Changes In Peripheral Blood Pressure Research Articles

Biomechanical remodeling of the murine descending thoracic aorta during late-gestation pregnancy

With the rise in maternal mortality rates and the growing body of epidemiological evidence linking pregnancy history to maternal cardiovascular health, it is essential to comprehend the vascular remodeling that occurs during gestation. The maternal body undergoes significant hemodynamic alterations which are believed to induce structural remodeling of the cardiovascular system. Yet, the effects of pregnancy on vascular structure and function have not been fully elucidated. Such a knowledge gap has limited our understanding of the etiology of pregnancy-induced cardiovascular disease. Towards bridging this gap, we measured the biaxial mechanical response of the murine descending thoracic aorta during a normotensive late-gestation pregnancy. Non-invasive hemodynamic measurements confirmed a 50% increase in cardiac output in the pregnant group, with no changes in peripheral blood pressure. Pregnancy was associated with significant wall thickening ( ∼14%), an increase in luminal diameter ( ∼6%), and material softening in both circumferential and axial directions. This expansive remodeling of the tissue resulted in a reduction in tensile wall stress and intrinsic tissue stiffness. Collectively, our data indicate that an increase in the geometry of the vessel may occur to accommodate for the increase in cardiac output and blood flow that occurs in pregnancy. Similarly, wall thickening accompanied by increased luminal diameter, without a change in blood pressure may be a necessary mechanism to decrease the tensile wall stress, and avoid pathophysiological events following late gestation.

Changes in peripheral arterial blood pressure after resuscitative endovascular balloon occlusion of the aorta (REBOA) in non-traumatic cardiac arrest patients

BackgroundResuscitative endovascular balloon occlusion of the aorta (REBOA) may be an adjunct treatment to cardiopulmonary resuscitation (CPR). Aortic occlusion may increase aortic pressure and increase the coronary perfusion pressure and the cerebral blood flow. Peripheral arterial blood pressure is often measured during or after CPR, however, changes in peripheral blood pressure after aortic occlusion is insufficiently described. This study aimed to assess changes in peripheral arterial blood pressure after REBOA in patients with out of hospital cardiac arrest.MethodsA prospective observational study performed at the helicopter emergency medical service in Trondheim (Norway). Eligible patients received REBOA as adjunct treatment to advanced cardiac life support. Peripheral invasive arterial blood pressure and end-tidal CO2 (EtCO2) was measured before and after aortic occlusion. Differences in arterial blood pressures and EtCO2 before and after occlusion was analysed with Wilcoxon Signed Rank test.ResultsFive patients were included to the study. The median REBOA procedural time was 11 min and median time from dispatch to aortic occlusion was 50 min. Two patients achieved return of spontaneous circulation. EtCO2 increased significantly 60 s after occlusion, by a mean of 1.16 kPa (p = 0.043). Before occlusion the arterial pressure in the compression phase were 43.2 (range 12–112) mmHg, the mean pressure 18.6 (range 4–27) mmHg and pressure in the relaxation phase 7.8 (range − 7 – 22) mmHg. After aortic occlusion the corresponding pressures were 114.8 (range 23–241) mmHg, 44.6 (range 15–87) mmHg and 14.8 (range 0–29) mmHg. The arterial pressures were significant different in the compression phase and as mean pressure (p = 0.043 and p = 0.043, respectively) and not significant in the relaxation phase (p = 0.223).ConclusionThis study is, to our knowledge, the first to assess the peripheral invasive arterial blood pressure response to aortic occlusion during CPR in the pre-hospital setting. REBOA application during CPR is associated with a significantly increase in peripheral artery pressures. This likely indicates improved central aortic blood pressure and warrants studies with simultaneous peripheral and central blood pressure measurement during aortic occlusion.Trial registrationThe study is registered in ClinicalTrials.gov (NCT03534011).

Effect of dietary salt restriction on central blood pressure: A systematic review and meta-analysis of the intervention studies.

Central blood pressure (cBP) is highly associated with cardiovascular risk. Although reduction of salt intake leads to lower peripheral blood pressure (BP), the studies on cBP provided inconsistent results. Therefore, we performed a systematic review and a meta-analysis of the available intervention trials of salt reduction on cBP values to reach definitive conclusions. A systematic search of the online databases available (up to December 2018) was conducted including the intervention trials that reported non-invasively assessed cBP changes after two different salt intake regimens. For each study, the mean difference and 95% confidence intervals were pooled using a random-effect model. Sensitivity, heterogeneity, publication bias, subgroup, and meta-regression analyses were performed. Fourteen studies met the pre-defined inclusion criteria and provided 17 cohorts with 457 participants with 1-13weeks of intervention time. In the pooled analysis, salt restriction was associated with a significant reduction in augmentation index (9.3%) as well as central systolic BP and central pulse pressure. There was a significant heterogeneity among studies (I2 =70%), but no evidence of publication bias. Peripheral BP changes seemed to partially interfere on the relationship between salt restriction and cBP. The results of this meta-analysis indicate that dietary salt restriction reduces cBP. This effect seems to be, at least in part, independent of the changes in peripheral BP.

