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). RESULTS
Seventeen participants (88% men, median age 60 years and peripheral CD4(+) T lymphocyte count 625 cells/mm(3)) 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.