Device-guided Slow Breathing Research Articles

VASODILATION IS THE PREDOMINANT FACTOR OF BLOOD PRESSURE LOWERING DURING DEVICE-GUIDED SLOW BREATHING– ANALYSIS BY WAVE SHAPE PARAMETERS OF PULSE WAVE ANALYSIS

Objective: There is evidence that device-guided slow breathing with direct biofeedback of pulse arrival time (PAT) leads to favorable changes (increase) in PAT and blood pressure (decrease). Slow breathing modulates peripheral blood flow and may decrease blood pressure by vasodilation. The objectives of the study presented here was to identify hemodynamic mechanisms of the blood pressure lowering effect of device-guided breathing observed in a previously published study (Mengden Blood Pressure Monitoring 2023). Design and method: Patients with a systolic BP 130-160 mmHg or treated essential hypertension (21 females / 23 males) were trained to perform repeated and unattended device guided slow breathing exercises for 10 minutes and 5 minutes cool down over 5 days. Furthermore, they were skilled to perform a self-measurement of blood pressure before and after the breathing exercise using a validated upper-arm device. A simple device was used to measure pulse arrival time by electrocardiography and photoplethysmography connected with a smartphone or tablet to provide biofeedback. Using pulse wave analysis, time to systolic peak (tsys) and time to dicrotic notch (tnotch) were measured and normalized to RR interval, i.e., as tsys / tT and tnotch / tT. Results: Oscillometric self measured blood pressure showed a reproducible decrease in systolic blood pressure of 5 mmHg (p<0.01, SD 8 mmHg). Absolute tsys increased by 13ms (p<0.001, SD 36 ms) and relative tsys / tT increased by 0.013 (p<0.001, SD 0.033) by the end of the exercise compared to baseline after cooling down (15 min). Similarly absolute tnotch increased by 11ms (p<0.001, SD 31 ms) as well as relative tnotch / tT in total by 0.011 (p<0.001, SD 0.036) compared to baseline. Conclusions: The delayed arrival of the first pulse wave maximum and the prolonged ejection time after adjustment for heart rate can be assumed here as a surrogate of a decreasing afterload. It is thus evident from this perspective that vasodilation is an important factor of blood pressure lowering during device-guided breathing.

Exploring mechanisms of blood pressure regulation in response to device-guided and non-device-guided slow breathing: A mini review.

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 (4weeks to 3months) 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.

Device-guided slow breathing with direct biofeedback of pulse wave velocity - acute effects on pulse arrival time and self-measured blood pressure.

There isevidence that device-guided slow breathing using biofeedback acutely reduces blood pressure (BP) and pulse wave velocity [i.e. increased pulse arrival time (PAT)]. The objectives of the study presented here were to test whether the results of changes observed in PAT in earlier studies are reproducible over 1 week and how changes in pulse wave velocity/PAT translate into absolute self-measured BP changes. Patients with a systolic BP 130-160 mmHg or treated essential hypertension (21 females/23 males) were trained to perform unattended device-guided slow breathing exercises for 10 min daily over 5 days. Furthermore, they were skilled to perform self-measurement of BP before and after the breathing exercise using a validated upper-arm device. Office BP at screening [median (1, 3. Q)] was 137 (132, 142)/83 (79, 87) mmHg. We observed a significant ( P < 0.05) increase in PAT of 5 ms (SD 12.5 ms) on average after 10 min of guided breathing and an additional 1 ms ( P < 0.05, SD 8 ms) during the following 5 min of spontaneous breathing compared to baseline. PAT before the exercise remained constant over 5 days paralleled by constant self-measured BP before the exercise. Device-guided breathing was associated with a significant reduction of self-measured SBP of 5 mmHg ( P < 0.01, SD 8 mmHg). Data furthermore demonstrated that these changes were highly reproducible over 1 week. Device-guided slow breathing and biofeedback lead to reproducible and favorable changes (increase) in PAT and SBP (decrease).

Device-guided slow breathing alters postprandial oxidative stress in young adult males: A randomized sham-controlled crossover trial

Background and aimsSlow, deep breathing (SDB) lowers blood pressure (BP) though the underlying mechanisms are unknown. Redox improvements could facilitate hemodynamic adjustments with SDB though this has not been investigated. The purpose of this randomized, sham-controlled trial was to examine the acute effects of SDB on oxidative stress and endothelial function during a physiological perturbation (high-fat meal) known to induce oxidative stress. Methods and resultsSeventeen males (ages 18–35 years) were enrolled, and anthropometric measurements and 7-day physical activity monitoring were completed. Testing sessions consisted of 24-h diet recalls (ASA24), blood sample collection for superoxide dismutase (SOD) and thiobarbituric acid reactive substances (TBARS) analysis, and flow-mediated dilation (FMD). High-fat meals were ingested and 2-min breathing exercises (SDB or sham control breathing) were completed every 15 min during the 4-h postprandial phase. Blood sample collection and FMD were repeated 1-, 2-, and 4-h post meal consumption. Mean body mass index and step counts were 25.6 ± 4.3 kg/m2 and 8165 ± 4405 steps per day, respectively. Systolic and diastolic BP and nutrient intake 24 h prior were similar between conditions. No time or time by condition interaction effects were observed for FMD. The total area under the curve (AUC) for SOD was significantly lower during SDB compared to the sham breathing condition (p < 0.01). No differences were observed in TBARS AUC (p = 0.538). ConclusionsFindings from the current investigation suggest that SDB alters postprandial redox in the absence of changes in endothelial function in young, healthy males. Clinical trial registration number: NCT04864184. Clinical trials identifierNCT04864184.

