The effect of left ventricular contractility on arterial hemodynamics: A model-based investigation.
Ontology highlight
ABSTRACT:
SUBMITTER: Pagoulatou S
PROVIDER: S-EPMC8328319 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:To evaluate the relationships of right ventricular (RV) and left ventricular (LV) myocardial perfusion reserves with ventricular function and pulmonary hemodynamics in patients with pulmonary arterial hypertension (PAH) by using adenosine stress perfusion cardiac magnetic resonance (MR) imaging.This HIPAA-compliant study was institutional review board approved. Twenty-five patients known or suspected to have PAH underwent right heart catheterization and adenosine stress MR imaging on the same day. Sixteen matched healthy control subjects underwent cardiac MR imaging only. RV and LV perfusion values at rest and at adenosine-induced stress were calculated by using the Fermi function model. The MR imaging-derived RV and LV functional data were calculated by using dedicated software. Statistical testing included Kruskal-Wallis tests for continuous data, Spearman rank correlation tests, and multiple linear regression analyses.Seventeen of the 25 patients had PAH: 11 with scleroderma-associated PAH, and six with idiopathic PAH. The remaining eight patients had scleroderma without PAH. The myocardial perfusion reserve indexes (MPRIs) in the PAH group (median RV MPRI, 1.7 [25th-75th percentile range, 1.3-2.0]; median LV MPRI, 1.8 [25th-75th percentile range, 1.6-2.1]) were significantly lower than those in the scleroderma non-PAH (median RV MPRI, 2.5 [25th-75th percentile range, 1.8-3.9] [P = .03]; median LV MPRI, 4.1 [25th-75th percentile range, 2.6-4.8] [P = .0003]) and control (median RV MPRI, 2.9 [25th-75th percentile range, 2.6-3.6] [P < .01]; median LV MPRI, 3.6 [25th-75th percentile range, 2.7-4.1] [P < .01]) groups. There were significant correlations between biventricular MPRI and both mean pulmonary arterial pressure (mPAP) (RV MPRI: ρ = -0.59, Bonferroni P = .036; LV MPRI: ρ = -0.79, Bonferroni P < .002) and RV stroke work index (RV MPRI: ρ = -0.63, Bonferroni P = .01; LV MPRI: ρ = -0.75, Bonferroni P < .002). In linear regression analysis, mPAP and RV ejection fraction were independent predictors of RV MPRI. mPAP was an independent predictor of LV MPRI.Biventricular vasoreactivity is significantly reduced with PAH and inversely correlated with RV workload and ejection fraction, suggesting that reduced myocardial perfusion reserve may contribute to RV dysfunction in patients with PAH.
| S-EPMC3009386 | biostudies-other
Project description:Key pointsThe strength, functional significance and origins of parasympathetic innervation of the left ventricle remain controversial. This study tested the hypothesis that parasympathetic control of left ventricular contractility is provided by vagal preganglionic neurones of the dorsal motor nucleus (DVMN). Under ?-adrenoceptor blockade combined with spinal cord (C1) transection (to remove sympathetic influences), systemic administration of atropine increased left ventricular contractility in rats anaesthetized with urethane, confirming the existence of a tonic inhibitory muscarinic influence on cardiac inotropy. Increased left ventricular contractility in anaesthetized rats was observed when DVMN neurones were silenced. Functional neuroanatomical mapping revealed that vagal preganglionic neurones that have an impact on left ventricular contractility are located in the caudal region of the left DVMN. These neurones provide functionally significant parasympathetic control of left ventricular inotropy.AbstractThe strength, functional significance and origins of direct parasympathetic innervation of the left ventricle (LV) remain controversial. In the present study we used an anaesthetized rat model to first confirm the presence of tonic inhibitory vagal influence on LV inotropy. Using genetic neuronal targeting and functional neuroanatomical mapping we tested the hypothesis that parasympathetic control of LV contractility is provided by vagal preganglionic neurones located in the dorsal motor nucleus (DVMN). It was found that under systemic ?-adrenoceptor blockade (atenolol) combined with spinal cord (C1) transection (to remove sympathetic influences), intravenous administration of atropine increases LV contractility in rats anaesthetized with urethane, but not in animals anaesthetized with pentobarbital. Increased LV contractility in rats anaesthetized with urethane was also observed when DVMN neurones targeted bilaterally to express an inhibitory Drosophila allatostatin receptor were silenced by application of an insect peptide allatostatin. Microinjections of glutamate and muscimol to activate or inhibit neuronal cell bodies in distinct locations along the rostro-caudal extent of the left and right DVMN revealed that vagal preganglionic neurones, which have an impact on LV contractility, are located in the caudal region of the left DVMN. Changes in LV contractility were only observed when this subpopulation of DVMN neurones was activated or inhibited. These data confirm the existence of a tonic inhibitory muscarinic influence on LV contractility. Activity of a subpopulation of DVMN neurones provides functionally significant parasympathetic control of LV contractile function.
