Arterial Pressure Signals Research Articles

Autonomic dysfunction precede hemodynamic and metabolic changes in an experimental model of hypertension submitted to fructose overload

The aim this study was to evaluate the effects of 7 days of fructose overload on metabolic, hemodynamic and autonomic parameters in spontaneous hypertensive rats. Male Wistar rats and SHR rats were divided into control (C), hypertensive (H) and hypertensive submitted to fructose overload (HF). The fructose overload (100g/L in drinking water) was started with 30 days of life of the animals. Arterial pressure (AP) signals were directly recorded. Cardiovascular autonomic modulation was evaluated by spectral analysis. Regarding metabolic evaluations, the glucose, insulin resistance and triglycerides were similar between studied groups. The mean arterial pressure, systolic AP and diastolic arterial pressure were higher in hypertensive animals (mean AP, H: 124±2 and HF: 123±3 mmHg) compared to the C group (mean AP: 95±2 mmHg). There was no difference in heart rate among groups. However, the HF group showed lower vagal modulation than C group, evidenced by a reduction in variance of pulse interval (HF: 12±2 vs. C: 37±8 ms2) and RMSSD index (HF: 5.9±0.7 vs. C: 3.3±0.3 ms). Additionally, the HF group showed increase in variance of systolic arterial pressure compared to the C and H group (28 ± 4 vs. C: 13 ± 1 and H: 18 ± 2 mmHg2). In conclusion, only 7 days of fructose overload was able to induce impairment in cardiac vagal modulation and vascular sympathetic modulation with no alteration on metabolic or hemodynamic parameters, suggesting that autonomic modulation dysfunction precede cardiometabolic changes in this experimental model of metabolic syndrome.Support or Funding InformationFAPESP ‐ 2015/11223‐6; CAPES‐PROSUP – 1277269; UNINOVE, CNPq.

Abstract P167: Combined Exercise Training is Better than Isolated Aerobic and Resistance Exercise Training for an Experimental Model of Metabolic Syndrome and Menopausal Rats

The aim of this study was to verify the effects of three different moderate exercise training protocols (aerobic, resistance and combined (aerobic + resistance)) in a model of metabolic syndrome and menopause on a cardiovascular parameter and oxidative stress. Female SHR rats were divided into (n=8): hypertensive (H), hypertensive ovariectomized submitted to fructose overload (100g/L in drinking water) (HFO), aerobic trained hypertensive ovariectomized submitted to fructose overload (AHOF), resistance trained hypertensive ovariectomized submitted to fructose overload (RHOF) and combined trained hypertensive ovariectomized submitted to fructose overload (CHOF). Arterial pressure (AP) signals were directly recorded. Vascular autonomic modulation was evaluated by spectral analysis. The cardiac oxidative stress was evaluated by lipoperoxidation (LPO) determination. The association of fructose overload and hormone deprivation promoted an increase in AP (HOF: 174±4 vs. H: 146±4 mmHg), heart rate (HOF: 393±10 vs. H: 352±13 bpm), VAR-SAP (HOF: 77.8±11.9 vs H: 31.1±2.6 mmHg2), LF-SAP (HOF: 10.6±2.3 vs H: 5.0±0.9 mmHg2) and LPO, and reduced baroreflex sensitivity (tachycardia response: HOF: 1.06±0.06 vs. H: 1.91±0.17 bpm/mmHg). All exercise training protocols were able to reduce LPO and LF-SAP. It was noted that only the combined exercise training was able in reducing AP (CHOF: 158±4 mm Hg) and heart rate (CHOF: 303±5 bpm). The AP reduction noted only in the CHOF group may be associated with an improve in baroreflex sensitivity, represented by an increase of tachycardic response observed only in the CHOF (1.62±0.1 bpm/mmHg) and in the AHOF (1.54 ±0.07 bpm/mmHg) groups and a reduction of VAR-PAS observed only in the CHOF (30.31±3.85 mmHg 2 ) and in the RHOF (31±2.65 mmHg 2 ) groups. In conclusion, fructose overload induced impairment in hemodynamic, vascular autonomic control and increased oxidative stress in hypertensive rats submitted to ovarian hormones deprivation. However, all exercise training protocols showed a beneficial role. Moreover, the combined exercise training showed additional improvement, suggesting that this could be a better approach than isolated aerobic and resistance training.

