Increase In Aortic Pressure Research Articles

Hemodynamics with mechanical circulatory support devices using a cardiogenic shock model

Mechanical circulatory support (MCS) devices, including veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and Impella, have been widely used for patients with cardiogenic shock (CS). However, hemodynamics with each device and combination therapy is not thoroughly understood. We aimed to elucidate the hemodynamics with MCS using a pulsatile flow model. Hemodynamics with Impella CP, VA-ECMO, and a combination of Impella CP and VA-ECMO were assessed based on the pressure and flow under support with each device and the pressure–volume loop of the ventricle model. The Impella CP device with CS status resulted in an increase in aortic pressure and a decrease in end-diastolic volume and end-diastolic pressure (EDP). VA-ECMO support resulted in increased afterload, leading to a significant increase in aortic pressure with an increase in end-systolic volume and EDP and decreasing venous reservoir pressure. The combination of Impella CP and VA-ECMO led to left ventricular unloading, regardless of increase in afterload. Hemodynamic support with Impella and VA-ECMO should be a promising combination for patients with severe CS.

Evening and Morning-After Aortic Wave Reflection Responses to Binge Alcohol Consumption

Binge alcohol consumption acutely increases blood pressure and disrupts sleep. Recently, sleep irregularity has been linked to increases in aortic blood pressure. Increases in aortic wave reflection (i.e., aortic augmentation index) are associated with hypertension and cardiovascular risk. The purpose of the present study was to investigate the acute and next morning effects of evening binge alcohol consumption on aortic wave reflection. We tested the hypothesis that aortic augmentation index normalized to 75 heart beats per minute (AIx@75) and aortic pulsatile load (APL) would be increased acutely after binge drinking in the evening (study 1), and also the morning-after binge drinking compared to the morning after fluid control (study 2). Participants (n=33; 52% women; age 25±1 years; BMI 27±1 kg/m2) arrived at the laboratory at 4:00pm for baseline blood pressure and SphygmoCor (CPVH, Sydney, Australia) measures, and were provided a standardized meal verified by a registered dietitian. In a randomized order, separated by one month, participants completed a binge alcohol protocol (4-5 alcoholic drink equivalents within 2 hours) or fluid control. Alcohol or fluid control doses were administered in two equal allocates at 8 and 9 pm, and participants were provided 15 min to consume during each period. Binge alcohol consisted of a 1:3 mixture of 190 proof grain ethanol and fruit juice (i.e., Orange or Cranberry Juice) based on body weight and sex (1g/kg men, 0.85g/kg women), while the fluid control was only fruit juice in equal volume. Study 1 examined blood pressure, heart rate, aortic pulse pressure, APL, and AIx@75 before the standardized meal and then thirty minutes post-consumption of each allocated beverage using repeated measures ANOVA with condition (alcohol vs. fluid control) and time (baseline, post-drink 1, and post-drink 2) as within-subjects factors. Study 2 examined the same variables as study 1, but within 15 minutes of waking the morning after binge alcohol or fluid control using paired T-tests. Means were considered significantly different when p<0.05. In study 1, fluid control decreased HR and APL after doses one and two, while HR and APL were increased after the second dose of alcohol (time x cond. p<0.001). In study 2, morning-after HR was increased with binge alcohol compared to fluid control (57±1 vs. 63±2 beats/min; p<0.001). Morning-after APL (1857±66 vs. 2060±82 a.u.; p=0.012) and AIx@75 (2.9±2.5 vs. 6.5±2.4%; p=0.042) were also elevated in the binge alcohol condition. Our results indicate binge alcohol consumption acutely increases HR and APL the evening of consumption and increases HR, APL, and AIx@75 the morning after. These findings highlight a potential key physiological contributor to the known associations between binge alcohol consumption and cardiovascular risk. NIH (AA-024892). 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.

TABERNACL: Temporary Hemodynamic Stabilization In Vivo.

Acute aortic regurgitation is life-threatening with few nonsurgical options for immediate stabilization. We propose Trans-Aortic Balloon to Ease Regurgitation Applying Counter-Pulsation (TABERNACL), a simple, on-table temporary valve using commercially available equipment to temporize acute severe aortic regurgitation. We hypothesize that an appropriately sized commercial balloon dilatation catheter-straddling the aortic annulus and connected to a counterpulsation console-can serve as a temporizing valve to restore hemodynamic stability in acute aortic regurgitation. We performed benchtop testing of valvuloplasty, angioplasty, and sizing balloons as counterpulsation balloons. TABERNACL was assessed in vivo in a porcine model of acute aortic regurgitation (n=8). We also tested a static undersized, continuously inflated transvalvular balloon as a spacer intended physically to obstruct the regurgitant orifice. Benchtop testing identified that Tyshak II and PTS sizing (NuMed Braun) balloon catheters performed adequately as temporary valves (ie, complete inflation and deflation with each cycle) and resisted fatigue, in contrast to others. When TABERNACL was used in the acute severe regurgitation animals, there was immediate hemodynamic improvement, with a significant 35% increase in diastolic aortic pressure by 16 mm Hg ([95% CI, 7-25] P=0.0056), 34% reduction in left ventricular end-diastolic pressure by -7 mm Hg ([95% CI, -10 to -5] P=0.0006), improvement in the aortic diastolic index by 0.28 ([95% CI, 0.18-0.39] P=0.0009), and reversal of electrocardiographic myocardial ischemia. As an alternative, static balloon inflation across the aortic valve stabilized regurgitation hemodynamics at the expense of a new aortic gradient and caused excessive ectopy from balloon movement in the left ventricular outflow tract. TABERNACL improves hemodynamics and reduces coronary ischemia by electrocardiography in animals with acute severe aortic regurgitation. TABERNACL valves obstruct the diastolic regurgitant orifice without systolic obstruction. This may prove a lifesaving bridge to definitive valve replacement therapy.

