Immune markers, diurnal blood pressure profile and cardiac function in virologically suppressed HIV-infected patients.

PURPOSE: Non-dipping nocturnal blood pressure (BP) pattern has been reported prevalent among HIV-infected patients and is associated with adverse cardiovascular outcomes. The aims of this observational study were to identify predictors of nocturnal BP decline, and to explore whether diurnal BP profile is associated with alterations in cardiac structure and function. MATERIALS AND METHODS: A total of 108 treated HIV-infected patients with suppressed viremia underwent ambulatory BP measurement, 51 of these patients also underwent echocardiography. RESULTS: Non-dipping nocturnal BP pattern was present in 51% of the patients. Decreased nocturnal decline in systolic BP (SBP) correlated with lower CD4 count (rsp = 0.21, p = 0.032) and lower CD4/CD8 ratio (rsp = 0.26, p = 0.008). In multivariate linear regression analyses, lower BMI (p = 0.015) and CD4/CD8 ratio <0.4 (p = 0.010) remained independent predictors of nocturnal decline in SBP. Nocturnal decline in SBP correlated with impaired diastolic function, e' (r = 0.28, p = 0.049) as did nadir CD4 count (rsp = 0.38, p = 0.006). In multivariate linear regression analyses, nadir CD4 count <100 cells/µL (p = 0.037) and age (p < 0.001) remained independent predictors of e'. CONCLUSIONS: Compromised immune status may contribute to attenuated diurnal BP profile as well as impaired diastolic function in well-treated HIV infection.

Hypertension and antihypertensive treatment in HIV-infected individuals. A longitudinal cohort study.

OBJECTIVES: Hypertension is a significant contributor to cardiovascular disease in HIV-infected individuals. The purposes of this study were to assess the development of new-onset hypertension and the use of antihypertensive treatment and blood pressure (BP) control. METHODS: In a longitudinal study of 434 HIV-infected individuals (43±11 years, 72% males, follow-up 3.4±0.8 years), standardized BP recordings were undertaken at three clinical visits both at baseline and at follow-up, and cardiovascular risk factors were monitored. Adjusted odds ratio (OR) for new-onset hypertension (systolic BP≥140 and/or diastolic BP≥90 mmHg or initiation of antihypertensive treatment) was calculated using multiple logistic regression analyses. RESULTS: New-onset hypertension occurred with an incidence of 29.8 per 1000 person-years (95% CI 20.3-42.2). HIV duration (OR=1.10, 95% CI 1.01-1.20), mean BP (1.24, 95% CI 1.13-1.35) and abnormal urinary albumin excretion (OR=5.47, 95% CI 1.07-27.85) were independent predictors for new-onset hypertension after adjustment. Use of antihypertensive treatment increased threefold from 17% to 49% in hypertensive patients. Adequate BP control was obtained in 22% of patients on antihypertensive therapy. CONCLUSIONS: HIV duration predicted new-onset hypertension, which could suggest involvement of low-grade inflammation; this hypothesis needs to be further explored. Despite increased use of antihypertensive treatment, enhanced awareness and adequate treatment of hypertension are still warranted in HIV-infected individuals.

Effect of HIV duration on ambulatory blood pressure in HIV-infected individuals with high office blood pressure.

OBJECTIVE: There is a scarcity of data on ambulatory blood pressure (ABP) in HIV-infected individuals. The aim of the study was to identify possible predictors of ABP in HIV-infected individuals. METHODS: From a cohort of 542 HIV-infected patients, ABP monitoring was undertaken in 77 patients with high office blood pressure (BP) readings and without antihypertensive treatment. RESULTS: 24-h and daytime ABPs were associated with HIV duration (r=0.24-0.33, p=0.004-0.033), but not with duration of combined antiretroviral therapy. In multivariate linear regression analyses with the different ABPs as dependent variables, HIV duration (unstandardized beta=0.41-0.89, p=0.008-0.045) and log-transformed urinary albumin excretion (p=0.003-0.043) were predictors of all 24-h and daytime ABPs. Multiple logistic regression analysis revealed HIV duration (OR=1.14/year (95% CI 1.03-1.26)) as predictor of hypertension defined according to daytime ABP. Nocturnal hypertension was observed in 81%, white coat hypertension was present in 26%. CONCLUSIONS: HIV duration was an independent predictor of ABP and hypertension in a selected group of HIV-infected individuals. Nocturnal hypertension was prevalent, and white coat hypertension was present in one fourth of the patients.

