Arterial Pressure Variability Research Articles

Physical Training Protects Against Release of Pro‐Inflammatory Cytokines and Prevents Alterations in Cardiac Autonomic Modulation in NA Experimental Model of COPD

Respiratory chronic diseases are one of the most important causes of morbidity and mortality, and Chronic Obstructive Pulmonary Disease (COPD) stands out between the others. This disease is caracterized by a limitation to airflow, which is not completely reversible, beside importants systemics effects, like damages in cardiac autonomic modulation and an overreacted inflammatory cells associated with an increased secretion of cytokines. Physical training (PT) has been well‐marked as an important therapeutic tool. However, the influence of PT in the development of this disease is not completely described, especially as a preventive method. Thus, the aim of this study was to evaluate the impact of an PT in the inflammatory profile and autonomic modulation before the establishment of COPD. Experiments were executed in 2 steps. First, 28 mice C57Bl/6 were divided in 4 groups: G1(control, n=7); G2 (COPD, n=7); G3 (PT, n=7); and G4 (COPD+PT, n=7) to analise cellularity and the levels of TNF‐alfa, IL‐6, IL‐10, TGF‐beta, CXCL‐1 and CCL2. Then, 28 mice were divided into the same groups to analise the autonomic aspects. G1 were kept without intervention for 4 weeks, while G3 and G4 were trained in a treadmill for the same period (5 days/week, 1 hour/day). G2 and G4 (at the end of the PT) passed by the COPD induction, which were caracterized by 3 days with cigarette smoke (CS) exposion and the administration of an intranasal dose of LPS at the third day. 24 hours latter, mice were euthanized and the samples were collected. Animals that provided hemodynamics data had their carotid artery cannulated in the last day of the protocol, and 24 hours latter signals were registered. Inflammatory aspects showed that the model of CS+LPS was efficient to increase total and differential cellularity in the Bronchoalveolar Lavage Fluid, and, at the same time, PT decreased the same aspects. Pro‐inflammatory cytokines levels were also increased in COPD group. In the other hand, PT significantly prevented their increase in trained animals. TGF‐beta had their level increased in trained group, showing its “tissue‐protective” feature. About the hemodynamics aspects, the proposed model of COPD induction showed an increase in the sympathetic cardiac modulation and in the sympathovagal inbalance, while there was a decrease in the parasympathetic cardiac modulation. In COPD group, artherial pressure variability was also increased. PT was efficient to increase protective parameters, like parasympathetic cardiac modulation and arterial pressure variability, while it decreased sympathetic cardiac modulation and suited sympathovagal inbalance. In conclusion, aerobic PT was able to prevent a greater release of pro‐inflammatory cytokines and regulate the presence of protective molecules, like TGF‐beta. Also, PT acts like a protective tool to suit hemodynamics parameters, increasing positive aspects related to cardiac vagal tonus and decreasing the influence of sympathetic system.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Effect of Different Antihypertensive Classes on the Complexity of Heart Rate and Blood Pressure Variability

Hypertension is associated with several physiological dysfunctions, including changes in the neurohumoral control of heart and vessels. Different classes of antihypertensive drugs may have distinct effects on the autonomic system and body homeostasis, but their individual effects on the complexity of cardiovascular regulation are still not established. We investigated the effect of five different classes of antihypertensive on the complexity of pulse interval (PI) and arterial pressure (AP) variability in an experimental model of renal hypertension (2 kidney 1 clip, 2K1C) in the rat. Hypertensive rats were treated (by gavage) during 15 days with: water (N=12), ramipril (2 mg/kg/day; N=7), losartan (10 mg/kg/day; N=8), atenolol (90 mg/kg/day; N=9), amlodipine (10 mg/kg/day; N=7) or hydrochlorothiazide (20 mg/kg/day; N=8). A normotensive (sham‐operated) control group (N=10) received water for the same period. After the treatment, rats had their raw AP recorded and beat‐by‐beat series of systolic AP and PI were created. The complexity of AP and PI was assessed by multiscale entropy (MSE) and detrended fluctuation analysis (DFA). For PI series, hypertensive rats treated with water showed decreased MSE and increased DFA in the middle range of scales. For AP series, hypertensive rats untreated or treated with amlodipine have lower MSE at short and middle time scales. Hypertensive rats treated with amlodipine also showed altered DFA in comparison to the other groups. All antihypertensive drugs were efficient to restore AP to normal levels. Moreover, 2K1C untreated (water) rats presented the lowest cardiovascular complexity and all antihypertensive drugs, except for amlodipine, were capable to restore the cardiovascular complexity to normal levels. Therefore, amlodipine seems to have a deleterious effect on the cardiovascular integrative control, probably due to the increased sympathetic activity induced by amlodipine.Support or Funding InformationThis study was financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior ‐ Brasil (CAPES) ‐ Finance Code 001, São Paulo Research Foundation (FAPESP, Proc. 2013/20549‐7) and Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, Proc. 402076/2016‐8).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Short-term multiscale complexity analysis of cardiovascular variability improves low cardiac output syndrome risk stratification after coronary artery bypass grafting