Device and non-device-guided slow breathing to reduce blood pressure in hypertensive patients: a systematic review and meta-analysis

Abstract Backgroud Hypertension (HTN) is a multifactorial chronic disease. Considering the high prevalence rates of this disease, treatment of HTN is necessary, not only to reduce BP levels, but also to prevent the development of cardiovascular, cerebrovascular and kidney diseases. This treatment can be medication and/or non-farmacological, like device-guided slow breathing (DGSB) or non-device-guided slow breathing (NDGSB). Purpose The aim of this systematic review and meta-analysis is to summarize the effects of DGSB and NDGSB on blood pressure levels of patients with hypertension. Methods This study is systematic review and meta-analysis of randomized clinical trials, about hypertensive patients, with or without comorbidity, over 18 years old, of both sexes, with or without hypertensive medication. The selected studies showed comparisons between groups that performed DGSB and/or NDGSB with control conditions. The primary outcome was the value of systolic blood pressure (SBP) and diastolic blood pressure (DBP) after the interventions. Results Twenty-two studies involving 17,214 participants were included in the quantitative analysis. Considerable heterogeneity was revealed between studies. Using random effect model, it was found that DGSB did not significantly reduce SBP and DBP compared to usual care, both in terms BP values and in relation to their variations (SBP, MD −2.13 mmHg, [95% CI −12.71 to 8.44], 288 individuals; I2=93%, high heterogenity: DBP, MD −0.90, 95% CI −3.97 to 2.11, 288 individuals; I2=63%, substantial heterogenity. SBP variations MD −2.42, 95% CI −7.24 to 2.40, 443 individuals; I2=85% high heterogenity/DBP variations MD −1.67, 95% CI −4.57 to 1.24, 443 individuals; I2=80%, high heterogenity). Conclusion Based on these results it appears that DGSB did not reduce blood pressure in hypertensive patients and NDGSB is a new path for future. Funding Acknowledgement Type of funding sources: None.

Attractor Reconstruction for Quantifying the Arterial Pulse Wave Morphology During Device-Guided Slow Breathing

Attractor reconstruction is a new way to quantify the morphology of a cardiovascular waveform by plotting all data points in the three-dimensional phase space, generating a trajectory of overlapping loops. The aim of this study is to show the feasibility of an automatic approach to quantify pulse wave attractors from a device-guided breathing study, and to link attractor features to pulse waveform features. The recently developed feature extraction technique is applied to arterial pulse waveform data of 30 patients with treated hypertension. The patients performed a device-guided slow breathing exercise. The generated attractors were categorized into three different shapes: triangular attractors, bent attractors and attractors with overlapping arms. The average height of the attractors continuously and progressively dropped from 41.8 [35.4, 55.1] AU to 34.5 [25.4, 47.3] AU (p < 0.001) during the breathing exercise. We have shown that the novel approach to quantify pulse wave attractors is feasible and can be used to detect changes in the morphology of arterial pulse waveforms. Device-guided slow breathing exercise has a shrinking effect on the average height of the attractors, which may indicate a reduction in blood pressure.

Device and nondevice-guided slow breathing to reduce blood pressure in hypertensive patients: A systematic review and meta-analysis.

Backgroud and AimsHypertension (HTN) is a multifactorial chronic disease. Considering the high prevalence rates of this disease, treatment of HTN is necessary, not only to reduce blood pressure (BP) levels but also to prevent the development of cardiovascular, cerebrovascular, and kidney diseases. This treatment can be through medication, which will be determined according to the BP values, obtained either in medical consultations or at home; presence of cardiovascular risk factors, and the presence of target organ damage identified during anamnesis. The aim of this systematic review and meta‐analysis is to summarize the effects of device‐guided slow breathing (DGSB) and nondevice‐guided slow breathing (NDGSB) on BP levels of patients with HTN.MethodsThis study is a systematic review and meta‐analysis of randomized clinical trials, pertaining to hypertensive patients, with or without comorbidity, over 18 years old, of both sexes, and with or without hypertensive medication. The selected studies showed comparisons between groups that performed DGSB and/or NDGSB with control conditions. The primary outcome was the value of systolic blood pressure (SBP) and diastolic blood pressure (DBP) after the interventions.ResultsTwenty‐two studies involving 17,214 participants were included in the quantitative analysis. Considerable heterogeneity was revealed between studies. Using random effect model, it was found that DGSB did not significantly reduce SBP and DBP compared to usual care, both in terms BP values and in relation to their variations (SBP, mean difference [MD]: −2.13 mmHg, (95% confidence interval [CI]: −12.71 to 8.44), 288 individuals; I 2 = 93%, high heterogenity: DBP, MD: −0.90, 95% CI: −3.97 to 2.11, 288 individuals; I 2 = 63%, substantial heterogenity. SBP variations MD: −2.42, 95% CI: −7.24 to 2.40, 443 individuals; I 2 = 85% high heterogenity/DBP variations MD: −1.67, 95% CI: −4.57 to 1.24, 443 individuals; I 2 = 80%, high heterogenity).ConclusionBased on these results it appears that DGSB did not reduce BP in hypertensive patients and NDGSB is a new path for the future.

