title: Telmisartan increases vascular reparative capacity in older HIV-infected adults: a pilot study.
abstract: 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.
  
  
  
  To assess telmisartan's effects on EPC number and immunophenotype in older HIV + adults at risk for CVD.
  
  
  
  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).
  
  
  
  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.
  
  
  
  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.
authors.affiliation: a Division of Infectious Diseases, Department of Medicine , University of California , Los Angeles , CA , USA.
authors.forename: Jordan E
authors.initials: JE
authors.lastname: Lake
authors.affiliation: a Division of Infectious Diseases, Department of Medicine , University of California , Los Angeles , CA , USA.
authors.forename: Sophie
authors.initials: S
authors.lastname: Seang
authors.affiliation: a Division of Infectious Diseases, Department of Medicine , University of California , Los Angeles , CA , USA.
authors.forename: Theodoros
authors.initials: T
authors.lastname: Kelesidis
authors.affiliation: a Division of Infectious Diseases, Department of Medicine , University of California , Los Angeles , CA , USA.
authors.forename: Judith S
authors.initials: JS
authors.lastname: Currier
authors.affiliation: a Division of Infectious Diseases, Department of Medicine , University of California , Los Angeles , CA , USA.|b Department of Microbiology, Immunology, and Molecular Genetics , University of California , Los Angeles , CA , USA.|c AIDS Healthcare Foundation , Los Angeles , CA , USA.
authors.forename: Otto O
authors.initials: OO
authors.lastname: Yang
mesh_terms: D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D023241:Antiretroviral Therapy, Highly Active; D001562:Benzimidazoles / Q000494:pharmacology*; D001565:Benzoates / Q000494:pharmacology*; D015415:Biomarkers; D018791:CD4 Lymphocyte Count; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000378:metabolism*; D002452:Cell Count; D066026:Endothelial Progenitor Cells / Q000187:drug effects* / Q000378:metabolism*; D005260:Female; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D010865:Pilot Projects; D011446:Prospective Studies; D012307:Risk Factors; D000077333:Telmisartan; D013997:Time Factors
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001565:Benzoates; D015415:Biomarkers; D000077333:Telmisartan
keywords: Endothelial dysfunction; Endothelial progenitor cells; HIV; Telmisartan