Background: Low cardiac output syndrome (LCOS) is a myocardial dysfunction leading to systemic hypoperfusion, favored by particular conditions of the autonomic nervous system. LCOS is one of the adverse events that might occur after cardiac surgery. Objective: The aim is to test the hypothesis that short-term multiscale complexity (MSC) analysis of heart period (HP) and systolic arterial pressure (SAP) variability series in the frequency bands typical of cardiovascular control could be fruitfully exploited in identifying subjects at risk of developing LCOS after coronary artery bypass graft (CABG). Approach: HP and SAP beat-to-beat series were derived from electrocardiogram (ECG) and invasive arterial pressure (AP) signal acquired in 128 patients scheduled for CABG before (PRE) and after (POST) the induction of general anesthesia with propofol and remifentanil. Subjects were labeled as LCOS (n = 14) and noLCOS (n = 114) according to the LCOS development. MSC markers were calculated as the complement to 1 of the modulus of the average position of the poles dropping in the low-frequency (LF, 0.04–0.15 Hz) and high-frequency (HF, 0.15–0.5 Hz) bands as derived from the autoregressive model of HP and SAP series. Traditional time and frequency domain indexes were also calculated. Main results: Traditional parameters were able to assess the depression of the cardiovascular regulation induced by general anesthesia, but showed weak performances in differentiating LCOS and noLCOS groups. Conversely, HP complexity in LF band and SAP complexity in HF band assessed during POST remained associated with LCOS even after entering a multivariate logistic regression model adjusted for clinical and demographic factors. Significance: The MSC approach can be fruitfully applied to improve risk stratification for LCOS after CABG likely because MSC markers describe the dysfunction of the sympathetic control and the impairment of the mechanical properties of the heart in the LCOS group.

Multiscale information storage of linear long-range correlated stochastic processes.

Information storage, reflecting the capability of a dynamical system to keep predictable information during its evolution over time, is a key element of intrinsic distributed computation, useful for the description of the dynamical complexity of several physical and biological processes. Here we introduce a parametric approach which allows one to compute information storage across multiple timescales in stochastic processes displaying both short-term dynamics and long-range correlations (LRC). Our analysis is performed in the popular framework of multiscale entropy, whereby a time series is first "coarse grained" at the chosen timescale through low-pass filtering and downsampling, and then its complexity is evaluated in terms of conditional entropy. Within this framework, our approach makes use of linear fractionally integrated autoregressive (ARFI) models to derive analytical expressions for the information storage computed at multiple timescales. Specifically, we exploit state space models to provide the representation of lowpass filtered and downsampled ARFI processes, from which information storage is computed at any given timescale relating the process variance to the prediction error variance. This enhances the practical usability of multiscale information storage, as it enables a computationally reliable quantification of a complexity measure which incorporates the effects of LRC together with that of short-term dynamics. The proposed measure is first assessed in simulated ARFI processes reproducing different types of autoregressive dynamics and different degrees of LRC, studying both the theoretical values and the finite sample performance. We find that LRC alter substantially the complexity of ARFI processes even at short timescales, and that reliable estimation of complexity can be achieved at longer timescales only when LRC are properly modeled. Then, we assess multiscale information storage in physiological time series measured in humans during resting state and postural stress, revealing unprecedented responses to stress of the complexity of heart period and systolic arterial pressure variability, which are related to the different role played by LRC in the two conditions.