Device- and Nondevice-Guided Slow Breathing to Reduce Blood Pressure in Patients with Hypertension: Protocol for a Systematic Review and Meta-analysis.

BackgroundPhysiotherapy can include both device-guided slow breathing (DGSB) and nondevice-guided slow breathing (NDGSB) in the treatment of systemic arterial hypertension.ObjectiveThe aim of this study is to summarize the effects of DGSB on blood pressure levels of patients with hypertension based on the published literature to date.MethodsA systematic search of all published randomized controlled trials (RCTs) on the effects of device-guided and nondevice-guided slow breathing in patients with hypertension, without language restriction, was carried out up to a publication date of January 2020 in nine databases: PubMed/MEDLINE, Latin American and Caribbean Health Sciences Literature (LILACS), EMBASE, CENTRAL (Cochrane Central Register of Controlled Trials), Physiotherapy Evidence Database (PEDro), CINAHL (Cumulative Index to Nursing and Allied Health Literature), Scopus, Web of Science, and Livivo. Clinical trial records databases (ClinicalTrials.gov), and bases for the open gray literature, including Gray Literature Report and ProQuest Central (Citation, or Indexing, and Dissertations and Theses), were also searched for potentially eligible RCTs. The quality assessment of the included studies will be performed using the Cochrane Risk of Bias Tool for Randomized Trials. The overall quality of the evidence for each outcome will be assessed using the GRADE (Grading of Recommendations, Development and Evaluation) system.ResultsAs of December 2021, the review was completed and all data from continuous variables referring to blood pressure values (mmHg) were synthesized.ConclusionsThis systematic review will provide a summary of the current evidence on the effects of both DGSB and NDGSB on blood pressure levels. This information can contribute to decision-making by health professionals related to the use of these interventions in patients with hypertension.Trial RegistrationPROSPERO (Prospective International Register of Systematic Reviews) CRD42020147554; https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=147554International Registered Report Identifier (IRRID)RR1-10.2196/33579

Long-Term Effect of Device-Guided Slow Breathing on Blood Pressure Regulation and Chronic Inflammation in Patients with Essential Hypertension Using a Wearable ECG Device.

Hypertension is related to autonomic nervous system (ANS) dysfunction, atherosclerosis and chronic inflammation. The stimulation of baroreflex regulation by slow-breathing exercise may improve the interplay among these systems. The objective of this study was to investigate the effect of device-guided slow breathing on ANS, cardiovascular system and chronic inflammation in hypertensive patients. We prospectively collected 36 essential hypertension patients who were requested to practice slow-breathing exercise 5 times per day for 3 months. The breathing exercise was guided by a cellphone app with a wearable electrocardiography device and a rhythm of 6 cycles per minute. Cardiovascular indicators including heart rate variability (HRV), blood pressure, pulse wave velocity and baroreflex indexes were sampled 3 times: at the first visit, and 1 month and 3 months after the intervention. The levels of blood inflammatory biomarkers, including tumor necrosis factor-alpha (TNF-α), interleukin-6, interleukin-1 receptor antagonist and C-reactive protein were also collected at all 3 visits. The longitudinal differences in these variables and their correlations were tested. There was a significant decrease in blood pressure after 1 month of exercise. A significantly continuous decrease in TNF-α was also observed. The baroreflex indexes were significantly increased in the acute intervention of slow-breathing but not in the longitudinal effect. The HRV variables did not show differences with time. There were positive correlations between sympathetic index and TNF-α and galectin-3. The effect of slow-breathing exercise on blood pressure and chronic inflammation was significant. HRV indexes may also be used to assess chronic inflammation.

