Telmisartan increases vascular reparative capacity in older HIV-infected adults: a pilot study.

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/mm) 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.