The additional impact of type 2 diabetes on baroreflex sensitivity of coronary artery disease patients might be undetectable in presence of deterioration of mechanical vascular properties.

Both deterioration of the mechanical vascular properties of barosensitive vessels and autonomic derangement lead to modification of baroreflex sensitivity (BRS) in coronary artery disease (CAD) individuals. Type 2 diabetes (T2D) reduces BRS as well even in absence of cardiac autonomic neuropathy. The aim of the study is to clarify whether, assigned the degree of mechanical vascular impairment and without cardiac autonomic neuropathy, the additional autonomic dysfunction imposed in CAD patients by T2D (CAD-T2D) decreases BRS further. We considered CAD (n = 18) and CAD-T2D (n = 19) males featuring similar increases of average carotid intima media thickness (ACIMT) and we compared them to age- and gender-matched healthy (H, n = 19) subjects. BRS was computed from spontaneous beat-to-beat variability of heart period (HP) and systolic arterial pressure (SAP) at supine resting (REST) and during active standing (STAND). BRS was estimated via methods including time domain, spectral, cross-spectral, and model-based techniques. We found that (i) at REST BRS was lower in CAD and CAD-T2D groups than in H subjects but no difference was detected between CAD and CAD-T2D individuals; (ii) STAND induced an additional decrease of BRS visible in all the groups but again BRS estimates of CAD and CAD-T2D patients were alike; (iii) even though with different statistical power, BRS markers reached similar conclusions with the notable exception of the BRS computed via model-based approach that did not detect the BRS decrease during STAND. In presence of a mechanical vascular impairment, indexes estimating BRS from spontaneous HP and SAP fluctuations might be useless to detect the additional derangement of the autonomic control in CAD-T2D without cardiac autonomic neuropathy compared to CAD, thus limiting the applications of cardiovascular variability analysis to typify CAD-T2D individuals. Graphical abstract Graphical representation of the baroreflex sensitivity (BRS) estimated from spontaneous fluctuations of heart period and systolic arterial pressure via transfer function (TF) in low frequency (LF) band (from 0.04 to 0.15Hz). BRS was reported as a function of the group (i.e., healthy (H), coronary artery disease (CAD) and CAD with type 2 diabetes (CAD-T2D) groups) at REST (black bars) and during STAND (white bars). Values are shown as mean plus standard deviation. The symbol "*" indicates a significant difference between conditions within the same group (i.e., H, CAD, or CAD-T2D) and the symbol "§" indicates a significant difference between groups within the same experimental condition (i.e., REST or STAND). BRS cannot distinguish CAD and CAD-T2D groups both at REST and during STAND, while it is useful to distinguish experimental conditions and separate pathological groups from H subjects.

Sigh maneuver to enhance assessment of fluid responsiveness during pressure support ventilation

BackgroundAssessment of fluid responsiveness is problematic in intensive care unit (ICU) patients, in particular for those undergoing modes of partial support, such as pressure support ventilation (PSV). We propose a new test, based on application of a ventilator-generated sigh, to predict fluid responsiveness in ICU patients undergoing PSV.MethodsThis was a prospective bi-centric interventional study conducted in two general ICUs. In 40 critically ill patients with a stable ventilatory PSV pattern and requiring volume expansion (VE), we assessed the variations in arterial systolic pressure (SAP), pulse pressure (PP) and stroke volume index (SVI) consequent to random application of 4-s sighs at three different inspiratory pressures. A radial arterial signal was directed to the MOSTCARE™ pulse contour hemodynamic monitoring system for hemodynamic measurements. Data obtained during sigh tests were recorded beat by beat, while all the hemodynamic parameters were averaged over 30 s for the remaining period of the study protocol. VE consisted of 500 mL of crystalloids over 10 min. A patient was considered a responder if a VE-induced increase in cardiac index (CI) ≥ 15% was observed.ResultsThe slopes for SAP, SVI and PP of were all significantly different between responders and non-responders (p < 0.0001, p = 0.0004 and p < 0.0001, respectively). The AUC of the slope of SAP (0.99; sensitivity 100.0% (79.4–100.0%) and specificity 95.8% (78.8–99.9%) was significantly greater than the AUC for PP (0.91) and SVI (0.83) (p = 0.04 and 0.009, respectively). The SAP slope best threshold value of the ROC curve was − 4.4° from baseline. The only parameter found to be independently associated with fluid responsiveness among those included in the logistic regression was the slope for SAP (p = 0.009; odds ratio 0.27 (95% confidence interval (CI95) 0.10–0.70)). The effects produced by the sigh at 35 cmH20 (Sigh35) are significantly different between responders and non-responders. For a 35% reduction in PP from baseline, the AUC was 0.91 (CI95 0.82–0.99), with sensitivity 75.0% and specificity 91.6%.ConclusionsIn a selected ICU population undergoing PSV, analysis of the slope for SAP after the application of three successive sighs and the nadir of PP after Sigh35 reliably predict fluid responsiveness.Trial registrationAustralian New Zealand Clinical Trials Registry, ACTRN12615001232527. Registered on 10 November 2015.

