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Aims Precapillary pulmonary hypertension (pPH) affects left ventricular (LV) function by ventricular interdependence. Since LV ejection fraction (EF) is commonly preserved, LV dysfunction should be assessed with more sensitive techniques. Left atrial (LA) strain and estimation of LV intraventricular pressure gradients (IVPG) may be valuable in detecting subtle changes in LV mechanics; however, the value of these techniques in pPH is unknown. Therefore, the aim of our study is to evaluate LA strain and LV-IVPGs from cardiovascular magnetic resonance (CMR) cines in pPH patients. Methods and results In this cross-sectional study, 31 pPH patients and 22 healthy volunteers underwent CMR imaging. Feature-tracking LA strain was measured on four- and two-chamber cines. LV-IVPGs (from apex–base) are computed from a formulation using the myocardial movement and velocity of the reconstructed 3D-LV (derived from long-axis cines using feature-tracking). Systolic function, both LV EF and systolic ejection IVPG, was preserved in pPH patients. Compared to healthy volunteers, diastolic function was impaired in pPH patients, depicted by (i) lower LA reservoir (36 ± 7% vs. 26 ± 9%, P < 0.001) and conduit strain (26 ± 6% vs. 15 ± 8%, P < 0.001) and (ii) impaired diastolic suction (−9.1 ± 3.0 vs. ‒6.4 ± 4.4, P = 0.02) and E-wave decelerative IVPG (8.9 ± 2.6 vs. 5.7 ± 3.1, P < 0.001). Additionally, 11 pPH patients (35%) showed reversal of IVPG at systolic–diastolic transition compared to none of the healthy volunteers (P = 0.002). Conclusions pPH impacts LV function by altering diastolic function, demonstrated by an impairment of LA phasic function and LV-IVPG analysis. These parameters could therefore potentially be used as early markers for LV functional decline in pPH patients. [ABSTRACT FROM AUTHOR]

Background: The various conditions causing a chronic increase of RV pressure greatly differ in the occurrence of RV failure, and in clinical outcome. To get a better understanding of the differences in outcome, RV remodeling, longitudinal function, and transverse function are compared between patients with pulmonary stenosis (PS), those with a systemic RV and those with pulmonary hypertension (PH). Materials and methods: This cross-sectional study prospectively enrolled subjects for cardiac magnetic resonance imaging (CMR), functional echocardiography and cardiopulmonary exercise testing. The study included: controls (n = 37), patients with PS (n = 15), systemic RV (n = 19) and PH (n = 20). Statistical analysis was performed using Analysis of Variance (ANOVA) with posthoc Bonferroni. Results: PS patients had smaller RV volumes with higher RV ejection fraction (61.1±9.6%; p<0.05) compared to controls (53.8±4.8%). PH and systemic RV patients exhibited dilated RVs with lower RV ejection fraction (36.9±9.6% and 46.3±10.1%; p<0.01 versus controls). PH patients had lower RV stroke volume (p = 0.02), RV ejection fractions (p<0.01) and VO2 peak/kg% (p<0.001) compared to systemic RV patients. Mean apical transverse RV free wall motion was lower and RV free wall shortening (p<0.001) was prolonged in PH patients–resulting in post-systolic shortening and intra-ventricular dyssynchrony. Apical transverse shortening and global longitudinal RV deformation showed the best correlation to RV ejection fraction (respectively r = 0.853, p<0.001 and r = 0.812, p<0.001). Conclusions: RV remodeling and function differed depending on the etiology of RV pressure overload. In contrast to the RV of patients with PS or a systemic RV, in whom sufficient stroke volumes are maintained, the RV of patients with PH seems unable to compensate for its increase in afterload completely. Key mediators of RV dysfunction observed in PH patients, were: prolonged RV free wall shortening, resulting in post-systolic shortening and intra-ventricular dyssynchrony, and decreased transverse function. [ABSTRACT FROM AUTHOR]

