pericardial adipose tissue volume and to explore possible HIV-specific risk factors. Methods Persons with HIV (PWH) were recruited from the Copenhagen Comorbidity in HIV Infection (COCOMO) Study and matched 1:1 on age and sex to uninfected controls. Pericardial adipose tissue volume was measured using cardiac computed tomography. Results A total of 587 PWH and 587 controls were included. Median age was 52 years, and 88% were male. Human immunodeficiency virus status was independently associated with 17 mL (95% confidence interval [CI], 10–23; P < .001) larger pericardial adipose tissue volume. Larger pericardial adipose tissue volume was associated with low CD4+ nadir and prior use of stavudine, didanosine, and indinavir. Among PWH without thymidine analogue or didanosine exposure, time since initiating combination antiretroviral treatment (per 5-year use) was associated with l6 mL (95% CI, −6 to −25; P = .002) lower pericardial adipose tissue volume. Conclusions Human immunodeficiency virus status was independently associated with larger pericardial adipose tissue volume. Severe immunodeficiency, stavudine, didanosine, and indinavir were associated with larger pericardial adipose tissue volume. Persons with HIV with prior exposure to these drugs may constitute a distinct cardiovascular risk population.
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Pasca, Sergiu, Shiyu Wang, Susan Langan, Aparna Pallavajjala, Lisa Haley, Christopher D. Gocke, Wendy S. Post, et al. "Clonal Hematopoiesis Is More Common in People Living with HIV and May be Associated with Increased Prevalence of Cardiovascular Disease." Blood 138, Supplement 1 (November 5, 2021): 4298. http://dx.doi.org/10.1182/blood-2021-152860.
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Abstract Background: Cardiovascular disease (CVD) is more common in people living with HIV (PLWH) and may be related to abnormal immune activation. With aging, the expansion of mutated hematopoietic clones or clonal hematopoiesis (CH) has been associated with CVD events in the general population and is hypothesized to be driven by systemic inflammation. We investigated whether CH was more common in PLWH compared to those without HIV, whether the distribution of CH mutations differed by HIV status, and whether CH was associated with subclinical coronary atherosclerosis in PLWH. Methods: Study participants were selected from men in the Baltimore -Washington DC center of the Multicenter AIDS Cohort Study (MACS) who had had coronary CT angiography (CTA) as part of the MACS Cardiovascular Study 2. The MACS is a prospective study of the natural history of HIV infection in men who have sex with men, and includes both PLWH and HIV-uninfected men. Since the prevalence of CH increases with age, the oldest participants were preferentially included in this study. To detect CH, DNA extracted from viably frozen peripheral blood mononuclear cells or cell pellets was subjected to targeted, error-corrected, ultra-deep next generation sequencing (NGS) which included 70 genes frequently mutated in hematologic malignancies. CTA results and inflammatory biomarker levels were already available from MACS data. Results: The current analysis was a cross-sectional study involving 118 participants: 86 (72.9%) PLWH and 32 (27.1%) HIV-uninfected men (HIV-). The groups were well-balanced in terms of known major risk factors for CH such as age and smoking. The median age was 53 and 54 years for PLWH and HIV- men, respectively (p=0.147). Caucasians represented 37 (43.0%) of PLWH and 21 (65.6%) of HIV- men. Out of 86 PLWH, 72 (83.7%) were on antiretroviral therapy (ART) at the time of the assessment; 41 (47.7%) on a PI-containing regimen and 31 (36.0%) on an NNRTI-containing regimen. The HIV viral load was under 400 copies/mL in 77 (89.5%) of PLWH, and the median (IQR) CD4+ count was 585 (397, 745)/mL. The prevalence of coronary artery stenosis of 50% or more was 12 (14.3%) in PLWH and 5 (16.1%) in HIV- men (p = 0.774). Since the minimum size of the biologically relevant CH is unknown, we applied variant allele frequency (VAF) cut-offs of > 0.5% and > 1%. For both cutoffs, CH was significantly more frequent in PLWH than in HIV- men (p=0.012 