Rheumatoid Arthritis Ku, Ivy A.; Imboden, John B.; Hsue, Priscilla Y. ...
Circulation Journal,
06/2009, Letnik:
73, Številka:
6
Journal Article
Recenzirano
Odprti dostop
Similarities between the inflammatory pathways in atherosclerosis and rheumatoid arthritis (RA) are striking. Chronic systemic inflammation in RA patients leads to cardiovascular (CV) events beyond ...traditional cardiac risk factors. Clinicians typically focus on treating the joint manifestations of RA while neglecting to eliminate systemic inflammation, which leaves RA patients vulnerable to adverse CV events. In this review we provide an understanding of how systemic inflammation in RA accelerates atherosclerosis. This knowledge should guide therapeutic targets to minimize CV risk in RA, and may lead to insights into the inflammatory mechanisms of atherosclerosis in general. (Circ J 2009; 73: 977-985)
Although a substantial proportion of ischemic strokes in persons with HIV infection (PWH) is related to large artery disease, studies evaluating elevated cerebrovascular risk in PWH have focused ...primarily on microvascular disease. We compared the burden of intracranial large artery disease on vessel wall MRI (VW-MRI) in PWH and HIV-uninfected individuals.
Cross-sectional study.
We recruited antiretroviral therapy-treated PWH with undetectable plasma viral load and HIV-uninfected individuals. All participants were at least 40 years of age and at moderate-to-high cardiovascular risk. We used Poisson and mixed effects logistic regression models to compare the number and associated characteristics of enhancing intracranial arteries on VW-MRI by HIV status.
Of 46 participants (mean age 59 years), 33 were PWH. PWH had nearly four-fold as many enhancing intracranial arteries on VW-MRI than HIV-uninfected individuals (rate ratio 3.94, 95% CI 1.57-9.88, P = 0.003). The majority of wall enhancement was eccentric (76%) and short-segment (93%), suggestive of intracranial atherosclerotic disease (ICAD). Sixty-nine percent of enhancing arteries were not associated with luminal narrowing on magnetic resonance angiography (MRA). None of these characteristics differed significantly by HIV status.
In persons at moderate-to-high cardiovascular risk, HIV infection, even when well controlled, may be associated with a greater burden of intracranial large artery disease and, specifically, of ICAD. Studies of the mechanisms underlying higher rates of ischemic stroke in PWH should include evaluation for intracranial large artery disease. VW-MRI provides added value as an adjunct to traditional luminal imaging when evaluating cerebrovascular risk in PWH.
OBJECTIVE:To determine the associations of markers of immune activation with atherosclerosis and mortality, in participants with treated and suppressed HIV infection.
DESIGN:Observational study of ...149 HIV-infected participants with virologic suppression on antiretroviral therapy.
METHODS:Cryopreserved mononuclear cells and plasma were used to evaluate markers of T cell and monocyte activation, inflammation and coagulopathy. Carotid artery intima–media thickness (CIMT) was measured by high-resolution ultrasound at the common, bifurcation and internal carotid regions. Associations of immunologic markers with CIMT and all-cause mortality were assessed using multivariable linear regression and Cox proportional hazards regression.
RESULTS:The majority of participants were men (93%) and white (67%), median age of 48.5 years and median CD4 T-cell count of 522 cells/μl. The median baseline IMT was 1.0 mm. Over a median of 8.3-year follow-up, 12 deaths occurred. In multivariate analysis, adjusted for traditional cardiovascular risk factors, higher monocyte C-C motif chemokine receptor 5 (CCR5) expression 5.4%, P = 0.001 was associated with greater common CIMT. Higher plasma IL-6 was associated with greater bifurcation 8.0%, P = 0.007 and overall mean IMT 5.2%, P = 0.026. Finally, higher plasma IL-6 hazard ratio 1.9, P = 0.030, internal carotid hazard ratio 4.1, P = 0.022 and mean IMT hazard ratio 5.2, P = 0.026 were individually associated with all-cause mortality.
CONCLUSION:Higher monocyte CCR5 expression and plasma IL-6 were associated with atherosclerosis, independent of traditional cardiovascular risk factors. IL-6 and CIMT were individually associated with all-cause mortality. The impact of therapies targeting immune activation in cardiovascular disease in treated HIV infection merits additional investigation.
The aim of this study was to evaluate the association of HIV infection with outcomes among people hospitalized with COVID-19.
A prospectively planned analysis of the American Heart Association's ...COVID-19 Cardiovascular Disease Registry.
One hundred and seven academic and community hospitals in the United States from March through December 2020.
Consecutive sample of 21 528 adults hospitalized with COVID-19 at participating hospitals.
Primary outcome was predefined as in-hospital mortality. We used hierarchical mixed effects models to assess the association of HIV with in-hospital mortality accounting for patient demographics, comorbidities, and clustering by hospital. Secondary outcomes included major adverse cardiac events (MACE), severity of illness, and length of stay (LOS).