Abstract 218: Effect of Airway Pressure and Localized Sternal Compression Upon Hemodynamics During Cardiopulmonary Resuscitation

Background: During cardiopulmonary resuscitation (CPR), chest compression (CC) and mechanical ventilation are cyclic in nature and each modulate the intrathoracic pressure (ITP). ITP is increased during the compression phase of CC, causing an increase in aortic pressure (AoP) and right atrial pressure (RAP) to drive forward blood flow. Similarly, positive pressure ventilation increases ITP during the inspiratory phase as pressure is transmitted through the lungs, which also has an impact on hemodynamics. The purpose of this analysis was to examine differences in hemodynamics during ventricular fibrillation (VF) arrest due to ventilation alone and during localized sternal CC of varying depths in a porcine model of cardiac arrest. Methods: Domestic swine (n = 8) underwent electrically induced VF with ten-minute downtime, followed by resuscitation with mechanical ventilation and CC with active lift to neutral chest position. Mechanical ventilation was delivered using pressure-controlled synchronized intermittent mandatory ventilation (SIMV) mode (Vt 10 mL/kg, 10 bpm, trigger -6 cmH 2 O, PEEP 5 cmH 2 O, FiO 2 100). CPR was initiated with three minutes of ventilation only, followed by one minute of break-in CC at 1.0 in and 1.5 in prior to increase to depth of 2.0 in. AoP, RAP, esophageal pressure (Pes), and airway pressure (Paw) were examined over the ventilation cycle to determine the effect of each treatment upon parameters. Results: Positive pressure ventilation caused similar changes to the Pes, RAP, and AoP values (3-5 mmHg). CC caused similar changes to Pes (3-5 mmHg), but much larger changes to the RAP and AoP (10-130 mmHg) depending on compression depth. Conclusions: The ITP is not uniform during CC, creating only modest changes to Pes. This suggests that CC generate blood pressures, and presumably flows, through mechanisms other than ITP modulation. Understanding this interaction could improve our understanding of blood flow during CPR.

Cardioprotective Effects of a Selective c-Jun N-terminal Kinase Inhibitor in a Rat Model of Myocardial Infarction.

Activation of c-Jun N-terminal kinases (JNKs) is involved in myocardial injury, left ventricular remodeling (LV), and heart failure (HF) after myocardial infarction (MI). The aim of this research was to evaluate the effects of a selective JNK inhibitor, 11H-indeno [1,2-b]quinoxalin-11-one oxime (IQ-1), on myocardial injury and acute myocardial ischemia/reperfusion (I/R) in adult male Wistar rats. Intraperitoneal administration of IQ-1 (25 mg/kg daily for 5 days) resulted in a significant decrease in myocardial infarct size on day 5 after MI. On day 60 after MI, a significant (2.6-fold) decrease in LV scar size, a 2.2-fold decrease in the size of the LV cavity, a 2.9-fold decrease in the area of mature connective tissue, and a 1.7-fold decrease in connective tissue in the interventricular septum were observed compared with the control group. The improved contractile function of the heart resulted in a significant (33%) increase in stroke size, a 40% increase in cardiac output, a 12% increase in LV systolic pressure, a 28% increase in the LV maximum rate of pressure rise, a 45% increase in the LV maximum rate of pressure drop, a 29% increase in the contractility index, a 14% increase in aortic pressure, a 2.7-fold decrease in LV end-diastolic pressure, and a 4.2-fold decrease in LV minimum pressure. We conclude that IQ-1 has cardioprotective activity and reduces the severity of HF after MI.

The COSEVAST Study Outcome: Evidence of COVID-19 Severity Proportionate to Surge in Arterial Stiffness.

BackgroundThe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection affects the cardiovascular system at many levels. It initially infects endothelial cells, inducing marked endothelial damage and inflammation. However, there was no empirical evidence of functional compromise of arterial walls.Aims and objectiveOur primary objective was to study functional arterial damage in coronavirus disease 2019 (COVID-19) and establish the noninvasive measurement of arterial stiffness as an independent marker of disease severity.Materials and methodsWe recorded the arterial stiffness of 23 mild, 21 moderate, and 20 severe COVID-19 patients grouped on the latest National Institute of Health (NIH) severity criteria. We observed arterial stiffness of COVID-19 patients with standard parameters like noninvasive estimated carotid–femoral pulse wave velocity (cfPWV), age-normalized increase in cfPWV (ANI_cfPWV), age-normalized increase in aortic augmentation pressure (ANI_AugP), and heart rate-normalized augmentation index (HRN_ AIx). All the parameters were also corrected for statistically significant confounding factors.ResultsModerate and severe COVID-19 patients have extremely significantly elevated arterial stiffness than mild patients. In mild patients, cfPWV (829.1 ± 139.2 cm/second) was significantly lower than both moderate (1067 ± 152.5 cm/second, p <0.0001) and severe (1416 ± 253.9 cm/second, p <0.0001) patients. ANI_cfPWV in moderate and severe patients was significantly higher than mild patients (mild: 101.2 ± 126.1 cm/second; moderate: 279 ± 114.4 cm/second; severe: 580.1 ± 216.4 cm/second; intergroup p <0.0001). The results even after correction for significant confounding factors did not show any considerable change in the increasing trend of arterial stiffness.ConclusionThis study establishes the functional deterioration of arteries in proportion to the severity of COVID-19.How to cite this articleKumar N, Kumar S, Kumar A, Bhushan D, Kumar A, Kumar A, et al. The COSEVAST Study Outcome: Evidence of COVID-19 Severity Proportionate to Surge in Arterial Stiffness. Indian J Crit Care Med 2021;25(10):1113–1119.