OP.1C.02] SPECTRAL ESTIMATION OF PETERSON'S MODULUS VARIABILITY FROM ARTERIAL BLOOD PRESSURE AND WAVELET ANALYSIS

Objective: Arterial stiffness is mainly characterized by its Peterson's Modulus (EP). Increased values of EP are associated with a reduced heart function and an increased arterial blood pressure. Assessment of EP requires simultaneous measurements of arterial diameter and pressure signals. However, instantaneous determination of arterial diameter signals implies optical and ultrasonic techniques and neither of them are portables. Aims: To evaluate a novel method for estimating the Ep spectral variability of arterial stiffness, without arterial diameter signals. Design and method: Arterial pressure (Konigsberg micro-transducer) was measured in 10 sheeps (25–35 kg) during 24 hours. Instantaneous cardiac cycle of pressure signals were determined using five–level multi-resolution wavelet analysis and decomposition. A state machine processed and analysed different linear combinations of details d3, d4 and d5 of mother wavelet Symlet11. EP spectral estimation assessment involved the study of various temporal locations of the fiducial elasticity starting point within each beat. Moreover, discard criteria were added from the heart rate variability studio and coherence index between systolic pressure and beat to beat intervals around 0.1 Hz. Agreement between the actual direct measurement of EP and the proposed method of spectral stiffness estimation was analyzed according to the Bland–Altman approach. Results: Results showed a high coherence (more than 70%) between the actual and proposed method for a wide frequency range (0 to 0.5 Hz). Bland & Altman test showed a standard deviation of the mean less of 10% between the proposed methodology and the direct assessment of EP. Conclusions: The methodology presented in this work evidenced high levels of spectral coherence in EP variability studios and no significantly difference between the actual and the proposed estimation method. So, this novel method is able to estimate the Peterson's modulus spectral variability by solely using the arterial blood pressure signal.

Cardiac signal estimation based on the arterial and venous pressure signals of a hemodialysis machine

Continuous cardiac monitoring is usually not performed during hemodialysis treatment, although a majority of patients with kidney failure suffer from cardiovascular disease. In the present paper, a method is proposed for estimating a cardiac pressure signal by combining the arterial and the venous pressure sensor signals of the hemodialysis machine. The estimation is complicated by the periodic pressure disturbance caused by the peristaltic blood pump, with an amplitude much larger than that of the cardiac pressure signal. Using different techniques for combining the arterial and venous pressure signals, the performance is evaluated and compared to that of an earlier method which made use of the venous pressure only. The heart rate and the heartbeat occurrence times, determined from the estimated cardiac pressure signal, are compared to the corresponding quantities determined from a photoplethysmographic reference signal. Signals from 9 complete hemodialysis treatments were analyzed. For a heartbeat amplitude of 0.5 mmHg, the median absolute deviation between estimated and reference heart rate was 1.3 bpm when using the venous pressure signal only, but dropped to 0.6 bpm when combining the pressure signals. The results show that the proposed method offers superior estimation at low heartbeat amplitudes. Consequently, more patients can be successfully monitored during treatment without the need of extra sensors. The results are preliminary, and need to be verified on a separate dataset.

Enhancement of Arterial Pressure Pulsatility by Controlling Continuous-Flow Left Ventricular Assist Device Flow Rate in Mock Circulatory System.

Continuous-flow left ventricular assist devices (CF-LVADs) generally operate at a constant speed, which reduces pulsatility in the arteries and may lead to complications such as functional changes in the vascular system, gastrointestinal bleeding, or both. The purpose of this study is to increase the arterial pulse pressure and pulsatility by controlling the CF-LVAD flow rate. A MicroMed DeBakey pump was used as the CF-LVAD. A model simulating the flow rate through the aortic valve was used as a reference model to drive the pump. A mock circulation containing two synchronized servomotor-operated piston pumps acting as left and right ventricles was used as a circulatory system. Proportional-integral control was used as the control method. First, the CF-LVAD was operated at a constant speed. With pulsatile-speed CF-LVAD assistance, the pump was driven such that the same mean pump output was generated. Continuous and pulsatile-speed CF-LVAD assistance provided the same mean arterial pressure and flow rate, while the index of pulsatility increased significantly for both arterial pressure and pump flow rate signals under pulsatile speed pump support. This study shows the possibility of improving the pulsatility of CF-LVAD support by regulating pump speed over a cardiac cycle without reducing the overall level of support.