Non-invasive quantification of the effect of device-guided slow breathing with direct feedback to the patient to reduce blood pressure

Objective: Slow breathing is a relaxation exercise recommended for lowering blood pressure (BP). Biofeedback may improve patient adherence and enhance BP lowering effects. Since the pulse arrival time (PAT) is inversely proportional to BP, it can be used to estimate BP changes. Approach: In this pilot study, 30 patients (age 62.9 (SD 7.7) years, 11 F/19 M, Sys. BP 133.0 (SD 17.1) mmHg, Dia. BP 83.8 (SD 10.6) mmHg) performed a device-guided slow breathing exercise. PAT was measured by ECG and plethysmography and immediately presented to the patient, and respiratory sinus arrhythmia (RSA) was calculated retrospectively to measure the adherence to the instructed respiratory rate. Main results: Respiratory rate was 13.6 (SD 1.9) bpm at baseline and 5.4 (SD 1.0) bpm during guided breathing. PAT continuously and progressively increased from 231.5 (SD 20.3) to 237.3 (SD 18.5) ms (p 0.001). The median deviation of RSA from the guided respiratory rate was 0.06 (IQR 0.19) bpm. In three patients, a deviation of > 0.20 bpm was detected, and two of them showed no increase in PAT. In total, 25 patients responded with increase in PAT. Significance: In this pilot study we have shown that biofeedback of PAT and RSA are feasible and can further improve motivation and adherence. Furthermore, we have shown that the exercise increased PAT, which indicates a reduction in BP. Due to its ease of use, this method is ideal for home use and self-monitoring.

Eight weeks of device-guided slow breathing decreases sympathetic nervous reactivity to stress in posttraumatic stress disorder.

Posttraumatic stress disorder (PTSD) is characterized by increased risk for developing hypertension and cardiovascular disease. We recently showed that device-guided slow breathing (DGB) acutely lowers blood pressure (BP) and muscle sympathetic activity (MSNA) and improves baroreflex sensitivity (BRS) in PTSD. The aim of this study was to assess the long-term benefits of DGB on autonomic function at rest and during stress. We hypothesized that long-term DGB improves arterial BRS and lowers BP and MSNA in PTSD. Twenty-five veterans with PTSD were studied and randomized to either 8 wk of daily DGB (n = 12) or 8 wk of sham device (Sham; n = 13). BP, heart rate (HR), and MSNA were measured at rest and during mental math. Arterial BRS was assessed using the modified Oxford technique. Resting MSNA, BP, and heart rate (HR) remained comparable before and after 8 wk in both groups (DGB and Sham). Likewise, the change in sympathetic and cardiovagal BRS was not different between the groups. Interestingly, DGB significantly decreased MSNA reactivity to mental math when expressed as burst frequency (P = 0.012) or burst incidence (P = 0.008) compared with Sham, suggesting a sustained effect of DGB on sympathetic reactivity to stress in PTSD. Contrary to our hypothesis, long-term DGB did not lower systolic BP, diastolic BP, or HR responses to stress compared with Sham. Likewise, pulse pressure reactivity after 8 wk (P = 0.121) was also comparable. In summary, these data suggest that long-term use of DGB may lead to a sustained dampening of sympathetic reactivity to mental stress in PTSD.

Long‐term Device Guided Slow Breathing Decreases Sympathetic Nervous Reactivity to Stress in Post‐Traumatic Stress Disorder

Posttraumatic stress disorder is characterized by augmented sympathetic reactivity, impaired baroreflex sensitivity, and an increased risk for developing hypertension and cardiovascular disease. We recently showed that device‐guided slow breathing (DGB), in which breathing rates are lowered to subphysiologic levels using a biofeedback device, acutely lowers blood pressure (BP) and muscle sympathetic activity (MSNA) and improves sympathetic baroreflex sensitivity (BRS) in post‐traumatic stress disorder (PTSD). The aim of this study was to assess the potential long‐term benefits of DGB on MSNA, hemodynamics, and BRS in patients with PTSD at rest and during stress. We hypothesized that long‐term DGB will further improve sympathetic BRS, lower BP and MSNA in PTSD. Twenty five young adults, clinically diagnosed with PTSD, were studied and randomized to either 8 weeks of DGB (n=12; age, 36±2 years; BMI, 30±2 Kg/m2) or 8 weeks of an identically looking Sham device (n=13; age, 34±2 years; BMI, 28±2 Kg/m2). DGB guided the participants to a breathing rate of 5–6 breaths/min while Sham guided breathing to 14 breaths/min. BP, heart rate (HR) and MSNA was measured at rest and during 3 min of mental arithmetic. Sympathetic and cardiovagal BRS were assessed using the modified oxford technique. Measurements were done during two laboratory visits, before and after 8 weeks of 15 min of at‐home breathing daily. Both groups (DGB and Sham) were matched for age, BMI, resting MSNA, BP and heart rate (HR). Resting MSNA, BP and HR remain comparable (condition*device, p&gt;0.05) before and after the 8 weeks (condition effect) in both breathing groups. Likewise, the change in sympathetic and cardiovagal BRS was not different between the two groups (condition*device, p&gt;0.05). Interestingly, 8 weeks of DGB significantly decreased minute by minute (time effect) MSNA reactivity to mental arithmetic when expressed as burst frequency (time*condition*device, p= 0.006) or burst incidence (time*condition*device, p= 0.004) compared to 8 weeks of sham, suggesting a sustained effect of chronic DGB on sympathetic reactivity to mental stress in PTSD. Contrary to our hypothesis, long term DGB did not lower (time*condition*device, p&gt;0.05) systolic BP, diastolic BP or HR responses to stress compared to sham. However, DGB but not sham tended to decrease pulse pressure reactivity after 8 weeks of intervention (time*condition*device, p= 0.06), due to the tendency for low systolic BP reactivity post DBG. In summary, our data suggest that the long‐term use of DGB leads to a sustained dampening of sympathetic reactivity and trend towards improved pulse pressure reactivity to mental stress. Taken together, these results suggest that long term use of DGB may have beneficial effects on neurocardiovascular reactivity in individuals with PTSD.Support or Funding InformationThis work was supported by National Institutes of Health (NIH) Grant R01 HL135183; NIH R61 AT010457, VA Merit I01CX001065, the Department of Veterans Affairs, Veterans Health Administration and the Office of Research and Development, Decatur, Georgia.

