CV Risk Factors and Cognitive Performance in HIV Patients
Objectives The aim of the study was to investigate the relationship between metabolic comorbidities, cardiovascular risk factors or common carotid intima-media thickness (cIMT) and cognitive performance in HIV-infected patients.
Methods Asymptomatic HIV-infected subjects were consecutively enrolled during routine out-patient visits at two clinical centres. All patients underwent an extensive neuropsychological battery and assessment of metabolic comorbidities and cardiovascular risk factors. Moreover, cIMT was assessed by ultrasonography. Cognitive performance was evaluated by calculating a global cognitive impairment (GCI) score obtained by summing scores assigned to each test (0 if normal and 1 if pathological).
Results A total of 245 patients (median age 46 years; 84.1% with HIV RNA < 50 copies/mL; median CD4 count 527 cells/μL) were enrolled in the study. Cardiovascular risk factors were highly prevalent in our population: the most frequent were dyslipidaemia (61.2%), cigarette smoking (54.3%) and hypertension (15.1%). cIMT was abnormal (≥ 0.9mm) in 31.8% of patients. Overall, the median GCI score was 2 [interquartile range (IQR) 1–4]; it was higher in patients with diabetes (P = 0.004), hypertension (P = 0.030) or cIMT ≥ 0.9 mm (P < 0.001). In multivariate analysis, it was confirmed that diabetes (P = 0.007) and cIMT ≥ 0.9 mm (P = 0.044) had an independent association with lower cognitive performance. In an analysis of patients on combination antiretroviral therapy (cART), abacavir use was independently associated with a better cognitive performance (P = 0.011), while no association was observed for other drugs or neuroeffectiveness score.
Conclusions Diabetes, cardiovascular risk factors and cIMT showed a strong association with lower cognitive performance, suggesting that metabolic comorbidities could play a relevant role in the pathogenesis of HIV-associated neurocognitive disorders in the recent cART era.
Although combination antiretroviral therapy (cART) has markedly changed the prognosis of HIV-infected patients by reducing AIDS-related morbidity and mortality, HIV-associated neurocognitive disorders (HANDs) are increasingly recognized in such populations. In particular, while the incidence of HIV-associated dementia (HAD) has significantly decreased in recent years, the prevalence of milder forms of HAND has gradually increased. Several factors may contribute to these epidemiological changes, such as a lower mortality leading to aging and a longer duration of HIV infection, a poor central nervous system (CNS) penetration of some antiretroviral agents, a potential neurotoxicity of cART, poor adherence and drug resistance, but also comorbidities.
HIV-infected patients show a high prevalence of cardiovascular (CV) risk factors (including diabetes, hypertension, obesity, dyslipidaemia, atherosclerosis and coronary heart disease) which can contribute to the increased mortality of a such population. These factors have been linked to a lower cognitive performance in the general population. It has been postulated that subclinical cerebrovascular disease, accelerated by CV risk factors and metabolic comorbidities, may be the basis for initial cognitive decline. In support of this hypothesis, recent data have shown that carotid intima-media thickness (cIMT), a subclinical marker of atherosclerosis, can predict reduced cognitive performance in patients without clinical vascular disease.
However, it is not exactly known if, in the recent cART era, the role of HIV-related variables (e.g. viral load, CD4 count) in the pathogenesis of HAND can be at least partially overshadowed by CV risk factors.
The aim of our study was to investigate the relationship between metabolic comorbidities, CV risk factors or cIMT and cognitive performance in HIV-infected patients, in order to obtain further insights into the pathogenesis of HAND.
Abstract and Introduction
Abstract
Objectives The aim of the study was to investigate the relationship between metabolic comorbidities, cardiovascular risk factors or common carotid intima-media thickness (cIMT) and cognitive performance in HIV-infected patients.
Methods Asymptomatic HIV-infected subjects were consecutively enrolled during routine out-patient visits at two clinical centres. All patients underwent an extensive neuropsychological battery and assessment of metabolic comorbidities and cardiovascular risk factors. Moreover, cIMT was assessed by ultrasonography. Cognitive performance was evaluated by calculating a global cognitive impairment (GCI) score obtained by summing scores assigned to each test (0 if normal and 1 if pathological).
Results A total of 245 patients (median age 46 years; 84.1% with HIV RNA < 50 copies/mL; median CD4 count 527 cells/μL) were enrolled in the study. Cardiovascular risk factors were highly prevalent in our population: the most frequent were dyslipidaemia (61.2%), cigarette smoking (54.3%) and hypertension (15.1%). cIMT was abnormal (≥ 0.9mm) in 31.8% of patients. Overall, the median GCI score was 2 [interquartile range (IQR) 1–4]; it was higher in patients with diabetes (P = 0.004), hypertension (P = 0.030) or cIMT ≥ 0.9 mm (P < 0.001). In multivariate analysis, it was confirmed that diabetes (P = 0.007) and cIMT ≥ 0.9 mm (P = 0.044) had an independent association with lower cognitive performance. In an analysis of patients on combination antiretroviral therapy (cART), abacavir use was independently associated with a better cognitive performance (P = 0.011), while no association was observed for other drugs or neuroeffectiveness score.
Conclusions Diabetes, cardiovascular risk factors and cIMT showed a strong association with lower cognitive performance, suggesting that metabolic comorbidities could play a relevant role in the pathogenesis of HIV-associated neurocognitive disorders in the recent cART era.
Introduction
Although combination antiretroviral therapy (cART) has markedly changed the prognosis of HIV-infected patients by reducing AIDS-related morbidity and mortality, HIV-associated neurocognitive disorders (HANDs) are increasingly recognized in such populations. In particular, while the incidence of HIV-associated dementia (HAD) has significantly decreased in recent years, the prevalence of milder forms of HAND has gradually increased. Several factors may contribute to these epidemiological changes, such as a lower mortality leading to aging and a longer duration of HIV infection, a poor central nervous system (CNS) penetration of some antiretroviral agents, a potential neurotoxicity of cART, poor adherence and drug resistance, but also comorbidities.
HIV-infected patients show a high prevalence of cardiovascular (CV) risk factors (including diabetes, hypertension, obesity, dyslipidaemia, atherosclerosis and coronary heart disease) which can contribute to the increased mortality of a such population. These factors have been linked to a lower cognitive performance in the general population. It has been postulated that subclinical cerebrovascular disease, accelerated by CV risk factors and metabolic comorbidities, may be the basis for initial cognitive decline. In support of this hypothesis, recent data have shown that carotid intima-media thickness (cIMT), a subclinical marker of atherosclerosis, can predict reduced cognitive performance in patients without clinical vascular disease.
However, it is not exactly known if, in the recent cART era, the role of HIV-related variables (e.g. viral load, CD4 count) in the pathogenesis of HAND can be at least partially overshadowed by CV risk factors.
The aim of our study was to investigate the relationship between metabolic comorbidities, CV risk factors or cIMT and cognitive performance in HIV-infected patients, in order to obtain further insights into the pathogenesis of HAND.
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