and p=0.036, respectively) (Figure 1A). Mutations in epigenetic modifiers (DNMT3A, TET2) were the most common mutations among both PLWH and HIV- men. Interestingly, DNMT3A mutations were more frequent in PLWH (Figure 1B). For both VAF cut-offs, PLWH had significantly more somatic mutations than HIV-uninfected men (p = 0.043 and 0.033, respectively) (Figure 1C). Since inflammation-mediated complications of CH become more apparent in people with larger clones, we focused on CH with VAF > 1% in order to determine the clinical consequences of CH in PLWH. As CH is known to be a risk factor for accelerated CVD in the general population, we asked whether CH was also associated with subclinical atherosclerosis in PLWH. Coronary artery stenosis > 50% (moderate/severe) was significantly more frequent in PLWH with CH compared to PLWH without CH (p = 0.032) (Figure 1 D). This difference remained significant in multivariable logistic regression models that adjusted for the Framingham coronary heart disease 10-year risk (p=0.017) and for the Framingham hard coronary heart disease 10-year risk (p<0.01). Additionally, we examined the association of serum concentrations of several inflammatory markers such as CRP, IL-1b, IL-6, as well as white blood cell count, with the presence of CH in PLWH, but we found no significant associations. Conclusions: CH was more common in PLWH compared to HIV-uninfected men, and PLWH had more somatic mutations. Moreover, the presence of CH was significantly associated with the presence of coronary artery stenosis > 50% (moderate/severe) in PLWH, even after adjusting for known CVD risk factors. The results from our exploratory analysis may provide a potential explanation for increased CVD in PLWH. Larger studies are warranted to further delineate the etiology of increased CH in PLWH and its impact on accelerated CVD. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
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Wallet, Mark, Sofia Appelberg, Caroline Reist, Giorgio Guiulfo, John Sleasman, and Maureen Goodenow. "Reduction of HIV-1 innate immune activation by protease inhibitors (154.15)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 154.15. http://dx.doi.org/10.4049/jimmunol.186.supp.154.15.
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Abstract HIV-1-associated innate immune activation is caused by viral replication and/or microbial substances that leak from the gut lumen into the circulation (microbial translocation). Consequences of the ensuing HIV-1-associated inflammation range from neurocognitive impairment to cardiovascular disease where macrophages play a central role. HIV-1 therapy is evaluated based on suppression of viremia and restoration of CD4 T cells, while the effects of therapy on innate immune activation are rarely considered. The current study assessed the effects of protease inhibitors on macrophage activation ex vivo and in vivo. Nelfinavir [NFV] and tipranavir [TPV] inhibited LPS activation of human macrophages ex vivo as measured by reduced secretion of LPS-binding protein soluble CD14 [sCD14] and pro-inflammatory cytokines IL-6 and TNF. Cytokine secretion was inhibited prior to transcription by modulation of toll-like receptor signaling pathways. In vivo, NFV-treated HIV-1-infected patients presented with significantly reduced monocyte/macrophage activation as measured by a greater reduction in sCD14 plasma levels compared to those treated with indinavir or ritonavir. These data suggest that anti-inflammatory effects of NFV or TPV may augment efficacy of HIV-1 treatment by targeting HIV-1-assocated innate immune activation. Delineation of cellular targets of NFV or TPV will lead to novel approaches to suppress innate immune activation in HIV-1, other infectious diseases or autoimmunity.
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Stubblefield Park, Samantha, Hannah Sung, Nicholas Funderburg, Jon Meddings, and Alan Levine. "Increased small intestinal and colonic permeability, and loss of villus tip surface area, correlates with microbial translocation and immune activation in HIV (71.5)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 71.5. http://dx.doi.org/10.4049/jimmunol.188.supp.71.5.
