Cardiovascular implications from untreated human immunodeficiency virus infection

Area of Science:

• Cardiology
• Infectious Diseases
• Immunology

Background:

• Atherosclerotic cardiovascular disease (CVD) is a leading cause of death in human immunodeficiency virus (HIV)-infected individuals, particularly with improved life expectancy due to antiretroviral therapy (ART).
• Traditional CVD risk factors are prevalent in the HIV population, necessitating continued application of established prevention strategies.
• Untreated HIV infection exacerbates CVD risk through immune activation, inflammation, coagulation abnormalities, and altered lipoprotein profiles.

Purpose of the Study:

• To review the multifaceted mechanisms contributing to accelerated atherosclerosis in HIV-infected individuals.
• To evaluate the dual impact of antiretroviral therapy (ART) on CVD risk, including viral suppression benefits and potential toxicities.
• To highlight the need for novel therapeutic approaches to reduce premature CVD in the context of HIV infection.

Main Methods:

• Literature review of recent studies on HIV, cardiovascular disease, and antiretroviral therapy.
• Analysis of mechanisms linking HIV infection and immune activation to atherogenesis.
• Examination of the effects of ART on viral load, immune status, and cardiovascular risk factors.

Main Results:

• HIV infection independently promotes pro-atherogenic processes beyond traditional risk factors.
• ART partially mitigates HIV-driven atherogenic mechanisms but can introduce its own CVD risks.
• A complex interplay exists between HIV, ART, inflammation, and cardiovascular health.

Conclusions:

• Despite ART, HIV-infected individuals remain at elevated risk for premature atherosclerotic CVD.
• Current prevention strategies are insufficient to fully address the unique CVD risks in this population.
• Adjunctive therapies targeting inflammation and other HIV-specific pathways are crucial for mitigating CVD in treated HIV patients.