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Published on: June 30, 2013
Pathogenesis of cardiovascular disease in HIV infection
1St Vincent's Hospital and University of New South Wales, Sydney, Australia. acarr@stvincents.com.au
Insights
Effective antiretroviral therapy that suppresses HIV without metabolic side effects is key to reducing cardiovascular disease (CVD) risk in adults. Understanding HIV
Area of Science:
- Cardiology
- Infectious Diseases
- Pharmacology
Background:
- Cardiovascular disease (CVD) is a leading cause of mortality in adults with HIV infection.
- Understanding the mechanisms of CVD in HIV is crucial for effective management strategies.
Purpose of the Study:
- To review the pathogenesis of cardiovascular disease in HIV-infected adults.
- To identify factors contributing to CVD risk in the context of HIV infection and its treatment.
Main Methods:
- Review of current literature on HIV, antiretroviral therapy (ART), and cardiovascular disease.
- Analysis of the metabolic and direct effects of HIV and ART on cardiovascular health.
Main Results:
- Certain antiretroviral therapies, particularly older protease inhibitors and thymidine analogues, are linked to dyslipidemia and insulin resistance.
- While current protease inhibitors have modest adverse glycemic effects, about half of ART-associated CVD risk remains unexplained by lipid abnormalities.
- Untreated HIV infection is associated with increased pro-inflammatory markers (D-dimer) and potential direct vascular effects.
Conclusions:
- Antiretroviral therapy that effectively suppresses HIV with minimal metabolic impact is associated with the lowest CVD risk.
- Further research is needed to fully elucidate the direct effects of HIV on vascular tissue and their clinical significance.
Purpose Of Review:
Cardiovascular disease (CVD) is one of the most common causes of death in HIV-infected adults. Understanding the pathogenesis of cardiovascular disease in the setting of HIV infection is essential for the development of appropriate management strategies.
Recent Findings:
Antiretroviral therapy with most protease inhibitors and thymidine nucleoside analogue reverse transcriptase inhibitors has been linked to dyslipidaemia and insulin resistance. The adverse glycaemic effects of longer term, current generation protease inhibitors, however, appear relatively modest. Nevertheless, about half of the risk associated with antiretroviral therapy remains unexplained by lipid abnormalities. More recently, HIV has been associated with increased risk of cardiovascular disease. HIV nef inhibits HDL efflux from macrophages and so may directly lower HDL cholesterol levels. Untreated HIV infection is also associated with increased levels of D-dimer, a pro-inflammatory and pro-thrombotic marker of cardiovascular disease, and HIV has direct effects on vascular tissue in vitro that remains of uncertain clinical significance.
Summary:
Antiretroviral therapy without metabolic effects that suppresses HIV effectively is likely to be associated with the lowest risk of cardiovascular disease.
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