A randomized controlled trial to assess the central hemodynamic response to exercise in patients with transient ischaemic attack and minor stroke

Early exercise engagement elicits meaningful changes in peripheral blood pressure in patients diagnosed with transient ischaemic attack (TIA) or minor stroke. However, central hemodynamic markers may provide clinicians with important diagnostic and prognostic information beyond that provided by peripheral blood pressure readings. The purpose of this single-centre, randomized, parallel-group clinical trial was to determine the effect of a 12-week aerobic exercise intervention on central and peripheral hemodynamic variables in patients with TIA or minor stroke. In this study, 47 participants (66±10 years) completed a baseline assessment, which involved the measurement of central and peripheral hemodynamic parameters, undertaken in the morning, in a fasted state. Participants were randomized to either a 12-week exercise or control group on completion of the baseline assessment. An identical follow-up assessment was completed post intervention. Central hemodynamic variables were assessed using an oscillometric device at both assessments. Analysis of covariance demonstrated a significant interaction for central and peripheral blood pressure and augmentation index (all P<0.05; ηp2.09–.11), with the exercise group presenting lower values than the control group post intervention (118±17 vs 132±28 mm Hg for central blood pressure; 125±19 vs 138±28 mm Hg for peripheral blood pressure; 104±49 vs 115±67% for augmentation index). The present study demonstrates that participation in an exercise program soon after stroke/TIA diagnosis may elicit significant beneficial changes to a patient’s central systolic blood pressure and augmentation index. This may positively impact upon the treatment strategies implemented by clinicians in the care of patients with TIA and minor stroke.

Influence of Oxidative Stress on Blood Pressure among Japanese Community- Dwelling Persons

Introduction: Blood pressure (BP) is one of the most significant manifestations of aging and vascular disease. Oxidative stress is thought to be involved in the development of vascular dysfunction, however, the effect on baseline and changes in peripheral BP is unknown. We investigated whether baseline and changes in the oxidative stress marker, malondialdehyde-modified low density lipoprotein (MDA-LDL) are associated with baseline and change in BP, by a 12-week exercise among Japanese community-dwelling persons. Methods: The subjects comprised 10 men and 76 women aged 70 ± 7 (range, 61-82) and 67 ± 7 (range, 53-81) years, respectively. Before and at the end of the 12-week training program, metabolic variables including MDA-LDL, and systolic BP (SBP) anddiastolic BP (DBP) were obtained. Results: Gender, baseline TG, and MDL-LDL correlated significantly with baseline SBP; gender, age, BMI, TG, MDA-LDL, hsCRP, GGT, and HMA-IR correlated significantly with DBP. Stepwise linear regression analysis for baseline BP status showed that baseline BMI and MDA-LDL are significantly and independently associated with SBP, and age while baseline GGT significantly and independently associated with DBP. After the 12-week Nordic walking exercise, change in MDA-LDL significantly correlated with changes in SBP and DBP. Stepwise multivariate linear regression analysis for changes in BP parameters showed that reduction in MDA-LDL was significantly and independently associated with reduction in SBP. Conclusions:These results suggest that reduction in MDA-LDL may be a predictor for reduction in SBP after a 12-week exercise in community-dwelling persons.

Improvement in arterial stiffness following cardiac rehabilitation

BackgroundExercise has been shown to beneficially alter arterial stiffness in selected clinical settings. However, the effects of a standardized exercise protocol – “cardiac rehabilitation (CR)” – on measures of arterial stiffness in patients with established coronary heart disease (CHD) has not been well studied. MethodsUsing applanation tonometry, we studied arterial vascular properties in 26 men and 22 women (mean age 60.5±10.8years) with established CHD over a 20week CR program. All patients continued to receive their anti-anginal and vasoactive medications. In addition to standard hemodynamics we estimated central aortic pressure, central arterial pulsatility, augmentation index and arterial pulse wave velocity (PWV). ResultsAfter 20weeks of CR, there were no significant changes in resting heart rate or peripheral blood pressure. In 33 patients with at least two follow-up visits, central aortic systolic pressure was consistently lower than peripheral arterial blood pressure and decreased over the CR program time (baseline, 109±16mmHg; final, 105±14mmHg. p=0.01). Both carotid–radial (n=12) and carotid–femoral (n=21) — derived PWV decreased over the CR program (carotid–radial: baseline, 7.3±1.2m/s; final, 6.6±1.2m/s, p=0.028. carotid–femoral: baseline, 7.2±1.4m/s; final, 6.5±1.3m/s, p=0.02). ConclusionsIn this group of patients with established CHD, arterial PWV was noted to significantly decrease over a 20week CR program. This change occurred in the absence of detectable changes in peripheral blood pressure or heart rate. Decreases in PWV may serve as a sensitive indicator of improved arterial stiffness in patients with atherosclerotic arterial disease notwithstanding ongoing medical therapy.