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Abstract As early diagnosis and viremic control of HIV becomes more prevalent, the clinical focus has turned to preventing co-morbidities that include cardiovascular, hepatic, neurological, and metabolic abnormalities and immune exhaustion. Immune activation, as measured by leukocyte activation and soluble inflammatory mediators in circulation, is increased in HIV patients, even those on effective HAART therapy, and is a better predictor of disease progression and of all-cause mortality than viral load. Intestinal permeability, which often leads to microbial products in the bloodstream, may provide a cause for chronic inflammation in HIV patients. Here, we provide corroborating evidence of small intestinal and colonic permeability in a cohort of HIV patients with increased LPS, determined by measuring the excretion of various saccharides. Levels of lactulose and mannitol (small intestinal permeability) and sucralose (colonic permeability) were elevated (p=0.0014 and p<0.001, respectively) in the urine of HIV patients, independent of HAART status. Further analysis of the saccharide excretion profile revealed that HIV patients have a loss of villus tip surface area in the small intestine as compared to controls (p<0.001). These results were correlated to markers of bowel damage and microbial translocation (LPS Binding Protein, EndoCAb, sCD14, I-FABP) and immune activation (CRP, IL-6, IFN-α) and to clinical parameters in hopes of identifying key risk factors for disease progression.
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Falasca, K., C. Ucciferri, L. Manzoli, P. Mancino, E. Pizzigallo, P. Conti, and J. Vecchiet. "Metabolic Syndrome and Cardiovascular Risk in HIV-Infected Patients with Lipodystrophy." International Journal of Immunopathology and Pharmacology 20, no. 3 (July 2007): 519–27. http://dx.doi.org/10.1177/039463200702000310.
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In this cross-sectional study, we evaluate potential predictors of Metabolic Syndrome (MS) in a group of 54 Caucasian chronically HIV-infected patients with lipodystrophy. According to ATP-III criteria, 22 patients were affected by MS and 32 were not. The mean age of the sample was 41.2 ± 8.6 years, and most patients were males (74.1%); the two groups were homogeneous for gender, age, viro-immunologic status and the duration of antiviral therapy. The independent association between MS and several factors including demographic characteristics, type of highly-active antiviral therapy (HAART), viro-immunologic response, common cardiovascular risk factors (including Framingham scores), and selected cytokines (IFN-γ, TNF-α, IL-2, IL-4, IL-6, IL-10 and IL-18), was investigated using stepwise forward logistic regression. At multivariate analysis, the only independent predictors of the metabolic syndrome were triglycerides and IL-18. A10 mg/dL increase in triglycerides corresponds to an adjusted risk ratio for MS of 1.11 (95% IC: 1.04–1.19); and patients in the top tertile of IL-18 (those with IL-18 ≥ 530 pg/L) had more than three times the likelihood of MS, as compared to the bottom and medium fertiles of IL-18 (patients with IL-18 < 530 pg/L). This relationship was not attenuated by the inclusion of any other variable in the multivariate model. However, the association between metabolic syndrome and IL-18 is no longer significant when IL-18 is treated as a continuous variable (trend p = 0.087). Our results on HIV patients with lipodystrophy confirm previous findings on a strong independent association between IL-18 and MS in the general population. Further research is needed to clarify the mechanism of this association and its role in the development of cardiovascular disease in HIV patients.
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Mwakyandile, Tosi, Grace Shayo, Sabina Mugusi, Bruno Sunguya, Philip Sasi, Candida Moshiro, Ferdinand Mugusi, and Eligius Lyamuya. "Effect of aspirin on HIV disease progression among HIV-infected individuals initiating antiretroviral therapy: study protocol for a randomised controlled trial." BMJ Open 11, no. 11 (November 2021): e049330. http://dx.doi.org/10.1136/bmjopen-2021-049330.
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IntroductionAn increase in cardiovascular disease (CVD) among people living with HIV infection is linked to platelet and immune activation, a phenomenon unabolished by antiretroviral (ARV) drugs alone. In small studies, aspirin (acetylsalicylic acid [ASA]) has been shown to control immune activation, increase CD4+ count, halt HIV disease progression and reduce HIV viral load (HVL). We present a protocol for a larger ongoing randomised placebo controlled trial on the effect of an addition of ASA to ARV drugs on HIV disease progression.Methods and analysisA single-centre phase IIA double-blind, parallel-group randomised controlled trial intends to recruit 454 consenting ARV drug-naïve, HIV-infected adults initiating ART. Participants are randomised in blocks of 10 in a 1:1 ratio to receive, in addition to ARV drugs, 75 mg ASA or placebo for 6 months. The primary outcome is the proportion of participants attaining HVL of <50 copies/mL by 8, 12 and 24 weeks. Secondary outcomes include proportions of participants with HVL of >1000 copies/mL at week 24, attaining a >30% rise of CD4 count from baseline value at week 12, experiencing adverse events, with normal levels of biomarkers of platelet and immune activation at weeks 12 and 24 and rates of morbidity and all-cause mortality. Intention-to-treat analysis will be done for all study outcomes.Ethics and disseminationEthical approval has been obtained from institutional and national ethics review committees. Findings will be submitted to peer-reviewed journals and presented in scientific conferences.Trial registration numberPACTR202003522049711.