Chronic maternal hypercortisolemia models stress-induced adverse birth outcome and altered cardiac function in newborn lambs.

Maternal stress in pregnancy is thought to be a contributing factor in adverse pregnancy outcomes, including stillbirth and prematurity. Previous studies in our laboratory have shown that chronic elevation in maternal cortisol concentration in ewes (by maternal infusion of 1 mg/kg/day) during the late gestation increased the incidence of stillbirth and altered fetal heart rate and blood pressure at birth. We designed the current study to test the effect of chronically elevated maternal cortisol on fetal cardiac adaption from in utero life to ex utero life. The combined risk of stillbirth or prematurity was significantly greater in the pregnancies with maternal hypercortisolemia; in this cohort, 40% of the lambs of cortisol-infused ewes died in utero or at birth compared with 25% of lambs of control ewes, and 24% of lambs of cortisol-infused ewes were born preterm, whereas no lamb was born preterm in the control group. Compared with control lambs, the lambs of cortisol-infused ewes born at full term exhibited a significant increase in mean aortic pressure just before birth and a significant decrease in mean aortic pressure that was evident during the first 9 h after birth. The QT interval was decreased before birth and increased immediately after birth in the newborns of cortisol-treated ewes compared with control lambs. These findings suggest that excess in utero corticosteroid exposure adversely affects fetal cardiac adaptation to extrauterine life and that chronic maternal stress or hypersecretion of corticosteroids may contribute to adverse obstetric outcomes.

Microbeam Irradiation of the Beating Rodent Heart: An Ex Vivo Study of Acute and Subacute Effects on Cardiac Function

Microbeam radiation therapy (MRT) has shown several advantages compared with conventional broad-beam radiation therapy in small animal models, including a better preservation of normal tissue function and improved drug delivery based on a rapidly increased vascular permeability in the target region. Normal tissue tolerance is the limiting factor in clinical radiation therapy. Knowledge of the normal tissue tolerance of organs at risk is therefore a prerequisite in evaluating any new radiation therapy approach. With an irradiation target in the thoracic cavity, the heart would be the most important organ at risk. We used the ex vivo beating rodent heart in the Langendorff perfusion system at the synchrotron to administer microbeam irradiation (MBI) with a peak dose of 40 or 400 Gy. By continuously recording the electrocardiogram, the left ventricular pressure, and the aortic pressure before, during and after MBI, we were able to assess acute and subacute effects of MBI on electrophysiological and mechanical cardiac function. In addition, we analyzed histologic and ultrastructural sequelae caused by MBI. There were no significant changes in heart rate, heart rate variability, systolic increase of left ventricular pressure or aortic pressure. Moreover, the changes of heart rate, left ventricular pressure and aortic pressure by adding 10-5 mol/L norepinephrine to the perfusate, were also not significant between MBI and sham experiments. However, the rate-pressure product as a surrogate marker for maximum workload after MBI was significantly lower compared with sham-irradiated controls. On the structural level, no severe membranous, sarcomeric, mitochondrial or nuclear changes caused by MBI were detected by desmin immunohistochemistry and electron microscopy. With respect to acute and subacute toxicity, an MBI peak dose up to 400Gy did not result in severe changes in cardiac electrophysiology or mechanics.

АRTERIAL STIFFNESS AND CENTRAL AORTAL PRESSURE AS SIGNIFICANT PREDICTORS OF COMPLICATIONS AFTER OFF-PUMP CORONARY ARTERY BYPASS GRAFTING

Some studies have shown that an increase in arterial stiffness and central aortic pressure increase the risk of postoperative complications for off-pump coronary artery bypass grafting (off-pump CABG). AIM: To determine the significance of arterial stiffness and central aortic pressure indicators for predicting acute kidney injury (AKI) and cardiac events in patients after off-pump CABG. MATERIALS AND METHODS: An analysis of off-pump CABG outcomes was carried out in 196 patients (mean age 62.7 ± 5.3 years) without clinical signs of chronic kidney disease. The patients were divided into a test (n = 56) and control (n = 140) groups, depending on the presence or absence of AKI, acute coronary syndrome (ACS), or cardiac arrhythmias in the early postoperative period. Pulse wave velocity indicators (PWV) were processed on the carotidfemoral (cf PWV) and brachio-ankle (baPWV) segments, and the results of measuring central aortic pressure (CAP). RESULTS: It has been proven that the incidence of AKI is significantly higher in patients with higher cf PWV (n &lt;0.001), baPWV (n = 0.034) and systolic aortic pressure (SAP) (n = 0.013). ACS was more often observed in patients with higher SAP (n &lt;0.001) and diastolic (DAP) (n = 0.005) aortic pressure, and cardiac arrhythmias in patients with higher SAP and office systolic pressure (n &lt; 0.001). Based on the results of logistic regression analysis, it was determined (by regression coefficients — B) that an increase in cf PWV by 1 m/s increases the risk of AKI by 85.0%. An increase in SAP by one unit significantly increases the risk of ACS by 111.0% and cardiac arrhythmias by 58.0%. It was shown that the measurement of CAP has a greater diagnostic value than the office measurement of blood pressure. CONCLUSION: Arterial stiffness is an independent predictor of AKI for off-pump CABG. A decrease in PWV value is accompanied by a decrease in the incidence of AKI. CAP indices have a more significant prognostic value with respect to the likelihood of cardiac events after an off-pump CABG than the data of measurement of blood pressure.

