Targeting thrombogenicity and inflammation in chronic HIV infection

Autor: Meagan O’Brien, Gabriela Rodriguez-Caprio, Jose C. Rodriguez, M. Urooj Zafar, Alan D. Weinberg, Juan J. Badimon, Karen Cavanagh, Gines Escolar, Alex Heyison, Judith A. Aberg, Ibeawuchi Okoroafor
Rok vydání: 2018
Předmět:
Male
Platelet Aggregation
Anti-Inflammatory Agents
Lipopolysaccharide Receptors
Gene Expression
HIV Infections
030312 virology
Monocytes
0302 clinical medicine
Coronary thrombosis
Antiretroviral Therapy
Highly Active
Antithrombotic
030212 general & internal medicine
Research Articles
0303 health sciences
Aspirin
Multidisciplinary
virus diseases
SciAdv r-articles
Middle Aged
Clopidogrel
3. Good health
Receptors
Tumor Necrosis Factor
Type I
Tumor necrosis factor alpha
Female
medicine.symptom
medicine.drug
circulatory and respiratory physiology
Research Article
Adult
Blood Platelets
Thrombogenicity
Inflammation
Placebo
Fibrin Fibrinogen Degradation Products
03 medical and health sciences
medicine
Humans
Receptors
Tumor Necrosis Factor
Type II
cardiovascular diseases
Health and Medicine
business.industry
Coronary Thrombosis
Immunity
Innate
Cross-Sectional Studies
Immunology
business
Biomarkers
Platelet Aggregation Inhibitors
Zdroj: Science Advances
ISSN: 2375-2548
Popis: Patients with HIV have higher thrombogenicity that correlates with markers of inflammation; both respond to clopidogrel treatment.
Persons with HIV infection (PWH) have increased risk for cardiovascular disease (CVD), but the underlying mechanisms remain unclear. Coronary thrombosis is known to provoke myocardial infarctions, but whether PWH have elevated thrombotic propensity is unknown. We compared thrombogenicity of PWH on antiretroviral therapy versus matched controls using the Badimon chamber. Measures of inflammation, platelet reactivity, and innate immune activation were simultaneously performed. Enrolled PWH were then randomized to placebo, aspirin (81 mg), or clopidogrel (75 mg) for 24 weeks to assess treatment effects on study parameters. Thrombogenicity was significantly higher in PWH and correlated strongly with plasma levels of D-dimer, soluble TNF receptors 1 and 2, and circulating classical and nonclassical monocytes in PWH. Clopidogrel significantly reduced thrombogenicity and sCD14. Our data suggest that higher thrombogenicity, interacting with inflammatory and immune activation markers, contributes to the increased CVD risk observed in PWH. Clopidogrel exhibits an anti-inflammatory activity in addition to its antithrombotic effect in PWH.
Databáze: OpenAIRE
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