The influence of mindfulness meditation on inattention and physiological markers of stress on students with learning disabilities and/or attention deficit hyperactivity disorder

BackgroundOver recent decades, the number of students diagnosed with learning disabilities and/or attention deficit hyperactivity disorders has substantially increased. These students face various challenges and experience stress when receiving higher education. AimsThe purpose of this study was to compare two non-pharmacological interventions: mindfulness and device-guided slow breathing, with a control group. MethodsSeventy-three students (age = 25.76, std. dev = 3.10) with attention problems and/or learning disabilities were randomly assigned to three groups: mindfulness meditation, device guided breathing practice and waiting-list control. Before and after the intervention physiological and psychological measures were collected. ResultsOur results show that only mindfulness practice improved awareness of the present moment and decreased hyperactivity and inattention. Furthermore, both mindfulness and practice with device-guided breathing were associated with stress reduction, as shown by an increase in the galvanic skin response only in the control group. ConclusionsImplementation of the study results may lead to an advance in treating attention deficit disorders and learning disabilities, especially among higher education students.

Abstract P3056: The Effect of Device Guided Slow Breathing With Biofeedback on Pulse Transit Time and Respiratory Sinus Arrhythmia

Slow breathing is a relaxation exercise with class B, IIa recommendation by the AHA for lowering blood pressure (BP). Biofeedback on the effect of the exercise may improve patient adherence and enhance the BP lowering effect. Conversely, standard BP measurements with occlusion cuffs interfere with relaxation. Hence, the pulse transit time (PTT) is used as a surrogate to estimate BP changes. Thirty patients treated for essential hypertension (age 62.9 (SD 7.7) years, 11F/19M, Sys. BP 133.0 (SD 17.1) mmHg, Dia. BP 83.8 (SD 10.6) mmHg) performed a device-guided slow breathing relaxation exercise for 10 minutes, with respiratory rate guided by instructions on a tablet computer. The PTT was measured by ECG and plethysmography and immediately presented on the same display. Respiratory sinus arrhythmia (RSA) was detected as the most prominent frequency in the interbeat intervals. Respiratory rate was reduced from 13.6/min (SD 1.9/min) at baseline to 5.4/min (SD 1.0/min) during guided breathing. We observed a continuous and progressive increase of PTT from 231.5 (SD 20.3) to 237.3 (SD 18.5) ms (p &lt; 0.001, fig.). Of the 30 patients, 25 responded with increase in PTT. The overall deviation of RSA from the guided respiratory rate was 0.06/min (IQR 0.19/min). In 3 subjects, an individual deviation of &gt;0.20/min was detected. Two of those 3 did not respond with increased PTT. Real-time biofeedback of PTT during device-guided slow breathing results in an increased PTT, indicating a BP reduction. Feedback of the RSA as indicator of the respiratory rate is feasible and may further improve adherence and motivation. The procedure may serve as a user-friendly, self-managed alternative for lowering BP.

Device-guided slow breathing reduces blood pressure and sympathetic activity in young normotensive individuals of both sexes.