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Albino, Elinette, Lenin Godoy, and Martin Hill. "Markers of Chronic Immune Activation in HIV Patients Receiving Antiretroviral Therapy." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 217.39. http://dx.doi.org/10.4049/jimmunol.196.supp.217.39.
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Abstract Antiretroviral therapy (ART) prolongs the lifespan of HIV-infected individuals but does not reduce chronic immune activation and inflammation. While ART typically decreases both immune activation and inflammation markers, recent studies showed these markers remain elevated in many HIV-infected patients. Over time, this heightened inflammation state may increase the rate of cardiovascular disease in HIV-infected individuals. In this study we characterize the inflammatory monocyte subsets in HIV positive subjects taking HAART and correlate this information with innate and inflammatory cytokines levels in plasma. Blood samples were taken from 50 subjects including: HIV positive subjects under ART, untreated HIV positive subjects healthy subjects taking HAART and healthy controls. Nine cytokines were measured in plasma using a Magnetic Luminex technology. In addition, fresh monocytes were separated from peripheral blood mononuclear cells (PBMCs) by CD14/CD16 monoclonal antibodies. Levels inflammatory cytokines were associated with health status parameters and self reported lifestyles. HIV-1 infected subjects had increased levels of both CD14/CD16 cells and inflammatory cytokines compare to the rest of the subjects enrolled in the study. A plasma inflammatory biomarker signature consisting of CD14, IL-6, IL-15, CD163 and IL-12 p70 corresponded with immune activation after prolonged exposition to ART. These findings suggest that increased inflammatory cytokines levels could be a consequence of antiretroviral use, yet the specific role of these inflammatory markers in disease state remains to be determined.
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Mitchell, Brooks I., Elizabeth I. Laws, Dominic C. Chow, Ivo N. Sah Bandar, Louie Mar A. Gangcuangco, Cecilia M. Shikuma, and Lishomwa C. Ndhlovu. "Increased Monocyte Inflammatory Responses to Oxidized LDL Are Associated with Insulin Resistance in HIV-Infected Individuals on Suppressive Antiretroviral Therapy." Viruses 12, no. 10 (October 5, 2020): 1129. http://dx.doi.org/10.3390/v12101129.
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Despite long term antiretroviral therapy (ART), insulin resistance (IR) is common among people living with HIV/AIDS (PLWHA) exposing this population to a greater risk of cardiometabolic complications when compared to their uninfected counterparts. We previously identified an expansion in monocyte subpopulations in blood that were linked to the degree of IR in persons with HIV on stable ART. In this study, we directly assessed monocyte inflammatory functional properties from PLWHA on ART (n = 33) and HIV-uninfected controls (n = 14) of similar age, gender, and cardiovascular disease risk and determined the relationship with IR (homeostatic model assessment-insulin resistance (HOMA-IR)), calculated from fasting blood glucose and insulin measurements. Peripheral blood mononuclear cells were stimulated with oxidized low-density lipoproteins (oxLDL) and polyfunctional monocyte cytokine responses (IL-1β, IL-6, IL-8, or TNF-α) were determined by flow cytometry. Higher monocyte IL-1β and IL-8 responses to oxLDL were associated with higher IR in PLWHA but not in the control group. We observed that higher basal monocyte cytokine responses were associated with both duration since HIV diagnosis and ART initiation. In the management of IR in chronic HIV, strategies lowering monocyte IL-1β and IL-8 responses should be considered in addition to ART in order to limit adverse cardio-metabolic outcomes.