Effects of Left Ventricular Versus Traditional Chest Compressions in a Traumatic Pulseless Electrical Activity Model.

Prehospital cardiopulmonary resuscitation has commonly been considered ineffective in traumatic cardiopulmonary arrest because traditional chest compressions do not produce substantial cardiac output. However, recent evidence suggests that chest compressions located over the left ventricle (LV) produce greater hemodynamics when compared to traditional compressions. We hypothesized that chest compressions located directly over the LV would result in an increase in return of spontaneous circulation (ROSC) and hemodynamic variables, when compared to traditional chest compressions, in a swine model of traumatic pulseless electrical activity (PEA). Transthoracic echocardiography was used to mark the location of the aortic root (traditional compressions) and the center of the LV on animals (n = 34) that were randomized to receive chest compressions in one of the two locations. Animals were hemorrhaged to mean arterial pressure <20 to simulate traumatic PEA. After 5 minutes of PEA, basic life support (BLS) with mechanical cardiopulmonary resuscitation was initiated and performed for 10 minutes followed by advanced life support for an additional 10 minutes. Hemodynamic variables were averaged over the final 2 minutes of BLS and advanced life support periods. Six of the LV group (35%) achieved ROSC compared to eight of the traditional group (47%) (P = .73). There was an increase in aortic systolic blood pressure (P < .01), right atrial systolic blood pressure (P < .01), and right atrial diastolic blood pressure (P = .02) at the end of BLS in the LV group compared to the traditional group. In our swine model of traumatic PEA, chest compressions performed directly over the LV improved blood pressures during BLS but not ROSC.

Patient-specific computational flow modelling for assessing hemodynamic changes following fenestrated endovascular aneurysm repair

ObjectiveThis study aimed to develop an accessible patient-specific computational flow modelling pipeline for evaluating the hemodynamic performance of fenestrated endovascular aneurysm repair (fEVAR), with the hypothesis that computational flow modelling can detect aortic branch hemodynamic changes associated with fEVAR graft implantation. MethodsPatients who underwent fEVAR for juxtarenal aortic aneurysms with the Cook ZFEN were retrospectively selected. Using open-source SimVascular software, preoperative and postoperative visceral aortic anatomy was manually segmented from computed tomography angiograms. Three-dimensional geometric models were then discretized into tetrahedral finite element meshes. Patient-specific pulsatile in-flow conditions were derived from known supraceliac aortic flow waveforms and adjusted for patient body surface area, average resting heart rate, and blood pressure. Outlet boundary conditions consisted of three-element Windkessel models approximated from physiologic flow splits. Rigid wall flow simulations were then performed on preoperative and postoperative models with the same inflow and outflow conditions. We used SimVascular's incompressible Navier-Stokes solver to perform blood flow simulations on a cluster using 72 cores. ResultsPreoperative and postoperative flow simulations were performed for 10 patients undergoing fEVAR with a total of 30 target vessels (20 renal stents, 10 mesenteric scallops). Postoperative models required a higher mean number of mesh elements to reach mesh convergence (3.2 ± 1.8 × 106 vs 2.6 ± 1.1 × 106; P = .005) with a longer mean computational time (10.3 ± 6.3 hours vs 7.8 ± 3.5 hours; P = .04) compared with preoperative models. fEVAR was associated with small but statistically significant increases in mean peak proximal aortic arterial pressure (140.3 ± 11.0 mm Hg vs 136.9 ± 8.7 mm Hg; P = .02) and peak renal artery pressure (131.6 ± 14.8 mm Hg vs 128.9 ± 11.8 mm Hg; P = .04) compared with preoperative simulations. No differences were observed in peak pressure in the celiac, superior mesenteric, or distal aortic arteries (P = .17-.96). When measuring blood flow, the only observed difference was an increase in peak renal flow rate after fEVAR (17.5 ± 3.8 mL/s vs 16.9 ± 3.5 mL/s; P = .04). fEVAR was not associated with changes in the mean pressure or the mean flow rate in the celiac, superior mesenteric, or renal arteries (P = .06-.98). Stenting of the renal arteries did not induce significant changes time-averaged wall shear stress in the proximal renal artery (23.4 ± 8.1 dynes/cm2 vs 23.2 ± 8.4 dynes/cm2; P = .98) or distal renal artery (32.7 ± 13.9 dynes/cm2 vs 29.6 ± 11.8 dynes/cm2; P = .23). In addition, computational visualization of cross-sectional velocity profiles revealed low flow disturbances associated with protrusion of renal graft fabric into the aortic lumen. ConclusionsIn a pilot study involving a selective cohort of patients who underwent uncomplicated fEVAR, patient-specific flow modelling was a feasible method for assessing the hemodynamic performance of various two-vessel fenestrated device configurations and revealed subtle differences in computationally derived peak branch pressure and blood flow rates. Structural changes in aortic flow geometry after fEVAR do not seem to affect computationally estimated renovisceral branch perfusion or wall shear stress adversely. Additional studies with invasive angiography or phase contrast magnetic resonance imaging are required to clinically validate these findings. (JVS–Vascular Science 2021;2:53-69.) Clinical RelevanceUsing a computational flow modelling for assessing the hemodynamic performance of fenestrated endovascular aneurysm repair (fEVAR), this real-world, patient-specific study included 10 participants and found that structural changes in aortic flow geometry after fEVAR did not seem to adversely impact estimated renal or visceral branch perfusion metrics (eg, peak and mean arterial pressure and flow rates) or wall shear stress. These findings overall support the ongoing clinical use of commercially available fEVAR devices for repair of juxtarenal aortic aneurysms, and provides a computational framework for future evaluation of fEVAR configurations in a preoperative or postoperative settings.