The effects of ventricular drainage on the intracranial pressure signal and the pressure reactivity index.

In subarachnoid hemorrhage (SAH) patients intracranial pressure (ICP) is usually monitored via an extraventricular drain (EVD), which can produce false readings when the drain is open. It is established that both the ICP cardiac pulse frequency and long term trends over several hours are often seriously corrupted. The aim of this study was to establish whether or not the intermediate frequency bands [respiratory, Mayer wave and very low frequency (VLF)] were also corrupted. The VLF range is of special interest because it is important in cerebral autoregulation studies. Using a pattern recognition algorithm we retrospectively identified 718 cases of EVD opening in 80 SAH patients. An analysis of differences between closed and open-drain periods showed that ICP amplitude decreased significantly in all of the three lower frequency bands when the EVD was open. A similar analysis of systemic arterial pressure signal revealed similar changes in the same frequency bands that were positively correlated with the ICP changes. Therefore we concluded that the changes in the ICP signal represented real, physiological changes and not artifact. Pressure reactivity index (PRx) values were also computed during closed and open-drain periods. We found a small but statistically significant decrease during open-drain periods. Based on analysis of the change in the PRx distribution during open drainage we concluded that this decrease also represented physiological changes rather than artifact. In summary the ICP respiratory, Mayer wave, and VLF frequency bands are not corrupted when the EVD is open, and it safe to use these for autoregulation studies.

An innovative peak detection algorithm for photoplethysmography signals: an adaptive segmentation method

The purpose of this paper is twofold. The first purpose is to detect M-peaks from raw photoplethysmography (PPG) signals with no preprocessing method applied to the signals. The second purpose is to estimate heart rate variability (HRV) by finding the peaks in the PPG signal. HRV is a measure of the fluctuation of the time interval between heartbeats and is calculated based on time series between strokes derived from electrocardiogram (ECG), arterial pressure (AP), or PPG signals, separately. PPG is a method widely used to measure blood volume of tissue on the basis of blood volume change in every heartbeat. In the estimation of the HRV signal from the PPG signal, HRV is calculated by measuring the time intervals between the peak values in the PPG signal. In the present paper, a novel peak detection algorithm was developed for PPG signals. Finding peak values correctly from PPG signals, the HRV signal can be estimated. This peak detection algorithm has been called an adaptive segmentation method (ASM). In this method, the PPG signals are first separated into segments with sample sizes and then the peak points in these signals are detected by comparing with maximum points in these segments. To evaluate the estimated pulse rate and HRV signals from PPG, Poincar\'{e} plots and time domain features including minimum, maximum, mean, mode, standard deviation, variance, skewness, and kurtosis values were used. Our experimental results demonstrated that ASM could be even used both in the estimation of HRV signals and to detect the peaks from raw and noisy PPG signals without a pre-processing method.

In Response.