Microbial translocation and cardiometabolic risk factors in HIV infection.

The widespread access to antiretroviral treatment during the past decades has transformed HIV infection from a lethal disease to a chronic condition, in which the relative burden of non-AIDS-related chronic disorders such as cardiovascular disease, malignancy, renal, liver, and bone disease has increased. The adjusted relative risk for myocardial infarction is reported to be around 2-fold compared to that of the general population, which over time is likely to translate into increased absolute risk in an aging population. Thus, delineating potentially HIV-specific pathogenetic mechanisms is crucial in order to tailor novel strategies for prophylaxis and treatment. This review will focus on advances in the field that possibly link HIV-induced alterations of the gut mucosa and consequent microbial translocation to cardiometabolic risk factors in HIV infection. Recent work suggests that markers of microbial translocation are closely associated with several cardiovascular risk factors such as dyslipidemia, insulin resistance, hypertension, coagulation abnormalities, endothelial dysfunction, and carotid atherosclerosis. Future studies should investigate whether associations between microbial translocation and cardiovascular risk factors will translate into increased risk of acute events, and whether strategies to target gut microbiota and microbial translocation might reduce such a risk.

Monocyte activation, but not microbial translocation, is independently associated with markers of endovascular dysfunction in HIV-infected patients receiving cART.

BACKGROUND: Microbial translocation has been suggested as a driver of cardiovascular disease in HIV infection. We hypothesized that microbial translocation and the resulting monocyte activation would be associated with markers of endovascular dysfunction. METHODS: In 60 HIV-infected patients on combination antiretroviral therapy, plasma levels of lipopolysaccharide, soluble CD14 (sCD14), asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA) were measured. RESULTS: ADMA and SDMA were associated with sCD14 but not lipopolysaccharide. There was a significant increase in ADMA and SDMA through tertiles of sCD14, and both markers were associated with sCD14 in multivariate linear regression analyses. CONCLUSIONS: Monocyte activation as measured by sCD14 is associated with endovascular dysfunction in HIV infection.

Low nadir CD4 cell count predicts sustained hypertension in HIV-infected individuals.

Hypertension is associated with cardiovascular disease in the human immunodeficiency virus (HIV)-infected population. The authors aimed to test the hypothesis whether advanced immunosuppression with low nadir CD4 lymphocyte cell count is a predictor of sustained hypertension in HIV-infected individuals. In a longitudinal study of an HIV cohort of 434 patients (43±11 years, 72% men, 71% Caucasians), standardized blood pressure was measured in duplicate during 3 clinical visits both at baseline and after 3.4±0.8 years. The lowest CD4 cell count in the individual history was recorded as nadir CD4. Both nadir CD4 cell count<50 cells/µL and duration of antiretroviral therapy (ART) were associated with sustained hypertension, and the highest proportion of hypertensive patients was observed in those who had both nadir CD4 cell count<50 cells/µL and prolonged ART duration. Nadir CD4 cell-count<50 cells/µL was an independent predictor of hypertension (adjusted odds ratio [OR], 2.48; 95% confidence interval [CI], 1.27-4.83), as was ART duration (adjusted OR, 1.13; 95% CI, 1.03-1.24). The predictive power of ART duration was more pronounced in patients with nadir CD4 cell count<50 cells/µL. Delaying ART initiation until a state of advanced immunosuppression might add to and even fuel the cardiovascular risk associated with ART.