Cardiology and ART

HIV infection by itself increases some CVD risk factors.
People with HIV have:
  • Higher rates of CVD than the general population -explained partly by higher rates of smoking and an aging HIV population.
  • A notable inter-individual variability in lipid response to ART.
  • An increased risk of MI and CVD associated with ART, in particular the PI drug class (lopinavir and indinavir), recently also abacavir.

Facts about ART and Cardiovascular Disease

 

  • ART can increase blood fats (cholesterol and triglycerides)
  • ART can contribute to diabetes and insulin resistance
  • HIV decreases good cholesterol and increases triglycerides
  • HIV causes inflammation -which can also contribute to CVD

Because HIV and its treatment can increase the risk of CVD in several ways, people with HIV should evaluate their CVD risk. If it is high, they may need to take special measures to reduce it. The Framingham Risk Evaluation tool is available to calculate individual risk of developing CVD. 

Over the last decade several metabolic side effects have been identified and are reported to be associated with different cART regimens. Those include insuln resistance (IR) and diabetes mellitus (DM), dyslipidemia, abdominal fat accumulation, and subcutaneous fat loss.

Our knowledge about these side effects reveals a complex picture with side effects relating to both individual drug-classes (class effect) and to the individual drugs. The same metabolic side effect, eg dislipidemia, can thus be caused by drugs from different drug classes1,2.

In addition to this, there is a notable inter-individual variability in lipid response to ART classes1,9,10. More recent data have suggested an increased risk of MI and CVD associated with ART, in particular the PI drug class (lopinavir and indinavir) recently also abacavir9,10.

The role of HIV per se in the development of CVD remains to be determined. It is well-known that inflammation is an important risk factor for and contributor to atherosclerosis and CVD. Uncontrolled HIV infection with high viral loads is hypothesized to be involved in the pathogenesis of CVD in HIV-infected individuals. The SMART study is an RCT addressing the risks and benefits of reducing ART exposure by giving intermittent drug therapy, guided by the CD4 count, in one arm and continued drug therapy in the other arm3.

The SMART study used validated clinical end-points and reported increased CVD in patients treatment interruption (TI) as compared to patients remaining on therapy. Speculations are ongoing if this is due to low HDL found in patients in the TI arm, in particular in those off NNRTI treatment or if it is due to increased vascular inflammation, as also suggested by others4.


It is important to emphasize that the traditional risk factors of CVD in the general population, eg. age, is also of key importance in the HIV positive population. The risk for CVD increases with 6-9% per 1 year older in both HIV positive and HIV negative individuals. Extremely high rates of smoking- up to 72%- in HIV-infected populations have been reported. These rates are generally higher than those in the local populations and in HIV-uninfected controls5,6.

The prevalence of MI ranges from 3.5 - 11.1 per 1000 PY and increased rates of MI have been found in HIV positive compared to HIV negative individuals7,8. Increased numbers of MI is to be expected as the HIV population ages, and due to efficient cART more people are expected to live longer thus reaching an age where their risk for CHD increases significantly.

Jens D. Lundgren from the University of Copenhagen and Rigshospitalet in Denmark presented Risk of Myocardial Infarction with Exposure to Specific ARV from the PI, NNRTI, and NRTI Drug Classes: The D:A:D Study at CROI 2009

Jens D. Lundgren explains why HIV and its medications seem to be causing more heart attacks.
Watch the interview