Differential Effects of Sound Intervention and Rest on Cardiovascular Parameters in Cancer Patients: A Randomized Cross-over Trial.

Background:Music therapy or sound interventions were shown to confer beneficial effects in patients with cancer for instance in terms of pain or fear relief and improvement of other patient reported outcomes. Cardiovascular parameters, especially heart rate variability (HRV) were found to have prognostic implications in cancer patients. In this trial we aimed to investigate the effects of a sound intervention on cardiovascular parameters compared to rest in patients with cancer.Methods and results:Using a randomized cross-over design, 52 patients (male 13, female 39) with cancer were recruited to receive both a 15-minute sound intervention and a 15-minute rest intervention within 4 weeks with at least a one-week blanking period. Cardiovascular parameters (among others HRV, aortic pulse wave velocity [PWV], augmentation index [Aix], aortic blood pressure [BP], heart rate [HR]) were assessed immediately before (pre) and after (post) the intervention had taken place. HRV (Root mean square of successive RR interval differences [RMSSD, ms]) significantly increased, during sound intervention (median RMSSD pre 24 [range 5-112] vs post 22 [range 9-141], P = .03). Likewise, median PWV, as a direct marker of arterial stiffness, was significantly reduced by sound intervention ([m/s] pre 8.5 [range 5.6-19.6] vs post 8.3 [range 5.6-15.6], P = .04). For both parameters no statistically significant change during rest was observed. HR was lowered by both, rest (P < .0001) and sound intervention (P = .02), with a more pronounced effect by rest. A significant increase in systolic aortic blood pressure was shown by rest ([mmHg] median 101 [range 78-150] vs post median 103 [range 71-152], P = .04) but not during sound intervention (P = .59), while rest intervention led to a decrease in resistance index (pre median 33 [range 13-92] vs post median 32 [11-84], P = .02).Conclusion:In comparison with rest, a single sound intervention in patients with cancer improved cardiovascular parameters commonly associated with increased stress levels. Studies with longer follow-up and multiple interventions are warranted.Trial Registration:ISRCTN registry 70947363.

Time-Resolved Echo-Particle Image/Tracking Velocimetry Measurement of Interactions Between Native Cardiac Output and Veno-Arterial ECMO Flows.

Determination of optimal hemodynamic and pressure-volume loading conditions for patients undergoing veno-arterial extracorporeal membrane oxygenation (VA-ECMO) would benefit from understanding the impact of ECMO flow rates (QE) on the native cardiac output in the admixing zone, i.e., aortic root. This study characterizes the flow in the aortic root of a pig with severe myocardial ischemia using contrast-enhanced ultrasound particle image/tracking velocimetry (echo-PIV/PTV). New methods for data preprocessing are introduced, including autocontouring to remove surrounding tissues, followed by blind deconvolution to identify the centers of elongated bubble traces in images with low signal to noise ratio. Calibrations based on synthetic images show that this procedure increases the number of detected bubbles and reduces the error in their locations by 50%. Then, an optimized echo-PIV/PTV procedure, which integrates image enhancement with velocity measurements, is used for characterizing the time-resolved two-dimensional (2D) velocity distributions. Phase-averaged and instantaneous flow fields show that the ECMO flow rate influences the velocity and acceleration of the cardiac output during systole, and secondary flows during diastole. When QE is 3.0 L/min or higher, the cardiac ejection velocity, phase interval with open aortic valve, velocity-time integral (VTI), and mean arterial pressure (MAP) increase with decreasing QE, all indicating sufficient support. For lower QE, the MAP and VTI decrease as QE is reduced, and the deceleration during transition to diastole becomes milder. Hence, for this specific case, the optimal ECMO flow rate is 3.0 L/min.

Acute effects of transcatheter aortic valve replacement on the ventricular-aortic interaction.

Transcatheter aortic valve replacement (TAVR) is increasingly used to treat severe aortic stenosis (AS) patients. However, little is known regarding the direct effect of TAVR on the ventricular-aortic interaction. In the present study, we aimed to investigate changes in central hemodynamics after successful TAVR. We retrospectively examined 33 cases of severe AS patients (84 ± 6 yr) who underwent TAVR. Invasive measurements of left ventricular and aortic pressures as well as echocardiographic aortic flow were acquired before and after TAVR (maximum within 5 days). We examined alterations in key features of central pressure and flow waveforms, including the aortic augmentation index (AIx), and performed wave separation analysis. Arterial parameters were determined via parameter-fitting on a two-element Windkessel model. Resolution of AS resulted in direct increase in the aortic systolic pressure and maximal aortic flow (131 ± 22 vs. 157 ± 25 mmHg and 237 ± 49 vs. 302 ± 69 mL/s, P < 0.001 for all), whereas the ejection duration decreased (P < 0.001). We noted a significant decrease in the AIx (from 42 ± 12 to 19 ± 11%, P < 0.001). Of note, the arterial properties remained unchanged. There was a comparable increase in both forward (61 ± 20 vs. 77 ± 20 mmHg, P < 0.001) and backward (35 ± 14 vs. 42 ± 10 mmHg, P = 0.013) pressure wave amplitudes, while their ratio, i.e., the reflection coefficient, was preserved. Our results highlight the impact of TAVR on the ventricular-aortic interaction by affecting the amplitude, shape, and related attributes of the aortic pressure and flow pulse and challenge the interpretation of AIx as a solely vascular measure in AS patients.NEW & NOTEWORTHY Transcatheter aortic valve replacement (TAVR) is linked with an immediate increase in aortic systolic blood pressure and maximal flow, as well as steeper aortic pressure and flow wave upstrokes. After TAVR, the forward wave pumped by the heart is enhanced. Although the arterial properties remain unchanged, the central augmentation index (AIx) is markedly decreased after TAVR. This challenges the interpretation of AIx as a solely vascular measure in patients with aortic valve stenosis.

