Left Ventricular Interaction Research Articles

Assessment and diagnosis of right ventricular failure-retrospection and future directions.

The right ventricle (RV) has a critical role in hemodynamics and right ventricular failure (RVF) often leads to poor clinical outcome. Despite the clinical importance of RVF, its definition and recognition currently rely on patients' symptoms and signs, rather than on objective parameters from quantifying RV dimensions and function. A key challenge is the geometrical complexity of the RV, which often makes it difficult to assess RV function accurately. There are several assessment modalities currently utilized in the clinical settings. Each diagnostic investigation has both advantages and limitations according to its characteristics. The purpose of this review is to reflect on the current diagnostic tools, consider the potential technological advancements and propose how to improve the assessment of right ventricular failure. Advanced technique such as automatic evaluation with artificial intelligence and 3-dimensional assessment for the complex RV structure has a potential to improve RV assessment by increasing accuracy and reproducibility of the measurements. Further, noninvasive assessments for RV-pulmonary artery coupling and right and left ventricular interaction are also warranted to overcome the load-related limitations for the accurate evaluation of RV contractile function. Future studies to cross-validate the advanced technologies in various populations are required.

Venoarterial Extracorporeal Membrane Oxygenation.

Venoarterial Extracorporeal Membrane Oxygenation.

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.

Right and left ventricular interactions, strain, and remodeling in repaired pulmonary stenosis patients with preserved right ventricular ejection fraction: A cardiac magnetic resonance study.

Right ventricular dilation and dysfunction is a common long-term complication in patients with repaired pulmonary stenosis (rPS). Additionally, abnormal right and left ventricular interactions have been reported in right-sided heart defect after intervention, including in pulmonary stenosis. To analyze ventricular strain, remodeling, and left and right ventricular interactions in rPS patients with preserved right ventricular ejection fraction (RVEF) compared with healthy children using cardiac magnetic resonance. A cross-sectional study. In all, 34 rPS patients and 10 healthy children volunteers (controls). 3.0T/2D balanced steady-state free precession (2D b-SSFP) cine, late gadolinium enhancement (LGE), and 2D phase contrast (2D-PC). Pulmonary regurgitation (PR) fractions of the main pulmonary artery, biventricular volumes, masses, function, and cardiac strain. Mann-Whitney U-test, t-test, Pearson correlation coefficients, Spearman's correlation coefficients, and intraclass correlation coefficients analysis were performed. For group analysis, the right ventricular (RV) global circumferential strain and radial strain were significantly increased in patients when compared with controls (-13.57 ± 2.69 vs. -5.91 ± 3.16, P < 0.001; 25.31 ± 8.12 vs. 9.87 ± 5.32, P < 0.001, respectively). The fraction of PR displayed moderate correlation with right ventricular end-diastolic volume index (RVEDVi) (r = 0.452, P = 0.022). RVEDVi and mass index were larger in patients vs. control (104.92 ± 27.46 vs. 85.15 ± 11.98, P = 0.016; 18.28 ± 4.95g/m2 vs. 11.67 ± 2.14 g/m2 , P < 0.001, respectively). Patients presented with preserved left ventricular ejection function, but was lower than healthy controls (60.89% ± 4.89% vs. 65.95% ± 4.56%, P = 0.006). Regional circumferential strain of segment 3 of left ventricle (LV) were significantly decreased in patients (-7.79 ± 6.52 vs. -13.56 ± 3.22, P = 0.003). Compensated increased RV strain, myocardial remodeling of RV, and adverse right and left ventricular interactions occur in rPS patients with preserved RVEF. The decreased interventricular septum strain may lead to impaired LV function due to RV dilation as a result of PR. 3 Technical Efficacy Stage: 3 J. Magn. Reson. Imaging 2020;52:129-138.

Right and left ventricular interaction in pulmonary hypertension: Insight from velocity vector imaging.

