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 (43AE11 years, 72% men, 71% Caucasians), standardized blood pressure was measured in duplicate during 3 clinical visits both at baseline and after 3.4AE0.8 years. The lowest CD4 cell count in the individual history was recorded as nadir CD4. Both nadir CD4 cell count <50 cells ⁄ lL 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 ⁄ lL and prolonged ART duration. Nadir CD4 cellcount <50 cells ⁄ lL 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 ⁄ lL. Delaying ART initiation until a state of advanced immunosuppression might add to and even fuel the cardiovascular risk associated with ART. J Clin Hypertens (Greenwich). 2013; 15:101-106 Ó2012 Wiley Periodicals, Inc.

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.

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.

Monocyte activation as measured by sCD14 is associated with endovascular dysfunction in HIV infection.

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.

Compromised immune status may contribute to attenuated diurnal BP profile as well as impaired diastolic function in well-treated HIV infection.

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