Hemodynamic Indices Research Articles

Effect of low-volume combined aerobic and resistance high-intensity interval training on vascular health in people with type 2 diabetes: a randomised controlled trial

PurposeWe compared the effects of low-volume combined aerobic and resistance high-intensity interval training (C-HIIT), combined moderate-intensity continuous training (C-MICT) and waitlist control (CON) on vascular health after 8-weeks of supervised training, and an additional 10-months of self-directed training, in adults with type 2 diabetes (T2D).MethodsSixty-nine low active adults with T2D were randomised to 8-weeks of supervised C-HIIT (3 times/week, 78-min/week), C-MICT (current exercise guidelines, 4 times/week, 210-min/week) or CON. CON underwent usual care for 8-weeks before being re-randomised to C-HIIT or C-MICT. This was followed by 10-months of self-directed training for participants in C-HIIT and C-MICT. Vascular outcomes were evaluated at baseline, 8-weeks, and 12-months.ResultsAfter 8-weeks, supervised C-HIIT significantly improved relative flow-mediated dilation (FMD) compared with CON (mean difference [MD] 0.8% [0.1, 1.4], p = 0.025). Although not significantly different from CON, the magnitude of change in relative FMD following 8-weeks of supervised C-MICT was similar (MD 0.8% [–0.1, 1.7], p = 0.080). There were no differences in haemodynamic indices, carotid-femoral pulse wave velocity (cfPWV), or aortic reservoir pressure between groups at 8-weeks. After 12-months, there was a significant reduction in haemodynamic indices (time effect, p < 0.05) for both C-HIIT and C-MICT, with no between-group difference. The reduction in cfPWV over 12-months was significantly greater in C-MICT than C-HIIT (group × time effect, p = 0.018). There was no difference in FMD over time or between groups at 12-months.ConclusionsShort-term supervised C-HIIT and C-MICT both increased brachial artery FMD compared with CON. Long-term C-HIIT and C-MICT were beneficial for improving haemodynamic indices, but not brachial artery FMD. C-MICT was superior to C-HIIT for improving cfPWV at 12-months.Trial Registration: Australian New Zealand Clinical Trials Registry Identifier ACTRN12615000475549.

Analysis of the effect of continuous blood purification combined with xuebijing in the treatment of sepsis and its impact on inflammatory factors and hemodynamic indicators in patients.

Analysis of the effect of continuous blood purification combined with xuebijing in the treatment of sepsis and its impact on inflammatory factors and hemodynamic indicators in patients.

PM2.5 toxicity in blood impairs cardiac redox balance and promotes mitochondrial dysfunction in rat heart that further aggravates ischemia reperfusion injury by modulating PI3K/AKT/mTOR/NF-kB signaling axis.

According to the pathophysiological mechanisms linking particulate matter (PM2.5) exposure and cardiovascular diseases, PM2.5 may directly translocate into the blood stream and remote target organs and thereby induce cardiovascular effects. The toxicity of PM2.5 is known to induce oxidative stress in pulmonary tissue, but its impact on the redox state in heart (distant organ) is unknown and how it modulates the cardiac response to ischemia reperfusion (IR) remains unclear. In the present study, we evaluated the toxic effect of PM2.5 on cardiac physiology in the presence and absence of IR after introducing PM2.5 into the blood. Female Wistar rats were injected with diesel particulate matter (DPM) via i.p & i.v routes at a concentration of 10 µg/ml. The toxic impact of PM2.5 not only adversely affects the cardiac ultra-structure (leading to nuclear infiltration, edema, irregularities in heart muscle and nuclear infiltration), but also altered the cellular redox balance, elevated inflammation and promoted the upregulation of proapoptotic mediator genes at the basal level of myocardium. The results showed alterations in cardiac ultrastructure, elevated oxidative stress and significant redox imbalance, increased inflammation and proapoptotic mediators at the basal level of myocardium. Moreover, the cardioprotective pro survival signaling axis was declined along with an increased NF-kB activation at the basal level. IR inflicted further injury with deterioration of cardiac hemodynamic indices (Heart rate [HR], Left ventricular developed pressure [LVDP], Left ventricular end-diastolic pressure [LVEDP] and rate pressure product [RPP]) along with prominent inactivation of signaling pathways. Furthermore, the levels of GSH/GSSG, NADH/NAD, NADPH/NADP were significantly low along with increased lipid peroxidation in mitochondria of PM2.5 treated IR rat hearts. This observation was supported by downregulation of glutaredoxin and peroxiredoxin genes in the myocardium. Similarly the presence of oxidative stress inducing metals was found at a higher concentration in cardiac mitochondria. Thus, the toxic impact of PM2.5 in heart augment the IR associated pathological changes by altering the physiological response, initiating cellular metabolic alterations in mitochondria and modifying the signaling molecules.

