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Central regulation of heart rate and blood pressure provides the bases for a neurogenic mechanism of hypertension (HTN). Post menopause (PM) age coincides with changes in resting state functional brain connectivity (rsFC) as well as increased risk for HTN. Whether the neural networks underpinning cardioautonomic control differ between PM women with and without HTN is unclear. Phenotypic and functional neuroimaging data from the Nathan Kline Institute was first evaluated for group differences in intrinsic network connectivity between 22 HTN post menopausal women and 22 normotensive controls. Intrinsic rsFC of the midbrain-brainstem-cerebellar network with bilateral mid-anterior insula was lower in women with HTN (FWE-corrected, p

Depression and chronic inflammation are common in persons infected with the human immunodeficiency virus (HIV+). Although depression and response to inflammatory challenge are shown to reflect activity in common neural networks, little is known regarding sub-clinical presentation in persons chronically infected with HIV. The relationship of resting-state functional connectivity (rsFC) between the subgenual anterior cingulate cortex (sgACC) and bilateral amygdala to Beck Depression Inventory-1 (BDI) scores were compared within a group of 23 HIV+ and 23 HIV-negative comparison adults. An interaction was found wherein lower rsFC between the sgACC and both right and left amygdala was associated with higher BDI scores in HIV+ individuals. Total BDI scores and plasma levels of IL-6, IL-8, TNF-α, and IL-10 made available from 10 of the HIV+ patients were regressed upon an index of spontaneous whole-brain activity at rest; i.e., the amplitude of low-frequency fluctuations (ALFFs). Elevated levels of depression and IL-6 were associated with increased ALFF in a cluster of voxels on the medial portion of the ventral surface of the frontal lobe (Brodmann Area 11). Within this sample of HIV+ individuals lower rsFC of the sgACC with subcortical limbic regions predicts greater burden of depressive symptomology whereas elevated activity in the adjacent BA 11 may reflect sickness, indexed by elevated IL-6, and associated depressive behaviors.

The increasing prevalence of cardiovascular disease comorbidity in persons infected with the HIV has become a global concern. The electrocardiogram (ECG) is increasingly being utilized to provide clinically relevant information regarding cardiac arrhythmias and cardio-autonomic dysfunction. The purpose of this review is to summarize the latest research comparing QT and R-to-R interval length as a function of HIV+ status or antiretroviral therapy (ART) regimen.Prolongation of the corrected QTc interval may be acquired in HIV+ ART-naive individuals, exacerbated by various classes of ART drugs, and is generally predictive of lethal cardiac arrhythmias, with effects observed from childhood to adulthood. Recent literature also suggests the trend of lower heart rate variability in HIV is indicative of cardiorespiratory and inflammatory-immune dysfunction.These emergent studies support the clinical relevance of the ECG across the age and HIV disease spectrum. Furthermore, the reported findings have implications for the management of cardiovascular and chronic inflammatory disease comorbidity in persons living with HIV.

Peripheral blood mononuclear cell derived endothelial progenitor cells (EPCs) are associated with cardiovascular function and their numbers decline with older age hypertensive risk and HIV infectionisease burden. Emergent evidence suggests that their functionality and presence may be related to cardio-autonomic and psychological functioning. This study examined whether in a sample of post-menopausal (PM) women (n = 5 HIV+/HTN + mean PM age = 53, n = 11 HIV+/HTN- mean PM age = 57, n = 6 HIV-/HTN + mean PM age = 53, or n = 14 HIV-/HTN- mean PM age = 53) ex vivo expansion of EPC counts derived from peripheral blood mononuclear cells covary with measures of high and low frequency heart rate variability. Mononuclear cells were isolated from each subject’s blood sample and incubated for 15 days in a fibronectin coated flask at 37 degrees Celsius, with the EPC medium changed every 2–3 days. Total cell, cluster, and spindle counts were recorded every 5 days for 2 weeks at 3 different time points labeled (t1, t2, and t3). After 10 days, EPC counts were significantly lower in HIV + HTN + and HIV + HTN- women compared to HIV-HTN+ (ps

