Search results

Hypertension is more prevalent among HIV‐infected subjects than in the general population, contributing to increased cardiovascular risk in HIV+ patients. The angiotensin II receptor blocker telmisartan is also a partial peroxisome proliferator activated receptor (PPAR)‐γ agonist, with documented effects on improving hypertension, lipid metabolism and renal function. Therefore telmisartan was found to be the first choice for treatment of HIV+ hypertensive patients. Aim of this study was to evaluate the durability on 144 weeks of treatment with telmisartan in HIV+ patients. 13 HIV+ Caucasian male patients treated with combined antiretroviral therapy (cART) and discovered to be naïve hypertensive, were given 80 mg telmisartan daily. Systolic (SBP) and diastolic (DBP) blood pressure, viro‐immunological, lipid and metabolic parameters, including triglycerides, cholesterol, insulin resistance (HOMA‐IR), inflammatory markers, C‐reactive protein (CRP), erythrocyte sedimentation rate (ESR), indexes of renal function and cardiovascular risk, microalbuminuria, cystatin C, were measured at baseline (T0), and after 24 (T24), 48 (T48), 72 (T72), 96 (T96), 120 (T120) and 144 (T144) weeks. Treatment with telmisartan decreased SBP and DBP levels during the 144 weeks of observation. We also observed improved HDL‐cholesterol, HOMA‐IR, microalbuminuria and cystatin C at the end of study. Triglycerides and total cholesterol significantly decreased and HDL‐cholesterol significantly increased. Total cholesterol/HDL cholesterol ratio improved significantly. Throughout in the course of the trial our patients showed a significant improvement of the percentage of CD4+ and CD8+. Eventually in all 144 weeks of therapy with telmisartan 80 mg/day have not observed adverse events or dropouts. Telmisartan was effective in improving hypertension, lipid metabolism and renal function in 144 weeks of evaluation. It determines the improvement of cystatin C and microalbuminuria, markers of renal function and cardiovascular risk. Telmisartan doesn't interfere with cART, not interfering with the recovery of immunological HIV patients. Telmisartan has confirmed durability and effectiveness, excellent tolerability and an high persistance with a good blood pressure control. Therefore telmisartan reveals the first choice in the treatment of hypertension in HIV+ because of significant morbidity in this group of patients.

Atherosclerotic cardiovascular disease is an increasing concern for patients with human immunodeficiency virus (HIV) infection. We investigated carotid intima‐media thickness (IMT), flow‐mediated dilation (FMD), pulse wave velocity (PWV) and the augmentation index (AIx), evaluated as indices of subclinical atherosclerosis, in HIV‐infected patients compared to uninfected subjects. We enrolled 80 HIV‐infected patients, 68 of whom treated with combined antiretroviral therapy (cART) and 12 therapy‐naïve, matched with 82 healthy subjects for age, systolic and diastolic blood pressure. We investigated IMT, FMD, PWV, AIx, viro‐immunological parameters, inflammatory markers, microalbuminuria and other biochemical parameters. Compared with uninfected subjects, HIV‐infected subjects had higher IMT, PWV and AIx values (all P=0.0001); and lower FMD (P=0.001). In the HIV+ group, naïve patients had statistically lower levels of IMT (P=0.02), and AIx (P=0.042) and higher FMD (P=0.032) compared with cART‐treated patients. In the HIV+group, IMT values was significantly related to the number of CD4+ (r=−0.31, P=0.008) and CD8+ cells (r=0.261, P=0.025), interleukin‐6 (r=0.284, P=0.015) and endothelin‐1 (r=0.302, P=0.009). Vascular dysfunction evaluated as IMT, FMD and arterial stiffness is increased in HIV‐infected subjects than in healthy subjects. Furthermore, cART‐treated patients showed higher IMT and AIx and lower FMD values than naïve patients. Our data support the hypothesis that both HIV infection and cART treatment are risk factors for accelerated arteriosclerosis.