MiR-92b-3p Protects against Myocardial Ischemia-Reperfusion Injury by Inhibiting MAP3K2 in a Mouse Model.

MicroRNAs are well-known RNA regulators modulating biological functions in complex signaling networks. This work aims to explore the impact of microRNA-92b-3p (miR-92b-3p) on myocardial ischemia-reperfusion (I/R) injury. The I/R model was established by left anterior descending coronary artery ligation in mice. The hemodynamic parameters were detected through a multichannel physiological recorder. Myocardial injury markers: serum cardiac troponin I, myocardial kinase isoenzyme (creatine kinase-MB), and serum inflammatory factors (tumor necrosis factor-α, interleukin [IL]-1β, and IL-6) were evaluated by enzyme-linked immunosorbent assay. Cardiac tissue oxidative stress-related factors (malondialdehyde, glutathione peroxidase, total antioxidation capability, and superoxide dismutase) were assessed by colorimetry, myocardial pathology was observed by hematoxylin-eosin staining, and cardiomyocyte apoptosis was measured by triphosphate nick end-labeling staining, as well as the expression of miR-92b-3p and mitogen-activated protein kinase kinase kinase 2 (MAP3K2) in cardiac tissues were determined by reverse transcription quantitative polymerase chain reaction or western blot assay. The targeting relationship between miR-92b-3p and MAP3K2 was verified by bioinformatics, RNA immunoprecipitation, and luciferase reporter assays. miR-92b-3p was lowly expressed and MAP3K2 was highly expressed in myocardial I/R injury mice. Upregulation of miR-92b-3p improved hemodynamic indices, decreased serum levels of myocardial injury biomarkers, inhibited serum inflammatory response, alleviated cardiac tissue oxidative stress, relieved myocardial pathology, and reduced cardiomyocyte apoptosis during the myocardial I/R injury in mice. MAP3K2 was a direct target gene of miR-92b-3p. This research suggests that miR-92b-3p protects against myocardial I/R injury by inhibiting MAP3K2, which may provide novel candidates for treatment of myocardial I/R injury.

Cardiomyocyte Specific MLK3 Deletion Opposes LV Dysfunction and Cardiac Fetal Gene Re-Expression