Slow breathing (SLOWB) is recommended for use as an adjuvant treatment for hypertension. However, the extent to which blood pressure (BP) responses to SLOWB differ between men and women are not well-established. Therefore, we tested the hypothesis that an acute bout of SLOWB would induce larger decreases in BP in males than in females, given that males typically have higher resting BP. We also examined autonomic contributors to reduced BP during SLOWB; that is, muscle sympathetic nerve activity and spontaneous cardiovagal (sequence method) and vascular sympathetic baroreflex sensitivity. We tested normotensive females (n = 10, age: 22 ± 2 y, body mass index: 22 ± 2 kg/m2) and males (n = 12, age: 23 ± 3 y, body mass index: 26 ± 4 kg/m2). Subjects were tested at baseline and during the last 5 min of a 15-min RESPeRATE-guided SLOWB session. Overall, SLOWB reduced systolic BP by 3.2 ± 0.8 mmHg (main effect, P < 0.01). Females had lower systolic BP (main effect, P = 0.02); we observed no interaction between sex and SLOWB. SLOWB also reduced muscle sympathetic nerve activity burst incidence by -5.0 ± 1.4 bursts/100 heartbeats (main effect, P < 0.01). Although females tended to have lower burst incidence (main effect, P = 0.1), there was no interaction between sex and SLOWB. Cardiovagal baroreflex sensitivity improved during SLOWB (21.0 vs. 36.0 ms/mmHg, P = 0.03) with no effect of sex. Despite lower overall BP in females, our data support a lack of basement effect on SLOWB-induced reductions in BP, as SLOWB was equally effective in reducing BP in males and females. Our findings support the efficacy of the RESPeRATE device for reducing BP in both sexes, even in young, normotensive individuals.NEW & NOTEWORTHY We provide support for the effectiveness of device-guided slow breathing for blood pressure reduction in young normotensive women and men. Despite having lower baseline blood pressure and sympathetic nerve activity, women experienced equivalent reductions in both measures in response to RESPeRATE-guided slow breathing as men. Thus, slow breathing appears to be effective in young healthy normotensive individuals of both sexes and may be an ideal preventative therapy against future hypertension.

PULSE TRANSIT TIME AND RESPIRATION RATE ADHERENCE IN DEVICE-GUIDED SLOW BREATHING WITH BIOFEEDBACK TO THE PATIENT

Objective: Device-guided slow breathing is a non-invasive exercise with a class B, IIa recommendation by the American Heart Association for lowering blood pressure (BP), as it improves the arterial baroreflex sensitivity. Immediate biofeedback on the respiration rate and the effect of the exercise may improve adherence and further enhance the BP lowering effect. Pulse wave velocity (PWV) correlates to BP and is inversely related to the pulse transit time (PTT). Therefore, PTT is a non-invasive and non-interfering method to estimate BP changes. Design and method: In this study, 30 treated patients with essential hypertension (age 62.9 (SD 7.7) years, 11F/19 M, systolic BP 133.0 (SD 17.1) mmHg, diastolic BP 83.8 (SD 10.6) mmHg) performed a 10 min-session of device-guided slow breathing. Using ECG and finger-plethysmography, the PTT was calculated as the time interval from R-wave to pulse arrival and presented to the patient on the display of a tablet computer. Furthermore, the patients’ respiration rate was guided by individual instructions on the same display. Retrospectively, the actual respiration rate was evaluated using spectral analysis of the intervals between successive heartbeats in blocks of 60 seconds. Results: The subjects’ spontaneous respiration rate before the breathing exercise started was 13.6/min (SD 1.9/min). During the device-guided slow breathing exercise, it was reduced to 5.4/min (SD 1.0/min). We observed a continuous and progressive increase of PTT from 231.5 (SD 20.3) to 237.3 (SD 18.5) ms (p < 0.001, figure). Of the 30 patients, 25 responded with an increase in PTT. An overall median deviation from the guided breathing rate of 0.06/min (IQR 0.19/min) was detected. In only 3 subjects, an individual median deviation of more than 0.20/min was detected. Two of those 3 did not respond with increased PTT.Conclusions: In essential hypertensives, real-time biofeedback of PTT during device-guided slow breathing is feasible. It results in a continuous increase in PTT, indicating a BP reduction. Furthermore, biofeedback of the actual respiration rate is possible and may improve patients’ adherence and motivation. The procedure may serve as a user-friendly, self-managed, App-based alternative for lowering BP.

A randomized cross-over study on the blood pressure lowering effect of the combined passive head-up and -down movement with Device-Guided slow breathing

Purpose: Baroreflex emerges as a therapeutic target of hypertension. We investigated blood pressure (BP) lowering effect of the combined passive head-up and -down movement with device-guided slow breathing in untreated mild hypertension or high-normal BP.Methods: In a randomized, cross-over trial, untreated subjects with an ambulatory systolic/diastolic BP of 125–140/80–90 mmHg and a clinic BP of 130–150/80–90 mmHg were randomized to intervention treatment with head movement and slow breathing or sham control, and then crossed over. Both treatments consisted of 1-week preparation, 2-week treatment, and 1-week recovery. During the 2-week treatment, subjects were treated for a session of 20 min/day. BP, pulse rate and respiration were measured before and after each treatment session. Ambulatory BP monitoring was performed at baseline and the end of the 2-week treatments’ period, and home BP monitoring in the morning and evening for the whole 8-week follow-up period.Results: 14 subjects completed the study. The intervention treatment, compared to control, reduced respiration rate by −2.1 breaths/min (95% CI −2.9 to −1.2, p = .0001), but not clinic BP and pulse rate (p ≥ .67). The intervention treatment, compared to control, significantly reduced nighttime systolic/diastolic blood pressure by −5.63/−3.82 mm Hg (p ≤ .01) but not 24-h or daytime ambulatory blood pressure (p ≥ .69). Home BP decreased with the intervention treatment, but the between-treatment difference was not statistically significant (p ≥ .27).Conclusions: The combined head movement with slow breathing did not influence 24-h BP, but reduced nighttime BP in untreated mild hypertension or high-normal BP.