Atripla is a fixed‐dose drug combining FTC/TDF/EFV into a single pill and may increase adherence. To our knowledge, there is little data comparing the durability of Atripla vs. other regimens. Our first aim was to compare the durability of Truvada (TVD)/EFV or TVD/PIr or Atripla started when ART‐naïve, in terms of time to virological failure (VF first of 2 consecutive values>50 and>200 copies/mL), time to discontinuation of any drug in the regimens, or both. Then, we aimed to compare the incidence of virological rebound (VR)>200 copies/mL in patients (pts) currently receiving these same regimens after achieving a viral load (VL)≤80 copies/mL. Pts in the Icona Foundation Study who started for the first time a cART regimen with TVD/EFV or TVD/PIr or Atripla, either while ART‐naïve (analysis 1) or while with a VL≤80 (analysis 2) were included. In analysis 1, pts' follow‐up accrued from cART initiation to the date of the event (VF or discontinuation of any drug in the regimen) or to the date of last available visit/VL. In the TVD/EFV group a switch to Atripla was not counted as an event. Survival analysis employing KM curves and Cox regression model was used. In analysis 2, follow‐up accrued from the date of first VL≤80 (which could be achieved with any cART) to VR or last VL and only person years (PY) on the regimens of interest were considered. Rates were calculated as number of VR per 1000 PY and relative rates (RR) compared using a Poisson regression model. In analysis 1, 515 pts starting TVD/EFV, 1001 TVD/PIr and 160 Atripla when ART‐naïve on average in 2010 (IQR: 2008–2011) were included. PI/r were LPV (33%), ATV (38%) fos‐APV (4%) and DRV (24%). Median age was 38 years, 19% females, 40% heterosexuals. Pts starting Atripla were younger, less likely to be female, IDU, HCV co‐infected, to have AIDS and they had higher CD4 count (334 vs. 280). By 2 years, 48% (95% CI: 43–53) of those initiating TVD/PIr experienced the composite endpoint of VF or drug discontinuation vs. 20% in the other groups (p=0.0001). Median time to switch from TVD to Atripla in the EFV group was 17 months (95% CI: 12–23). The table shows the results of the Cox regression analysis. In analysis 2 (n=1,425), the rates of VR were 16.8 per 1000 PY for TVD/PIr, 11.17 for TVD/EFV and 5.3 for Atripla (adjusted RR vs. TVD/PIr=0.51, 95% CI: 0.19–1.34). Durability of Atripla was comparable to that of TVD/EFV and potentially longer than that of TVD/PIr. Unmeasured confounding cannot be ruled out.












Crude and adjusted relative hazards from fitting a Cox regression


Outcomes
No. with event (%)
Crude RH (95% CI)
p‐value
Adjusted* RH (95% CI)
p‐value




VL>50 copies/mL


Truvada+PI/r
131 (13%)
1.00

1.00



Truvada+EFV
54 (10%)
0.60 (0.43,0.83)
0.002
0.61 (0.42,0.89)
0.009


Atripla
8 (5%)
0.66 (0.32,1.37)
0.265
1.15 (0.54,2.48)
0.716


Stop of any drug







Truvada+PI/r
322 (32%)
1.00

1.00



Truvada+EFV
79 (15%)
0.37 (0.29, 0.47)
<.001
0.33 (0.25,0.44)
<.001


Atripla
23 (14%)
0.50 (0.32,0.77)
0.002
0.50 (0.31,0.80)
0.004


VL>200 copies / mL or stop of any drug


Truvada+PI/r
314 (31%)
1.00

1.00



Truvada+EFV
84 (16%)
0.39 (0.31,0.50)
<.001
0.37 (0.28,0.49)
<.001


Atripla
23 (14%)
0.52 (0.33,0.80)
0.003
0.57 (0.35,0.91)
0.017





*adjusted for age, gender, nation of birth, mode of HIV tranmission, hepatitis co‐infection status, AIDS diagnosis, baseline CD4 count and viral load an year of starting cART and stratified by clinical centre