To evaluate whether global peak systolic strain (PSS) and peak systolic strain rate (PSSR) derived from velocity vector imaging (VVI) allow early recognition of regional and global right ventricular (RV) dysfunction and the impact of this on left ventricular (LV) function in patients with pulmonary hypertension (PHT). RV function is an important determinant of prognosis in patients with heart failure, pulmonary hypertension, heart transplant, and congenital heart diseases. However, evaluation of the right ventricle is often limited by its complex geometry and inadequate visualization of RV free wall. Furthermore, the impact of RV dysfunction on the LV function is not well elucidated. Ninety-nine participants, 35 control patients with normal RV systolic pressure (RVSP) (<30mm Hg) and 64 patients with PHT (25 with mild-to-moderate increase in RVSP [≥36 and <60mm Hg] and 39 with severe increase in RVSP [≥60mm Hg]), underwent comprehensive echo-Doppler assessment and velocity vector imaging (VVI) for strain rate analysis. RV regional peak systolic and diastolic tangential velocity, strain, and strain rate were obtained from the basal, mid and apical segments of the RV free wall and interventricular septum (IVS) from apical 4-chamber view at end-expiration. Similar data were obtained from eighteen LV segments from apical 4-chamber, 2-chamber, and long-axis views. Peak systolic strain, strain rate, and tangential velocity at all segments in the RV free wall and IVS were decreased compared to controls in patients with PHT (P<0.001). Significant correlation (r>0.60; P<0.001) was noted between RVSP and systolic and diastolic strain and strain rate at basal segment in IVS and global RV function. Peak early diastolic strain rate at all segments was also decreased in PHT patients compared with control patients (P<0.01). Furthermore, RV systolic and diastolic strain and strain rate were lower in group 2 with mild-to-moderate hypertension while the conventional echo parameters were normal. Except for IVS segments, other LV segments had no statistical differences in systolic and diastolic velocity, strain, and strain rate compared to controls. However, they were lower than the published normal range. Strain and strain rate derived from VVI demonstrates early recognition of systolic and diastolic RV dysfunction in patients with PHT compared to controls. PHT is associated with global and regional RV systolic and diastolic dysfunction. Systolic and diastolic strain and strain rate from LV was lower compared to controls but were not statistically significant. This may indicate subclinical LV dysfunction in these patients, suggesting that conventional LV function parameters may not be sensitive to recognize subclinical LV dysfunction.

Temporal changes in interpapillary muscle dynamics as an active indicator of mitral valve and left ventricular interaction in ischemic mitral regurgitation.

Regional subpapillary myocardial hypokinesis may impair lateral reduction in the interpapillary muscle distance (IPMD) from diastole to systole, and adversely affect mitral valve geometry and tethering. The goal of this study was to investigate the impact of impaired lateral shortening in the interpapillary muscle distance on mitral valve geometry and function in ischemic heart disease. To quantify ventricular size/shape, regional myocardial contraction, lateral shortening of the IPMD, mitral valve geometry, and severity of mitral regurgitation, 67 patients with ischemic heart disease underwent cardiac magnetic resonance imaging, and a correlation analysis of measured parameters was performed. The impact of reduced IPMD shortening on mitral valve (dys)function was confirmed in swine and in a physiological computational mitral valve model. Lateral shortening of the IPMD from diastole to systole was severely reduced in patients with moderate/severe ischemic mitral regurgitation (9.6 ± 2.8 mm), but preserved in mild IMR (11.5 ± 3.4 mm). Left ventricular size and ejection fraction did not differ between the groups. In swine with subpapillary infarction and impaired IPMD, mitral regurgitation was evident within 1 week, compared to those pigs with a nonpapillary infarction and preserved IPMD. In the controlled computational valve model, IPMD had the maximal impact on regurgitation, and was exacerbated with additional annular dilation. By using cardiac magnetic resonance imaging in humans, we demonstrated that it is the impairment of lateral shortening between the papillary muscles, and not passive ventricular size, that governs the severity of mitral regurgitation. Loss of lateral shortening of IPMD tethers the leaflet edges and impairs their systolic closure, resulting in mitral regurgitation, even in small ventricles. Understanding the lateral dynamics of ventricular-valve interactions could aid the development of new repair techniques for ischemic mitral regurgitation.

