HIV can destroy or substantially affect essential cells (CD4+ T cells or T helper cells) of the immune system, which ordinarily help combat diseases. The virus spreads through the exchange of certain bodily fluids such as blood or as a result of unprotected sex. HIV affects more than 34 million people in the world according to WHO statistics, and more than 3.3 million North Americans aged 13 years and older, according to CDC statistics ( Centers for Disease Control and Prevention, 2015). There is no cure for this disease, and if left untreated, it can progress to AIDS (acquired immune deficiency syndrome, defined as 200 or fewer CD4+ cells/µl); however, medication to control HIV exists (antiretroviral therapy) which can prolong the lives of patients ( Song et al., 2017; WHO, 2011).

Patients with HIV can develop symptoms that vary depending on the disease stage. The most common symptoms are fever, fatigue, weight loss, swollen lymph nodes and shingles, amongst others. Typically, neurological complications, such as difficulty walking, are often seen in patients with advanced stages of HIV or AIDS. Nevertheless, there is one symptom that is not often mentioned, which it is known to affect HIV patients: orthostatic hypotension (OH) ( Cohen et al., 1991; Robinson-Papp et al., 2013; Song et al., 2017; WHO, 2011).

By definition, OH is a reduction in blood pressure (BP) of at least 20 mmHg systolic or 10 mmHg diastolic after either 1 or 3 minutes of standing when the patient moves from supine or to the upright position. Symptoms of OH are often associated with medications, dehydration, and infections, as explained by Cohen et al., 1991. One theory of why OH may affect patients with HIV is due to impairments in the autonomic nervous system (ANS), which is typically responsible for the modulation of numerous functions, including heart rate and vasomotor tone ( Robinson-Papp et al., 2013).

Although neurologic complications due to HIV are well characterized in the central and peripheral nervous systems, it is not entirely understood in the ANS due to its complexity. However, studies show that autonomic dysfunctions ( Cohen et al., 1991) and autonomic neuropathy ( Robinson-Papp et al., 2013) are common in patients with HIV. The symptoms of autonomic neuropathy, therefore, could include orthostatic dizziness or fainting, among others ( Robinson-Papp et al., 2013).

Although there is some evidence of a connection between OH and impairments to the ANS, this connection is unclear and poorly understood. Therefore, the objective of this study is to evaluate OH during balance sensory condition tests (SCTs) and to assess the function of the cardiac autonomic system, such as BP and heart rate (HR), during a balance task. We hypothesized that BP and HR would rise with a change in postural positioning, thus revealing ANS dysfunction.

We analyzed eight subjects of different genders and years of HIV diagnosis from a health center in San Juan, Puerto Rico ( Table 1). Raw data of heart rate, SBP and DBP is reported in Table 2. The average of BP and HR measurements for each subject before and after standing to observe possible ANS deficits associated with HIV ( Table 2– Table 3).

We assessed HR ( Figure 1), and SBP ( Figure 2) and DSB ( Figure 3) to determine whether there were ANS alterations in these participants.

All comparison are reported in Table 4. Results revealed no difference in BP and HR in sitting versus standing. However, there was a significant increase in SBP (mean ± SD) (SP, 136.5±17.8; BT, 153.7±16.5; P<0.01) and HR (SP, 73.9±10.1; BT, 109.7±13.9; P<0.05) when subjects changed positions from standing to standing during the SCT (see Figure 2). Additionally, in our last comparison, standing versus standing during the SCT, there was a significant increase in SBP (SP, 139.4±16.2; BT, 153.8±16.5; P<0.01) and HR (SP, 78.9±14.7; BT, 109.7±1.9; P<0.05).

We hypothesized that BP and heart rate would increase with changes in postural positioning, thus revealing ANS dysfunction. The key findings of our study were that participants demonstrated an increase in SBP and HR when going from sitting to standing while performing the SCT. There was also an increase in SBP and HR from standing to standing while carrying out the SCT. Therefore, our hypothesis was accepted. The present study provides support for the presence of autonomic dysfunction in persons with HIV.

The fact that SBP and HR changed from sitting and standing (on foam) could, by themselves, be causing alterations in the cardiovascular system. When we stand, muscles in charge of venous return in the lower extremities are activated ( Recek, 2013). It is possible that muscle weakness is responsible for improper venous return, thus causing an increase in HR as a compensatory mechanism ( Dymarek et al., 2014). However, the fact that BP and HR changed from standing to standing while performing the SCT was surprising. Head movements during the SCT could be affecting the carotid body (baroreceptor), thus resulting in fluctuation of BP and HR ( Ogoh et al., 2003). However, it is important to point out that normal head tilts or movements do not cause BP changes ( Ogoh et al., 2006) like the ones observed in the present study of subjects with HIV.

Venous return can also be influenced by the difficulty experienced by individuals standing on a foam/complaint surface or their inability to do so. Lower extremities muscles will co-contract, thus increasing muscle activity to maintain the standing position. ( Shumway-Cook & Woollacott, 2007).

Previous studies suggest that ANS alterations in patients with HIV are linked to the use of medications to control the HIV virus itself ( Cohen et al., 1991). Other studies also show that there are neurologic deficits in people with HIV, specifically with the ANS. Although the ANS regulates many different bodily functions, we were most interested in identifying alterations within the ANS during balance tests and the cardiac autonomic response (BP and HR) during the same task. However, there is a lack of evidence concerning why OH affects many people with HIV.

An initial study by Cohen et al. in 1991 suggests that patients with HIV will have OH as a feature of ANS impairments. An update is needed to address the recent data related to OH and HIV. Therefore, we studied BP and HR in patients with HIV to reveal OH alteration. In our initial results, there was an increase in BP when participants were asked to go from a sitting to standing position, albeit not a significant one. It is possible that with these changes in BP and HR our participants with HIV are exhibiting ANS alterations or dysfunctions. Despite the different methodology used in this study, our results had similar findings compared to the information available in the literature ( Cohen et al., 1991).

In this study, there was a significant increase (p<0.01) in HR when standing compared to HR when standing and performing the SCT. These results were surprising because such values have never been reported before. This study shows that the ANS may be impaired in people with HIV; however, more research is needed to confirm these findings.

Some of the clinical implications of this study indicate the need for further investigation of the neuromuscular activation of lower extremity muscles responsible for antero-posterior sway (tibialis anterior/gastrocnemius) and venous return (gastrocnemius). Additionally, peripheral neuropathy testing should be considered when evaluating ANS changes in persons with HIV. Towards identifying ANS dysfunctions in this population, clinicians should observe changes in HR and BP during functional movements, such as moving from a supine position to sitting, and from sitting to standing.

All data underlying the results are available as part of the article and no additional source data are required.