Guided imagery for treating hypertension in pregnancy.

Hypertension (high blood pressure) in pregnancy carries a high risk of maternal morbidity and mortality. Although antihypertensive drugs are commonly used, they have adverse effects on mothers and fetuses. Guided imagery is a non-pharmacological technique that has the potential to lower blood pressure among pregnant women with hypertension. Guided imagery is a mind-body therapy that involves the visualisation of various mental images to facilitate relaxation and reduction in blood pressure. To determine the effect of guided imagery as a non-pharmacological treatment of hypertension in pregnancy and its influence on perinatal outcomes. We searched the Cochrane Pregnancy and Childbirth Group's Trials Register, and two trials registers (October 2018). We also searched relevant conference proceedings and journals, and scanned the reference lists of retrieved studies. We included randomised controlled trials (RCTs). We would have included RCTs using a cluster-randomised design, but none were identified. We excluded quasi-RCTs and cross-over trials.We sought intervention studies of various guided imagery techniques performed during pregnancy in comparison with no intervention or other non-pharmacological treatments for hypertension (e.g. quiet rest, music therapy, aromatherapy, relaxation therapy, acupuncture, acupressure, massage, device-guided slow breathing, hypnosis, physical exercise, and yoga). Three review authors independently assessed the trials for inclusion, extracted data, and assessed risk of bias for the included studies. We checked extracted data for accuracy, and resolved differences in assessments by discussion. We assessed the certainty of the evidence using the GRADE approach. We included two small trials (involving a total of 99 pregnant women) that compared guided imagery with quiet rest. The trials were conducted in Canada and the USA. We assessed both trials as at high risk of performance bias, and low risk of attrition bias; one trial was at low risk for selection, detection, and reporting bias, while the other was at unclear risk for the same domains.We could not perform a meta-analysis because the two included studies reported different outcomes, and the frequency of the intervention was slightly different between the two studies. One study performed guided imagery for 15 minutes at least twice daily for four weeks, or until the baby was born (whichever came first). In the other study, the intervention included guided imagery, self-monitoring of blood pressure, and thermal biofeedback-assisted relaxation training for four total hours; the participants were instructed to practice the procedures twice daily and complete at least three relief relaxation breaks each day. The control groups were similar - one was quiet rest, and the other was quiet rest as bed rest.None of our primary outcomes were reported in the included trials: severe hypertension (either systolic blood pressure of 160 mmHg or higher, or diastolic blood pressure of 110 mmHg or higher); severe pre-eclampsia, or perinatal death (stillbirths plus deaths in the first week of life). Only one of the secondary outcomes was measured.Low-certainty evidence from one trial (69 women) suggests that guided imagery may make little or no difference in the use of antihypertensive drugs (risk ratio 1.27, 95% confidence interval 0.72 to 2.22). There is insufficient evidence to inform practice about the use of guided imagery for hypertension in pregnancy.The available evidence for this review topic is sparse, and the effect of guided imagery for treating hypertension during pregnancy (compared with quiet rest) remains unclear. There was low-certainty evidence that guided imagery made little or no difference to the use of antihypertensive drugs, downgraded because of imprecision.The two included trials did not report on any of the primary outcomes of this review. We did not identify any trials comparing guided imagery with no intervention, or with another non-pharmacological method for hypertension.Large and well-designed RCTs are needed to identify the effects of guided imagery on hypertension during pregnancy and on other relevant outcomes associated with short-term and long-term maternal and neonatal health. Trials could also consider utilisation and costs of health service.

Sympathetic and Cardiovascular Response to Device Guided Slow Breathing Acutely Depends on Post‐Traumatic Stress Disorder (PTSD) Severity