Study Objective: To determine the cardiac myocyte (CM) and blood pressure-independent effects of Mixed lineage kinase 3 (MLK3) in the regulation of left ventricular (LV) function at baseline and in response to pathological stress. Background: MLK3 functions as a direct substrate effector of cGMP-dependent protein kinase 1α (PKG1α). Whole-body MLK3 deletion in mice increases cardiac dysfunction and remodeling after pressure overload and prevents the therapeutic effect of cGMP augmentation on LV function. However, MLK3 deletion also causes hypertension, which may confound these findings. Hypothesis: MLK3 opposes LV dysfunction through a blood pressure-independent function in the cardiac myocyte (CM). Methods: We generated mice harboring LoxP sites flanking the MAP3K11 gene encoding MLK3 (MLK3fl/fl) and crossed them with αMHC-Cre transgenic mice, enabling constitutive postnatal cardiac myocyte-specific MLK3 deletion (CMKO). Male and female 3- and 6-month-old MLK3 CMKO and control MLK3 intact (MLK3fl/fl Cre-) littermates were studied in the basal state. We also performed transaortic constriction (TAC) or sham surgery for 4 weeks on 3-month-old male mice. We assessed LV structure and function by organ mass, echocardiography, pressure volume loop analysis, qPCR, and immunoblot. In basal and TAC studies, we used age-matched αMHC-Cre x MLK3+/+ (non-floxed) mice as additional controls. Results: MLK3 gene excision in CMs was confirmed by PCR. By 6 months of age, MLK3 CMKO mice displayed: progressive reduction in LV ejection fraction; increase in LV internal diameter; and LV hypertrophy, indicating LV dysfunction and pathological remodeling, compared with littermate controls or with αMHC-Cre x MLK3+/+ non-floxed mice. This effect was more prominent in females than in males. LV fetal gene expression did not differ between genotypes at 3 months. At 6 months of age, however, the fetal genes nppa, RCAN, and CTGF were significantly upregulated in both male and female MLK3 CMKO mice, compared with MLK3 intact, indicating pathological remodeling. After 4-week TAC, MLK3 CMKO LVs developed more severe reduction in LV systolic function compared with MLK3 intact littermates as assayed by echocardiographic measures of LV ejection fraction; and invasive hemodynamic indices of preload recruitable stroke work, maximum LV pressure and LV developed pressure. The MLK3 CMKO LVs also demonstrated a more eccentric remodeling phenotype in which LV mass/tibia length, LV end diastolic and end systolic diameters increased more severely in CMKO mice, with corresponding reduced LV wall thicknesses. Finally, lung mass/tibia length was elevated in the MLK3 CMKO TAC mice compared to MLK3 intact TAC littermates, indicating overt heart failure. Conclusion: (1) MLK3 functions as a tonic inhibitor of LV dysfunction and pathological remodeling through a role in the CM, possibly through sex-specific mechanisms. (2) Intact MLK3 is required for normal LV compensation and concentric remodeling in response to pressure overload. These findings have important clinical implications, as drugs which activate PKG1 in heart failure improve outcomes but are limited by excess hypotension. As a myocardial PKG1 substrate which opposes pathological LV remodeling through blood pressure-independent mechanisms, MLK3 may represent a candidate therapeutic target for heart failure. NIH 1R01HL162919. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Abstract 1145: A Computational Fluid Dynamics Analysis Of Hemodynamic Differences In Patients With High Grade Asymptomatic Carotid Artery Stenosis

Introduction: Current assessment/management of internal carotid artery (ICA) stenosis is based on estimation of percentage (%) stenosis which does not account for trans-lesional flow, pressure gradient (PG), wall shear stress (WSS), or oscillatory shear index (OSI). Computation fluid dynamics (CFD) can be used to characterize such indices. Hypothesis: We hypothesize that patients asymptomatic &gt;70% ICA stenosis will have hemodynamic differences that are independent of % stenosis. Aims: Evaluate hemodynamic indices in patients with asymptomatic &gt;70% ICA stenosis via CFD. Methods: Patients with asymptomatic &gt;70% ICA stenosis were included. 3D time-of-flight (TOF) and phase-contrast (PC) magnetic resonance imaging (MRI) sequences were obtained. CRIMSON was used to generate CFD models containing the carotid artery (CCA), ICA, and external carotid artery (ECA). PC MRI-derived flow waveforms were prescribed to the CCA and ECA. The ICA outlet was coupled to a three-element Windkessel model. Blood was modeled as an incompressible Non-Newtonian fluid with a dynamic viscosity of 0.004 kg m –1 s –1 and a density of 1,060 kg m -3 . Incompressible Navier-Stokes equations were used to solve for velocity and pressures. Results: Eight patients (average age 73.8 years, 62.5% male) with asymptomatic high-grade ICA stenosis (62.5% left) were included. Hypertension (87.5%), tobacco use (87.5%), and hyperlipidemia (75%) were common. Most patients were medically optimized with anti-hypertensive (100%), statin (87.5%), and aspirin (87.5%). Three patients (37.5%) underwent ICA intervention.. Mean peak systolic velocity was 406 cm/s and mean end-diastolic velocity was 127 cm/s. There was large variability in trans-lesional ICA flow, PG, WSS, and OSI (Table 1). Conclusions: Asymptomatic patients with the same % stenosis have differences in trans-lesional ICA flow, PG, WSS, and OSI. Future work is needed to determine the prognostic value of such differences.

Does cardiac impairment develop in ischemic renal surgery in rats depending on the reperfusion time?

