Lower Right Ventricular Fractional Area Change Research Articles

RIGHT VENTRICULAR FUNCTION ASSESSMENT BY SPECKLE TRACKINGECHOCARDIOGRAPHY IN PATIENTS ON REGULAR HEMODIALYSIS WITH PRESERVED LEFT VENTRICULAR EJECTION FRACTION

Aims: To investigate right ventricular function in hemodialysis patients with preserved left ventricular ejection fraction (LVEF) using twodimensional speckle tracking echocardiography.
 Methods: Patients with end-stage kidney disease (ESKD) who were on regular hemodialysis and had preserved LVEF and a group of age- and sex-matched control subjects were recruited for the study in Bach Mai Hospital. All subjects were interviewed and examined comprehensively. Echocardiography was performed in all patients and controls. Right ventricular function was evaluated using conventional and speckletracking echocardiography. Estimate glomerular filtration rate (eGFR) was calculated according to the MDRD GFR equation.
 Results: From 6/2022 to 11/2022, a total of 61 ESKD receiving hemodialysis regularly and 32 controls were evaluated. The mean age of the hemodialysis patients was 51.2±13.8. Men account for 54.1% (33/61). Hemodialysis patients had larger right ventricular diameters, lower RV fractional area change (FAC) and tricuspid annular plane systolic excursion (TAPSE), and decreased S velocities of the tricuspid valve compared to the controls (p<0.05 for all). Systolic pulmonary artery pressure (sPAP) of the hemodialysis group was higher when compared to the controls (p<0.05 for all). Absolute values of right ventricular global strain (RVGS) and right ventricular free wall strain (RVFWS) were significantly lower in the hemodialysis group than in the control (p<0.05 for all). Absolute values of RVGS and RVFWS inversely correlated to LV mass index (r = -0.42, p<0.05 and r=-0.46, p<0.05, respectively) while they positively correlated to eGFR (r = 0.57, p<0.05 and r = 0.59, p<0.05, respectively), hemoglobin level (r = 0.41, p<0.05 and r = 0.43, p<0.05, respectively), RVFAC (r = 0.54, p<0.05 and r = 0.51, p<0.05, respectively).
 Conclusion: Right ventricular function assessed by speckle tracking echocardiography reduced in hemodialysis patients. Right ventricular myocardial strain strongly correlated with glomerular filtration rate, RVFAC, and moderately correlated with hemoglobin level and LV mass index..

111 POST-OPERATIVE OUTCOME OF ADULT PATIENTS WITH PRE-TRICUSPID SHUNT UNDERGOING DEFECT CLOSURE

Abstract Background patients with pulmonary arterial hypertension (PAH) associated with corrected congenital heart disease (CHD) have a worse prognosis than other 3 groups of patients with PAH associated with CHD (Eisenmenger, small defect, prevalent systemic-to-pulmonary shunt). For this reason, in CHD the indication and timing of defect repair should be evaluated carefully. Current recommendations rely essentially on pulmonary vascular resistance (PVR) when deciding about defect closure, but this may be insufficient as PAH may develop even in cases of normal pre-operative PVR. In particular, patients with PVR below 3 WU are usually deemed operable and patients between 3 and 5 WU (gray zone) are deemed operable in case of significant persistence of left-to-right shunt. Detecting preoperative characteristics of patients who developed PAH after pre-tricuspid shunt repair can be helpful when deciding about CHD correction. Methods we enrolled adult patients referred to our centre for the suspicious of PAH after pre-tricuspid shunt correction from 2006 to 2021. We evaluated clinical, echocardiographic and hemodynamic parameters before and after defect repair (a post-correction hemodynamic evaluation was performed only in case of non-invasive signs of PAH) and PAH after defect closure was defined by the concomitant occurrence of a mean pulmonary artery pressure (mPAP) >25 mmHg and PVR >3 WU. Continuous variables were summarized using mean and standard deviation and Student's t-test was used for comparisons. Results sixty patients were included in the final analysis. After shunt repair, 10 patients (16.6%) were diagnosed with PAH during the long-term follow-up, with no differences given by the type of defect or type of correction. As expected, these patients already had an abnormal baseline hemodynamic profile: 7 had a clear PAH diagnosis before the correction [mPAP >25 mmHg with PVR between 3 and 5 WU and with a pulmonary/systemic cardiac output ratio of at least 1.5] while 3 had pulmonary hypertension related to high pulmonary blood flow (mPAP >25 mmHg and PVR <3 WU). At the baseline hemodynamic evaluation, patients with PAH after shunt repair had higher mPAP (39±6 vs 24±10 mmHg, p <0.001) and PVR (3.7±1.2 vs 1.5±0.9, p <0.001) and lower mixed venous oxygen saturation (81±3 vs 87±3, p <0.001). At the baseline echocardiographic evaluation, patients with PAH after shunt repair had a greater right ventricular hypertrophy (RV wall thickness 0.7±0.1 vs 0.5±0.2 cm, p= 0.011), tricuspid regurgitation jet velocity (424±63 vs 319±62 cm/s, p <0.001) and a significant lower RV fractional area change (34±8 vs 43±9%, p= 0.009). Conclusions currently there are no established evidence-based algorithms to predict the development of PAH after defect correction. Our study shows that this condition may persist or develop even when PVR values are lower than 5 WU despite a significant left-to-right shunt before defect closure. Patients with grey zone PVR values require a global clinical, instrumental and hemodynamic assessment that takes into account more than bare calculated PVR that, especially in patients with a high pulmonary blood flow, can be less reliable.