| S-EPMC4945717 | biostudies-literature
Project description:Pulmonary arterial hypertension (PAH) is a complex disease involving increased resistance in the pulmonary arteries and subsequent right ventricular (RV) remodeling. Ventricular-arterial interactions are fundamental to PAH pathophysiology but are rarely captured in computational models. It is important to identify metrics that capture and quantify these interactions to inform our understanding of this disease as well as potentially facilitate patient stratification. Towards this end, we developed and calibrated two multi-scale high-resolution closed-loop computational models using open-source software: a high-resolution arterial model implemented using CRIMSON, and a high-resolution ventricular model implemented using FEniCS. Models were constructed with clinical data including non-invasive imaging and invasive hemodynamic measurements from a cohort of pediatric PAH patients. A contribution of this work is the discussion of inconsistencies in anatomical and hemodynamic data routinely acquired in PAH patients. We proposed and implemented strategies to mitigate these inconsistencies, and subsequently use this data to inform and calibrate computational models of the ventricles and large arteries. Computational models based on adjusted clinical data were calibrated until the simulated results for the high-resolution arterial models matched within 10% of adjusted data consisting of pressure and flow, whereas the high-resolution ventricular models were calibrated until simulation results matched adjusted data of volume and pressure waveforms within 10%. A statistical analysis was performed to correlate numerous data-derived and model-derived metrics with clinically assessed disease severity. Several model-derived metrics were strongly correlated with clinically assessed disease severity, suggesting that computational models may aid in assessing PAH severity.
| S-EPMC9490558 | biostudies-literature
Project description:BackgroundCardiac CT (CCT) is well suited for a detailed analysis of heart structures due to its high spatial resolution, but in contrast to MRI and echocardiography, CCT does not allow an assessment of intracardiac flow. Computational fluid dynamics (CFD) can complement this shortcoming. It enables the computation of hemodynamics at a high spatio-temporal resolution based on medical images. The aim of this proposed study is to establish a CCT-based CFD methodology for the analysis of left ventricle (LV) hemodynamics and to assess the usability of the computational framework for clinical practice.Materials and methodsThe methodology is demonstrated by means of four cases selected from a cohort of 125 multiphase CCT examinations of heart failure patients. These cases represent subcohorts of patients with and without LV aneurysm and with severe and no mitral regurgitation (MR). All selected LVs are dilated and characterized by a reduced ejection fraction (EF). End-diastolic and end-systolic image data was used to reconstruct LV geometries with 2D valves as well as the ventricular movement. The intraventricular hemodynamics were computed with a prescribed-motion CFD approach and evaluated in terms of large-scale flow patterns, energetic behavior, and intraventricular washout.ResultsIn the MR patients, a disrupted E-wave jet, a fragmentary diastolic vortex formation and an increased specific energy dissipation in systole are observed. In all cases, regions with an impaired washout are visible. The results furthermore indicate that considering several cycles might provide a more detailed view of the washout process. The pre-processing times and computational expenses are in reach of clinical feasibility.ConclusionThe proposed CCT-based CFD method allows to compute patient-specific intraventricular hemodynamics and thus complements the informative value of CCT. The method can be applied to any CCT data of common quality and represents a fair balance between model accuracy and overall expenses. With further model enhancements, the computational framework has the potential to be embedded in clinical routine workflows, to support clinical decision making and treatment planning.
| S-EPMC8980692 | biostudies-literature
Project description:BACKGROUND:Continuous-flow left ventricular assist devices (LVADs) improve the hemodynamics of patients with advanced heart failure. However, the longitudinal trajectories of hemodynamics in patients after LVAD implantation remain unknown. The aim of this study was to investigate the trends of hemodynamic parameters following LVAD implantation. METHODS AND RESULTS:We retrospectively reviewed patients who underwent LVAD implantation between April 2014 and August 2018. We collected hemodynamic parameters from right heart catheterizations. Of 199 consecutive patients, we enrolled 150 patients who had both pre- and postimplant right heart catheterizations. They had 3 (2, 4) postimplant right heart catheterizations during a follow-up of 2.3 (1.3, 3.1) years. The mean age was 57 ± 13 years, and 102 patients (68%) were male. Following LVAD implantation, pulmonary arterial pressure and pulmonary capillary wedge pressure decreased, and cardiac index increased significantly, then remained unchanged throughout follow-up. Right atrial pressure decreased initially and then gradually increased to preimplant values. The pulmonary artery pulsatility index decreased initially and returned to preimplant values, then progressively decreased over longer follow-up. Subgroup analysis showed significant differences in the trajectories of the pulmonary artery pulsatility index based on gender. CONCLUSIONS:Despite improvement in left-side filling pressures and cardiac index following LVAD implantation, right atrial pressure increased and the pulmonary artery pulsatility index decreased over time, suggesting progressive right ventricular dysfunction.
