| Summary: | Hypertension is among the leading causes of mortality and an important contributor toward disability-adjusted life years worldwide. Several factors contribute toward individuals’ risk to develop hypertension. Stress is considered an important pathogenic component affecting blood pressure regulation. However, systematic reviews examining the effect of psychosocial stressors and anxiety on hypertension produced spurious results. The observed heterogeneity in the operationalization of stress and subsequent reactivity hindered the characterization of the evidence for the association between exposure, physiological reactivity, and risk for hypertension. This is of paramount importance as physiological reactivity constitutes a biological interface mechanism through which stressors affect blood pressure regulation. The neural substrates of vagally mediated heart rate variability (VM-HRV) indicate that it is able to assimilate such an interfacing mechanism. Large-scale epidemiological studies provided substantial evidence linking decreases in VM-HRV with the development and progression of hypertension, indicating that individuals’ reactivity to stressors, as measured via VM-HRV, increases individuals’ risk for the development and progression of hypertension. As such, VM-HRV can reinforce current screening initiatives and support treatment-related prognosis. Self-regulation techniques, like heart rate variability biofeedback (HRVB), and neuromodulation techniques, like cranial electrotherapy stimulation (CES), are able to enhance VM-HRV and the associated parasympathetic modulation of cardiovascular outcomes, and thus address autonomic imbalances associated with hypertension. Copyright: © 2021. Christou-Champi.
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