Regional Cerebral Oxygen Saturation Decreases During Primary Hip Arthroplasty: An Analysis of Perioperative Regional Cerebral Oxygenation (rSO2), S100 Calcium-Binding Protein B (S100B) and Glial Fibrillary Acidic Protein (GFAP) Values. A Pilot Study.

BackgroundThe incidence of postoperative cognitive dysfunction (POCD) after major joint arthroplasty is high. In the etiology of POCD, many factors have been cited, including thromboembolic complications. The incidence of cerebral embolization after lower extremity arthroplasty may be as high as 40–60%. The potential events of cerebral embolization could lead to a decrease in the regional cerebral oxygenation (rSO2) and increased serum levels of biochemical markers of brain damage. The objective of the study was to test whether there are any changes in the rSO2 values and serum markers of brain damage in patients who underwent total hip arthroplasty.Material/MethodsFifteen patients who underwent primary hip arthroplasty under spinal anesthesia were analyzed. The rSO2 was monitored using infrared spectroscopy. Biochemical analyses of S100 calcium-binding protein B (S100B) protein and fibrillary acidic protein (GFAP) serum concentrations were performed using immunoassay methods.ResultsThe values of rSO2 decreased during the surgery, but this was not related to mean arterial pressure variations or hemoglobin saturation. The concentration of S100B was increased compared to its preoperative values, and there were no changes in GFAP values. The changes in rSO2 readings correlated with the biomarkers’ levels just after the surgery.ConclusionsOur results suggest that S100B may be a more specific marker of astroglial damage in patients after primary total hip arthroplasty. The decrease in rSO2 readings may be due to micro-thromboembolic events that occurred during the surgery. However, the results of this study are preliminary, and further studies are needed to establish its clinical efficacy.

Maternal dyslipidemia during pregnancy and lactation increases blood pressure and disrupts cardiorespiratory and glucose hemostasis in female rat offspring.

Hypertension and metabolic disorders evidenced in adults who have been exposed to nutritional insults during early life may be sex-dependent. We evaluated if blood pressure (BP), cardiorespiratory control, and metabolic parameters are affected in female offspring (FO) from dams fed a dyslipidaemic diet during pregnancy and lactation. FO was obtained from dams who received control (CTL) or dyslipidaemic diets during pregnancy and lactation. The effects of a maternal dyslipidaemic diet on BP, cardiorespiratory control, and biochemical parameters were assessed at 30 and 90 days of age. The experimental protocol based on a dyslipidaemic diet intervention was effective in developing maternal dyslipidemia. At 30 days of age, the FO from dyslipidaemic dams displayed disordered respiratory pattern, enhanced ventilatory response to hypercapnia (P < 0.05), and increased serum levels of total cholesterol and triglycerides (P < 0.05) when compared with CTL female offspring. At 90 days of age, FO from dyslipidaemic dams had augmented BP (P < 0.05), exacerbated cardiorespiratory responses to hypercapnia (P < 0.05), enhanced pressor responses to peripheral chemoreflex activation (P < 0.05), impaired baroreflex (P < 0.05), and larger delta variations in arterial pressure after ganglionic blockade (P < 0.05). Furthermore, during oral glucose and insulin tolerance tests, FO from dyslipidaemic dams exhibited altered glucose tolerance and insulin sensitivity (P < 0.05) when compared with FO from CTL dams. Altered breathing linked to enhanced central and peripheral chemosensitivity, impaired baroreflex, and augmented sympathetic tone may be predisposing factors for increased BP and metabolic disorders in female offspring from dyslipidaemic dams.