| S-EPMC7259826 | biostudies-literature
Project description:Heart failure is a global epidemic. Left ventricular assist devices provide added cardiac output for severe cases but cause infection and thromboembolism. Proposed direct cardiac compression devices eliminate blood contacting surfaces, but no group has optimized the balance between hemodynamic benefit and excessive ventricular wall strains and stresses. Here, we use left ventricular simulations to apply compressions and analyze hemodynamics as well as regional wall mechanics. This axisymmetric model corresponds with current symmetric bench prototypes. At nominal pressures of 3.1 kPa applied over the epicardial compression zone, hemodynamics improved substantially. Ejection fraction changed from 17.6% at baseline to 30.3% with compression and stroke work nearly doubled. Parametric studies were conducted by increasing and decreasing applied pressures; ejection fraction, peak pressure, and stroke work increased linearly with changes in applied compression. End-systolic volume decreased substantially. Regional mechanics analysis showed principal stress increases at the endocardium, in the middle of the compression region. Principal strains remained unchanged or increased moderately with nominal compression. However, at maximum applied compression, stresses and strains increased substantially providing potential constraints on allowable compressions. These results demonstrate a framework for analysis and optimization of cardiac compression as a prelude to biventricular simulations and subsequent animal experiments.
| S-EPMC6822737 | biostudies-literature
Project description:BackgroundCardiac resynchronization therapy (CRT) with biventricular epicardial (BV-CS) or endocardial left ventricular (LV) stimulation (BV-EN) improves LV hemodynamics. The effect of CRT on right ventricular function is less clear, particularly for BV-EN. Our objective was to compare the simultaneous acute hemodynamic response (AHR) of the right and left ventricles (RV and LV) with BV-CS and BV-EN in order to determine the optimal mode of CRT delivery.MethodsNine patients with previously implanted CRT devices successfully underwent a temporary pacing study. Pressure wires measured the simultaneous AHR in both ventricles during different pacing protocols. Conventional epicardial CRT was delivered in LV-only (LV-CS) and BV-CS configurations and compared with BV-EN pacing in multiple locations using a roving decapolar catheter.ResultsBest BV-EN (optimal AHR of all LV endocardial pacing sites) produced a significantly greater RV AHR compared with LV-CS and BV-CS pacing (P < 0.05). RV AHR had a significantly increased standard deviation compared to LV AHR (P < 0.05) with a weak correlation between RV and LV AHR (Spearman rs = -0.06). Compromised biventricular optimization, whereby RV AHR was increased at the expense of a smaller decrease in LV AHR, was achieved in 56% of cases, all with BV-EN pacing.ConclusionsBV-EN pacing produces significant increases in both LV and RV AHR, above that achievable with conventional epicardial pacing. RV AHR cannot be used as a surrogate for optimizing LV AHR; however, compromised biventricular optimization is possible. The beneficial effect of endocardial LV pacing on RV function may have important clinical benefits beyond conventional CRT.
| S-EPMC4913734 | biostudies-literature
Project description:Intermittent hypoxia (IH) commonly occurs in patients with obstructive sleep apnea and can cause a wide range of pathology, including reduced left ventricular (LV) ejection fraction in rats as determined by echocardiography, in rodent models. We utilized echocardiography and pressure-volume (PV) loop analyses to determine whether LV contractility was decreased in inbred C57BL/6J mice exposed to IH and whether blockade of beta-adrenergic receptors modified the response to hypoxia. Adult male 9- to 10-wk-old mice were exposed to 4 wk of IH (nadir inspired O(2) 5-6% at 60 cycles/h for 12 h during the light period) or intermittent air (IA) as control. A second group of animals were exposed to the same regimen of IH or IA, but in the presence of nonspecific beta-blockade with propranolol. Cardiac function was assessed by echocardiography and PV loop analyses, and mRNA and protein expression in ventricular homogenates was determined. Contrary to our expectations, we found with PV loop analyses that LV ejection fraction (63.4 +/- 3.5 vs. 50.5 +/- 2.6%, P = 0.015) and other measures of LV contractility were increased in IH-exposed animals compared with IA controls. There were no changes in contractile proteins, atrial natriuretic peptide levels, LV posterior wall thickness, or heart weight with IH exposure. However, cAMP levels were elevated after IH, and propranolol administration attenuated the increase in LV contractility induced by IH exposure. We conclude that, contrary to our hypothesis, 4 wk of IH exposure in C57BL/6J mice causes an increase in LV contractility that occurs independent of ventricular hypertrophy and is, in part, mediated by activation of cardiac beta-adrenergic pathways.
