An in silico study of the effects of left ventricular assist device on right ventricular function and inter-ventricular interaction.

BACKGROUND: Left ventricular assist device (LVAD) is associated with a high incidence of right ventricular (RV) failure, which is hypothesized to be caused by the occurring inter-ventricular interactions when the LV is unloaded. Factors contributing to these interactions are unknown. METHODS: We used computer modeling to investigate the impact of the HeartMate 3 LVAD on RV functions. The model was first calibrated against pressure-volume (PV) loops associated with a heart failure (HF) patient and validated against measurements of inter-ventricular interactions in animal experiments. The model was then applied to investigate the effects of LVAD on (1) RV chamber contractility indexed by V 60 derived from its end-systolic PV relationship, and (2) RV diastolic function indexed by V 20 derived from its end-diastolic PV relationship. We also investigated how septal wall thickness and regional contractility affect the impact of LVAD on RV function. RESULTS: The impact of LVAD on RV chamber contractility is small at a pump speed lower than 4k rpm. At a higher pump speed between 4k and 9k rpm, however, RV chamber contractility is reduced (by ~3% at 6k rpm and ~10% at 9k rpm). The reduction of RV chamber contractility is greater with a thinner septal wall or with a lower myocardial contractility at the LV free wall, septum, or RV free wall. CONCLUSION: RV chamber contractility is reduced at a pump speed higher than 4k rpm, and this reduction is greater with a thinner septal wall or lower regional myocardial contractility. Findings here may have clinical implications in identifying LVAD patients who may suffer from RV failure.

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

BACKGROUND: 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. PURPOSE: 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. STUDY TYPE: A cross-sectional study. POPULATION: In all, 34 rPS patients and 10 healthy children volunteers (controls). FIELD STRENGTH/SEQUENCE: 3.0T/2D balanced steady-state free precession (2D b-SSFP) cine, late gadolinium enhancement (LGE), and 2D phase contrast (2D-PC). ASSESSMENT: Pulmonary regurgitation (PR) fractions of the main pulmonary artery, biventricular volumes, masses, function, and cardiac strain. STATISTICAL TESTS: Mann-Whitney U-test, t-test, Pearson correlation coefficients, Spearman's correlation coefficients, and intraclass correlation coefficients analysis were performed. RESULTS: 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). DATA CONCLUSION: 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. LEVEL OF EVIDENCE: 3 Technical Efficacy Stage: 3 J. Magn. Reson. Imaging 2020;52:129-138.

Neo-aortic Root Dilatation, Aortic Stiffness, and Ventricular interactions in Long-Term Follow-Up After the Ross Procedure in Childhood.

Patients after the Ross procedure are at risk for right (RV) and left ventricular (LV) dysfunction due to neo-aortic and pulmonary dysfunction. While neo-aortic root dilatation has been related to LV dysfunction, the potential contributions of aortic stiffness and ventricular interactions have not been evaluated. Patients status post Ross procedure up to age 18 years with cardiac magnetic resonance (CMR) exam from 2007 to 2018 were retrospectively reviewed. Aortic pulse wave velocity (PWV) was calculated from phase contrast and angiogram images. RV and LV peak global longitudinal (GLS) and circumferential strain (GCS) were measured using tissue tracking software. Multivariable regression was performed for variables associated with parameters of LV function. In 58 patients (median age 20.5 years at CMR exam), male gender, longer time since Ross procedure, aortic root dilatation, and lower RV ejection fraction (EF) were associated with decreased LV EF. There was no association with LV late gadolinium enhancement or neo-aortic or conduit regurgitation. LV GCS and GLS also correlated with RV GCS, RV GLS and PWV. In multivariable analysis, the relation of RV and LV systolic function, but not aortic measurements, remained significant. In conclusion, in long-term follow-up after pediatric Ross procedure, RV function rather than aortic root size or aortic stiffness most closely relates to LV function. Ventricular interactions may impact decision-making on timing of conduit intervention, which could differ from established criteria in populations with only aortic or pulmonary valve disease. Further study is warranted to evaluate possible association with clinical outcome.