Left ventricular rotation and right–left ventricular interaction in congenital heart disease: the acute effects of interventional closure of patent arterial ducts and atrial septal defects

Left ventricular rotation is physiologically affected by acute changes in preload. We investigated the acute effect of preload changes in chronically underloaded and overloaded left ventricles in children with shunt lesions. A total of 15 patients with atrial septal defects (Group A: 7.4 ± 4.7 years, 11 females) and 14 patients with patent arterial ducts (Group B: 2.7 ± 3.1 years, 10 females) were investigated using 2D speckle-tracking echocardiography before and after interventional catheterisation. The rotational parameters of the patient group were compared with those of 29 matched healthy children (Group C). Maximal torsion (A: 2.45 ± 0.9°/cm versus C: 1.8 ± 0.8°/cm, p < 0.05), apical peak systolic rotation (A: 12.6 ± 5.7° versus C: 8.7 ± 3.5°, p < 0.05), and the peak diastolic torsion rate (A: -147 ± 48°/second versus C: -110 ± 31°/second, p < 0.05) were elevated in Group A and dropped immediately to normal values after intervention (maximal torsion 1.5 ± 1.1°/cm, p < 0.05, apical peak systolic rotation 7.2 ± 4.1°, p < 0.05, and peak diastolic torsion rate -106 ± 35°/second, p < 0.05). Patients in Group B had decreased maximal torsion (B: 1.8 ± 1.1°/cm versus C: 3.8 ± 1.4°/cm, p < 0.05) and apical peak systolic rotation (B: 8.3 ± 6.1° versus C: 13.9 ± 4.3°, p < 0.05). Defect closure was followed by an increase in maximal torsion (B: 2.7 ± 1.4°/cm, p < 0.05) and the peak diastolic torsion rate (B: -133 ± 66°/second versus -176 ± 84°/second, p < 0.05). Patients with chronically underloaded left ventricles compensate with an enhanced apical peak systolic rotation, maximal torsion, and quicker diastolic untwisting to facilitate diastolic filling. In patients with left ventricular dilatation by volume overload, the peak systolic apical rotation and the maximal torsion are decreased. After normalisation of the preload, they immediately return to normal and diastolic untwisting rebounds. These mechanisms are important for understanding the remodelling processes.

Significance of force transfer in mitral valve–left ventricular interaction: In vivo assessment

The objective of this study was to assess the combined force transfer from the papillary muscle tips to the mitral valve through the chordae tendineae invivo, and thereby quantify the force transmitted through the papillary-chordal complex to augment left ventricular ejection. In an acute porcine model (n=8), force transfer between papillary muscles and the mitral valve was recorded on the anterior and posterior papillary muscle tip using dedicated force transducers. Ultrasound sonomicrometry was utilized to record and calculate left ventricular long-axis shortening and mitral annular geometry. The closing force acting on the mitral valve leaflets was calculated as mitral annular area multiplied by the transmitral pressure difference throughout systole. Mitral valve competence was verified before measurements with color Doppler ultrasound. Peak force in the anterior and posterior papillary muscle was 5.9 ± 0.6 N and 5.8 ± 0.7 N (mean ± standard error of the mean), respectively, and peak closing force was 6.8 ± 0.3 N all at a transmitral pressure of 90 mm Hg. Peak rate of left ventricular contraction coincided with peak papillary muscle force. This study is the first to assess the magnitude and time course of the longitudinal force transmitted through the papillary-chordal complex to the left ventricular wall during ejection. The study also demonstrates a significant force transfer to the closing force acting on the mitral valve leaflets that constitutes an essential component of valvular-ventricular interaction to enhance left ventricular systolic pump performance. The magnitude of the combined papillary muscle force component emphasizes the crucial role of preserving mitral valve-left ventricular continuity in mitral valve surgery.