Background: Tricuspid valve (TV) regurgitation (TR) is a common complication of pulmonary hypertension and right-sided congenital heart disease, associated with increased morbidity and mortality. Estimation of TR severity by echocardiography and conventional cardiovasvular magnetic resonance (CMR) is not well validated and has high variability. 4D velocity- encoded (4D-flow) CMR was used to measure tricuspid flow in patients with complex right ventricular (RV) geometry and varying degrees of TR. The aims of the present study were: 1) to assess accuracy of 4D-flow CMR across the TV by comparing 4D-flow CMR derived TV effective flow to 2D-flow derived effective flow across the pulmonary valve (PV); 2) to assess TV 4D-flow CMR reproducibility, and 3) to compare TR grade by 4D-flow CMR to TR grade by echocardiography. Methods: TR was assessed by both 4D-flow CMR and echocardiography in 21 healthy subjects (41.2 ± 10.5 yrs., female 7 (33%)) and 67 RV pressure-load patients (42.7 ± 17.0 yrs., female 32 (48%)). The CMR protocol included 4D-flow CMR measurement across the TV, 2D-flow measurement across the PV and conventional planimetric measurements. TR grading on echocardiographic images was performed based on the international recommendations. Bland-Altman analysis and intra-class correlation coefficients (ICC) were used to asses correlations and agreement. Results: TV effective flow measured by 4D-flow CMR showed good correlation and agreement with PV effective flow measured by 2D-flow CMR with ICC = 0.899 (p < 0.001) and mean difference of -1.79 ml [limits of agreement -20.39 to 16.81] (p = 0.084). Intra-observer agreement for effective flow (ICC = 0.981; mean difference - 1.51 ml [-12.88 to 9.86]) and regurgitant fraction (ICC = 0.910; mean difference 1.08% [-7.90; 10.06]) was good. Inter-observer agreement for effective flow (ICC = 0.935; mean difference 2.12 ml [-15.24 to 19.48]) and regurgitant fraction (ICC = 0.968; mean difference 1.10% [-7.96 to 5.76]) were comparable. In 25/65 (38.5%) TR grade differed by at least 1 grade using 4D-flow CMR compared to echocardiography. Conclusion: TV effective flow derived from 4D-flow CMR showed excellent correlation to PV effective flow derived from 2D-flow CMR, and was reproducible to measure TV flow and regurgitation. Twenty-five out of 65 patients (38.5%) were classified differently by at least one TR grade using 4D-flow CMR compared to echocardiography. [ABSTRACT FROM AUTHOR]

Right ventricular ( RV) pressure overload has a vastly different clinical course in children with idiopathic pulmonary arterial hypertension ( iPAH) than in children with pulmonary stenosis ( PS). While RV function is well recognized as a key prognostic factor in iPAH, adverse ventricular-ventricular interactions and LV dysfunction are less well characterized and the pathophysiology is incompletely understood. We compared ventricular-ventricular interactions as hypothesized drivers of biventricular dysfunction in pediatric iPAH versus PS. Eighteen iPAH, 16 PS patients and 18 age- and size-matched controls were retrospectively studied. Cardiac cycle events were measured by M-mode and Doppler echocardiography. Measurements were compared between groups using ANOVA with post hoc Dunnet's or ANCOVA including RV systolic pressure ( RVSP; iPAH 96.8 ± 25.4 mmHg vs. PS 75.4 ± 18.9 mmHg; P = 0.011) as a covariate. RV-free wall thickening was prolonged in iPAH versus PS, extending beyond pulmonary valve closure (638 ± 76 msec vs. 562 ± 76 msec vs. 473 ± 59 msec controls). LV and RV isovolumetric relaxation were prolonged in iPAH ( P < 0.001; LV 102.8 ± 24.1 msec vs. 63.1 ± 13.7 msec; RV 95 [61-165] vs. 28 [0-43]), associated with adverse septal kinetics; characterized by rightward displacement in early systole and leftward displacement in late RV systole (i.e., early LV diastole). Early LV diastolic filling was decreased in iPAH (73 ± 15.9 vs. PS 87.4 ± 14.4 vs. controls 95.8 ± 12.5 cm/sec; P = 0.004). Prolonged RVFW thickening, prolonged RVFW isovolumetric times, and profound septal dyskinesia are associated with interventricular mechanical discoordination and decreased early LV filling in pediatric iPAH much more than PS. These adverse mechanics affect systolic and diastolic biventricular efficiency in iPAH and may form the basis for worse clinical outcomes. We used clinically derived data to study the pathophysiology of ventricular-ventricular interactions in right ventricular pressure overload, demonstrating distinct differences between pediatric pulmonary arterial hypertension ( iPAH) and pulmonary stenosis ( PS). Altered timing of right ventricular free wall contraction and profound septal dyskinesia are associated with interventricular mechanical discoordination and decreased early LV filling in iPAH much more than PS. These adverse mechanics affect systolic and diastolic biventricular efficiency, independent of right ventricular systolic pressure. [ABSTRACT FROM AUTHOR]