Long-term effects of an intensive intervention in HIV-infected patients with moderate-high atherosclerotic cardiovascular risk.

Abstract

To evaluate the 5 year effects of an intensive intervention versus the standard-of-care intervention on cardiovascular risk factors in HIV-infected patients on antiretroviral therapy (ART). This was a longitudinal study including virologically suppressed patients with at least two cardiovascular risk factors or a Framingham risk score ≥10%. Intensive and standard-of-care interventions aimed for low-density lipoprotein cholesterol (LDL-C) <100 and <130 mg/dL, respectively, by using lipid-lowering drugs. In the intensive group, switching ART when needed to achieve the LDL-C target and low-dose aspirin were used. Achievement of LDL-C targets and changes in carotid intima-media thickness (cIMT) and cardiovascular biomarkers were compared between groups at different timepoints through a 5 year period. Twenty-two and 25 patients in the intensive and standard intervention groups, respectively, were followed up. At 5 years, pre-specified LDL-C targets were achieved in 82% (intensive) and 81% (standard of care) of patients. The median (IQR) change in LDL-C in the intensive and standard intervention groups was -78 (-96/-39.7) and -49 (-72/-3) mg/dL, respectively (P = 0.04), and in the Framingham score was -4% (-8%/-1%) and 0% (-4%/6.5%), respectively (P = 0.01). There were no significant intra- or between-group changes in cIMT measurements. A significant decrease was observed in the intensive and standard groups in interleukin 6 (P = 0.001 and P = 0.002, respectively) and in tumour necrosis factor α (P = 0.023 and P = 0.052, respectively). Asymptomatic creatine phosphokinase elevations were observed in two patients assigned to the standard intervention group. An intensive intervention on cardiovascular risk factors in HIV-infected patients on ART was feasible, safe and capable of achieving LDL-C targets in the long term. Both intensive and standard interventions were accompanied by antiatherosclerotic changes in inflammatory cytokines and lack of cIMT progression.