Effect of Short-Term Cold Exposure on Central Aortic Blood Pressure in Patients with CKD

Objectives: Study determined effects of arterial hypertension and impaired kidney function on acute cold exposure induced changes in peripheral and central aortic blood pressure (BP). Methods: Five-six subjects were divided into 3 groups including 20 hypertensive patients with normal kidney function (AH-non-CKD), 20 patients with hypertension and CKD (AH-CKD) stage 3b–4 and 16 healthy normotensive subjects (C). Baseline BP, central BP, and central pulse pressure, unadjusted augmentation index (AI) and central augmented pressure were assessed by applanation tonometry (SphygmoCor) before entering the room with constant temperature −10°C (°C), after 10 min in the cold room and in same conditions in room temperature. Results: Cold exposure led to significant increase of central aortic, systolic, and diastolic BP in both AH-non-CKD (p < 0.01) and AH-CKD (p < 0.001). The central aortic BP did not change in healthy subjects. The increase of central aortic systolic blood pressure was significantly larger in AH-CKD compared to AH-non-CKD group (p = 0.0002). Increase of aortic central and brachial systolic and diastolic BP was significantly larger in AH-CKD and AH-non-CKD patients than in controls. AI increased and subendocardial viability ratio and heart rate decreased after cold exposure in all groups. Central aortic and brachial rate pressure product increased by approximately 2,300 bpm × mm Hg (p < 0.001) and 1,600 bpm × mm Hg (p < 0.001), respectively, in the AH-CKD group and by 1,000 bpm × mm Hg (p = 0.007) and 500 bpm × mm Hg (p = 0.19) in AH-non-CKD group after cold exposure. Conclusion: Short-term cold exposure induces larger increase of brachial and central aortic BP in patients with arterial hypertension than in healthy subjects. The changes in central aortic pressure are augmented in hypertensive patients with impaired kidney function.

The Influence of Non-Alc oholic Fatty Liver Disease on Indicators of Arterial Stiffness and Risk of Cardiovascular Complications in Patients with Arterial Hypertension

Aim. To determine the value of concomitant non-alcoholic fatty liver disease in patients with arterial hypertension in the progression of rigidity of the main arteries and in increase of risk of cardiovascular complications. Material and methods. A cross-sectional comparative study was conducted. Group 1 (n=50, 35(70%) women, average age 57,4±6,9 years) included patients with arterial hypertension and non-alcoholic fatty liver disease, group 2 (n=50, 40(80%) women, average age 56,5±7,0 years) included patients with arterial hypertension only. The groups were comparable in the main clinical and demographic indicators (p&gt;0,05). A comparative analysis of pulse wave velocity, central aortic pressure, vascular age and a 10-year risk of developing cardiovascular complications in both groups was performed.Results. There is a statistically larger number of patients with metabolic index&gt;7,0 (58,0% vs 28,0%, p=0,0019). It was also established that systolic (121,9±10,9 mm Hg vs 115,9±8,9 mm Hg) and diastolic (82,5±9,3 mm Hg vs 77,4±8,9 mm Hg) aortic pressure, as well as the augmentation index (26,5±8,5% vs 18,6±4,2%), were significantly higher in patients with arterial hypertension and non-alcoholic fatty liver disease than in patients with isolated arterial hypertension. In the 1st group, a statistically significant increased pulse wave velocity was found both in muscular (12,0±3,1 m/s vs 10,6±1,8 m/s) and elastic (10,4±2,8 m/s vs 9,1±1,7 m/s) vessels, which indicates an increase in arterial stiffness. In addition, there was an increase in post-occlusal pulse wave velocity in this category of patients (11,0±3,3 m/s vs 9,4±1,9 m/s, p=0,0037). A significant increase in vascular age in relation to the passport age (60,4 [56,0:68,0] years vs 58,0 [53,0:60,0] years) and an increase in the 10-year fatal risk was detected (2,15 [1,42: 4,63] and 1,05 [0,52: 2,82] %, p = 0,0043 ) were also revealed in patients with arterial hypertension and non-alcoholic fatty liver disease compared to patients with isolated arterial hypertension. Significantly more patients with a high (13 (26,0%) vs 5 (10,0%), p = 0,0332) total cardiovascular risk were observed in group 1 than in group 2.Conclusions. Arterial stiffness was significantly higher in patients with arterial hypertension and non-alcoholic fatty liver disease than in patients with isolated arterial hypertension, which is confirmed by a statistically significant increase in pulse wave velocity and central aortic pressure. Comorbid patients have pronounced endothelial dysfunction, which is confirmed by a significant increase in the post-occlusion rate of the pulse wave. An increase in vascular age in relation to the passport age indicates earlier aging of blood vessels in the 1st group compared with the 2nd group. Patients in the main group have a higher incidence of a high 10-year risk of developing cardiovascular events compared with patients in the control group.

Dynamic right and left ventricular interactions in the pig.