We thank Jan Vos et al.1 for their interest in our study recently published in Anesthesia & Analgesia.2 It is important to understand the physiological differences between dynamic arterial elastance (Eadyn) and arterial elastance (Ea). Edyn is not arterial elastance but a functional parameter relating changes in pulse pressure variations (PPVs) to stroke volume variations (SVVs): PPV/SVV. Edyn has been reported as being able to predict changes in arterial pressure after a change in volume. Unlike Ea, Eadyn has a significant central component that is independently influenced by left ventricular dP/dt, because central vascular impedance is not linear. Thus, paradoxically vasopressors may decrease Eadyn and inodilators increase it. Eadyn is primarily a central parameter, whereas Ea is a lumped sum parameter of both central and peripheral tone.3 As these authors correctly pointed out, spontaneously breathing is a known limitation for assessing fluid responsiveness using the functional hemodynamic parameters of PPV or SVV.4 The impact of varying tidal volumes, ventricular interdependence, and the small changes in intrathoracic pressure during spontaneous breathing diminishes the usefulness of these parameters for assessing preload dependency.5,6 However, Eadyn is the instantaneous ratio between PPV and SVV, not the determinants of each; thus, the effects of nonuniform ventilation should have no effect on their ratio. Consequently, it is logical to assume that spontaneous breathing is not a limitation for Eadyn estimation. SVV is the main determinant of PPV. Because aortic impedance remains constant during a respiratory cycle, discrepancies between PPV and SVV should be primarily related to how left ventricular stroke volume dynamically interacts with the arterial system.7,8 It is noteworthy, however, that very low PPV and SVV values resulting from small variations in intrathoracic pressure, as seen during spontaneous breathing, could reduce the reliability of the Eadyn for defining the slope in the PPV–SVV relationship because the changes in both PPV and SVV would be small. Jan Vos et al.1 also point out a possible issue with mathematical coupling in the estimation of Eadyn. With this regard, it is important to differentiate how mathematical coupling can affect the calculation of PPV and SVV and how it can affect the ratio between the 2 (Eadyn). In the article by Cecconi et al.,2 PPV was measured by the Nexfin monitor (BMEYE, Amsterdam, The Netherlands) from the noninvasive assessment of arterial pressure using the Clamp method described by Penáz et al.,9 whereas SVV was computed using the Nexfin-CO algorithm.10 Still, both parameters were obtained from the same arterial pressure signal, and hence, some degree of mathematical coupling cannot be excluded. Importantly, García et al.11 previously confirmed the physiological assumptions and the clinical usefulness of Eadyn for predicting arterial pressure response to fluid administration and found a similar threshold value of <0.89 for the PPV/SVV, and they calculated SVV (esophageal Doppler) and PPV (obtained from an arterial line) independently. Regarding the second point about mathematical coupling, if the PPV/SVV ratio was mathematically coupled, it would not be expected to discriminate between responders and nonresponders. In practice, when using pulse pressure analysis, the reliability of Eadyn relies on the robustness of the algorithm to estimate stroke volume and its changes over a respiratory cycle.12 As long as this estimation is trustworthy enough, this assumption should allow the calculation of a valid Eadyn. This raises another issue regarding the external validity of studies performed with a specific monitor. Because Eadyn relies on the robustness of the algorithm, it is important to study and validate the reliability of Eadyn for different monitors. Finally, although the clinical applicability of Eadyn seems now purely limited by the technological boundaries, the impact of its implementation during hemodynamic resuscitation in a patient’s outcome has yet to be determined.12 Maurizio Cecconi, MD, FRCA, FFICM, MD St. George’s Healthcare NHS Trust and St. George’s University of London Tooting, London, United Kingdom [email protected] Manuel Ignacio Monge García, MD St. George’s Healthcare NHS Trust and St. George’s University of London Tooting, London, United Kingdom Servicio de Cuidados Intensivos y Urgencias Hospital SAS de Jerez Jerez de la Frontera, Spain Michael R. Pinsky, MD Department of Critical Care Medicine University of Pittsburgh Pittsburgh, Pennsylvania Andrew Rhodes, FRCP, FRCA, FFICM, MD St. George’s Healthcare NHS Trust and St. George’s University of London Tooting, London, United Kingdom

Abstract P078: Cardiovascular Autonomic Impairment Triggers Cardiometabolic Dysfunction in an Experimental of Metabolic Syndrome

The aim was evaluate on time-course of changes in cardiometabolic dysfunction model. Male Wistar and SHR rats were divided: Control (C), hypertensive (H), hypertensive + fructose (HF). The fructose overload (100g/L) was initiated at 30 days (d) of life. All evaluations were at 37, 45, 60 and 90 d of age. Arterial pressure (AP) signals were directly recorded. The baroreflex sensitivity was evaluated by the tachycardic (TR) and bradycardic (BR) responses to AP changes. Cardiovascular autonomic modulation was evaluated by spectral analysis. Inflammatory markers were evaluated in adipose tissue. No differences were observed in glycemia and triglycerides between the groups. The SHR groups showed increased systolic (SAP), diastolic (DAP) and mean arterial pressure (MAP) compared to control groups in all times of evaluation. Additionally, SHR groups progressively increased AP during the time course evaluation. The HF group showed additionally increased in DAP and MAP (90: MAP: C: 114±1, H: 165±3, HF: 179±3 mmHg) vs. H group. The cardiac parasympathetic modulation (HF-IP) was decreased H group in 37 d and HF group in 37, 90 d vs. C group. The VAR-PAS was higher in SHR groups vs. C group in all times evaluated. The HF group showed additionally increase in VAR-PAS during the time course evaluation (45, 90 vs. 37 d). The vascular sympathetic modulation (LF-PAS) was higher H group in 60, 90 d vs. C group. The HF group showed increased LF-PAS in 45, 60, 90 d vs. C group, and vs. 37 d in the same group; and showed additionally increased in 90 d vs. H group (90: C: 3.7±0.6 H: 6.2±0.9 HF: 8.7±0.5 mmHg2). The spontaneous baroreflex sensitivity was lower in SHR groups all the times evaluated (90: C: 0.80±0.1 H: 0.51±0.05 HF: 0.32±0.02 ms/mmHg). The H group showed decreased BR in 60, 90 d vs. C group, the HF group showed decreased in 37, 45, 60, 90 d vs. C group (90: C: 1.15±0.1 H: 0.80±0.05 HF: 0.77±0.07 bpm/mmHg). The HF group showed decreased TR in 60, 90 d vs. C group. Increased TNF alpha and IL-6 were observed only in 45 and 60 d in HF group. The results showed that cardiometabolic dysfunctions are time-dependent in SHR, and fructose overload induces additional dysfunctions in this model. Furthermore, the baroreflex impairment seems to precede hemodynamic, metabolic and inflammatory changes in this model.