BackgroundRenal dysfunction is known to cause heart failure. However, renal dysfunction associated with kidney surgeries (mediated by reperfusion injury) that affects the cardiac physiological function, especially during the recovery and repair phase of renal surgery is unknown. MethodMale Wistar rats (238 ± 18 g) were subjected to renal sham and ischemia-reperfusion (IR-bilateral clamping for 15 min/45 min and reperfusion for 24 h/48 h/7 days) surgeries. At the end of the experiment, the heart was isolated from the animal (to exclude neurohormonal influence) and perfused for 60 min with Krebs-Hanseleit buffer to study the physiological changes. ResultRenal artery bilateral occlusion for 45 min that creates ischemia, followed by 24 h of reperfusion did not impart any significant cardiac physiological functional decline but 48 h of reperfusion exhibited a significant decline in cardiac hemodynamic indices (Rate pressure product in x104 mmHg*beats/min: Sham- 3.53 ± 0.19, I45_R48–2.82 ± 0.21) with mild tissue injury. However, 7 days of reperfusion inflict significant physiological decline (Rate pressure product in x104 mmHg*beats/min - 2.5 ± 0.14) and tissue injury (Injury score- 4 ± 1.5) in isolated rat hearts. Interestingly, when the renal artery bilateral occlusion time was reduced to 15 min the changes in the hearts were negligible after 7 days. Cellular level exploration reveals a positive relation between functional deterioration of mitochondria and elevated mitochondrial oxidative stress and inflammation with cardiac physiological decline and injury linked with renal ischemia-reperfusion surgery. ConclusionCardiac functional decline associated with renal surgery is manifested during renal repair or recovery. This decline depends on cardiac mitochondrial health, which is negatively influenced by the renal IR mediators and kidney function.

Hemodynamic gain index and risk of ventricular arrhythmias: a prospective cohort study.

Objectives: Hemodynamic gain index (HGI), a novel hemodynamic index obtained from cardiopulmonary exercise testing (CPX), is associated with adverse cardiovascular outcomes. However, its specific relationship with ventricular arrhythmias (VAs) is unknown. We aimed to assess the association of HGI with risk of VAs in a prospective study. Design: Hemodynamic gain index was estimated using heart rate and systolic blood pressure (SBP) responses ascertained in 1945 men aged 42-61 years during CPX from rest to maximum exercise, using the formula: [(Heart ratemax x SBPmax) - (Heart raterest x SBPrest)]/(Heart raterest x SBPrest). Cardiorespiratory fitness (CRF) was measured using respiratory gas exchange analysis. Hazard ratios (HRs) (95% confidence intervals, CIs) were estimated for VAs. Results: Over a median follow-up duration of 28.2 years, 75 cases of VA were recorded. In analysis adjusted for established risk factors, a unit (bpm/mmHg) higher HGI was associated with a decreased risk of VA (HR 0.72, 95% CI: 0.55-0.95). The results remained consistent on adjustment for lifestyle factors and comorbidities (HR 0.72, 95% CI: 0.55-0.93). Comparing the top versus bottom tertiles of HGI, the corresponding adjusted HRs (95% CIs) were 0.51 (0.27-0.96) and 0.52 (0.28-0.94), respectively. The associations were attenuated on addition of CRF to the model. HGI improved risk discrimination beyond established risk factors but not CRF. Conclusions: Higher HGI is associated with a reduced risk of VAs in middle-aged and older Caucasian men, but dependent on CRF levels. Furthermore, HGI improves the prediction of the long-term risk for VAs beyond established risk factors but not CRF.

OMX: A NOVEL OXYGEN DELIVERY BIOTHERAPEUTIC IMPROVES OUTCOMES IN AN OVINE MODEL OF CONTROLLED HEMORRHAGIC SHOCK.

