Coronary Artery Disease in Patients with HIV Infection: An Update
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REVIEW ARTICLE
Coronary Artery Disease in Patients with HIV Infection: An Update Amish A. Patel1,2 · Matthew J. Budoff1 Accepted: 30 October 2020 © Springer Nature Switzerland AG 2020
Abstract Premature cardiovascular disease among the HIV-infected population is of great concern among clinicians. The increased life expectancy of HIV-infected individuals is mainly due to the early detection of infection and the advent of antiretroviral therapy. Once known as a deadly disease, HIV infection has transitioned into a chronic condition. Cardiovascular disease in this population is thought to progress early due to traditional and non-traditional risk factors. Early detection of subclinical atherosclerosis has become a center of focus in research as our complete understanding of this process it not yet well known. Advancements in cardiac computed tomography angiography has enabled the exploration of coronary artery disease by further evaluation of coronary stenosis and plaque analysis. An increase in cardiovascular event rates in this population is currently thought to be linked to antiretroviral therapy, Framingham risk factors, and HIV. We sought to present an updated comprehensive review of the available literature on HIV related to atherosclerosis and cardiovascular risk.
Key Points
1 Introduction
HIV increases the risk of cardiovascular disease (CVD), even when traditional risk factors are controlled.
The effect of antiretroviral therapy (ART) on individuals infected with human immunodeficiency virus (HIV) has dramatically shifted the paradigm of the disease. Initially regarded as a terminal condition, it is now considered a chronic manageable disease in regions with access to healthcare and ART. The evolution of this process has led to the increased prevalence of cardiovascular disease (CVD) due to a greater life expectancy and an increase in traditional CVD risk factors [1]. The association between HIV infection and CVD has been recognized for at least 2 decades, and possible mechanisms identified include vascular inflammation and endothelial dysfunction [2]. The complex interaction of HIV-related inflammation, immune activation, and procoagulant mechanism is core to the development of CVD [3]. The effects of ART, smoking, diabetes mellitus, hypertension, and dyslipidemia in various combinations accelerates the process of atherosclerosis further, and eventually leads to early development of acute coronary events [4, 5]. These factors have subsequently led to the increased prevalence of subclinical atherosclerosis in HIV-infected individuals compared with HIV-negative individuals in North American and European studies [6–8]. Current evidence suggests that even when traditional CVD risk factors are controlled, HIV-infected individuals remain at a twofold risk of developing CVD [9]. CVD is the second leading cause of nonAIDS-related mortality according to the Data collection on
Traditional CVD risk models underestimate risk in the HIV population. The acute myocardial infarction event rate among HIVinfected indi
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