Abstract
Evidence from epidemiological studies on the general population suggests that midlife cardiovascular disease (CVD) and/or metabolic syndrome (MetS) are associated with an increased risk of cognitive impairment and dementia later in life. In the modern combined antiretroviral therapy (cART) era, as in the general population, CVD and MetS were strongly and independently associated with poorer cognitive performances of sustained immunovirologically controlled persons living with human immunodeficiency viruses (PLHIVs). Those findings suggest that CV/metabolic comorbidities could be implicated in the pathogenesis of HIV-associated neurocognitive disorders (HAND) and might be more important than factors related to HIV infection or its treatment, markers of immunocompetence, or virus replication. The association between CVD/MetS and cognition decline is driven by still not well-understood mechanisms, but risk might well be the consequence of increased brain inflammation and vascular changes, notably cerebral small-vessel disease. In this review, we highlight the correspondences observed between the findings concerning CVD and MetS in the general population and virus-suppressed cART-treated PLHIVs to evaluate the real brain-aging processes. Indeed, incomplete HIV control mainly reflects HIV-induced brain damage described during the first decades of the pandemic. Given the growing support that CVD and MetS are associated with HAND, it is crucial to improve early detection and assure appropriate management of these conditions.
Highlights
Atrial fibrillation Acquired immunodeficiency syndrome Blood–brain barrier Body mass index Blood pressure systolic (SBP) and diastolic (DBP) Coronary artery disease Combined antiretroviral therapy Carotid intima–media thickness Cerebrospinal fluid Cerebral small-vessel disease Cardiovascular CV disease HIV-associated neurocognitive disorders Hepatitis C virus High-density lipoprotein cholesterol Human immunodeficiency virus Low-density lipoprotein cholesterol Metabolic syndrome Magnetic resonance imaging Plasma HIV load Person living with HIV Vascular cognitive impairment White-matter hyperintensity
With growing evidence that cardiovascular disease (CVD) and metabolic syndrome (MetS) probably contribute to cognitive impairment in Combined antiretroviral therapy (cART)-treated persons living with human immunodeficiency viruses (PLHIVs) with well-sustained virological control, it is essential to improve early detection and encourage appropriate management of these conditions
Their precise roles remain to be elucidated because several studies included PLHIVs not virologically suppressed and with major confounding cognitive impairment risk factors, e.g., ethnically diverse cohorts, heterogeneous ages at which reading was acquired and years of education, current hepatitis C virus (HCV) infection, or illicit drug abuse (Saloner and Cysique 2017; Marquine et al 2018; Haddow et al 2015)
Summary
The absolute CVD risk increases with aging, and a growing body of evidence is showing a heightened CVD risk for middle-aged PLHIVs, compared to age-matched HIV-uninfected individuals, even after correcting for traditional CVD risk factors (Boccara et al 2013). If the relative risk of all CVDs is ~1.5-fold higher for PLHIVs than age-matched, HIV-uninfected individuals, a trend toward its decline in virussuppressed PLHIVs has been observed over recent calendar periods in the modern cART era (Klein et al 2015). The more recent myocardial infarction incidence for cART-treated male and female PLHIVs in France is 1.12- and 1.99fold higher, respectively, than the general population (Baldé et al 2019). Both HIV-related factors and antiretrovirals might contribute independently to enhancing the CVD risk, together with overrepresentation of CVD risk factors (Lang et al 2012). PLHIVs with well-controlled infections and preexisting CVD had sixfold higher odds of having neurocognitive impairment, after adjustment for age, sex, race/ethnicity, education, location, prior acquired immunodeficiency syndrome (AIDS), and total cholesterol (Wright et al 2010)
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