Hemorrhagic shock is a major source of morbidity and mortality worldwide. While whole blood or blood product transfusion is a first-line treatment, maintaining robust supplies presents significant logistical challenges, particularly in austere environments. OMX is a novel nonhemoglobin (Hb)-based oxygen carrier derived from the H-NOX (heme-nitric oxide/oxygen binding) protein family. Because of their engineered oxygen (O 2 ) affinities, OMX proteins only deliver O 2 to severely hypoxic tissues. Additionally, unlike Hb-based oxygen carriers, OMX proteins do not scavenge nitric oxide in the vasculature. To determine the safety and efficacy of OMX in supporting tissue oxygen delivery and cardiovascular function in a large animal model of controlled hemorrhage, 2-3-week-old lambs were anesthetized, intubated, and mechanically ventilated. Hypovolemic shock was induced by acute hemorrhage to obtain a 50% reduction over 30 min. Vehicle (n = 16) or 400 mg/kg OMX (n = 13) treatment was administered over 15 min. Hemodynamics, arterial blood gases, and laboratory values were monitored throughout the 6-h study. Comparisons between groups were made using t tests, Wilcoxon rank sum test, and Fisher's exact test. Survival was assessed using Kaplan-Meier curves and the log-rank test. We found that OMX was well-tolerated and significantly improved lactate and base deficit trends, and hemodynamic indices ( P < 0.05). Median survival time was greater in the OMX-treated group (4.7 vs. 6.0 h, P < 0.003), and overall survival was significantly increased in the OMX-treated group (25% vs. 85%, P = 0.004). We conclude that OMX is well-tolerated and improves metabolic, hemodynamic, and survival outcomes in an ovine model of controlled hemorrhagic shock.

Deep-learning-based real-time individualization for reduce-order haemodynamic model

The reduced-order lumped parameter model (LPM) has great computational efficiency in real-time numerical simulations of haemodynamics but is limited by the accuracy of patient-specific computation. This study proposed a method to achieve the individual LPM modeling with high accuracy to improve the practical clinical applicability of LPM.Clinical data was collected from two medical centres comprising haemodynamic indicators from 323 individuals, including brachial artery pressure waveforms, cardiac output data, and internal carotid artery flow waveforms. The data were expanded to 5000 synthesised cases that all fell within the physiological range of each indicator. LPM of the human blood circulation system was established. A double-path neural network (DPNN) was designed to input the waveforms of each haemodynamic indicator and their key features and then output the individual parameters of the LPM, which was labelled using a conventional optimization algorithm. Clinically collected data from the other 100 cases were used as the test set to verify the accuracy of the individual LPM parameters predicted by DPNN.The results show that DPNN provided good convergence in the training process. In the test set, compared with clinical measurements, the mean differences between each haemodynamic indicator and the estimate calculated by the individual LPM based on the DPNN were about 10 %. Furthermore, DPNN prediction only takes 4 s for 100 cases.The DPNN proposed in this study permits real-time and accurate individualization of LPM's. When facing medical issues involving haemodynamics, it lays the foundation for patient-specific numerical simulation, which may be beneficial for potential clinical application.

Correlations between heart sound components and hemodynamic variables

Although the esophageal stethoscope is used for continuous auscultation during general anesthesia, few studies have investigated phonocardiographic data as a continuous hemodynamic index. In this study, we aimed to induce hemodynamic variations and clarify the relationship between the heart sounds and hemodynamic variables through an experimental animal study. Changes in the cardiac contractility and vascular resistance were induced in anesthetized pigs by administering dobutamine, esmolol, phenylephrine, and nicardipine. In addition, a decrease in cardiac output was induced by restricting the venous return by clamping the inferior vena cava (IVC). The relationship between the hemodynamic changes and changes in the heart sound indices was analyzed. Experimental data from eight pigs were analyzed. The mean values of the correlation coefficients of changes in S1 amplitude (ΔS1amp) with systolic blood pressure (ΔSBP), pulse pressure (ΔPP), and ΔdP/dt during dobutamine administration were 0.94, 0.96, and 0.96, respectively. The mean values of the correlation coefficients of ΔS1amp with ΔSBP, ΔPP, and ΔdP/dt during esmolol administration were 0.80, 0.82, and 0.86, respectively. The hemodynamic changes caused by the administration of phenylephrine and nicardipine did not correlate significantly with changes in the heart rate. The S1 amplitude of the heart sound was significantly correlated with the hemodynamic changes caused by the changes in cardiac contractility but not with the variations in the vascular resistance. Heart sounds can potentially provide a non-invasive monitoring method to differentiate the cause of hemodynamic variations.

Study Protocol of a Prospective, Monocentric, Single-Arm Study Investigating the Correlation of Endograft Properties with Aortic Stiffness in Abdominal Aortic Aneurysm Patients Subjected to Endovascular Aortic Repair.