Telemetric Recording of Renal and Carotid Blood Flow Velocity and Arterial Blood Pressure Simultaneously in Rats

Hypertension‐induced barotrauma without or with concomitant vasoconstriction, tissue ischemia and hypoxia has been postulated to initiate and drive the pathogenic cascades that lead to hypertension induced tissue injury. Yet the precise temporal relationship between arterial pressure and tissue blood flow over time as causative mechanisms for barotrauma remain unresolved and controversial. A major technical limitation has been the absence of methods allowing simultaneous high fidelity long‐term measurement of blood flow and arterial pressure in conscious animals. Transonic has developed a cutting edge technology to continuously evaluate arterial blood pressure and two blood flow velocity's simultaneously in conscious rats. Here, we report the first demonstration of recording renal and carotid blood flow and arterial pressure using this new multi‐variable telemetric system. A solid state pressure sensor was placed in the abdominal aorta and 0.8mm and 0.5mm in diameter flow probes were sutured on the renal and carotid artery, respectively, in Wistar rats. Both flow velocity signals correlated with the arterial pressure signal and exhibited constant lag times. After 5 min of carbogen breathing carotid vascular resistance decreased by 31±4% while renal vascular resistance decreased by 7±1%. These experiments demonstrate the feasibility of the technique for high fidelity temporal profiling of both blood pressure and blood flows to renal and carotid vascular beds simultaneously in conscious rats. British Heart Foundation funded research.

A Stochastic Delay Differential Model of Cerebral Autoregulation

Mathematical models of the cardiovascular system and of cerebral autoregulation (CAR) have been employed for several years in order to describe the time course of pressures and flows changes subsequent to postural changes. The assessment of the degree of efficiency of cerebral auto regulation has indeed importance in the prognosis of such conditions as cerebro-vascular accidents or Alzheimer. In the quest for a simple but realistic mathematical description of cardiovascular control, which may be fitted onto non-invasive experimental observations after postural changes, the present work proposes a first version of an empirical Stochastic Delay Differential Equations (SDDEs) model. The model consists of a total of four SDDEs and two ancillary algebraic equations, incorporates four distinct delayed controls from the brain onto different components of the circulation, and is able to accurately capture the time course of mean arterial pressure and cerebral blood flow velocity signals, reproducing observed auto-correlated error around the expected drift.

Cardiovascular autonomic dysfunction and oxidative stress induced by fructose overload in an experimental model of hypertension and menopause.

BackgroundMetabolic syndrome is characterized by the association of 3 or more risk factors, including: abdominal obesity associated with an excess of abdominal fat, insulin resistance, type 2 diabetes, dyslipidemia and hypertension. Moreover, the prevalence of hypertension and metabolic dysfunctions sharply increases after the menopause. However, the mechanisms involved in these changes are not well understood. Thus, the aim of this study was to assess the effects of fructose overload on cardiovascular autonomic modulation, inflammation and cardiac oxidative stress in an experimental model of hypertension and menopause.MethodsFemale SHR rats were divided into (n = 8/group): hypertensive (H), hypertensive ovariectomized (HO) and hypertensive ovariectomized undergoing fructose overload (100 g/L in drinking water) (FHO). Arterial pressure (AP) signals were directly recorded. Cardiac autonomic modulation was evaluated by spectral analysis. Oxidative stress was evaluated in cardiac tissue.ResultsAP was higher in the FHO group when compared to the other groups. Fructose overload promoted an increase in body and fat weight, triglyceride concentration and a reduction in insulin sensitivity. IL-10 was reduced in the FHO group when compared to the H group. TNF-α was higher in the FHO when compared to all other groups. Lipoperoxidation was higher and glutathione redox balance was reduced in the FHO group when compared to other groups, an indication of increased oxidative stress. A negative correlation was found between IL-10 and adipose tissue.ConclusionFructose overload promoted an impairment in cardiac autonomic modulation associated with inflammation and oxidative stress in hypertensive rats undergoing ovarian hormone deprivation.