Splitting the anterior mitral leaflet impairs left ventricular function in an ovine model.

OBJECTIVES: During mitral valve replacement, the anterior mitral leaflet is usually resected or modified. Anterior leaflet splitting seems the least disruptive modification. Reattachment of the modified leaflet to the annulus reduces the annulopapillary distance. The goal of this study was to quantify the acute effects on left ventricular function of splitting the anterior mitral leaflet and shortening the annulopapillary distance. METHODS: In 6 adult sheep, a wire was placed around the anterior leaflet and exteriorized through the left ventricular wall to enable splitting the leaflet in the beating heart. Releasable snares to reduce annulopapillary distance were likewise positioned and exteriorized. A mechanical mitral prosthesis was inserted to prevent mitral incompetence during external manipulations of the native valve. Instantaneous changes in left ventricular function were recorded before and after shortening the annulopapillary distance, then before and after splitting the anterior leaflet. RESULTS: After splitting the anterior leaflet, preload recruitable stroke work, stroke work, stroke volume, cardiac output, left ventricular end systolic pressure and mean pressure were significantly decreased by 26%, 23%, 12%, 9%, 15% and 11%, respectively. Shortening the annulopapillary distance was associated with significant decreases in the end systolic pressure volume relationship, preload recruitable stroke work, stroke work and left ventricular end systolic pressure by 67%, 33%, 15% and 13%, respectively. Shortening the annulopapillary distance after splitting the leaflet had no significant effect. CONCLUSIONS: Splitting the anterior mitral leaflet acutely impaired left ventricular contractility and haemodynamics in an ovine model. Shortening the annulopapillary distance after leaflet splitting did not further impair left ventricular function.

Incorporating the anterior mitral leaflet to the annulus impairs left ventricular function in an ovine model.

Objectives: Transcatheter mitral valve prostheses are designed to capture the anterior leaflet and surgical techniques designed to fully preserve the subvalvular apparatus at prosthetic valve insertion both serve to shorten the anterior mitral leaflet height, thus effectively incorporating it into the anterior annulus. This study quantifies the acute effects of incorporating the anterior mitral leaflet into the annulus on left ventricular function. Methods: Fourteen adult sheep (weight, 48.7 ± 6.2 kg) underwent a mechanical mitral valve insertion on normothermic beating-heart cardiopulmonary bypass, with full retention of the native mitral valve but with placement of exteriorized releasable snares around the anterior mitral leaflet. Continuous measurements of left ventricular mechano-energetics were recorded throughout, alternating incorporating and releasing of the anterior mitral leaflet to the mitral annulus. Echocardiography confirmed the incorporation into the annulus and release. Results: The independent indices of left ventricular contractility (ie, end systolic pressure volume relationship and preload recruitable stroke work) were both significantly impaired when the anterior mitral leaflet was incorporated to the annulus and restored after release, as were the hemodynamic parameters: cardiac output, stroke volume, stroke work, and left ventricular pressure decreased by 15%, 17%, 23%, and 11%, respectively. Echocardiography demonstrated increased sphericity of the left ventricle during anterior mitral leaflet incorporation. Conclusions: Incorporating the anterior mitral leaflet to the anterior annulus adversely affected left ventricular contractility, caused distortion of the left ventricle in the form of increased sphericity, and impaired hemodynamic parameters in normal ovine hearts.

Ventricular-ventricular interaction variables correlate with surrogate variables of clinical outcome in children with pulmonary hypertension.