Contribution of Vascular and Neural Segments to Baroreflex Sensitivity in Response to Postural Stress

Background/Aims: The baroreflex pathway has a vascular and a neural segment, both being modulated by variations in peripheral blood pressure (BP). Besides overall baroreceptor sensitivity (BRS), defined as the spectral relationship between changes in peripheral BP and R-R interval within the frequency band of 0.05–0.15 Hz, vascular and neural segment contributions to the overall BRS can be distinguished. We test the hypothesis that changes in overall BRS following a postural maneuver mainly originate from the vascular (peripheral pressure to carotid artery diameter) rather than the neural segment (carotid artery diameter to R-R interval). Methods: Peripheral pressure (Finapress), carotid artery diameter (ultrasound in B-/M-mode) and electrocardiogram values of 20 young subjects in supine and upright-seated postures were recorded simultaneously. Transfer gains were computed for the segmental and overall responses. Results:Postural change significantly increases peripheral BP and carotid artery diameter. The vascular segment has a uniform spectral distribution. Statistical analyses revealed that postural change decreased overall (p < 0.004) and vascular (p < 0.0001) transfer gains, but did not modify neural gain. Conclusions:Unlike the neural segment, the vascular segment is frequency non-specific. The decrease in overall BRS due to a postural change is mainly explained by the reduced transfer gain of the vascular segment.

Diurnal and Obstructive Sleep Apnea Influences on Arterial Stiffness and Central Blood Pressure in Men

Nocturnal and early morning elevation of blood pressure are common acute manifestations of obstructive sleep apnea (OSA) that do not always carry over into a sustained daytime hypertension. Using pulse wave analysis, we examined the effect of OSA on arterial stiffness and central aortic blood pressure to assess whether each would be elevated independent of diurnal changes in peripheral blood pressure. Cross-sectional sleep laboratory cohort study. Two university teaching hospitals. 57 male nonsmokers referred for suspected OSA and free of known cardiovascular disease or blood-pressure and lipid-lowering medications. The augmentation index, a quantification of augmentation of central aortic pressure due to the reflected component of the pulse pressure waveform, and brachial and aortic blood pressure were determined in the evening and early morning. The augmentation index consistently increased from evening to morning (P < .001) and was accompanied by an increase in central systolic blood pressure (P = .007) and a decrease in pulse pressure amplification (P < .001). However, these changes were unaccompanied by any changes in peripheral blood pressure. Overnight changes in mean blood pressure and heart rate were the only predictors of this effect, but they only accounted for a third of the variance (r2 = 0.339, P = .002). After adjustment for known confounders, the respiratory disturbance index was positively correlated with augmentation index at both time points (PM: P = .008, am: P = .016). The respiratory disturbance index did not correlate with any indexes of peripheral or central blood pressure. Systemic arterial stiffness is positively correlated with OSA severity and, in addition, is increased in magnitude in the early morning independent of OSA severity.

A beta vasoactivity in vivo.

Bilateral temporoparietal hypoperfusion has been frequently observed early in the Alzheimer's disease (AD) process. The beta-amyloid (A beta) peptide is believed to play a central role in the pathogenesis of AD. In vitro experiments have shown that freshly solubilized A beta enhances constriction of cerebral and peripheral vessels. We proposed that in vivo, A beta would also have vasoactive properties. To test this hypothesis, we intraarterially infused freshly solubilized A beta 1-40 in rats and observed changes in peripheral blood pressure, cerebral blood flow, and cerebrovascular resistance. We found that infusion of A beta in vivo significantly increased the blood pressure in hypotensive rats but not in normotensive and hypertensive rats. Moreover, A beta infusion also resulted in a decreased blood flow and increased vascular resistance specifically in cerebral cortex but not in heart or kidneys. These data suggest that A beta has a direct and specific constrictive effect on cerebral vessels in vivo, which may contribute to the cerebral hypoperfusion observed early in the AD process.