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Green, Samantha, Mindy Smith, Rebecca Hasley, David Stephany, Adam Harned, Kunio Nagashima, Tomozumi Imamichi, et al. "Increased activated platelet-T cell conjugates in patients with HIV infection: relationship between coagulation/inflammation and T cells. (VIR10P.1171)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 216.9. http://dx.doi.org/10.4049/jimmunol.194.supp.216.9.
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Abstract While antiretroviral therapies can successfully suppress HIV replication, there remains evidence of persistent immune activation, which is correlated with increased risks of all-cause mortality. Patients with elevated biomarkers of coagulation/inflammation such as IL-6, sCD14 and D-dimer (a fibrin bioproduct) are at an increased risk to develop non-AIDS defining illnesses such as cardiovascular disease. The interaction between the coagulation system and the immune system is critical for host defense; however, in HIV infection, the mechanisms underlying the ongoing activation of these pathways remains poorly understood. We hypothesized that interaction between platelets and T cells may play a role. We found that platelets from healthy controls and HIV infected patients bind to CD4 and CD8 T cells, preferentially to those with memory phenotypes. HIV infected patients showed a higher proportion of activated platelet (CD42b+CD62P+)-T cell conjugates and significantly correlated to the D-dimer levels. In vitro thrombin stimulation of PBMCs enhanced formation of platelet-T cell conjugates mediated in part by CD62P released by platelets. These data suggest that platelets can promote trafficking of T cells into injured tissues by upregulation of CD62P leading to enhanced rolling of leukocytes along vascular endothelium. In HIV infected patients, recruitment of T cells by this mechanism may promote a state of inflammation/coagulation and contribute to the pathology of the disease.
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Tong, Li, Marcel Schmidt, Ziang Zhu, Jinya Chen, Anton Wellstein, Jai Kumar, Princy Kumar, and Marta Catalfamo. "HIV infection drives immune activation of angiogenic T cells." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 120.24. http://dx.doi.org/10.4049/jimmunol.202.supp.120.24.
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Abstract In patients with HIV infection, chronic immune activation, systemic inflammation and endothelial dysfunction have been identified as the main drivers of cardiovascular risk/disease. In addition, recent reports have shown that, T cells with angiogenic properties (Tang) contribute to vascular repair by promoting new vessels formation in vivo and in vitro. In the present study, we hypothesized that HIV drives immune activation of Tang cells. We measured the frequency and phenotype of circulating Tang cells defined as CXCR4+CD31+. Patients with HIV infection and well controlled viral replication by cART (n= 25) showed a decreased proportion of both CD4 and CD8 Tangs cells when compared to healthy controls (n= 12), although this difference was more striking in the CD8 Tang subset. CD8 Tang but not CD4 Tang cells were significantly decreased in HIV negative patients whom are undergoing PrEP (Pre-Exposure Prophylaxis) therapy, (n=5). In addition, we found that: angiogenic T cells as defined by the surface markers CXCR4 and CD31 are a heterogenous population including naïve, memory and terminal effector memory phenotypes. Tang cells of HIV infected patients showed an activated phenotype with increased expression of granzymes A (GZA) and B (GZB) when compared to healthy controls. Lastly, CD4 and CD8 Tang cells show increased expression of CD49f (integrin a-6). The frequency of Tang GZA+GZB+ in patients with HIV infection was positively associated with 10yr cardiovascular risk score (ASCVD), CD4 Tang (R= 0.51, p= 0.02) and CD8 Tang (R= 0.6, p< 0.01). These results suggest that in the context of HIV infection, angiogenic T cells possess an immune activated phenotype with a proinflammatory potential that may alter their ability of vascular repair
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Dirajlal-Fargo, Sahera, Manjusha Kulkarni, Abdus Sattar, Nicholas Funderburg, and Grace A. McComsey. "933. Serum Albumin Is Associated With Higher Inflammation and Carotid Atherosclerosis in Treated HIV Infection." Open Forum Infectious Diseases 5, suppl_1 (November 2018): S32. http://dx.doi.org/10.1093/ofid/ofy209.073.