What is the central question of this study? Are the mechanisms that cause ventricular interdependence different when due to primary right to left ventricular pressure loading? What is the main finding and its importance? An instantaneous selective increase in aortic pressure causes an immediate increase in right ventricular end-systolic pressure independent of the pericardium, whereas a selective increase in pulmonary artery pressure decreases left ventricular diastolic compliance owing to a subsequent increasing right ventricular end-diastolic volume as a function of an intact pericardium limiting biventricular volume. Changes in contraction synchrony of either ventricle do not appear to be causing these effects. I characterized the dynamic factors determining ventricular interdependence with and without the pericardium. I measured right (RV) and left ventricular (LV) pressures and volumes simultaneously using conductance catheters in seven pentobarbitone-anaesthetized open-chested 5- to 7-week-old piglets. I studied these effects during apnoea, inferior vena caval occlusion and rapid partial aortic and pulmonary arterial occlusions. Conductance catheter-defined long-axis regional volumes were assessed to define regional contractile synchrony. Closed-pericardium measures were made from an initial (baseline) volume, then after two 20mlkg-1 fluid loads followed by an open-pericardium step. Baseline RV and LV volumes were similar. Aortic occlusion increased LV pressures and volumes and RV end-systolic pressure such that RV end-systolic elastance increased without changes in RV contraction synchrony, not affected by the pericardium. Pulmonary artery occlusion increased RV end-systolic pressure but not end-systolic volume. On the subsequent beat, RV end-diastolic pressure increased, whereas LV end-diastolic volume and diastolic compliance decreased. These effects were attenuated by opening the pericardium. Contraction synchrony across longitudinal segments was unaltered by either aortic or pulmonary artery occlusion. I conclude that the determinants of systolic and diastolic ventricular interdependence are different. Increasing RV pressures causes diastolic RV-to-LV interdependence, decreasing LV diastolic compliance and dependent on an intact pericardium. An increase in LV end-systolic pressure increases RV end-systolic elastance independent of the pericardium and has a minimal effect on RV diastolic function or contraction synchrony.

Patient-Specific Computational Flow Modelling for Assessing Hemodynamic Changes Following Fenestrated Endovascular Aneurysm Repair

Abstract Objective This study aimed to develop an accessible patient-specific computational flow modelling pipeline for evaluating the hemodynamic performance of fenestrated endovascular aneurysm repair (fEVAR), with the hypothesis that computational flow modelling can detect aortic branch hemodynamic changes associated with fEVAR graft implantation. Methods Patients who underwent fEVAR for juxtarenal aortic aneurysms with the Cook ZFEN were retrospectively selected. Using open-source SimVascular software, preoperative and postoperative visceral aortic anatomy was manually segmented from computed tomography angiograms. Three-dimensional geometric models were then discretized into tetrahedral finite element meshes. Patient-specific pulsatile in-flow conditions were derived from known supraceliac aortic flow waveforms and adjusted for patient body surface area, average resting heart rate, and blood pressure. Outlet boundary conditions consisted of three-element Windkessel models approximated from physiologic flow splits. Rigid wall flow simulations were then performed on preoperative and postoperative models with the same inflow and outflow conditions. We used SimVascular's incompressible Navier-Stokes solver to perform blood flow simulations on a cluster using 72 cores. Results Preoperative and postoperative flow simulations were performed for 10 patients undergoing fEVAR with a total of 30 target vessels (20 renal stents, 10 mesenteric scallops). Postoperative models required a higher mean number of mesh elements to reach mesh convergence (3.2 ± 1.8 × 106 vs 2.6 ± 1.1 × 106; P = .005) with a longer mean computational time (10.3 ± 6.3 hours vs 7.8 ± 3.5 hours; P = .04) compared with preoperative models. fEVAR was associated with small but statistically significant increases in mean peak proximal aortic arterial pressure (140.3 ± 11.0 mm Hg vs 136.9 ± 8.7 mm Hg; P = .02) and peak renal artery pressure (131.6 ± 14.8 mm Hg vs 128.9 ± 11.8 mm Hg; P = .04) compared with preoperative simulations. No differences were observed in peak pressure in the celiac, superior mesenteric, or distal aortic arteries (P = .17-.96). When measuring blood flow, the only observed difference was an increase in peak renal flow rate after fEVAR (17.5 ± 3.8 mL/s vs 16.9 ± 3.5 mL/s; P = .04). fEVAR was not associated with changes in the mean pressure or the mean flow rate in the celiac, superior mesenteric, or renal arteries (P = .06-.98). Stenting of the renal arteries did not induce significant changes time-averaged wall shear stress in the proximal renal artery (23.4 ± 8.1 dynes/cm2 vs 23.2 ± 8.4 dynes/cm2; P = .98) or distal renal artery (32.7 ± 13.9 dynes/cm2 vs 29.6 ± 11.8 dynes/cm2; P = .23). In addition, computational visualization of cross-sectional velocity profiles revealed low flow disturbances associated with protrusion of renal graft fabric into the aortic lumen. Conclusions In a pilot study involving a selective cohort of patients who underwent uncomplicated fEVAR, patient-specific flow modelling was a feasible method for assessing the hemodynamic performance of various two-vessel fenestrated device configurations and revealed subtle differences in computationally derived peak branch pressure and blood flow rates. Structural changes in aortic flow geometry after fEVAR do not seem to affect computationally estimated renovisceral branch perfusion or wall shear stress adversely. Additional studies with invasive angiography or phase contrast magnetic resonance imaging are required to clinically validate these findings. (JVS–Vascular Science 2021;▪:1-17.) Clinical Relevance Using a computational flow modelling for assessing the hemodynamic performance of fenestrated endovascular aneurysm repair (fEVAR), this real-world, patient-specific study included 10 participants and found that structural changes in aortic flow geometry after fEVAR did not seem to adversely impact estimated renal or visceral branch perfusion metrics (eg, peak and mean arterial pressure and flow rates) or wall shear stress. These findings overall support the ongoing clinical use of commercially available fEVAR devices for repair of juxtarenal aortic aneurysms, and provides a computational framework for future evaluation of fEVAR configurations in a preoperative or postoperative settings.