The number of endovascular aortic repairs (EVARs) has surpassed the number of open surgical repairs of abdominal aortic aneurysms (AAAs) worldwide. The available commercial endoprostheses are composed of materials that are stiffer than the native aortic wall. As a consequence, the implantation of stent-graft endoprostheses during EVAR increases aortic rigidity and thus aortic stiffness, resulting in a decrease in abdominal aorta compliance. EVAR has been found to have a possibly harmful effect not only on heart functions but also on other vascular beds, including kidney function, due to the decrease in aortic compliance that it causes. Aortic stiffness is measured by various hemodynamic indices like the pulse wave velocity (PWV), the central aortic pressure (CAP), and the augmentation index (AIx). In the literature, there are increasing numbers of studies investigating the properties of endografts, which are strongly related to increases in aortic stiffness. However, there is a lack of data on whether there is a correlation between the length of various endografts implanted during EVAR and the increase in the PWV, CAP, and AIx postoperatively compared to the preoperative values. The aim of this prospective, observational, monocentric, single-arm study is to investigate the correlation between endograft length and the postoperative increase in the PWV, CAP, and AIx in patients subjected to EVAR. Additionally, this study intends to identify other endograft properties related to increases in the PWV, CAP, and AIx. Other endpoints to be studied are the existence of immediate postoperative myocardial and kidney injury after EVAR. The prediction of cardiovascular events caused by endograft-related increased aortic stiffness could contribute to the improvement of various endograft properties so that the impact of endografts on the native aortic wall can be minimized.

Analysis of the effect of comprehensive physical and mental nursing for patients with acute cerebral infarction in intravenous thrombolytic therapy.

To evaluate the efficacy of comprehensive physical and mental nursing for patients with acute cerebral infarction (ACI) undergoing intravenous thrombolytic therapy and its impact on patients' quality of life and psychological state. A total of 200 patients with ACI, admitted to our hospital between December 2018 and December 2019, were included in the study. They were randomly assigned to either the control group or the experimental group using a random number table. The control group received routine care (basic care such as monitoring vital signs, assisting with daily activities, administering medications, and providing comfort measures), while the experimental group received comprehensive physical and mental nursing (physical care, phsycological surpport, education and conceling). Various parameters including quality of life index (QLI) scores, mental status scale in non-psychiatric settings (MSSNS) scores, self-rating anxiety scale (SAS) scores, self-rating depression scale (SDS) scores, National Institute of Health Stroke Scale (NIHSS) scores, changes in hemodynamic indicators, and incidence of adverse events during intravenous thrombolysis were compared between the two groups. The experimental group had higher QLI scores and lower MSSNS, SAS, SDS, and NIHSS scores compared to the control group (p = 0.33, 0.22, 0.35, 0.26, 0.042). The experimental group also exhibited a lower incidence of adverse reactions during intravenous thrombolysis (p = 0.02). Comprehensive physical and mental nursing for patients with ACI undergoing intravenous thrombolysis improves nursing efficacy, nursing satisfaction, quality of life, and patients' psychological state. These findings highlight the importance of implementing holistic nursing interventions to optimize patient outcomes in ACI management.

Cholinergic anti-inflammatory pathway confers protective effects in septic shock rats

Background: Septic shock can lead to multiple organ dysfunction. The cholinergic anti-inflammatory pathway is known to prevent organ damage from infection by modulating the inflammatory response. However, the modulatory capacity of cholinergic anti-inflammatory pathways in septic shock remains unclear. Methods: Cecal ligation and puncture (CLP) was used to establish a rat model of septic shock. Bilateral cervical vagal nerve isolation, dual cervical vagotomy, and vagus nerve stimulation (VNS) were used to inhibit or activate cholinergic anti-inflammatory pathways. Tacrine and α-bungarotoxin groups were used to mimic the activation and shutdown of cholinergic anti-inflammatory pathways. The survival status, hemodynamic indicators, inflammatory cytokine content, and inflammatory response of liver and kidney tissues of the rats were detected. Results: Dual cervical vagotomy significantly exacerbated the hepatic (p &lt; 0.05) and renal (p &lt; 0.05) impairment in septic shock rats relative to the sham-operated group. Tacrine, a cholinergic potentiator, significantly alleviated liver (p &lt; 0.05) and kidney (p &lt; 0.05) damage in septic shock rats. Dual cervical vagotomy significantly promoted the expression of pro-inflammatory factors caused by septic shock in rat liver and kidney tissues (p &lt; 0.05), while Tacrine treatment inhibited the increase of inflammatory factors (p &lt; 0.05). Conclusions: Activation of the cholinergic anti-inflammatory pathway exerts protective effects on multiple organ dysfunction caused by septic shock. The cholinergic enhancer, Tacrine, and VNS effectively ameliorated liver and kidney damage, improved hemodynamic indicators, and enhanced survival rates in septic shock rats.

