BACKGROUND: The accurate selection of patients likely to respond to renal denervation (RDN) is crucial for optimizing treatment outcomes in patients with hypertension. This systematic review was designed to evaluate patient-specific factors predicting the RDN response.
RESULTS: We focused on individuals with hypertension who underwent RDN. Patients were categorized based on their baseline characteristics. The primary outcome was blood pressure (BP) reduction after RDN. Both randomized controlled trials and nonrandomized studies were included. We assessed the risk of bias using corresponding tools and further employed the Grading of Recommendations Assessment, Development, and Evaluation approach to assess the overall quality of evidence. A total of 50 studies were ultimately included in this systematic review, among which 17 studies were for meta-analysis. Higher baseline heart rate and lower pulse wave velocity were shown to be associated with significant antihypertensive efficacy of RDN on 24-hour systolic BP reduction (weighted mean difference, -4.05 [95% CI, -7.33 to -0.77]; weighted mean difference, -7.20 [95% CI, -9.79 to -4.62], respectively). In addition, based on qualitative analysis, higher baseline BP, orthostatic hypertension, impaired baroreflex sensitivity, and several biomarkers are also reported to be associated with significant BP reduction after RDN.
CONCLUSIONS: In patients with hypertension treated with the RDN, higher heart rate, and lower pulse wave velocity were associated with significant BP reduction after RDN. Other factors, including higher baseline BP, hypertensive patients with orthostatic hypertension, BP variability, impaired cardiac baroreflex sensitivity, and some biomarkers are also reported to be associated with a better BP response to RDN.

In resistant hypertensive patients acute carotid baroreflex stimulation is associated with a blood pressure (BP) reduction, believed to be mediated by a central sympathoinhbition.The evidence for this sympathomodulatory effect is limited, however. This meta-analysis is the first to examine the sympathomodulatory effects of acute carotid baroreflex stimulation in drug-resistant and uncontrolled hypertension, based on the results of microneurographic studies. The analysis included 3 studies assessing muscle sympathetic nerve activity (MSNA) and examining 41 resistant uncontrolled hypertensives. The evaluation included assessment of the relationships between MSNA and clinic heart rate and BP changes associated with the procedure. Carotid baroreflex stimulation induced an acute reduction in clinic systolic and diastolic BP which achieved statistical significance for the former variable only [systolic BP: -19.98 mmHg (90% CI, -30.52, -9.43), P < 0.002], [diastolic BP: -5.49 mmHg (90% CI, -11.38, 0.39), P = NS]. These BP changes were accompanied by a significant MSNA reduction [-4.28 bursts/min (90% CI, -8.62, 0.06), P < 0.07], and by a significant heart rate decrease [-3.65 beats/min (90% CI, -5.49, -1.81), P < 0.001]. No significant relationship was detected beween the MSNA, systolic and diastolic BP changes induced by the procedure, this being the case also for heart rate. Our data show that the acute BP lowering responses to carotid baroreflex stimulation, although associated with a significant MSNA reduction, are not quantitatively related to the sympathomoderating effects of the procedure. This may suggest that these BP effects depend only in part on central sympathoinhibition, at least in the acute phase following the intervention.

Blood pressure (BP) reduction occurs after a single bout of exercise, referred to as postexercise hypotension (PEH). The clinical importance of PEH has been advocated owing to its potential contribution to chronic BP lowering, and as a predictor of responders to exercise training as an antihypertensive therapy. However, the mechanisms underlying PEH have not been well defined. This study undertook a scoping review of research on PEH mechanisms, as disclosed in literature reviews. We searched the PubMed, Web of Science, Scopus, Cumulated Index to Nursing and Allied Health Literature (CINAHL), Cochrane Library, and Sport Discus databases until January 2023 to locate 21 reviews - 13 narrative, four systematic with 102 primary trials, and four meta-analyses with 75 primary trials involving 1566 participants. We classified PEH mechanisms according to major physiological systems, as central (autonomic nervous system, baroreflex, cardiac) or peripheral (vascular, hemodynamic, humoral, and renal). In general, PEH has been related to changes in autonomic control leading to reduced cardiac output and/or sustained vasodilation. However, the role of autonomic control in eliciting PEH has been challenged in favor of local vasodilator factors. The contribution of secondary physiological outcomes to changes in cardiac output and/or vascular resistance during PEH remains unclear, especially by exercise modality and population (normal vs. elevated BP, young vs. older adults). Further research adopting integrated approaches to investigate the potential mechanisms of PEH is warranted, particularly when the magnitude and duration of BP reductions are clinically relevant. (PROSPERO CRD42021256569).