The stop-flow arm equilibrium pressure in preoperative patients: Stressed volume and correlations with echocardiography.

The distending intravascular pressure at no flow conditions reflects the stressed volume. While this haemodynamic variable is recognised as clinically important, there is a paucity of reports of its range and responsiveness to volume expansion in patients without cardiovascular disease and no reports of correlations to echocardiographic assessments of left ventricular filling. Twenty-seven awake (13 male), spontaneously breathing patients without any history of cardiopulmonary, vascular or renal disease were studied prior to induction of anaesthesia. The no-flow equilibrium pressure in the arm following rapid circulatory occlusion (Parm ) was measured via a radial arterial catheter. Transthoracic echocardiography was used to measure left ventricular end diastolic area and volume as well as the diameter of the inferior vena cava. The Parm and echocardiographic variables were measured before and after administration of 500mL 0.9% NaCl over 10minutes. Changes were analysed by paired t test, Pearson's correlation and multiple linear regression. Parm increased overall from 22±5mmHg to 25±6mmHg (mean difference 3.0±4.5mmHg, P=0.002) following the fluid bolus with corresponding increases in arterial pressure and echocardiographic variables. Variability in the direction of the Parm response reflected concomitant changes in vascular compliance. Only weak correlations were observed between changes in Parm and inferior vena cava diameter indexed to body surface area (R2 =0.29, P=0.01). Preoperative measurements of Parm increased following acute expansion of the intravascular volume. Echocardiography demonstrated poor correlation with Parm .

Изучение питания и состава тела пациентов с диппинг- и нондиппинг-вариантами суточной регуляции артериального давления при артериальной гипертензии

Изучение питания и состава тела пациентов с диппинг- и нондиппинг-вариантами суточной регуляции артериального давления при артериальной гипертензии

Arterial blood pressure variability in pregnant women with placental insufficiency

Arterial blood pressure variability in pregnant women with placental insufficiency

Arterial Pulse Pressure Variation with Mechanical Ventilation

Fluid administration leads to a significant increase in cardiac output in only half of ICU patients. This has led to the concept of assessing fluid responsiveness before infusing fluid. Pulse pressure variation (PPV), which quantifies the changes in arterial pulse pressure during mechanical ventilation, is one of the dynamic variables that can predict fluid responsiveness. The underlying hypothesis is that large respiratory changes in left ventricular stroke volume, and thus pulse pressure, occur in cases of biventricular preload responsiveness. Several studies showed that PPV accurately predicts fluid responsiveness when patients are under controlled mechanical ventilation. Nevertheless, in many conditions encountered in the ICU, the interpretation of PPV is unreliable (spontaneous breathing, cardiac arrhythmias) or doubtful (low Vt). To overcome some of these limitations, researchers have proposed using simple tests such as the Vt challenge to evaluate the dynamic response of PPV. The applicability of PPV is higher in the operating room setting, where fluid strategies made on the basis of PPV improve postoperative outcomes. In medical critically ill patients, although no randomized controlled trial has compared PPV-based fluid management with standard care, the Surviving Sepsis Campaign guidelines recommend using fluid responsiveness indices, including PPV, whenever applicable. In conclusion, PPV is useful for managing fluid therapy under specific conditions where it is reliable. The kinetics of PPV during diagnostic or therapeutic tests is also helpful for fluid management.

A quantitative model of relation between respiratory-related blood pressure fluctuations and the respiratory sinus arrhythmia

In order to propose an interpretation of recent experimental findings concerning short-term variability of arterial blood pressure (ABP), heart rate variability (HRV), and their dependence on body posture, we develop a qualitative dynamical model of the short-term cardiovascular variability at respiratory frequency (HF). It shows the respiratory-related blood pressure fluctuations in relation to the respiratory sinus arrhythmia (RSA). Results of the model-based analysis show that the observed phenomena may be interpreted as buffering of the respiratory-related ABP fluctuations by heart rate (HR) fluctuations, i.e., the respiratory sinus arrhythmia. A paradoxical enhancement (PE) of the fluctuations of the ABP in supine position, that was found in experiment, is explained on the ground of the model, as an ineffectiveness of control caused by the prolonged phase shift between the the peak of modulation of the pulmonary flow and the onset of stimulation of the heart. Such phasic changes were indeed observed in some other experimental conditions. Up to now, no other theoretical or physiological explanation of the PE effect exists, whereas further experiments were not performed due to technical problems. Better understanding of the short-term dynamics of blood pressure may improve medical diagnosis in cardiology and diseases which alter the functional state of the autonomous nervous system.Graphical A simple mathematical model of cardiorespiratory dynamics. A novel class of mathematical models of blood pressure dynamics in humans allows to represent respiratory modulation of Arterial Blood Pressure. The model shows how the phase shift in neural control of the heart rate may produce Paradoxic Enhancement of respiratory Blood Pressure fluctuations. Observed in experiment. The model has many options for further development.