Abstract 472: Positive Role of Combined Exercise Training in a Model of Metabolic Syndrome and Menopause: Autonomic, Inflammatory and Oxidative Stress Evaluations

The aim of this study was to evaluate the effects of combined exercise training in hypertensive ovariectomized rats submitted to fructose overload. Wistar and spontaneously hypertensive (SHR) rats were divided into (n=8/group): control (C), hypertensive (H), hypertensive ovariectomized (HO), hypertensive ovariectomized submitted to fructose overload sedentary (HOF) and trained (HOFT). The combined exercise training was performed on a treadmill and ladder adapted to rats in alternated days, during 8 weeks. At the end of exercise protocol, arterial pressure (AP) signals were directly recorded. Cardiovascular autonomic modulation was evaluated by spectral analysis. Oxidative stress and inflammation were measured on cardiac tissue. The association of hypertension and ovariecyomy induced an increase in arterial pressure (AP) (HO: 164±5 vs. H: 146±6 mmHg) and body weight in relation to hypertensive rats. The association of risk factors (hypertension+ovariectomy+fructose) induced an additional increase in AP (HOF: 174±4 mmHg), increased heart rate (HOF: 403±12 vs. HOS: 348±16 bpm) and blood triglycerides (HOF: 160±8 vs. HO: 125±6.4 mg/dl), promoted impairment on the insulin sensitivity, cardiovascular autonomic modulation, oxidative stress (redox ratio of glutathione: HOF: 8.94±0.8 vs. HO: 13.00±1.4) and inflammation (TNF-α- HFO: 65.8±9.9 vs. HO: 31.7±8.6 pg/mg protein) of these animals. However, the combined exercise training was able to reduce the AP (HOFTc: 158±4 mmHg) and heart rate (HOFT: 303±5 bp), to normalize the triglyceride levels (HOFT: 137±4.7 mg/dL), insulin sensitivity and vascular autonomic modulation. Moreover, this approach reduced cardiac lipoperoxidation and increased antioxidant defense and redox balance of glutathione (HOFT: 11.94 ± 1.1), reduced TNF-α (HOFT: 33.1±4.9 mg/dL) and increased IL-10. The results of this study demonstrated that the association of risk factors promoted additional impairment in metabolic, cardiovascular, autonomic, inflammatory and oxidative stress parameters and the combined exercise training was able to reduce and/or normalize these dysfunctions.

Arterial pulsatility improvement in a feedback-controlled continuous flow left ventricular assist device: An ex-vivo experimental study

Continuous flow left ventricular assist devices (CF-LVADs) reduce arterial pulsatility, which may cause long-term complications in the cardiovascular system. The aim of this study is to improve the pulsatility by driving a CF-LVAD at a varying speed, synchronous with the cardiac cycle in an ex-vivo experiment. A Micromed DeBakey pump was used as CF-LVAD. The heart was paced at 140bpm to obtain a constant cardiac cycle for each heartbeat. First, the CF-LVAD was operated at a constant speed. At varying-speed CF-LVAD assistance, the pump was driven such that the same mean pump output was generated. For synchronization purposes, an algorithm was developed to trigger the CF-LVAD each heartbeat. The pump flow rate was selected as the control variable and a reference model was used for regulating the CF-LVAD speed. Continuous and varying-speed CF-LVAD assistance provided the same mean arterial pressure and flow rate, while the index of pulsatility doubled in both arterial pressure and pump flow rate signals under pulsatile pump speed support. This study shows the possibility of improving the pulsatility in CF-LVAD support by regulating pump speed over a cardiac cycle without compromising the overall level of support.