The registry included 220 people with HIV (PWH). PWH were younger and more likely to be male, Non-Hispanic Black, on Medicaid, and active tobacco users. Of the study population, 36 PWH (16.4%) died compared with 3290 (15.4%) without HIV risk ratio 1.06; 95% confidence interval (95% CI) 0.79-1.43; P = 0.71. After adjustment for age, sex, race, and insurance, HIV was not associated with in-hospital mortality (aOR 1.12; 95% CI 0.76-1.64; P = 0.58) with no change in effect after adding BMI and comorbidities (aOR 1.14; 95% CI 0.78-1.68; P = 0.51). HIV was not associated with MACE (aOR 0.99; 95% CI 0.69-1.44, P = 0.91), COVID severity (aOR 0.96; 95% CI 0.62-1.50; P = 0.86), or LOS (aOR 1.03; 95% CI 0.76-1.66; P = 0.21).
In the largest study of PWH hospitalized with COVID-19 in the United States to date, we did not find significant associations between HIV and adverse outcomes including in-hospital mortality, MACE, or severity of illness.
We sought to characterize atherosclerotic cardiovascular disease (ASCVD) risk and metrics of cardiovascular health in persons with HIV (PWH) eligible for primary prevention of ASCVD.
A ...cross-sectional study of PWH 40 years and older without documented ASCVD who received care at three HIV clinics in San Francisco from 2019 to 2022.
We used ICD-10 codes and electronic health record data to assess ASCVD risk and cardiovascular health, as defined by the American Heart Association's Life's Essential 8 (LE8) metrics for nicotine exposure, BMI, lipids, glucose, and blood pressure (BP).
Among 2567 PWH eligible for primary prevention of ASCVD, the median age was 55 years, 14% were women, and 95% were on antiretroviral therapy. Seventy-seven percent had undergone complete assessment of ASCVD risk factors, and 50% of these patients had intermediate-high ASCVD risk (≥7.5%). Of those with hypertension, 39% were prescribed an antihypertensive. Among those eligible, 43% were prescribed a statin. The mean LE8 cardiovascular health score 0--100 (best health) was 55.1 for nicotine exposure, 71.3 for BMI, 70.4 for lipids, 81.2 for blood glucose, 56.0 for BP, with an average score of 66.2 across the five metrics. Patients with Medicare insurance, black patients, and those with sleep apnea and chronic kidney disease had on average lower cardiovascular health scores; patients with undetectable viral loads had higher cardiovascular health scores.
We highlight opportunities for improving primary prevention of ASCVD among PWH, especially in the areas of guideline-based therapy, nicotine exposure, and BP control.
HIV-infected patients have accelerated atherosclerosis. Abacavir has been associated with increased risk of cardiovascular events, for reasons that remain to be elucidated. As endothelial dysfunction ...is central to the pathogenesis of atherosclerosis, we tested the hypothesis that current treatment with abacavir is associated with impaired endothelial function.
We studied a cohort of 61 antiretroviral-treated patients who had undetectable plasma HIV RNA levels. Endothelial function was assessed by measuring flow-mediated dilation (FMD) of the brachial artery. We compared FMD in patients treated with or without abacavir, while adjusting for traditional risk factors and HIV-specific characteristics.
The median age was 50 years (interquartile range 45-57). The median duration of HIV infection was 18 years, and the median CD4 cell count was 369 cells/microl. Thirty patients (49%) were receiving abacavir. Overall, the median FMD in the HIV-infected patients was low (3.5%; interquartile range 2.3-5.6%). The FMD was lower in the abacavir-treated patients than those not on abacavir (2.8 vs. 4.9%, P = 0.01). After adjustment for traditional risk factors, HIV-specific factors, and baseline brachial artery diameter, current abacavir use was independently associated with lower FMD (P = 0.017). Duration of therapy and CD4 cell count were not associated with reduced FMD.
Endothelial function, a central mechanism in atherosclerosis and a marker of cardiovascular risk, is impaired among antiretroviral-treated patients with undetectable viral loads. Current use of abacavir was independently associated with impaired endothelial function. This finding suggests that abnormal endothelial function may underlie the clinically observed increased risk in myocardial infarction among abacavir-treated patients.
Abstract
Interferon (IFN)–specific autoantibodies have been implicated in severe coronavirus disease 2019 (COVID-19) and have been proposed as a potential driver of the persistent symptoms ...characterizing “long COVID,” a type of postacute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We report that only 2 of 215 participants with convalescent SARS-CoV-2 infection tested over 394 time points, including 121 people experiencing long COVID symptoms, had detectable IFN-α2 antibodies. Both had been hospitalized during the acute phase of the infection. These data suggest that persistent anti-IFN antibodies, although a potential driver of severe COVID-19, are unlikely to contribute to long COVID symptoms in the postacute phase of the infection.
Within a cohort of individuals with well-characterized post–coronavirus disease 2019 (COVID-19) conditions, or “long COVID,” the authors identified only 2 with anti–interferon α2 autoantibodies, suggesting that these antibodies are unlikely to contribute to most cases of long COVID.
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