Etomidate-induced hypotension: a pathophysiological approach using arterial elastance

Introduction: Anaesthesia frequently induces hypotension. Several recent studies have analysed arterial elastance (Ea) in order to describe clinical variations of mean arterial pressure (MAP). The objective of the study was to assess Ea to explain MAP variation following etomidate induction.Methods: We conducted a prospective single-centre study. Inclusion criteria were patients undergoing elective cardiac surgery with invasive blood pressure monitoring. Ea was expressed as Pes/SV (Pes: end systolic pressure, SV: stroke volume). Cardiac index (CI), peripheral vascular resistance (PVR) and arterial compliance (C) was compared before and 2 minutes after etomidate induction. Arterial hypotension was defined as a decrease greater than 15% of the baseline MAP.Results: Of the 45 patients included, 24 (53%) had a preserved MAP and 21 (47%) had an etomidate-induced hypotension. Ea was similar before induction and decreased in the decreased MAP group 2 minutes after induction (2.0 mmHg.ml-1 [1.7-2.4] vs 1.4 mmHg.ml-1 [0.9-1.9]; p = 0.001). Arterial compliance (C) increased in the decreased MAP group 2 minutes after induction (0.8 ml. mmHg-1 [0.6-1.0] vs 0.5 ml. mmHg-1 [0.4-0.6], p < 0.0001). No significant change in CI or PVR was observed between patients with or without etomidate-induced hypotension.Conclusion: Etomidate-induced hypotension was associated to a decrease in Ea. Ea variations can mainly be explained by induced changes in arterial compliance.

Long-term stimulation of cardiac vagal preganglionic neurons reduces blood pressure in the spontaneously hypertensive rat.

Arterial hypertension is associated with autonomic nervous system dysfunction. Different interventional strategies have been implemented in recent years for the reduction of sympathetic activity in patients with hypertension. However, the therapeutic benefit of increasing vagal tone in hypertensive patients remains largely unexplored. Here, we describe the effects of long-term activation of vagal neural pathways on arterial pressure, heart rate arterial pressure variability and spontaneous baroreflex sensitivity in spontaneously hypertensive rats (SHR) and normotensive Wistar rats. Brainstem vagal preganglionic neurons residing in the dorsal vagal motor nucleus (DVMN) were targeted with a lentiviral vector to induce the expression of an artificial G(s) protein-coupled receptor termed designer receptors exclusively activated by designer drugs (DREADD-Gs). The transduced neurons were activated daily by systemic administration of otherwise inert ligand clozapine-n-oxide. Arterial pressure measurements were recorded in conscious freely moving animals after 21 consecutive days of DVMN stimulation. Resting arterial pressure was significantly lower in SHRs expressing DREADD-Gs in the DVMN, compared with control SHRs expressing enhanced green fluorescent protein. No changes in arterial pressure were detected in Wistar rats expressing DREADD-Gs compared with rats expressing enhanced green fluorescent protein in the DVMN. Pharmacogenetic activation of DREADD-Gs-expressing DVMN neurons in SHRs was accompanied with increased baroreflex sensitivity and a paradoxical decrease in cardio-vagal components of heart rate and systolic arterial pressure variability in SHRs. These results suggest that long-term activation of vagal parasympathetic pathways is beneficial in restoring autonomic balance in an animal model of neurogenic hypertension and might be an effective therapeutic approach for the management of hypertension.