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Abstract Background Lower serum albumin has recently been associated with cardiovascular disease and non-AIDS malignancies in HIV. This analysis explores the associations between serum albumin and markers of inflammation and atherosclerosis. Methods We conducted a nested study within in the SATURN-HIV trial in which 147 HIV+ adults on stable antiretroviral therapy (ART), were virally suppressed, and had an LDL-cholesterol level <130 mg/dL were randomized to 10 mg daily rosuvastatin or placebo. Measures of serum albumin, carotid intima media thickness (IMT, surrogate marker of atherosclerosis), inflammation, T-cell and monocyte immune activation were assessed at baseline, 24, 48, and 96 weeks later. Spearman correlations and linear-mixed effects models with random intercept and slope were conducted to assess associations with albumin. Results Mean age was 45 years, 80% were male, 69% were African American, and 46% were receiving protease inhibitors. Mean serum albumin was not significantly different between the groups at any time points (4.05–4.08 g/dL in statin arm vs. 4.01–4.11 g/dL in placebo arm, P = 0.08–0.35). Low serum albumin significantly correlated with elevated levels of interleukin-6 (IL6), d-dimer, fibrinogen, and high sensitivity C-reactive protein (hsCRP) at all time points (P ≤ 0.04). Low serum albumin also correlated with higher inflammatory monocytes (CD14+CD16+) at week 24 and week 96 (P ≤ 0.03) but not with markers of T-cell activation at any time point (P ≥ 0.10). Lower baseline albumin significantly predicted larger changes in IMT (P = 0.03), IL6, d-dimer, tumor necrosis factor-α receptor 1, fibrinogen, and hsCRP (P ≤ 0.02) over 96 weeks. After adjusting for age, gender, smoking, body mass index, vascular cell adhesion molecule and creatinine clearance, every 1 g/dL decrease in albumin remained associated with a 0.5 mm increase in IMT over 96 weeks (P = 0.05). Conclusion Lower serum albumin in controlled HIV is associated with higher markers of chronic inflammation, hypercoagulation, and monocyte activation, which could explain the prior observation that albumin predicts non-AIDS events in HIV. Our findings suggest that serum albumin may predict progression of carotid atherosclerosis independent of traditional risk factors. Disclosures G. A McComsey, Gilead: Consultant, Consulting fee and Research support. Merck: Consultant, Consulting fee and Research support. Viiv: Consultant, Consulting fee and Research support. Roche: Research Contractor, Research support. Astellas: Research Contractor, Research support.
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Wallis, Zoey K., and Kenneth C. Williams. "Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging." Viruses 14, no. 2 (February 17, 2022): 409. http://dx.doi.org/10.3390/v14020409.
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Before the antiretroviral therapy (ART) era, people living with HIV (PLWH) experienced complications due to AIDS more so than aging. With ART and the extended lifespan of PLWH, HIV comorbidities also include aging—most likely due to accelerated aging—as well as a cardiovascular, neurocognitive disorders, lung and kidney disease, and malignancies. The broad evidence suggests that HIV with ART is associated with accentuated aging, and that the age-related comorbidities occur earlier, due in part to chronic immune activation, co-infections, and possibly the effects of ART alone. Normally the immune system undergoes alterations of lymphocyte and monocyte populations with aging, that include diminished naïve T- and B-lymphocyte numbers, a reliance on memory lymphocytes, and a skewed production of myeloid cells leading to age-related inflammation, termed “inflamm-aging”. Specifically, absolute numbers and relative proportions of monocytes and monocyte subpopulations are skewed with age along with myeloid mitochondrial dysfunction, resulting in increased accumulation of reactive oxygen species (ROS). Additionally, an increase in biomarkers of myeloid activation (IL-6, sCD14, and sCD163) occurs with chronic HIV infection and with age, and may contribute to immunosenescence. Chronic HIV infection accelerates aging; meanwhile, ART treatment may slow age-related acceleration, but is not sufficient to stop aging or age-related comorbidities. Overall, a better understanding of the mechanisms behind accentuated aging with HIV and the effects of myeloid activation and turnover is needed for future therapies.
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Perkins, Megan V., Sarah Joseph, Dirk P. Dittmer, and Nigel Mackman. "Cardiovascular Disease and Thrombosis in HIV Infection." Arteriosclerosis, Thrombosis, and Vascular Biology, December 2022. http://dx.doi.org/10.1161/atvbaha.122.318232.
