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Eur J Hosp Pharm 20:A175 doi:10.1136/ejhpharm-2013-000276.484
  • Clinical pharmacy and clinical trials (including case series)

CPC-027 Cardiovascular Risk Profile of a Spanish HIV-Infected Cohort on Antiretroviral Therapy and the Effect of Protease Inhibitors

  1. H Esteban-Cartelle
  1. Complejo Hospitalario Universitario de Santiago de Compostela, Pharmacy, Santiago de Compostela, Spain

Abstract

Background There is evidence that antiretroviral therapy (ART) increases cardiovascular risk (CVR). The use of protease inhibitors (PIs), specially indinavir and lopinavir/ritonavir, has been associated with a higher incidence of myocardial infarction.

Purpose To characterise the CVR profile of an HIV-infected cohort on ART from the northwest of Spain. To determinate the effect of exposure to protease inhibitors (PIs) and exposure time (ET) to ART in CVR.

Materials and Methods Cross-sectional study including HIV patients on ART who were treated at our hospital between March and May 2012. We recorded demographics, ART history and CVR risk factors. CVR was estimated using the Framingham function calibrated for the Spanish population (REGICOR). CVR categories were: low (<5%); intermediate (5–9%); high (10–14%); very high (>15%). Five PI exposure groups were defined: a) no PI exposure (NoPI); b) exposure to PIs but not indinavir or lopinavir/ritonavir (PInoINDnoLPV/r); c) exposure to indinavir (IND); d) exposure to lopinavir/r (LPV/r); e) exposure to indinavir and lopinavir/r (IND+LPV/r).

Results 89 HIV patients were included in the study (83.1% males, mean age 47.4 ± 7.8 years). Smoking prevalence was 51.7%, hypertension 39.3%, dyslipidaemia 24.7%, low HDL cholesterol 67.4%, diabetes 4.5%. Mean global CVR was 4.01%±2.50. The proportion of patients with a low CVR was 70.8%; intermediate 25.8%; high 2.2%; very high 1.1%. Mean CVR according to PI exposure was 4.06 ± 2.60 (NoIP); 3.52 ± 2.29 (IPnoINDnoLPV/r); 5.05 ± 2.99 (IND); 3.50 ± 2.28 (LPV/r); 4.29 ± 1.50 (IND+LPV/r). Significant differences were found when we compared the group IND with the groups IPnoINDnoLPV/r (P = 0.02) and LPV/r (P = 0.03). The effect of ET was significant only for indinavir exposure (P = 0.02).

Conclusions Our HIV population presents low CVR. Smoking, hypertension and low HDL cholesterol are the outstanding modifiable risk factors in our cohort. Indinavir exposure and ET to indinavir increases CVR in our population, but no differences were found with lopinavir/r or other PIs.

No conflict of interest.

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