Effects of vagotomy on cardiovascular and heart rate variability alterations following chronic normobaric hypoxia in adult rabbits

Backgroundchronic hypoxia increases basal ventilation and pulmonary vascular resistance, with variable changes in arterial blood pressure and heart rate, but it’s impact on heart rate variability and autonomic regulation have been less well examined. We studied changes in arterial blood pressure, heart rate and heart rate variability (HRV) in rabbits subjected to chronic normobaric hypoxia (CNH; PB ~ 719 mmHg; FIO2 ~ 9.2%) for 14 days and assess the effect of autonomic control by acute bilateral vagal denervation.Resultsexposure to CNH stalled animal weight gain and increased the hematocrit, without affecting heart rate or arterial blood pressure. Nevertheless, Poincaré plots of the electrocardiographic R–R intervals showed a reduced distribution parallel to the line of identity, which interpreted as reduced long-term HRV. In the frequency domain, CNH reduced the very-low- (< 0.2 Hz) and high-frequency components (> 0.8 Hz) of the R–R spectrograms and produced a prominent component in the low-frequency component (0.2–0.5 Hz) of the power spectrum. In control and CNH exposed rabbits, bilateral vagotomy had no apparent effect on the short- and long-term HRV in the Poincaré plots. However, bilateral vagotomy differentially affected higher-frequency components (> 0.8 Hz); reducing it in control animals without modifying it in CNH-exposed rabbits.ConclusionsThese results suggest that CNH exposure shifts the autonomic balance of heart rate towards a sympathetic predominance without modifying resting heart rate or arterial blood pressure.

Role of arterial stiffness and blood pressure variability in the definition of SHATS (systemic hemodynamic atherothrombotic syndrome)

BackgroundCV risk exponentially increases as the number of damaged organs increases The Systemic Hemodynamic Atherosclerotic Syndrome (SHATS) represents a novel conceptualization of the CV continuum focusing on simultaneous multi-organ alteration. This is the first study operationally defining SHATS and aimed at identifying its determinants.MethodsLeft Ventricular Hypertrophy (echocardiography), Common Carotid Artery plaque and increased thickness (ultrasound), and Chronic Kidney Disease (estimated Glomerular Filtration Rate) indexed selective target organ damage. SHATS was operationally defined as their simultaneous presence in a patient. PWV was measured by Sphygmocor® and BP variability by 24 h ABPM.ResultsSHATS affected 19.9% of the 367 studied subjects. Subjects with SHATS had a similar prevalence in diabetes mellitus, but a greater prevalence of very stiff artery (84.9 vs 64.3 %, p < 0.01) and use of antihypertensive medications. In the presence of similar office BP, SHATS was associated with higher 24 h SBP and lower 24 h DBP (a greater pulsatile pressure!), reduced nighttime SBP fall, and a twofold greater prevalence of reverse dipper status (48.2 vs 20.2 %, p < 0.001). BMI (positive correlation) and DBP (negative correlation) were the only traditional CV risk factors significantly associated with the odds of having SHATS. Very stiff artery and BP variability were significant independent determinants of SHATS, with highly predictive accuracy.ConclusionSHATS, the simultaneous damage of multiple target organs, may easily operationally defined. Very stiff artery and BP variability represent key factors for SHATS. The present results support the hypothesis of SHATS as a systemic condition, needing further characterization.

Non-invasive determination of reference arterial blood pressure indices of healthy Alsatian and Boerboel dogs

In order to evaluate and manage Boerboels and Alsatians under critical and emergency care, knowledge of ranges and causes of variability of normal arterial blood pressure (ABP) indices is desirable. The systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and mean arterial pressure (MAP) of 30 healthy dogs were evaluated with human sphygmomanometer and neonatal cuff. The age, sex, breed, weight, height, weight to height ratio (WTH), of each dog was recorded. The mean and range of ABP values for Alsatians and Boerboels were similar to those of some other breeds. There were no age, breed and sex differences in ABP indices of dogs. The coefficient of variations and ranges of DAP and MAP were significantly higher than SAP measurements. In all dogs, SAP was influenced by breed and interaction of breed and sex when all confounders were controlled. The WTH and sex were found to independently influence SAP in presence of confounders. In Alsatian, WTH and sex interaction influenced all pressures in presence of confounders. The DAP was significantly influenced by heart rate and WTH in presence and absence of confounders respectively. Although age did not influence ABP in all dogs, it influenced SAP and DAP in females and Boerboel. The absence of age, sex, and breed differences in ABP of dogs may be due to multiple interactions between these factors. The human sphygmomanometer has the best precision for SAP measurements and WTH may be used as canine’s body mass index (BMI) because of its influence on ABP.Keywords: Blood pressure, dogs, breed, sex, age, oscillometry

Cerebral autoregulation in migraine with aura: A case control study.