Duration and magnitude of blood pressure below cerebral autoregulation threshold during cardiopulmonary bypass is associated with major morbidity and operative mortality

Optimizing blood pressure using near-infrared spectroscopy monitoring has been suggested to ensure organ perfusion during cardiac surgery. Near-infrared spectroscopy is a reliable surrogate for cerebral blood flow in clinical cerebral autoregulation monitoring and might provide an earlier warning of malperfusion than indicators of cerebral ischemia. We hypothesized that blood pressure below the limits of cerebral autoregulation during cardiopulmonary bypass would be associated with major morbidity and operative mortality after cardiac surgery. Autoregulation was monitored during cardiopulmonary bypass in 450 patients undergoing coronary artery bypass grafting and/or valve surgery. A continuous, moving Pearson's correlation coefficient was calculated between the arterial pressure and low-frequency near-infrared spectroscopy signals and displayed continuously during surgery using a laptop computer. The area under the curve of the product of the duration and magnitude of blood pressure below the limits of autoregulation was compared between patients with andwithout major morbidity (eg, stroke, renal failure, mechanical lung ventilation >48 hours, inotrope use >24 hours, or intra-aortic balloon pump insertion) or operative mortality. Of the 450 patients, 83 experienced major morbidity or operative mortality. The area under the curve ofthe product of the duration and magnitude of blood pressure below the limits of autoregulation was independently associated with major morbidity or operative mortality after cardiac surgery (odds ratio, 1.36; 95% confidence interval, 1.08-1.71; P=.008). Blood pressure management during cardiopulmonary bypass using physiologic endpoints such as cerebral autoregulation monitoring might provide a method of optimizing organ perfusion and improving patient outcomes from cardiac surgery.

Myocardial perfusion distribution and coronary arterial pressure and flow signals: clinical relevance in relation to multiscale modeling, a review

Coronary artery disease, CAD, is associated with both narrowing of the epicardial coronary arteries and microvascular disease, thereby limiting coronary flow and myocardial perfusion. CAD accounts for almost 2 million deaths within the European Union on an annual basis. In this paper, we review the physiological and pathophysiological processes underlying clinical decision making in coronary disease as well as the models for interpretation of the underlying physiological mechanisms. Presently, clinical decision making is based on non-invasive magnetic resonance imaging, MRI, of myocardial perfusion and invasive coronary hemodynamic measurements of coronary pressure and Doppler flow velocity signals obtained during catheterization. Within the euHeart project, several innovations have been developed and applied to improve diagnosis-based understanding of the underlying biophysical processes. Specifically, MRI perfusion data interpretation has been advanced by the gradientogram, a novel graphical representation of the spatiotemporal myocardial perfusion gradient. For hemodynamic data, functional indices of coronary stenosis severity that do not depend on maximal vasodilation are proposed and the Valsalva maneuver for indicating the extravascular resistance component of the coronary circulation has been introduced. Complementary to these advances, model innovation has been directed to the porous elastic model coupled to a one-dimensional model of the epicardial arteries. The importance of model development is related to the integration of information from different modalities, which in isolation often result in conflicting treatment recommendations.

Metabolic, hemodynamic and structural adjustments to low intensity exercise training in a metabolic syndrome model

BackgroundThe increase in fructose consumption is paralleled by a higher incidence of metabolic syndrome, and consequently, cardiovascular disease mortality. We examined the effects of 8 weeks of low intensity exercise training (LET) on metabolic, hemodynamic, ventricular and vascular morphological changes induced by fructose drinking in male rats.MethodsMale Wistar rats were divided into (n = 8 each) control (C), sedentary fructose (F) and ET fructose (FT) groups. Fructose-drinking rats received D-fructose (100 g/l). FT rats were assigned to a treadmill training protocol at low intensity (30% of maximal running speed) during 1 h/day, 5 days/week for 8 weeks. Measurements of triglyceride concentrations, white adipose tissue (WAT) and glycemia were carried out together with insulin tolerance test to evaluate metabolic profile. Arterial pressure (AP) signals were directly recorded. Baroreflex sensitivity (BS) was evaluated by the tachycardic and bradycardic responses. Right atria, left ventricle (LV) and ascending aorta were prepared to morphoquantitative analysis.ResultsLET reduced WAT (−37.7%), triglyceride levels (−33%), systolic AP (−6%), heart weight/body weight (−20.5%), LV (−36%) and aortic (−76%) collagen fibers, aortic intima-media thickness and circumferential wall tension in FT when compared to F rats. Additionally, FT group presented improve of BS, numerical density of atrial natriuretic peptide granules (+42%) and LV capillaries (+25%), as well as the number of elastic lamellae in aorta compared with F group.ConclusionsOur data suggest that LET, a widely recommended practice, seems to be particularly effective for preventing metabolic, hemodynamic and morphological disorders triggered by MS.