On the role of tissue mechanics in fluid–structure interaction simulations of patient‐specific aortic dissection

AbstractModeling an aortic dissection represents a particular challenge from a numerical perspective, especially when it comes to the interaction between solid (aortic wall) and liquid (blood flow). The complexity of patient‐specific simulations requires a variety of parameters, modeling assumptions and simplifications that currently hinder their routine use in clinical settings. We present a numerical framework that captures, among other things, the layer‐specific anisotropic properties of the aortic wall, the non‐Newtonian behavior of blood, patient‐specific geometry, and patient‐specific flow conditions. We compare hemodynamic indicators and stress measurements in simulations with increasingly complex material models for the vessel tissue ranging from rigid walls to anisotropic hyperelastic materials. We find that for the present geometry and boundary conditions, rigid wall simulations produce different results than fluid–structure interaction simulations. Considering anisotropic fiber contributions in the tissue model, stress measurements in the aortic wall differ, but shear stress‐based biomarkers are less affected. In summary, the increasing complexity of the tissue model enables capturing more details. However, an extensive parameter set is also required. Since the simulation results depend on these modeling choices, variations can lead to different recommendations in clinical applications.

Invasive haemodynamics predict outcomes in paediatric pulmonary artery hypertension.

Invasive haemodynamics are often performed for initiating and guiding pulmonary artery hypertension therapy. Little is known about the predictive value of invasive haemodynamic indices for long-term outcomes in children with pulmonary artery hypertension. We aimed to evaluate invasive haemodynamic data to help predict outcomes in paediatric pulmonary artery hypertension. Patients with pulmonary artery hypertension who underwent cardiac catheterisation (2006-2019) at a single centre were included. Invasive haemodynamic data from the first cardiac catheterisation and clinical outcomes were reviewed. The combined adverse outcome was defined as pericardial effusion (due to right ventricle failure), creation of a shunt for pulmonary artery hypertension (atrial septal defect or reverse Pott's shunt), lung transplant, or death. Among 46 patients with a median [interquartile range (IQR)] age of 13.2 [4.1-44.7] months, 76% had CHD. Median mean pulmonary artery pressure was 37 [28-52] mmHg and indexed pulmonary vascular resistance was 6.2 [3.6-10] Woods units × m2. Median pulmonary artery pulsatility index was 4.0 [3.0-4.7] and right ventricular stroke work index was 915 [715-1734] mmHg mL/m2. After a median follow-up of 2.4 years, nine patients had a combined adverse outcome (two had a pericardial effusion, one underwent atrial level shunt, one underwent reverse Pott's shunt, and six died). Patients with an adverse outcome had higher systolic and mean pulmonary artery pressures, higher diastolic and transpulmonary pressure gradients, higher indexed pulmonary vascular resistance, higher pulmonary artery elastance, and higher right ventricular stroke work index (p < 0.05 each). Invasive haemodynamics (especially mean pulmonary artery pressure and diastolic pressure gradient) obtained at first cardiac catheterisation in children with pulmonary artery hypertension predicts outcomes.

Impact of therapeutic hypothermia (TH) on echocardiography indices of pulmonary hemodynamics among neonates with hypoxic ischemic encephalopathy (HIE).

Impact of therapeutic hypothermia (TH) on echocardiography indices of pulmonary hemodynamics among neonates with hypoxic ischemic encephalopathy (HIE).

