Heart-brain interactions during social and cognitive stress in hypertensive disease: A multidimensional approach

Abstract

Hypertensive disease (HTD), a prominent risk factor for cardiovascular and cerebrovascular diseases, is characterized by elevated stress-proneness. Since stress levels are underpinned by both cardiac and neural factors, multidimensional insights are required to robustly understand their disruption in HTD. Yet, despite their crucial relevance, heart rate variability (HRV) and multimodal neurocognitive markers of stress in HTD remain controversial and unexplored respectively. To bridge this gap, we studied cardiodynamic as well as electrophysiological and neuroanatomical measures of stress in HTD patients and healthy controls. Both groups performed the Trier Social Stress Test (TSST), a validated stress-inducing task comprising a baseline and a mental stress period. During both stages, we assessed a sensitive HRV parameter (the low frequency/high frequency [LF/HF ratio]) and an online neurophysiological measure (the heartbeat-evoked potential [HEP]). Also, we obtained neuroanatomical data via voxel-based morphometry (VBM) for correlation with online markers. Relative to controls, HTD patients exhibited increased LF/HF ratio and greater HEP modulations during baseline, reduced changes between baseline and stress periods, and lack of significant stress-related HRV modulations associated with the grey matter volume of putative frontrostriatal regions. Briefly, HTD patients presented signs of stress-related autonomic imbalance, reflected in a potential basal stress overload and a lack of responsiveness to acute psychosocial stress, accompanied by neurophysiological and neuroanatomical alterations. These multimodal insights underscore the relevance of neurocognitive data for developing innovations in the characterization, prognosis and treatment of HTD and other conditions with autonomic imbalance. More generally, these findings may offer new insights into heart-brain interactions.

Keywords: heart rate variability; hypertension; psychosocial stress.

Figure 1.

(a) Differences in HRV during the TSST: Baseline and stress periods (superior row), subtraction between stress and baseline (inferior row). Significant differences are indicated with an asterisk (P < 0.05). Individual modulations are represented inside and outside the box as points. The middle box line indicates the group’s mean values. (b) HEP modulation in frontal ROI during the baseline and stress periods during the TSST: Differences between groups were calculated via Monte Carlo permutations analyses (5000 permutations, P < 0.05), point by point (Manly, 2006). Following previous reports, a minimum extension of five consecutive points was establish to ensure temporally robust results (García-Cordero et al., 2016; Salamone et al., 2018). Shadowed bars around ERP modulations indicate SEM. Grey boxes indicate significant differences. (c) Association between HEP modulation and HRV during the baseline and stress periods of the TSST: Significant correlations are indicated with an asterisk (P < 0.05). (d) Regressions between GM volume and HRV during the baseline and stress periods of the TSST: these analyses were conducted to identify regions in each group that were associated with the HRV during the TSST (P < 0.001 uncorrected, extent threshold = 30 voxels). Baseline (left), stress (right). HEP: Heart evoked potential; HRV: Heart rate variability; HTD: Hypertensive disease; TSST: Trier Stress Social Test.