Right ventricular–left ventricular interaction in adults with Tetralogy of Fallot: A combined cardiac magnetic resonance and echocardiographic speckle tracking study

Objectives To assess ventricular dysfunction and ventricular interaction after repair of Tetralogy of Fallot (ToF) employing echocardiography speckle-tracking and cardiac magnetic resonance imaging (CMR). Background Severe pulmonary regurgitation and right ventricular (RV) dysfunction are common after repair of ToF and may also affect the shape and function of the left ventricle (LV). Recent studies suggest that LV dysfunction may be of particular prognostic value. Methods and results Twenty-one consecutive adults with repaired ToF (15 male, mean age 38 ± 11 years, 7 with severe PR) underwent a comprehensive echocardiographic exam including speckle-tracking analysis, CMR and cardiopulmonary exercise testing. Twenty-one subjects without relevant heart disease served as controls. Echocardiographically measured RV diameters correlated with RV volumes obtained from CMR ( r = 0.63; p = 0.006). In addition, a close correlation was found between RV and LV function on CMR ( r = 0.74, p = 0.002), speckle-tracking LV and RV peak longitudinal 2D strain ( r = 0.66, p = 0.003) and mitral and tricuspid annular plain systolic excursion ( r = 0.71, p = 0.0003). While LV ejection fraction was normal in the majority of patients and not different from controls, LV longitudinal strain was significantly reduced in ToF patients (− 16.5 ± 3.3 vs. -20.5 ± 2.7%, p = 0.0001). Conclusion Left and right ventricular function both by CMR and speckle-tracking is interrelated in adults with repaired ToF. Despite normal LV ejection fraction, 2D longitudinal strain is significantly reduced in ToF patients, suggesting subclinical LV myocardial damage. Considering the potential prognostic value of LV dysfunction in ToF, this measurement may gain importance and should be included in future outcome studies.

44: Analysis of Implantable Left Ventricular Assist Device (LVAD) Acoustic Waveform by Fourier Transform and Empirical Mode Decomposition: Dependence on Rotation Speed, Device Design and Left Ventricular Interaction

44: Analysis of Implantable Left Ventricular Assist Device (LVAD) Acoustic Waveform by Fourier Transform and Empirical Mode Decomposition: Dependence on Rotation Speed, Device Design and Left Ventricular Interaction

16.47 Right and left ventricular interaction in chronic post-embolic pulmonary hypertension: a model for predicting the limits of normal left ventricular ejection fraction

16.47 Right and left ventricular interaction in chronic post-embolic pulmonary hypertension: a model for predicting the limits of normal left ventricular ejection fraction

A Closed-Loop Model of the Canine Cardiovascular System That Includes Ventricular Interaction

A closed-loop model of cardiopulmonary circulation has been developed for the study of right–left ventricular interaction under physiologically normal and altered conditions. The core model provides insight into the effects of ventricular interaction and pericardial mechanics on hemodynamics. The complete model contains realistic descriptions of (a) the interacting ventricular free walls and septum, (b) the atria, (c) the pericardium, and (d) the systemic and pulmonary vascular loads. The current analysis extends previous work on ventricular interaction and pericardial influence under isolated heart conditions to loading conditions imposed by a closed-loop model of the circulation. A nonlinear least-squares parameter identification method (Levenberg–Marquardt algorithm) is used, together with parameter sensitivity analysis, to estimate the values of key parameters associated with the ventricular and circulation models. Pressure measurements taken at several anatomical locations in the circulation during open-chest experiments on dogs are used as data in the identification process. The complete circulatory model, including septal and pericardial coupling, serves as a virtual testbed for assessing the global affects of localized mechanical or hemodynamic alterations. Studies of both direct and series ventricular interaction, as well as the effect of the pericardium on cardiac performance, are accomplished with this model. Alterations in model parameter values are used to predict the impact of disease and/or clinical interventions on steady-state hemodynamic performance. Additionally, a software package titled CardioPV has been developed to integrate the complete model with data acquisition tools and a sophisticated graphical user interface. The complete software package enables users to collect experimental data, use the data to estimate model parameters, and view the model outputs in an online setting.

