Jordan E Lake1, Sophie Seang1, Theodoros Kelesidis1, Judith S Currier1, Otto O Yang1,2,3. 1. a Division of Infectious Diseases, Department of Medicine , University of California , Los Angeles , CA , USA. 2. b Department of Microbiology, Immunology, and Molecular Genetics , University of California , Los Angeles , CA , USA. 3. c AIDS Healthcare Foundation , Los Angeles , CA , USA.
Abstract
BACKGROUND: Endothelial progenitor cells (EPCs) are bone marrow-derived cells that contribute to vascular repair. EPCs may be reduced in HIV-infected (HIV+) persons, contributing to cardiovascular disease (CVD). Telmisartan is an angiotensin receptor blocker that increases EPCs in HIV-uninfected adults. OBJECTIVE: To assess telmisartan's effects on EPC number and immunophenotype in older HIV + adults at risk for CVD. METHODS: HIV + persons ≥50 years old with HIV-1 RNA < 50 copies/mL on suppressive antiretroviral therapy and ≥1 CVD risk factor participated in a prospective, open-label, pilot study of oral telmisartan 80 mg daily for 12 weeks. Using CD34 and CD133 as markers of early maturity and KDR as a marker of endothelial lineage commitment, EPCs were quantified via flow cytometry and defined as viable CD3-/CD33-/CD19-/glycophorin- cells of four immunophenotypes: CD133+/KDR+, CD34+/KDR+, CD34+/CD133+, or CD34+/KDR+/CD133+. The primary endpoint was a 12-week change in EPC subsets (NCT01578772). RESULTS: Seventeen participants (88% men, median age 60 years and peripheral CD4+ T lymphocyte count 625 cells/mm3) enrolled and completed the study. After 6 and 12 weeks of telmisartan, frequencies of all EPC immunophenotypes were higher than baseline (all p < 0.10 except week 12 CD133+/KDR+ EPC, p = 0.13). Participants with lower baseline EPC levels had the largest gains. Additionally, the percentage of CD34+ cells with endothelial commitment (KDR+) increased. CONCLUSIONS: Our data suggest that telmisartan use is associated with an increase in circulating EPCs in older HIV + individuals with CVD risk factors. Further controlled studies are needed to assess whether EPC increases translate to a reduction in CVD risk in this population.
BACKGROUND: Endothelial progenitor cells (EPCs) are bone marrow-derived cells that contribute to vascular repair. EPCs may be reduced in HIV-infected (HIV+) persons, contributing to cardiovascular disease (CVD). Telmisartan is an angiotensin receptor blocker that increases EPCs in HIV-uninfected adults. OBJECTIVE: To assess telmisartan's effects on EPC number and immunophenotype in older HIV + adults at risk for CVD. METHODS: HIV + persons ≥50 years old with HIV-1 RNA < 50 copies/mL on suppressive antiretroviral therapy and ≥1 CVD risk factor participated in a prospective, open-label, pilot study of oral telmisartan 80 mg daily for 12 weeks. Using CD34 and CD133 as markers of early maturity and KDR as a marker of endothelial lineage commitment, EPCs were quantified via flow cytometry and defined as viable CD3-/CD33-/CD19-/glycophorin- cells of four immunophenotypes: CD133+/KDR+, CD34+/KDR+, CD34+/CD133+, or CD34+/KDR+/CD133+. The primary endpoint was a 12-week change in EPC subsets (NCT01578772). RESULTS: Seventeen participants (88% men, median age 60 years and peripheral CD4+ T lymphocyte count 625 cells/mm3) enrolled and completed the study. After 6 and 12 weeks of telmisartan, frequencies of all EPC immunophenotypes were higher than baseline (all p < 0.10 except week 12 CD133+/KDR+ EPC, p = 0.13). Participants with lower baseline EPC levels had the largest gains. Additionally, the percentage of CD34+ cells with endothelial commitment (KDR+) increased. CONCLUSIONS: Our data suggest that telmisartan use is associated with an increase in circulating EPCs in older HIV + individuals with CVD risk factors. Further controlled studies are needed to assess whether EPC increases translate to a reduction in CVD risk in this population.
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