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Cardiac strain is lower among women with HIV in relation to monocyte activation

BACKGROUND: Women with HIV (WWH) face heightened risks of heart failure; however, insights on immune/inflammatory pathways potentially contributing to left ventricular (LV) systolic dysfunction among WWH remain limited. SETTING: Massachusetts General Hospital, Boston, Massachusetts. METHODS: Global...

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Detalles Bibliográficos
Autores principales: Toribio, Mabel, Awadalla, Magid, Drobni, Zsofia D., Quinaglia, Thiago, Wang, Melissa, Durbin, Claudia G., Alagpulinsa, David A., Fourman, Lindsay T., Suero-Abreu, Giselle Alexandra, Nelson, Michael D., Stanley, Takara L., Longenecker, Christopher T., Burdo, Tricia H., Neilan, Tomas G., Zanni, Markella V.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9803182/
https://www.ncbi.nlm.nih.gov/pubmed/36584183
http://dx.doi.org/10.1371/journal.pone.0279913
Descripción
Sumario:BACKGROUND: Women with HIV (WWH) face heightened risks of heart failure; however, insights on immune/inflammatory pathways potentially contributing to left ventricular (LV) systolic dysfunction among WWH remain limited. SETTING: Massachusetts General Hospital, Boston, Massachusetts. METHODS: Global longitudinal strain (GLS) is a sensitive measure of LV systolic function, with lower cardiac strain predicting incident heart failure and adverse heart failure outcomes. We analyzed relationships between GLS (cardiovascular magnetic resonance imaging) and monocyte activation (flow cytometry) among 20 WWH and 14 women without HIV. RESULTS: WWH had lower GLS compared to women without HIV (WWH vs. women without HIV: 19.4±3.0 vs. 23.1±1.9%, P<0.0001). Among the whole group, HIV status was an independent predictor of lower GLS. Among WWH (but not among women without HIV), lower GLS related to a higher density of expression of HLA-DR on the surface of CD14+CD16+ monocytes (ρ = -0.45, P = 0.0475). Further, among WWH, inflammatory monocyte activation predicted lower GLS, even after controlling for CD4+ T-cell count and HIV viral load. CONCLUSIONS: Additional studies among WWH are needed to examine the role of inflammatory monocyte activation in the pathogenesis of lower GLS and to determine whether targeting this immune pathway may mitigate risks of heart failure and/or adverse heart failure outcomes. TRIAL REGISTRATION: Clinical trials.gov registration: NCT02874703.