| S-EPMC2756000 | biostudies-literature
Project description:BackgroundThe assessment of hemodynamics in patients supported with left ventricular assist devices (LVADs) is often challenging. Physical examination maneuvers correlate poorly with true hemodynamics. We assessed the value of novel transthoracic echocardiography (TTE)-derived variables to reliably predict hemodynamics in patients supported with LVAD.Methods and resultsA total of 102 Doppler-TTE images of the LVAD outflow cannula were obtained during simultaneous invasive right heart catheterization (RHC) in 30 patients supported with continuous-flow LVADs (22 HMII, 8 HVAD) either during routine RHC or during invasive ramp testing. Properties of the Doppler signal though the outflow cannula were measured at each ramp stage (RS), including the systolic slope (SS), diastolic slope (DS), and velocity time integral (VTI). Hemodynamic variables were concurrently recorded, including Doppler opening pressure (MAP), heart rate (HR), right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure (PCWP), Fick cardiac output (CO) and systemic vascular resistance (SVR). Univariate and multivariate regression analyses were used to explore the dependence of PCWP, CO, and SVR on DS, SS, VTI, MAP, HR, and RS. Multivariate linear regression analysis revealed significant contributions of DS on PCWP (PCWPpred = 0.164DS + 4.959; R = 0.68). Receiver operating characteristic (ROC) curve analysis revealed that PCWPpred could predict an elevated PCWP ≥18 mm Hg with a sensitivity (Sn) of 94% and specificity (Sp) of 85% (area under the ROC curve 0.88). CO could be predicted by RS, VTI, and HR (COpred = 0.017VTI + 0.016HR + 0.12RS + 2.042; R = 0.61). COpred could predict CO ≤4.5 L/min with Sn 73% and Sp 79% (AUC 0.81). SVR could be predicted by MAP, VTI, and HR (SVRpred = 15.44MAP - 5.453VTI - 6.349HR + 856.15; R = 0.84) with Sn 84% and Sp 79% (AUC 0.91) to predict SVR ≥1200 dyn-s/cm5.ConclusionsDoppler-TTE variables derived from the LVAD outflow cannula can reliably predict PCWP, CO, and SVR in patients supported with LVADs and may mitigate the need for invasive testing.
| S-EPMC6252054 | biostudies-literature
Project description:Through ventricular interdependence, pulmonary hypertension (PH) induces left ventricular (LV) dysfunction. We hypothesized that LV strain/strain rate, surrogate measures of myocardial contractility, are reduced in pediatric PH and relate to invasive hemodynamics, right ventricular strain, and functional measures of PH. At 2 institutions, echocardiography was prospectively performed in 54 pediatric PH patients during cardiac catheterization, and in 54 matched controls. Patients with PH had reduced LV global longitudinal strain (LS; -18.8 [-17.3 to -20.4]% versus -20.2 [-19.0 to -20.9]%; P=0.0046) predominantly because of reduced basal (-12.9 [-10.8 to -16.3]% versus -17.9 [-14.5 to -20.7]%; P<0.0001) and mid (-17.5 [-15.5 to -19.0]% versus -21.1 [-19.1 to -23.0]%; P<0.0001) septal strain. Basal global circumferential strain was reduced (-18.7 [-15.7 to -22.1]% versus -20.6 [-19.0 to -22.5]%; P=0.0098), as were septal and free-wall segments. Mid circumferential strain was reduced within the free-wall. Strain rates were reduced in similar patterns. Basal septum LS, the combined average LS of basal and mid interventricular septal segments, correlated strongly with degree of PH (r=0.66; P<0.0001), pulmonary vascular resistance (r=0.60; P<0.0001), and right ventricular free-wall LS (r=0.64; P<0.0001). Brain natriuretic peptide levels correlated moderately with septal LS (r=0.48; P=0.0038). PH functional class correlated moderately with LV free-wall LS (r=-0.48; P=0.0051). The septum, shared between ventricles and affected by septal shift, was the most affected LV region in PH. Pediatric PH patients demonstrate reduced LV strain/strain rate, predominantly within the septum, with relationships to invasive hemodynamics, right ventricular strain, and functional PH measures.
| S-EPMC4535191 | biostudies-literature