Normal human right and left ventricular mass, systolic function, and gender differences by cine magnetic resonance imaging.

Our objective was to establish normal ranges of left and right ventricular mass and function with cine magnetic resonance imaging (MRI) and to determine gender differences. Seventy-five healthy subjects (age range 8-55, mean 28 yr) were studied with cine MRI. Ten dogs were imaged for autopsy validation with a mean difference between actual and MRI-determined mass of 0.2 A +/- 8.4 g. Intraobserver and interobserver variability and interstudy variability were 5-6%. All parameters were significantly different between males and females except ejection fraction and the left ventricular mass to end-diastolic volume ratio. Agreement with published autopsy series, including gender differences, was excellent. This study presents normative MRI data that can be used for comparing individual patients and for further study of right and left ventricular interaction.

Systolic ventricular interaction in normal and diseased explanted human hearts

Objective: The purpose of this study was to quantify the magnitude of interaction between the right and left ventricles in conditions of heart failure. Methods: Human hearts were taken from transplant recipients diagnosed with dilated cardiomyopathy at the time of transplantation and were restored to beating condition with use of an isolated perfusion circuit. Left ventricular–right ventricular interaction was determined by ramping volume in the left ventricle while holding right ventricular volume constant. Right ventricular pressure gain was plotted against left ventricular pressure and the slope of the linear regression determined the left ventricular–right ventricular interaction. A similar procedure was used to determine right ventricular–left ventricular interaction. Two normal hearts were obtained from transplant donors not suitable for cardiac donation to serve as control hearts. Results: Mean left ventricular–right ventricular interaction was 0.22 in the hearts with dilated cardiomyopathy compared with 0.06 in the control hearts. Mean right ventricular–left ventricular interaction was 0.14 in the hearts with dilated cardiomyopathy compared with 0.09 in the control hearts. A marked increase in left ventricular–right ventricular interaction was noted in the hearts with dilated cardiomyopathy compared with control hearts. Although observed values of right ventricular–left ventricular interaction also correspond to previously published results, no significant increase was observed in the dilated cardiomyopathy condition. Conclusions: These studies confirm previously published values for systolic ventricular interaction obtained with animal models and demonstrate a marked increase in the dependence of the right ventricle on left ventricular function to maintain systolic pressure generation during conditions of dilated cardiomyopathy. (J Thorac Cardiovasc Surg 1997;113:1091-9)

Comparative significance in systolic ventricular interaction

The aim was to measure the systolic coupling between the ventricles and to determine the relative importance of ventricular interaction in the pressure development of each ventricle. Acute studies were done in dogs to measure the changes in right and left ventricular pressures (dPr, dPl) caused by sudden changes in left ventricular pressure (dPl') with release of an aortic constriction, and sudden changes in right ventricular pressure (dPr') with release of a pulmonary artery constriction, respectively. The instantaneous cross talk gain [dPr/dPl' (Klr) or dPl/dPr' (Krl)] was calculated during the ejection phase. The potential systolic pressure generated by the contralateral ventricle was evaluated as the cross talk gain multiplied by the contralateral systolic developed pressure. Studies were done in eight random source dogs (12-18 kg), anaesthetised with sodium pentobarbitone. The maximal Klr was lower than the maximal Krl, at 0.09 (SD 0.05) v 0.25 (0.06), and the mean Klr also was lower than the mean Krl, at 0.04 (0.02) v 0.10 (0.03), p less than 0.05. The potential right ventricular pressures developed by the left ventricle [maximum 10.3(5.6), mean 4.8(2.7) mm Hg] were not significantly different from the potential left ventricular pressures developed by the right ventricle [maximum 8.8(2.7), mean 3.4(0.7) mm Hg]. However, the ratio between the potential transmitted pressure and the measured developed pressure was greater in the right ventricle [maximum 39.0(21.1), mean 17.8(8.9)%] than in the left ventricle [maximum 11.1(7.1)%, p less than 0.05; mean 3.9(1.5)%, p less than 0.01]. This suggests that about 20-40% of the right ventricular systolic pressure may result from the left ventricle and about 4-10% of the left ventricular systolic pressure may result from right ventricle. Although the pressure coupling was greater in right to left ventricular interaction, right ventricular pressure generation may be more dependent on the left ventricle. Systolic ventricular interaction may be more important for right ventricular systolic function. Further, the parameters of right ventricular systolic function currently used may be considerably affected by the left ventricle.