Assessment of the physiological features of equine cardiohemodynamics by volumetric compression oscillometry

The cardiovascular system of humans and animals is a complex of organs that ensure the supply of all parts of the body (with a few exceptions) with necessary substances and remove waste products. It is the cardiovascular system that provides all parts of the body with the necessary oxygen and is the basis of life. Currently, research into the problems of maintaining an optimal level of well-being, assessing the functional state and improving the adaptive capabilities of animals continues to be relevant. A significant direction in this area is the study of the activity of the cardiovascular system (CVS), the parameters of which are characterized by high reactivity and an important role in the implementation of adaptive mechanisms of the animal body. Cardiovascular diseases remain the leading cause of death in most cases in both humans and animals. In many ways, the solution to this problem depends on timely and effective diagnosis of changes in the myocardium. The main goal of the research work is to establish indicators of cardiohemodynamic values and analyze them in horses. In our studies, to measure and further analyze indicators of central and peripheral hemodynamics, we used a hardware-software complex for non-invasive study of central hemodynamics using the method of volumetric compression oscillometry KAP TsGosm-“Globus” (oscillometric analyzer of blood circulation indicators). In horses, during the study, average numerical values of myocardial-hemodynamic parameters were obtained: different types of blood pressure, vascular characteristics and indicators of cardiac activity. Mathematical analysis of hemodynamic indicators established the values of cardiohemodynamic indicators. In this regard, it is advisable to include the assessment of these parameters in the basic set of methods for diagnosing heart diseases in horses. The study of the cardiovascular system is of great importance in veterinary treatment and prophylactic work.

Computational Analysis of Blood Flow in Healthy Pulmonary Arteries in Comparison to Repaired Tetralogy of Fallot Results: A Small Cohort Study

Characterization of the physiological hemodynamic environment in normal pulmonary arteries is a key factor in understanding pathological conditions. This study aimed to analyze the morphology and hemodynamics in the healthy adult pulmonary bifurcation in comparison to age-matched repaired Tetralogy of Fallot (rTOF) geometries. The pulmonary trunk of five healthy volunteers was reconstructed from 4D Flow-MRI data and was compared to rTOF results. Subject-specific boundary conditions were assigned in both the inlet and outlets of the models, and flow characteristics were analyzed computationally. The morphological and flow features were consistent among the healthy geometries, highlighting the ability of an averaged geometry derived from this small cohort to capture the main flow characteristics. A slightly higher mean time-averaged wall shear stress (TAWSS) was found in the right pulmonary artery, which was also the branch with a higher mean curvature and local Reynolds number. Compared to rTOF results, the averaged healthy geometry demonstrated more than an 8-fold lower value in TAWSS, with the individual patient-specific healthy volunteers showing further reduced TAWSS than the rTOF patients. These observations could be useful in clinical assessment and decision making based on hemodynamic indices.

Left atrial to coronary sinus shunting for treatment of heart failure with mildly reduced or preserved ejection fraction: The ALT FLOW Early Feasibility Study 1-year results.

Patients with heart failure and mildly reduced or preserved ejection fraction have limited therapeutic options. The ALT-FLOW Early Feasibility Study evaluated safety, haemodynamics and outcomes for the APTURE transcatheter shunt system, a novel left atrium to coronary sinus shunt in these patients. Safety and shunt implantation success was evaluated for all 116 enrolled patients. An analysis population of implanted patients with a left ventricular ejection fraction (LVEF) >40% (n = 95) was chosen to assess efficacy via paired comparison between baseline and follow-up haemodynamic (3 and 6 months), and echocardiographic, clinical and functional outcomes (6 months and 1 year). Health status and quality of life outcomes were assessed using the Kansas City Cardiomyopathy Questionnaire overall summary score (KCCQ-OSS). The primary safety endpoint, major adverse cardiac, cerebral, and renal events, and reintervention through 30 days, occurred in 3/116 patients (2.6%). All implanted shunts were patent at 1 year. In patients with LVEF >40%, the mean (95% confidence interval) reduction in exercise pulmonary capillary wedge pressure (PCWP) at 20 W was -5.7 (-8.6, -2.9) mmHg at 6 months (p < 0.001). At baseline, 8% had New York Heart Association class I-II status and improved to 68% at 1 year (p < 0.001). KCCQ-OSS at baseline was 39 (35, 43) and improved at 6 months and 1 year by 25 (20-30) and 27 (22-32) points, respectively (both p < 0.0001). No adverse changes in haemodynamic and echocardiographic indices of right heart function were observed at 1 year. Overall, the reduction in PCWP at 20 W and improvement in KCCQ-OSS in multiple subgroups were consistent with those observed for the entire population. In patients with heart failure and LVEF >40%, the APTURE shunt demonstrated an acceptable safety profile with significant sustained improvements in haemodynamic and patient-centred outcomes, underscoring the need for further evaluation of the APTURE shunt in a randomized trial.