Post‐traumatic stress disorder (PTSD) is associated with an increased risk for developing hypertension and cardiovascular disease. We previously showed that device guided slow breathing (DGB) using the RESPeRATE device acutely lowers muscle sympathetic nerve activity (MSNA) and improves baroreflex sensitivity and hemodynamics in patients with PTSD. However, it remains unclear whether the physiological responses to DGB depend on the severity of the disorder. We hypothesized that neural and cardiovascular response to acute DGB will be heightened in PTSD participants with a greater severity of PTSD symptoms. To test our hypothesis, we recruited 25 veterans (age 36 ± 2 years; BMI 29 ± 2 kg/m2) with PTSD. The clinician‐administered PTSD scale (CAPS) was used to confirm the diagnosis of PTSD (CAPS score ≥45) and the severity of PTSD symptoms. The CAPS scores in our sample ranged from 45 to 95 with a median score of 70 that was used to separate our study participants into two groups (group effect): Moderate (CAPS ≤70, n=13) and Severe (CAPS &gt;70, n=12). Within each group, participants were randomized to either breathing with the DGB device (at a rate of 5–6 breaths/min) or breathing with an identical Sham device (at 12–14 breaths/min) (device effect) for 15 minutes. In the Moderate group, 5 participants used DGB and 8 used Sham; while in the Severe group, 6 used DGB and 6 used Sham. Beat‐to‐beat blood pressure (BP) via finger plethysmography, heart rate (HR) via EKG, heart rate variability (HRV) and muscle sympathetic nerve activity (MSNA) using microneurography were measured continuously at baseline and after 10 minutes of breathing (time effect). Age, BMI, resting BP and HR (all p&gt;0.05) were similar between groups. In response to the breathing intervention, systolic BP (time*group*device, p=0.352) and diastolic BP (time*group*device, p=0.552) responses to DGB compared to Sham were comparable between the Moderate and Severe groups. However, as we hypothesized, HR decreased more with DGB (75 ± 4 to 62 ± 3 beats/min) than Sham (73 ± 6 to 75 ± 5 beats/min) in the Severe group when compared to the Moderate group (time*group*device, p=0.049). Likewise, MSNA decreased more (time*group*device, p=0.025) with DGB (38 ± 7 to 24 ± 4 bursts/min) compared to Sham (17 ± 2 to 14 ± 2 bursts/min) in the Severe group compared to the Moderate group. Unlike MSNA, HRV responses were not different between the groups. In summary, we found that DGB decreases HR and MSNA more in participants with a higher CAPS score, i.e. more severe PTSD. These results suggest that DGB may have greater beneficial effects on sympathetic overactivity and hemodynamics in PTSD patients with severe symptoms. Whether DGB leads to long‐term benefits on neural and cardiovascular function in severe PTSD should be studied in the future.Support or Funding InformationSupported by NIH HL‐098744, NIH DK‐00756, VA Merit I01CX001065, AHA 15CSA24340001This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Long‐Term Effects of Device‐Guided Slow Breathing on Autonomic Control of Blood Pressure at Rest and During Stress in Post‐Traumatic Stress Disorder

Post‐traumatic stress disorder (PTSD) is characterized by augmented sympathetic nervous system (SNS) reactivity, impaired baroreflex sensitivity (BRS), and an increased risk for developing hypertension and cardiovascular disease. We recently showed that device‐guided slow breathing (DGB) using the RESPeRATE device acutely lowers blood pressure (BP) and muscle sympathetic activity (MSNA) and improves sympathetic BRS in PTSD. The aim of this study was to determine if long‐term daily DGB leads to sustained improvements in resting MSNA, BP, sympathetic BRS, and neurocirculatory reactivity during mental stress in combat veterans with PTSD. 19 post 9/11 veterans with PTSD (age, 36±2 years) were enrolled and randomized to either 8 weeks of DGB (n=9) versus an identical Sham device (n=10) for 15 minutes daily. Using biofeedback and musical tones, DGB guided respiratory rate (RR) to a subphysiologic rate of 5–6 breaths/min, while Sham guided RR to a normal rate of 12–14 breaths/min. BP, heart rate (HR), RR and MSNA were measured at rest and during 3 minutes of mental arithmetic (MA). Sympathetic and cardiovagal BRS were assessed with pharmacologic manipulation of BP using the modified Oxford technique. All physiologic measures were obtained before, and after 8 weeks of breathing intervention. Age, BMI, BP and HR were similar between the groups, while baseline MSNA at rest was greater in the DGB group pre‐intervention (p=0.048). Contrary to our hypothesis, there was no difference in the change in resting systolic BP (visit*group, p=0.097), diastolic BP (visit*group, p=0.571), HR (visit*group, p=0.323) and RR (visit*group, p=0.304) after 8 weeks of DGB versus Sham. There was a trend towards a difference in change in resting MSNA between the groups (visit*group, p=0.081). However, contrary to our hypothesis, there was no change in resting MSNA from pre to post 8 weeks of DGB (19±4 vs 20±2 burst/min, p&gt;0.05), while there was an increase in resting MSNA after 8 weeks of Sham (9±2 vs 19±3 burst/min, p&lt;0.001). There was no difference in change in cardiovagal BRS between the groups (visit*group, p= 0.139). Meanwhile, sympathetic BRS (visit*group, p=0.031) was not altered by 8 weeks of DGB (−1.47±0.5 vs 1.13±0.4, p=0.401), but improved with 8 weeks of Sham (−0.63±0.3 vs 1.45±0.4, p=0.032). During stress, neural and hemodynamic responses to MA (time*visit*group, p &gt;0.05 for BP, HR and MSNA) were not different between the treatment groups. In summary, although our previous data showed that DGB acutely improves SNS activity and regulation in PTSD, we observed no sustained improvements in resting MSNA, BRS, hemodynamics, or neurocirculatory reactivity during mental stress with long‐term DGB in PTSD.Support or Funding InformationSupported by NIH HL‐098744, NIH DK‐00756, VA Merit I01CX001065, AHA 15CSA24340001This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.