Determination of biventricular dimensions, function, and ventricular-ventricular interactions (VVI) is an essential part of the echocardiographic examination in adults with pulmonary hypertension (PH); however, data from according pediatric studies are sparse. We hypothesized that left and right heart dimensions/function and VVI variables indicate disease severity and progression in children with PH. Left heart, right heart, and VVI variables (e.g. end-systolic LV eccentricity index [LVEI], right ventricular [RV]/left ventricular [LV] dimension ratio) were echocardiographically determined in 57 children with PH, and correlated with New York Heart Association (NYHA) functional class (FC), N-terminal-pro brain natriuretic peptide (NT-proBNP), and invasive hemodynamic variables (e.g. pulmonary vascular resistance index [PVRi]). Clinically sicker patients (higher NYHA FC) had lower LV ejection fraction (LVEF) and higher LVEI - a surrogate of LV compression. In PH children, the ratio of systolic pulmonary arterial pressure divided by systolic systemic arterial pressure (sPAP/sSAP) and the PVRi correlated well with the LVEI ( P < 0.001). Patients with more severe PH (sPAP/sSAP ratio, PVRi) had increased RV/LV and right-to-left atrial dimension ratios ( P < 0.01). When stratified using NYHA-FC, sicker PH children had greater RV and right atrial dimensions with lower exercise capacity, while the tricuspid annular plane systolic excursion as surrogate for longitudinal systolic RV function decreased. Consistent with previous studies, serum NT-proBNP correlated with both, sPAP/sSAP ratio ( P < 0.001) and NYHA FC ( P < 0.01). Taken together, the VVI variables LVEI and RV/LV dimension ratio are associated with lower FC, worse hemodynamics, and higher NT-proBNP levels, thus highlighting the importance of ventricular interdependence in pediatric PH.

Imaging Right-Left Ventricular Interactions.

The impact of one ventricle on the adjacent ventricle plays a key role in cardiac function. Ventricular-ventricular interactions are based on the arrangement in-series of the circulation and common pericardium, interventricular septum, and myocardial tracts. Imaging, in particular echocardiography, plays a central role in characterizing these interactions through geometric indices, septal configuration and motion, Doppler flow, timing of events in the ventricles and alterations in strain, remodeling, and diastolic filling with altered loading of the contralateral ventricle. Although standard echocardiography techniques are usually adequate to image ventricular-ventricular interactions, recent developments in automation, post-processing, and advanced techniques (e.g., 3-dimensional) could improve detection and understanding of interventricular interactions. Imaging findings must be analyzed in the context of the pathophysiology to correctly assess and understand ventricular-ventricular interactions. This paper reviews the imaging of ventricular-ventricular interactions in acquired and congenital heart disease, demonstrating their importance in a wide array of conditions.

Afterload- and preload-dependent interactions in the isolated biventricular working rat heart.

OBJECTIVES: The afterload- (AL) and preload- (PL) dependent interactions between the left and right ventricle (LV, RV, respectively) of an isolated biventricular ejecting rat heart were measured in terms of left (L) and right (R) intraventricular peak pressure (LP(max) and RP(max), respectively) and aortic and pulmonary flow (AF, PF, respectively). METHODS: Starting with standardized loading conditions, LVPL was varied in six steps for each of five distinct LVALs (n=28) and then RVPL was varied in seven steps for each of five distinct RVALs (n=37). Thus, the entire range of loading conditions was covered. RESULTS: Identification of AL-dependent systolic interactions revealed an important DeltaLP(max)-DeltaRP(max) gain of 0.25 (r(2)=0.78) and a still more dominant DeltaRP(max)-DeltaPF gain of 0.45 (r(2)=0.84). At least 26% of maximal PF were attributable to LV systolic function. In contrast, R-L systolic interaction impeded PF; there was no global crosstalk pressure gain and no ipsilateral pressure-flow gain. Reduction of RV activity augmented AF by at least 15%. PL-dependent L-R interactions were absent except for minimal LVAL. In contrast, the reverse interaction reflected an inverse correlation between RVPL and AF, which is coincidential with other studies (-11% AF for a doubling of the standard RVPL). For the minimal RVAL, there was a biphasic response of AF to RVPL. Unloading the maximally loaded RV revealed an overall inhibition of AF by 37% for the standardized LV. Unloading the standardized RV revealed a basal inhibition of AF by 6% for the standardized LV and a 4.5% augmentation for the highly loaded LV. Consequently, basal contribution of RV to LV performance depended on the conditions of LV loading. CONCLUSIONS: The authors suggest a unidirectional transseptal R-L mechanism for diastolic interactions, and transseptal L-R and paraseptal R-L mechanisms for systolic interactions.