OBJECTIVE: Non-invasive, beat-to-beat variations in physiological indices provide an opportunity for more accessible assessment of autonomic dysfunction. The potential association between the changes in these parameters and arterial stiffness in hypertension remains poorly understood. This systematic review aims to investigate the association between non-invasive indicators of autonomic function based on beat-to-beat cardiovascular signals with arterial stiffness in individuals with hypertension.
METHODS: Four electronic databases were searched from inception to June 2022. Studies that investigated non-invasive parameters of arterial stiffness and autonomic function using beat-to-beat cardiovascular signals over a period of > 5min were included. Study quality was assessed using the STROBE criteria. Two authors screened the titles, abstracts, and full texts independently.
RESULTS: Nineteen studies met the inclusion criteria. A comprehensive overview of experimental design for assessing autonomic function in terms of baroreflex sensitivity and beat-to-beat cardiovascular variabilities, as well as arterial stiffness, was presented. Alterations in non-invasive indicators of autonomic function, which included baroreflex sensitivity, beat-to-beat cardiovascular variabilities and hemodynamic changes in response to autonomic challenges, as well as arterial stiffness, were identified in individuals with hypertension. A mixed result was found in terms of the association between non-invasive quantitative autonomic indices and arterial stiffness in hypertensive individuals. Nine out of 12 studies which quantified baroreflex sensitivity revealed a significant association with arterial stiffness parameters. Three studies estimated beat-to-beat heart rate variability and only one study reported a significant relationship with arterial stiffness indices. Three out of five studies which studied beat-to-beat blood pressure variability showed a significant association with arterial structural changes. One study revealed that hemodynamic changes in response to autonomic challenges were significantly correlated with arterial stiffness parameters.
CONCLUSIONS: The current review demonstrated alteration in autonomic function, which encompasses both the sympathetic and parasympathetic modulation of sinus node function and vasomotor tone (derived from beat-to-beat cardiovascular signals) in hypertension, and a significant association between some of these parameters with arterial stiffness. By employing non-invasive measurements to monitor changes in autonomic function and arterial remodeling in individuals with hypertension, we would be able to enhance our ability to identify individuals at high risk of cardiovascular disease. Understanding the intricate relationships among these cardiovascular variability measures and arterial stiffness could contribute toward better individualized treatment for hypertension in the future.
BACKGROUND: PROSPERO ID: CRD42022336703. Date of registration: 12/06/2022.

This systematic review aimed to evaluate the effect of transcutaneous auricular vagus nerve stimulation on heart rate variability and baroreflex sensitivity in healthy populations.
PubMed, Scopus, the Cochrane Library, Embase, and Web of Science were systematically searched for controlled trials that examined the effects of transcutaneous auricular vagus nerve stimulation on heart rate variability parameters and baroreflex sensitivity in apparently healthy individuals. Two independent researchers screened the search results, extracted the data, and evaluated the quality of the included studies.
From 2458 screened studies, 21 were included. Compared with baseline measures or the comparison group, significant changes in the standard deviation of NN intervals, the root mean square of successive RR intervals, the proportion of consecutive RR intervals that differ by more than 50 ms, high-frequency power, low-frequency to high-frequency ratio, and low-frequency power were found in 86%, 75%, 69%, 47%, 36%, and 25% of the studies evaluating the effects of transcutaneous auricular vagus nerve stimulation on these indices, respectively. Baroreflex sensitivity was evaluated in six studies, of which a significant change was detected in only one. Some studies have shown that the worse the basic autonomic function, the better the response to transcutaneous auricular vagus nerve stimulation.
The results were mixed, which may be mainly attributable to the heterogeneity of the study designs and stimulation delivery dosages. Thus, future studies with comparable designs are required to determine the optimal stimulation parameters and clarify the significance of autonomic indices as a reliable marker of neuromodulation responsiveness.