Full textAbstract:
HIV infection has transitioned from an acute, fatal disease to a chronic one managed by antiretroviral therapy. Thus, the aging population of people living with HIV (PLWH) continues to expand. HIV infection results in a dysregulated immune system, wherein CD4 + T cells are depleted, particularly in the gastrointestinal tract, disrupting the gut epithelial barrier. Long-term HIV infection is associated with chronic inflammation through potentially direct mechanisms caused by viral replication or exposure to viral proteins and indirect mechanisms resulting from increased translocation of microbial products from the intestine or exposure to antiretroviral therapy. Chronic inflammation (as marked by IL [interleukin]-6 and CRP [C-reactive protein]) in PLWH promotes endothelial cell dysfunction and atherosclerosis. PLWH show significantly increased rates of cardiovascular disease, such as myocardial infarction (risk ratio, 1.79 [95% CI, 1.54–2.08]) and stroke (risk ratio, 2.56 [95% CI, 1.43–4.61]). In addition, PLWH have increased levels of the coagulation biomarker D-dimer and have a two to ten-fold increased risk of venous thromboembolism compared with the general population. Several small clinical trials analyzed the effect of different antithrombotic agents on platelet activation, coagulation, inflammation, and immune cell activation. Although some markers for coagulation were reduced, most agents failed to reduce inflammatory markers in PLWH. More studies are needed to understand the underlying mechanisms driving inflammation in PLWH to create better therapies for lowering chronic inflammation in PLWH. Such therapies can potentially reduce atherosclerosis, cardiovascular disease, and thrombosis rates in PLWH and thus overall mortality in this population.
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Chew, Kara W., Lei Hua, Debika Bhattacharya, Adeel A. Butt, Lorelei Bornfleth, Raymond T. Chung, Janet W. Andersen, and Judith S. Currier. "The Effect of Hepatitis C Virologic Clearance on Cardiovascular Disease Biomarkers in Human Immunodeficiency Virus/Hepatitis C Virus Coinfection." Open Forum Infectious Diseases 1, no. 3 (2014). http://dx.doi.org/10.1093/ofid/ofu104.
Full textAbstract:
Abstract Background. Successful hepatitis C virus (HCV) treatment may reduce cardiovascular disease (CVD) risk and improve levels of CVD biomarkers produced outside the liver (nonhepatic biomarkers). Methods. Stored serum or plasma from before and 24 weeks after end of HCV treatment (EOT) from human immunodeficiency virus (HIV)/HCV-coinfected subjects who received up to 72 weeks of peginterferon/ribavirin, 27 with and 27 without sustained virologic response (SVR) matched by race, ethnicity and sex, were tested for nonhepatic (soluble intercellular adhesion molecule-1 [sICAM-1], soluble P-selectin [sP-selectin], interleukin [IL]-6, d-dimer, and lipoprotein-associated phospholipase A2 [Lp-PLA2]) and hepatic (cholesterol and high-sensitivity C-reactive protein) CVD and macrophage activation markers (soluble CD163 [sCD163] and soluble CD14). Changes in biomarkers and their association with SVR were examined by t tests or Wilcoxon tests and regression models. Results. Of the 54 subjects, 30 were white, 24 were black, and 44 were male. Pretreatment levels of nonhepatic biomarkers were high: sICAM-1 overall median, 439.2 ng/mL (interquartile range [IQR], 365.6–592.8]; sP-selectin, 146.7 ng/mL (IQR, 94.1–209.9), and IL-6, 2.32 pg/mL (IQR, 1.61–3.49). Thirty-seven of 52 (71%) subjects had Lp-PLA2 >235 ng/mL. Sustained virologic response was associated with decrease in sICAM-1 (P = .033) and sCD163 (P = .042); this result was attenuated after controlling for changes in the alanine aminotransferase level. At 24 weeks after EOT, 17 (63%) SVRs had Lp-PLA2 >235 ng/mL vs 25 (93%) non-SVRs (P = .021). Conclusions. Hepatitis C virus clearance may reduce hepatic and, subsequently, systemic inflammation and CVD risk in HIV/HCV coinfection.