HIV-positive individuals are susceptible to expansion of the non-classical and intermediate pool of peripheral blood mononuclear cells (PBMCs). Persistent HIV-related inflammation contributes to neurodegeneration but effects on limbic brain centers are not well understood. Here, we compare PBMCs and their expression of pro-inflammatory cytokines to resting brain activity and mood within and between 19 HIV + and 19 HIV- (mean age = 54.5, SD = 5.68) post-menopausal women. Mean amplitude of low-frequency fluctuations (mALFF), Profile of Mood States Questionnaire (POMS) and PBMCs immunophenotyped by flow cytometry were collected on consecutive days. PBMCs were classified into classical (CD14++ CD16−), intermediate (CD14++ CD16+) and non-classical (CD14low/+ CD++) monocyte subsets. PBMCs underwent intracellular staining for IL-6, TNF-a, IL1-b and IL-10 cytokines. One sample t-tests indicated that, compared to classical PBMCs, there was greater nonclassical IL-6 and intermediate IL-6, IL1-b and IL-10 expression. Total mood disturbance correlated with intermediate (r = .474, p = .003) and non-classical (r = .425, p = .010) PBMCs (Bonferroni corrected). Percentage of intermediate PBMCs also predicted greater activity within the subgenual anterior cingulate cortex (sgACC), (T = 3.35, k = 50 p=.002, cluster thresholded), a region associated with sickness behavior and depression. However, using a 5-mm sphere surrounding the sgACC parameter estimates failed to correlate with mood disturbance (r = .196, p > .05). Our findings suggest that expansion of the intermediate monocyte pool may reflect increased activation within neurovisceral limbic regions.

Chronic infection with HIV is associated with impaired endothelial function and altered cerebral blood flow (CBF). Using fMRI Arterial Spin Labeling, we sought to determine 1) whether CBF in HIV+ postmenopausal women (n = 8, mean age = 55.13, SD = 5.38) differs from that of HIV- controls (n = 13, mean age = 53.77, SD = 6.41), and 2) whether a marker of angiogenic potential, i.e. endothelial progenitor cell (EPC) cluster formation, and time since HIV infection covary with CBF in HIV+ women (n = 8). After controlling for age, HIV+ individuals showed increased ventral perfusion extending from the inferior frontal lobes through the basal ganglia and cerebellar regions, k = 105271, p = .001, FWE-corrected (cluster). However, longer disease duration was associated with reduced perfusion to the right parahippocampal gyrus, k = 4,916, p = .001, uncorrected. Paradoxically, higher EPC clusters predicted greater CBF to the right parahippocampal gyrus, k = 10791, p .05, uncorrected. Post hoc correlational analyses revealed a trend towards lower numbers of ex vivo EPC clusters with longer disease duration in the HIV+ group, r = .576, p > .05. While longer disease duration places postmenopausal HIV+ women at risk of lower CBF to the parahippocampal gyrus, this effect may be mitigated by the angiogenic potential of peripheral blood mononuclear cell derived EPCs.

Human Immunodeficiency Virus (HIV-1) infection is associated with expansion of the non-classical monocyte pool. These monocytes transmigrate across the blood-brain-barrier and induce proliferation of pro-inflammatory cytokines. Although this expansion has been linked to HIV-associated neurocognitive impairment, associations with psychological functioning are unclear. Flow cytometric analysis yielded the proportion of gated non-classical, intermediate and classical monocytes in 22 post-menopausal women (11 HIV+ and 11 HIV-negative) aged 55.77 years (SD = 6.32). A regression model tested variance in the proportion of non-classical monocytes accounted for by HIV status and scores on the Profile of Mood States questionnaire. Accounting for HIV status, mood disturbance accounted for 28% of the variance in non-classical monocytes, R2 = 0.275, F(2,21) = 3.69, p = 0.047. For every 1 unit increase in mood disturbance, the proportion of non-classical monocytes increased by nearly 10%, B = 0.096, SE = 0.04, t = 2.59 p = 0.018. However, HIV status did not predict variance in the proportion of mononuclear cells B = 1.18, SE = 2.37, t = 0.498, p > 0.05, suggesting expansion of the non-classical monocyte pool is associated with increasing levels of mood disturbance, independent of HIV infection. More work is needed to determine whether peripheral or neural-inflammation resulting from activation of non-classical monocytes potentially drives and/or may be driven by distress in HIV positive individuals.