Hypertension is a widespread disease that, if persistent, increases the risks of coronary heart disease mortality and morbidity. Slow breathing is a recommended blood pressure-lowering strategy though the mechanisms mediating its effects are unknown.
This review aims to evaluate autonomic and vascular function as potential mediators driving BP adaptive responses with slow breathing.
We searched EBSCO host, Web of Science, Cochrane Central Register of Controlled Trials, and PubMed using key words for optimized search results.
Nineteen studies were included in this review (11 device-guided; 8 non-device-guided breathing). Though some studies showed increased vagally mediated components of heart rate variability during slow breathing, results from acute and long-term studies were incongruent. Increases in baroreflex sensitivity (BRS) following a single device-guided slow breathing bout were noted in normotensive and hypertensive adults. Long-term (4 weeks to 3 months) effects of slow breathing on BRS were absent. Device-guided breathing resulted in immediate reductions in muscle sympathetic nerve activity (MSNA) in normo- and hyper-tensive adults though results from long-term studies yielded inconsistent findings. Non-device-guided slow breathing posed acute and chronic effects on vascular function with reductions in arterial stiffness in adults with type I diabetes and increases in microvascular endothelial function in adults with irritable bowel syndrome. Non-device guided breathing also reduced pro-inflammatory cytokines in healthy and hypertensive adults in acute and chronic studies. No adverse effects or non-adherence to treatment were noted in these trials.
Device-guided slow breathing is a feasible and effective modality in improving BRS, HRV, and arterial stiffness though its long-term effects are obscure. Though less evidence exists supporting the efficacy of non-device-guided slow breathing, acute and chronic studies demonstrate improvements in vascular function and inflammatory cytokines. More studies are needed to further explore the long-term effects of slow breathing in general and non-device-guided breathing in particular.

Objective.To conduct a systematic review of the possible effects of passive heating protocols on cardiovascular autonomic control in healthy individuals.Approach.The studies were obtained from MEDLINE (PubMed), LILACS (BVS), EUROPE PMC (PMC), and SCOPUS databases, simultaneously. Studies were considered eligible if they employed passive heating protocols and investigated cardiovascular autonomic control by spontaneous methods, such as heart rate variability (HRV), systolic blood pressure variability (SBPV), and baroreflex sensitivity (BRS), in healthy adults. The revised Cochrane risk-of-bias tool (RoB-2) was used to assess the risk of bias in each study.Main results.Twenty-seven studies were included in the qualitative synthesis. Whole-body heating protocols caused a reduction in cardiac vagal modulation in 14 studies, and two studies reported both increased sympathetic modulation and vagal withdrawal. Contrariwise, local-heating protocols and sauna bathing seem to increase cardiac vagal modulation. A reduction of BRS was reported in most of the studies that used whole-body heating protocols. However, heating effects on BRS remain controversial due to methodological differences among baroreflex analysis and heating protocols.Significance.Whole-body heat stress may increase sympathetic and reduce vagal modulation to the heart in healthy adults. On the other hand, local-heating therapy and sauna bathing seem to increase cardiac vagal modulation, opposing sympathetic modulation. Nonetheless, further studies should investigate acute and chronic effects of thermal therapy on cardiovascular autonomic control.

