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 HIV and Hepatitis.com Coverage of the
5
th IAS Conference on HIV Pathogenesis, Treatment and Prevention (IAS 2009)
 July 19 - 22, 2009, Cape Town, South Africa
 The material posted on HIV and Hepatitis.com about IAS 2009 is not approved by nor is it a part of IAS 2009.
Intensive Cardiovascular Intervention Lowers Blood Lipids in HIV Patients on Antiretroviral Therapy

An intensive cardiovascular risk-reduction program lowered LDL cholesterol in HIV patients on HAART, though it did not lead to reduced levels of inflammatory biomarkers or carotid intima-media thickness, according to a study presented at the 5th International AIDS Society Conference on HIV Pathogenesis, Treatment, and Prevention this week in Cape Town, South Africa.

By Liz Highleyman

Most studies indicate that people with HIV have an elevated risk of cardiovascular disease compared with the general population, but the interplay of HIV infection itself, antiretroviral therapy (ART), and traditional risk factors is not fully understood. Preventive measures should be tailored to individual patients, but how best to manage cardiovascular risk in HIV positive people is not well-defined.

Spanish researchers designed a study to evaluate the effectiveness and safety of an intensive cardiovascular risk reduction intervention versus a standard-of-care intervention in HIV patients with moderate-to-high cardiovascular risk.

This small pilot study included 68 participants with stable viral suppression on ART. About 90% were men and the average age was about 50 years. About 40% were taking protease inhibitor (PI)-based regimens and nearly two-thirds were smokers.

Participants had 2 or more cardiovascular risk factors or a Framingham risk score of 10% or higher (mean of about 15%) and had a low-density lipoprotein (LDL or "bad") cholesterol level of 100 mg/dl or higher. At baseline, about half had plaques an indicator of atherosclerosis, or "hardening of the arteries" in the carotid arteries in the neck.

Participants were randomly assigned to the 2 study arms. Those receiving the standard-of-care intervention attempted to reduce LDL cholesterol below 130 mg/dl. Those in the intensive intervention group took steps to push LDL below 100 mg/dl, including:

Taking the lipid-lowering drug atorvastatin starting at 10 or 20 mg.
Adding ezetimibe if the LDL goal was not attained after doubling the dose of atorvastatin.
Using anti-platelet therapy (aspirin or clopidogrel) to reduce coagulation.
Strong encouragement to quit smoking.
Switching form other boosted PIs to atazanavir (boosted or unboosted), which had less effect on lipids than other drugs in its class.
Attempting to reach standard blood pressure and glycemic goals.

The primary study endpoint was progression of atherosclerosis, measured by changes in carotid intima-media thickness (cIMT), an indicator of plaque build-up in the carotid arteries. Secondary endpoints were achievement of LDL target levels, changes in levels of blood biomarkers associated with inflammation (including C-reactive protein, interleukin-6, and TNF-alpha), safety, and feasibility.

Results

After 12 months, the median proportional change in cIMT was +1.63% in the intensive intervention arm compared with +1.79% in the standard intervention arm, not a statistically significant difference (P = 0.59).
LDL cholesterol fell from 141 to 88 mg/dl in the intensive intervention arm, while remaining stable (131 to 126 mg/dl) in the standard intervention arm (P < 0.001).
60% of participants in the intensive intervention arm reached the LDL target level.
Levels of triglyceride and high-density lipoprotein (HDL or "good") cholesterol did not change significantly.
Framingham risk scores did not decrease significantly in either group.
Interleukin-6 levels fell more in the standard intervention group (-25.4 vs -7.2 pg/ml) while TNF-alpha fell more in the intensive intervention arm (-42.5 vs -11.7 pg/ml), but these differences were not statistically significant.
C-reactive protein fell in the intensive intervention arm while rising in the standard intervention arm (-1.4 vs +6/2 mg/l), with a trend toward statistical significance (P = 0.08).
A number of patients attempted to stop smoking, but only 1 remained abstinent at the end of the study.
Viral load remained suppressed and CD4 cell counts remained stable.
No significant adverse events were reported in either group during the follow-up period.

"An aggressive pharmacologic intervention on cardiovascular risk factors is feasible, safe, and effective in controlling LDL [cholesterol]," the investigators concluded. "However, the intervention did not influence cIMT progression nor inflammatory biomarkers after one year of follow-up."

The investigators have collected longer-term data through 3 years, which they are currently in the process of analyzing.

Session moderator Esteban Martinez noted that this type of study is needed to inform cardiovascular risk management guidelines for people with HIV, and expressed hope that some benefits might be seen with longer follow-up.

Hospital General Universitario de Elche, Unit Infectious Diseases and Clinical Laboratory Analysis, Alicante, Spain; Hospital Clinic-IDIBAPS, Barcelona, Spain.

7/24/09

Reference
M Masiá, E Bernal, S Padilla, and others. A randomized trial comparing an intensive versus a standard intervention in stable HIV-infected patients with moderate-high cardiovascular risk. 5th International AIDS Society Conference on HIV Pathogenesis, Treatment, and Prevention (IAS 2009). July 19-22, 2009. Cape Town, South Africa. Abstract TuAb201.

 

 

 

 

 

 

 

 

 

 

 

 

 

 




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