Assessing vascular endothelial function using frequency and rank order statistics

Using frequency and rank order statistics (FROS), this study analyzed the fluctuations in arterial waveform amplitudes recorded from an air pressure sensing system before and after reactive hyperemia (RH) induction by temporary blood flow occlusion to evaluate the vascular endothelial function of aged and diabetic subjects. The modified probability-weighted distance (PWD) calculated from the FROS was compared with the dilatation index (DI) to evaluate its validity and sensitivity in the assessment of vascular endothelial function. The results showed that the PWD can provide a quantitative determination of the structural changes in the arterial pressure signals associated with regulation of vascular tone and blood pressure by intact vascular endothelium after the application of occlusion stress. Our study suggests that the use of FROS is a reliable noninvasive approach to the assessment of vascular endothelial degeneration in aging and diabetes.

Correlation between cardiovascular autonomic control dysfunction and oxidative stress in an experimental model of hypertensive and menopause submitted to fructose overload

The aim of this study was to verify the effects of fructose overload in an experimental model of hypertensive and menopause on cardiovascular autonomic control and cardiac oxidative stress. Female SHR rats were divided into (n=8/group): hypertensive (H), hypertensive ovariectomized (HO) and hypertensive ovariectomized submitted to fructose overload (100g/L in drinking water) (FHO). Arterial pressure (AP) signals were directly recorded. Cardiovascular autonomic modulation was evaluated by spectral analysis. Oxidative stress was evaluated by chemiluminescence (CL), total reactive antioxidant potential (TRAP) and redox balance of glutathione (GSH/GSSG) determinations. AP was higher in FHO group (174±4 vs. H: 146±4 HO: 164±5 mmHg) than others groups. FHO group showed reduced vagal tonus (5±3 vs. H: 23±4; HO: 35±7 bpm) and increased sympathetic tonus (91±18 vs. H: 56±11; HO: 60±3 bpm) when compared to other groups. CL was higher in FHO group than other groups. GSH/GSSG was lower in FOH group (8.94±0.80 umol/g) than HO group (13.0±1.4 umol/g). Negative correlation was obtained between VAR‐SAP and TRAP (r: −0.71, p≤0.05) and a positive correlation between RMSSD index and GSH/GSSG (r: 0.68, p≤0.05). In conclusion, fructose overload induced impairment in cardiovascular autonomic control associated with increased oxidative stress in hypertensive rats submitted to ovarian hormones deprivation.

Multifractal Analysis of Hemodynamic Behavior

Physiologic instability is a common clinical problem in the critically ill. Many natural feedback systems are nonlinear, and seemingly random fluctuations may result from the amplification of external perturbations or even arise de novo as a consequence of their underlying dynamics. Characterization of the underlying nonlinear state may be of clinical importance, providing a technique to monitor complex physiology in real-time, guiding patient care and improving outcomes. We employ the wavelet modulus maxima technique to characterize the multifractal properties of heart rate and mean arterial pressure physiology retrospectively for four patients during open abdominal aortic aneurysm repair. We calculated point-estimates for the dominant Hölder exponent (hm, hm) and multifractal spectrum width-at-half-height for both heart rate and mean arterial pressure signals. We investigated how these parameters changed with the administration of an intravenous vasoconstrictor and examined how this varied with atropine pretreatment. Hypotensive patients showed lower values of hm, consistent with a more highly fluctuating and complex behavior. Treatment with a vasoconstrictor led to a transient increase in hm, revealing the appearance of longer-range correlations, but did not impact hm. On the other hand, prior treatment with atropine had no effect on hm behavior but did tend to increase hm. Hypotension leads to a reduction in dominant Hölder exponents for mean arterial pressure, demonstrating an increasing signal complexity consistent with the activation of important homeokinetic processes. Conversely, pharmacological interventions may also alter the underlying dynamics. Pharmacological restoration of homeostasis leads to system decomplexification, suggesting that homeokinetic mechanisms are derecruited as homeostasis is restored.