The COSEVAST Study Outcome: Evidence of COVID-19 Disease Severity Proportionate&amp;nbsp;To Surge in Arterial Stiffness

Background: Arterial stiffness has been established as an independent and specific marker of various chronic cardiovascular diseases. Based on the detailed review of available research and case studies reported in reputed international journals, it can be concluded that Endothelial Damage (Endotheliitis) both in small and large arteries may be an important factor of morbidity and mortality in COVID-19 patients. Despite the pathological evidence of structural damage due to Endotheliitis in COVID-19 patients, the functional deterioration of the vasculature was not yet studied.Hyper activated inflammation of the arteries may lead to sudden rise in arterial stiffness, the functional indicator of severity of cardiovascular impairment, which develops into Multiple Organ Dysfunction Syndrome (MODS) in COVID-19. Supervising and controlling the arterial Stiffness may be a way to mitigate the morbidities and mortalities caused due to COVID-19. Objective: Our primary objective was to study functional arterial damage in COVID-19 disease and establish the non-invasive measurement of Arterial Stiffness as an independent marker of disease severity.Methods: We recorded the Arterial Stiffness of 23 Mild, 21 Moderate and 20 Severe COVID-19 patients grouped on latest NIH severity criteria. Patients with pre-existing Diabetes and Hypertension were excluded. We observed Arterial Stiffness of COVID-19 patients with standard parameters like non-invasive Carotid-Femoral Pulse Wave velocity (cfPWV), Age-Normalized increase in cfPWV (ANI_cfPWV), Age-Normalized increase in Aortic Augmentation Pressure (ANI_AugP) and Heart rate-normalized Augmentation Index (HRN_ AIx).Results: Moderate and Severe COVID-19 patients have extremely significantly elevated arterial stiffness than Mild patients. In Mild patients, cfPWV (829.1 ± 139.2 cm/s) was significantly lower than both Moderate (1067 ± 152.5 cm/s, P Conclusion: This is the first study establishing the functional deterioration of vasculature in terms of abnormal increase in arterial stiffness in proportion with severity of COVID-19 disease. Our findings strongly suggest that arterial stiffness can be an independent and accurate marker for objective risk stratification and therapeutic alleviation of the acute cardiovascular complications like MODS in COVID-19.Trial Registration: The study design was registered with the Clinical Trials Registry of India (CTRI No. CTRI/2020/10/028489).Funding Statement: No external funding.Declaration of Interests: Authors declare no conflict of interest.Ethics Approval Statement: The study protocol, informed consents and other trial-related documents received the written approval of Institutional Ethics Committee (IEC No. AIIMS/Pat/IEC/2020/595).

P6514Head to head comparison of a pulsatile versus continuous flow left ventricular assist device in high-risk PCI setting: iVAC2L vs. Impella 2.5

Abstract Background To compare the hemodynamic and clinical performance between iVAC2L and Impella 2.5 in high-risk PCI. Patients and methods In 35 patients [8 female, age 75±8 years, left ventricular ejection fraction 45±12%] high-risk PCI was performed under Impella 2.5 (n=15) or IVAC2L (n=20) use. Aortic pressure and flow was collected before and after device placement and after PCI. Blood parameters of hemolysis were collected before and after PCI. Results Correct placement was achieved in 17 iVAC2L-patients and in 14 Impella-patients. PCI success was 97%. Support time was comparable between both groups. No early increase in aortic pressure occurred under full iVAC2L-support, but with prolonged support it increased significantly and kept higher level (Table 1). In contrast, aortic pressure increased significantly immediately under Impella, but the increase was comparable between the devices after PCI. Flow under Impella was significantly higher compared to iVAC2L (2.07±0.09l/min vs. 1.25±0.05l/min, p&lt;0.001). In five patients (iVAC2L n=3) critical events during PCI occurred, but both devices helped to stabilise hemodynamics. After PCI, one severe bleeding in each group and one stroke after iVAC2L occurred. Haptoglobin level after Impella showed signs of hemolysis (Table 1). Table 1 prePCI (no support) prePCI (full support) postPCI (full support) postPCI (no support) iVAC2L RRsyst Ao (mmHg, mean±SD) 123±29 125±21 142±28*§ 142±31# Impella 2.5 RRsyst Ao (mmHg, mean±SD) 137±23 148±29&amp;% 151±22 153±22% iVAC2L RRdiast Ao (mmHg, mean±SD) 57±16 59±14 68±18* 69±18# Impella 2.5 RRdiast Ao (mmHg, mean±SD) 60±12 76±15&amp;% 84±16* 76±17# iVAC2L RRmean Ao (mmHg, mean±SD) 81±17 83±16 97±21*§% 94±27# Impella 2.5 RRmean Ao (mmHg, mean±SD) 91±15 102±17&amp;% 109±16* 106±17# iVAC2L Haptoglobin (mg/l, mean±SD) 1485±689 1261±648 Impella 2.5 Haptoglobin (mg/l, mean±SD) 1456±570 894±371$ iVAC2L LDH (U/l, mean±SD) 240±90 241±68 Impella 2.5 LDH (U/l, mean±SD) 220±82 252±101 Ao = Aorta. *p&lt;0.05 prePCI (no support) vs. postPCI (full support); #p&lt;0.05 prePCI (no support) vs. postPCI (no support); §p&lt;0.05 prePCI (full support) vs. postPCI (full support); &amp;p&lt;0.05 prePCI (no support) vs. prePCI (full support); %p&lt;0.05 iVAC vs. Impella. Conclusion High-risk PCI under support of both devices is feasible and safe. Aortic pressure increases with both devices but earlier under Impella. Differences in outcome and hemodynamics between the 2 devices need to be evaluated in large multi-center studies.