Cardiodynamic effects of experimental right bundle branch block in canine hearts with normal and hypertrophied right ventricles

Cardiodynamic effects of acute experimental right bundle branch block (RBBB) were studied in canine hearts: group A included 15 normal hearts; group B-1 had seven hearts with mild right ventricular hypertrophy (RVH), and group B-2 had 11 hearts with marked RVH. The main sequential changes following RBBB were marked prolongation of the Q upstroke interval of the right ventricle and striking shortening of right ventricular systolic time that affected right and left ventricular interaction, particularly in the hearts with RVH. Hemodynamic changes were: the right ventricular end-diastolic pressure was elevated markedly (4.4 ± 2.2 → 9.8 ± 2.6 mm Hg, p < 0.001) in group B-2, moderately ( p < 0.01) in group B-1, and not at all in group A. The right ventricular positive peak dp dt decreased remarkably (1036 ± 151 → 827 ± 152 mm Hg/sec, p < 0.001) in group B-2 and negligibly in the other groups. A significant correlation existed between the percentage of decrease in right ventricular peak dp dt and the QRS duration of RBBB in each group ( p < 0.01). The left ventricular peak negative dp dt decreased distinctly (2570 ± 326 → ± 2055 ± 362 mm Hg/sec, p < 0.01) in group B-2 and not at all in the other groups. The atroke volume showed 12% decrease in group B-2 ( p < 0.001), 8% decrease in group B-1 (NS), and no decrease in group A. In the presence of RVH, acute RBBB causes significant impairment of right and left ventricular function. The magnitude of the impairment invariably depends upon both the prior degree of RVH and the width of the QRS complex.

Left ventricular interaction with arterial load studied in isolated canine ventricle.

We developed a framework of analysis to predict the stroke volume (SV) resulting from the complex mechanical interaction between the ventricle and its arterial system. In this analysis, we characterized both the left ventricle and the arterial system by their end systolic pressure (Ps)-SV relationships and predicted SV from the intersection of the two relationship lines. The final output of the analysis was a formula that gives the SV for a given preload as a function of the ventricular properties (Ees, V0, and ejection time) and the arterial impedance properties (modeled in terms of a 3-element Windkessel). To test the validity of this framework for analyzing the ventriculoarterial interaction, we first determined the ventricular properties under a specific set of control arterial impedance conditions. With the ventricular properties thus obtained, we used the analytical formula to predict SVs under various combinations of noncontrol arterial impedance conditions and four preloads. The predicted SVs were compared with those measured while actually imposing the identical set of arterial impedance conditions and preload in eight isolated canine ventricles. The predicted SV was highly correlated (P less than 0.0001) with the measured one in all ventricles. The average correlation coefficient was 0.985 +/- 0.004 (SE), the slope 1.00 +/- 0.04, and the gamma-axis intercept 1.0 +/- 0.2 ml, indicating the accuracy of the prediction. We conclude that the representations of ventricle and arterial system by their Ps-SV relationships are useful in understanding how these two systems determine SV when they are coupled and interact.

Dependence of ventricular distensibility on filling of the opposite ventricle.

Dependence of ventricular distensibility on filling of the opposite ventricle.