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Published on: September 26, 2011
Mechanisms of Cardiovascular Disease in the Setting of HIV Infection
1University of California San Francisco (UCSF), Zuckerberg San Francisco General Hospital, San Francisco, California, USA.
Insights
Advances in HIV treatment have shifted cardiovascular disease from pericardial issues to atherosclerosis. Chronic inflammation and immune activation persist despite therapy, contributing to heart conditions in people with HIV.
Area of Science:
- Immunology
- Cardiology
- Infectious Diseases
Background:
- Cardiovascular disease (CVD) is a significant concern in HIV infection, evolving from initial reports of pericardial disease to current issues like atherosclerosis and heart failure.
- Antiretroviral therapy has transformed HIV into a chronic condition, but the underlying mechanisms of HIV-associated CVD remain incompletely understood.
- The gut's role in HIV pathogenesis, including increased permeability and microbial translocation leading to chronic inflammation, is crucial.
Purpose of the Study:
- To explore the evolving landscape of cardiovascular disease in HIV-infected individuals.
- To understand the complex pathophysiology linking HIV, chronic inflammation, and cardiovascular complications.
- To identify potential therapeutic targets for mitigating cardiovascular risk in the context of HIV.
Main Methods:
- Review of existing literature on HIV, cardiovascular disease, and antiretroviral therapy.
- Analysis of the immunological and molecular mechanisms contributing to HIV-associated atherosclerosis.
- Correlation of persistent immune abnormalities with mortality and cardiovascular events in HIV.
Main Results:
- HIV treatment has shifted the spectrum of cardiovascular disease towards atherosclerosis and heart failure.
- Chronic inflammation and immune activation persist despite antiretroviral therapy, correlating with adverse outcomes.
- Antiretroviral therapy has complex effects on cardiovascular risk, reducing inflammation but potentially inducing lipid abnormalities like hypertriglyceridemia.
Conclusions:
- Chronic inflammation is a key factor in HIV-associated cardiovascular disease and a potential therapeutic target.
- Understanding the molecular mechanisms involving monocytes, macrophages, and platelets is vital for managing cardiovascular risk in HIV.
- Further research is needed to address the complex interplay between HIV, its treatment, and cardiovascular health.
Abstract:
Although the initial reports of increased cardiovascular (CV) disease in the setting of advanced AIDS were reported approximately 30 years ago, advances in antiretroviral therapy and immediate initiation of therapy on diagnosis have transformed what was once a deadly infectious disease into a chronic health condition. Accordingly, the types of CV diseases occurring in HIV have shifted from pericardial effusions and dilated cardiomyopathy to atherosclerosis and heart failure. The underlying pathophysiology of HIV-associated CV disease remains poorly understood, partly because of the rapidly evolving nature of HIV treatment and because clinical endpoints take many years to develop. The gut plays an important role in the early pathogenesis of HIV infection as HIV preferentially infects CD4+ T cells, 80% of which are located in gut mucosa. The loss of these T cells damages gut mucosa resulting in increased gut permeability and microbial translocation, which incites chronic inflammation and immune activation. Antiretroviral therapy does not cure HIV infection and immune abnormalities persist. These abnormalities correlate with mortality and CV events. The effects of antiretroviral therapy on CV risk are complex; treatment reduces inflammation and other markers of CV risk but induces lipid abnormalities, most commonly hypertriglyceridemia. On a molecular level, monocytes/macrophages, platelet reactivity, and immune cell activation, which play a role in the general population, may be heightened in the setting of HIV and contribute to HIV-associated atherosclerosis. Chronic inflammation represents an inviting therapeutic target in HIV, as it does in uninfected persons with atherosclerosis.
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