Treatment strategies that modulate autonomic tone through interventional and device-based therapies have been studied as an adjunct to pharmacological treatment of heart failure with reduced ejection fraction (HFrEF). The main objective of this study was to perform a meta-analysis of randomized controlled trials which evaluated the efficacy of device-based autonomic modulation for treatment of HFrEF. All randomized-controlled trials testing autonomic neuromodulation device therapy in HFrEF were included in this trial-level analysis. Autonomic neuromodulation techniques included vagal nerve stimulation (VNS), baroreflex activation (BRA), spinal cord stimulator (SCS), and renal denervation (RD). The prespecified primary endpoints included mean change and 95% confidence intervals (CI) of left ventricular ejection fraction (LVEF), NT pro-B-type natriuretic peptide (NT-proBNP), and quality of life (QOL) measures including 6-minute hall walk distance (6-MHWD), and Minnesota Living with Heart Failure Questionnaire (MLHFQ). New York Heart Association (NYHA) functional class improvement was reported as odds ratios and 95% CI of improvement by at least 1 functional class. Eight studies were identified that included 1037 participants (2 VNS, 2 BRA, 1 SCS, and 3 RD trials). This included 6 open-label, 1 single-blind, and 1 sham-controlled, double-blind study. The mean age (±SD) was 61 (±9.3) years. The mean follow-up time was 7.9 months. Twenty percent of the total patients were female, and the mean BMI (±SD) was 29.86 (±4.12). Autonomic neuromodulation device therapy showed a statistically significant improvement in LVEF (4.02%; 95% CI 0.24,7.79), NT-proBNP (-219.80 pg/ml; 95% CI -386.56, -53.03), NYHA functional class (OR 2.32; 95% CI 1.76, 3.07), 6-MHWD (48.39 m; 95% CI 35.49, 61.30), and MLHFQ (-12.20; 95% CI -19.24, -5.16) compared to control. In patients with HFrEF, the use of autonomic neuromodulation device therapy is associated with improvement in LVEF, reduction in NT-proBNP, and improvement in patient-centered QOL outcomes in mostly small open-label trials. Large, double-blind, sham-controlled trials designed to detect differences in hard cardiovascular outcomes are needed before widespread use and adoption of autonomic neuromodulation device therapies in HFrEF.

This review outlines the normal heart rate and blood pressure response to active standing, the physiological mechanisms governing these, and the effect of ageing on the responses.
A literature search was conducted to identify articles investigating the normal heart rate and/or blood pressure response to standing.
Heart rate when standing increases and then decreases and recovers to baseline. Blood pressure responses are inverse. Skeletal muscle contraction and the baroreceptor reflex drive this. With ageing, heart rate response attenuates and the initial blood pressure response increases.
Normal heart rate and blood pressure responses are attributed to the baroreceptor reflex and skeletal muscle contraction. Decreased muscle strength and baroreceptor sensitivity are associated with ageing, suggesting a possible benefit in improving skeletal muscle strength to maintain an efficient response. Understanding these responses and their variation with ageing is clinically relevant and may be beneficial in improving rehabilitation outcomes.

BACKGROUND: Increasing evidence suggests autonomic nervous system (ANS) dysfunction may occur following mild traumatic brain injury (mTBI). Measures of heart rate, heart rate variability, blood pressure and baroreceptor sensitivity can be used to evaluate ANS dysfunction following mTBI.
OBJECTIVE: Summarize the evidence for ANS dysfunction in adults following mTBI.
METHODS: A search of Embase, MEDLINE, Cochrane Central Register, PsycINFO, CINAHL and SPORTDiscus databases was conducted. Search topics included: mTBI and ANS. Identified abstracts were independently reviewed by 2 reviewers followed by full text screening. Risk of bias was assessed using a modified SIGN checklist. A structured synthesis was performed.
RESULTS: Thirty-nine studies (combined 1,467 participants diagnosed with mTBI) evaluating ANS function were included. ANS function was evaluated under various conditions including: rest, during exertion, cold pressor test, Valsalva maneuver, using face cooling and eyeball pressure paradigms. Short-term or ultra-short-term recordings were most common. The majority of studies (28/39) were rated as \"unacceptable\" for quality of evidence.
CONCLUSIONS: Altered parameters of ANS function have been reported in multiple conditions following mTBI, both acutely and in the post-acute/chronic stages of recovery. However, due to methodological limitations, conclusions regarding the severity and timing of ANS dysfunction following mTBI cannot be drawn.