Migraine with aura is independently associated with increased risk of ischemic stroke, especially in younger subjects. This association might be related to an impairment of cerebral autoregulation, which normally maintains cerebral blood flow independent of arterial blood pressure variations. Patients aged 30-55, fulfilling ICHD-3 beta criteria for migraine with aura, were prospectively enrolled and compared with gender- and age-matched healthy controls without a history of migraine. Patients and controls with a history of stroke or any disease potentially impairing cerebral autoregulation were excluded. We assessed cerebral autoregulation with two different methods: Transfer function analysis, and the correlation coefficient index Mx. The transfer function phase and gain reflect responses of cerebral blood flow velocities to relatively fast fluctuations of arterial blood pressure, whereas Mx also reflects responses to slower arterial blood pressure fluctuations. A total of 22 migraine with aura patients (median age [IQR]: 39.5 [12.5] years) and 22 controls (39 [9.75] years) were included. Transfer function parameters and Mx were not different between patients and controls. However, Mx was inversely correlated with age in patients (ρ = -0.567, p = 0.006) and not in controls (ρ = -0.084, p = 0.509). Mx was also inversely correlated with migraine with aura duration (ρ = -0.617, p = 0.002), suggesting improvement of cerebral autoregulation efficiency with disease duration. Cerebral autoregulation did not differ between patients and controls aged 30-55. However, cerebral autoregulation efficiency was strongly correlated with migraine with aura duration. Further studies in younger patients are needed to determine whether cerebral autoregulation is impaired early in the course of disease. NCT02708797.

Blood Pressure Coefficient of Variation and Its Association With Cardiac Surgical Outcomes.

Multiple studies completed in the ambulatory nonsurgical setting show a significant association between short- and long-term blood pressure variability and poor outcomes. However, perioperative blood pressure variability outcomes have not been well studied, especially in the cardiac surgical setting. In this study, we sought to assess whether systolic and mean arterial blood pressure variability were associated with 30-day mortality and in-hospital renal failure in patients undergoing cardiac surgery requiring cardiopulmonary bypass. Furthermore, blood pressure variability has not been evaluated specifically during each phase of surgery, namely in the pre-, intra- and postbypass phases; thus, we aimed also to assess whether outcomes were associated with phase-specific systolic and mean arterial blood pressure variability. All patients undergoing cardiac surgery from January 2008 to June 2014 were enrolled in this retrospective, single-center study. Demographic, intraoperative, and postoperative outcome data were obtained from the institution's Society of Thoracic Surgery database and Anesthesia Information Management System. Systolic and mean arterial blood pressure variability were assessed using the coefficient of variation (CV). The primary outcomes were 30-day mortality and in-hospital renal failure in relation to the entire duration of a case, while the secondary outcomes assessed phase-specific surgical periods. In an effort to control the family-wise error rate, P values <.0125 were considered significant for the primary outcomes. Of the 3687 patients analyzed, 2.7% of patients died within 30 days of surgery and 2.8% experienced in-hospital renal failure. After adjusting for significant covariates, we found a statistically significant association between increasing CV for systolic blood pressure (CVSBP) and 30-day mortality and in-hospital renal failure. For every 0.10 increase in CVSBP, there was a 150% increase in the odds of death (odds ratio, 2.50; 95% confidence interval, 1.60-3.92; P < .0001) and there was a 104% increase in odds of experiencing renal failure (odds ratio, 2.04; 95% confidence interval, 1.33-3.14; P = .001). The association with mortality was driven primarily by the prebypass period, because the association between CVSBP and mortality during the prebypass phase was significant (P = .01), and not during the postbypass phase (P = .08). There was no significant association between CV for mean arterial blood pressure and either death or renal failure during any period of surgery, including the bypass phase. Increasing systolic blood pressure variability was associated with 30-day mortality and development of renal failure, with surgery phase-specific relationships observed. Further research is required to determine how to prospectively detect blood pressure variability and elucidate opportunities for intervention.