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  • Review Article
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HIV infection and coronary heart disease: mechanisms and management

Abstract

Antiretroviral therapy has largely transformed HIV infection into a chronic disease condition. As such, physicians and other providers caring for individuals living with HIV infection need to be aware of the potential cardiovascular complications of HIV infection and the nuances of how HIV infection increases the risk of cardiovascular diseases, including acute myocardial infarction, stroke, peripheral artery disease, heart failure and sudden cardiac death, as well as how to select available therapies to reduce this risk. In this Review, we discuss the epidemiology and clinical features of cardiovascular disease, with a focus on coronary heart disease, in the setting of HIV infection, which includes a substantially increased risk of myocardial infarction even when the HIV infection is well controlled. We also discuss the mechanisms underlying HIV-associated atherosclerotic cardiovascular disease, such as the high rates of traditional cardiovascular risk factors in patients with HIV infection and HIV-related factors, including the use of antiretroviral therapy and chronic inflammation in the setting of effectively treated HIV infection. Finally, we highlight available therapeutic strategies, as well as approaches under investigation, to reduce the risk of cardiovascular disease and lower inflammation in patients with HIV infection.

Key points

  • As improvements to antiretroviral therapies have led to better control of HIV infection (although not cured it), individuals with HIV infection are now ageing, and cardiovascular disease is an important health concern in this patient population.

  • Traditional risk factors including dyslipidaemia, hypertension, cigarette smoking, diabetes mellitus and metabolic syndrome are common among people with HIV infection and increase the risk of cardiovascular disease.

  • In addition to traditional risk factors, characteristics related to HIV infection, including low CD4+ T cell count, nadir CD4+ T cell count and viral detectability, and some antiretroviral therapies are independently associated with increased risk of cardiovascular disease.

  • In the setting of treated suppressed HIV replication, chronic inflammation and immune activation persist and are strongly predictive of mortality and cardiovascular events.

  • Potential strategies to reduce the risk of cardiovascular disease in patients with HIV infection include targeting traditional risk factors, initiation of antiretroviral therapy to reduce inflammation and other approaches to lower inflammation, including gut-related interventions, statin therapy and immune modulators.

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Fig. 1: Overview of changes in HIV treatment and HIV-associated cardiovascular diseases.
Fig. 2: Pathophysiology and management of HIV-associated atherosclerotic cardiovascular disease.

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Glossary

CD4+ T cell counts

T cell subset that has a role in the immune system response against pathogens, infections and illnesses. A normal CD4+ T cell count is 500–1,500 cells per µl of plasma. CD4+ T cells are the main target cell of HIV, and the CD4+ T cell count is used to monitor the status of the HIV infection and the efficacy of the antiretroviral therapy.

Nadir CD4+ T cell count

The lowest CD4+ T cell count an individual has had, which serves as a marker for immunodeficiency.

Immunosenescence

Changes to the immune system that can be associated with age.

Viraemia

Presence of viral particles in the blood.

Latent HIV infection

A dormant or non-replicative HIV infection within a cell; in this state, the virus is not actively infecting other cells and individuals do not usually have noticeable symptoms.

Virological failure

Refers to the failure of the HIV treatment to supress the virus completely; the virus is detectable in the blood (>200 copies per ml). This failure can occur as a result of drug resistance, drug toxicity or noncompliance with antiretroviral therapy.

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Hsue, P.Y., Waters, D.D. HIV infection and coronary heart disease: mechanisms and management. Nat Rev Cardiol 16, 745–759 (2019). https://doi.org/10.1038/s41569-019-0219-9

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