Superior prognostic value of right ventricular free wall compared to global longitudinal strain in patients with repaired tetralogy of Fallot.

ObjectivesBoth right ventricular free wall longitudinal strain (RVFWLS) and right ventricular global longitudinal strain (RVGLS) using two-dimensional speckle tracking echocardiography (2D-STE) has been demonstrated to predict adverse outcomes in patients with repaired tetralogy of Fallot (r-TOF). However, RVGLS may be affected by left ventricular (LV) function owing to the fact that the interventricular septum is also a part of the left ventricle. Therefore, the aim of our study was to compare the predictive value of RVFWLS with that of RVGLS in patients with r-TOF.Materials and methodsA total of 179 patients with r-TOF were included in this study. RVFWLS, RVGLS, and left ventricle global longitudinal strain (LVGLS) were evaluated by 2D-STE. The adverse clinical events were death or r-TOF-related rehospitalization. Prognostic performance was evaluated by C-statistic and Akaike information criterion (AIC).ResultsThirty-one patients developed poor outcomes during a median follow-up period of 2.8 years. Compared with patients without end-point events, those with end-point events had higher incidence of moderate/severe pulmonary regurgitation, larger right heart sizes, and lower RV fractional area change (RVFAC), RVFWLS, RVGLS, and LVGLS than those without. Multivariate Cox regression analysis revealed that RVFAC, RVFWLS, RVGLS, and LVGLS were predictive of poor outcomes in patients with r-TOF after adjustment for transannular patch and QRS duration. A Cox model using RVFWLS (C index = 0.876, AIC = 228) was found to predict unfavorable outcomes more accurately than a model with RVGLS (C index = 0.856, AIC = 243), RVFAC (C index = 0.811, AIC = 248), and LVGLS (C index = 0.830, AIC = 248).ConclusionAlthough both RVGLS and RVFWLS are associated with adverse events, RVFWLS provides superior prognostic value than that of RVGLS in patients with r-TOF.

Prevalence, distribution, and determinants of pulmonary venous systolic flow reversal in severe mitral regurgitation.

This study aimed to evaluate the prevalence and distribution of pulmonary venous systolic flow reversal (PVSFR) in patients with severe mitral regurgitation (MR), and to examine the relationship between PVSFR profile and cardiac parameters. A total of 125 patients with severe MR who had transoesophageal echocardiography (TOE) performed were reviewed. Of these, 121 (96.8%) patients showed all four pulmonary venous (PV) flows by TOE. They were categorized into three groups by the MR aetiology: degenerative MR (DMR) (n = 72), ventricular functional MR (V-FMR) (n = 20), and atrial functional MR (A-FMR) (n = 16). Eighteen (16.7%) patients had PVSFR in all four PVs. Twenty-nine (26.9%) had PVSFR in three PVs, 23 (21.3%) in two PVs, and 23 (21.3%) in one PV. PVSFR appeared at right PVs more frequently compared with left PVs. A high number of PVSFR was significantly correlated with higher pulmonary capillary wedge pressure (PCWP) and 3D vena contracta area (3D-VCA). With regard to MR aetiology, the number of PVSFRs was correlated with high 3D-VCA in patients with DMR and A-FMR, while it was correlated with high PCWP in patients with V-FMR. Laminar-type PVSFR appeared more frequently in FMR compared with DMR, and it had a relationship with higher PCWP and lower right ventricular fractional area change (RVFAC). All four PV were detected in 96.8%, and 16.8% patients had PVSFR in all four PVs. PCWP and 3D-VCA were correlated with the number of PVSFRs in severe MR patients. Laminar-type PVSFR was related to higher PCWP and lower RVFAC.

Cardiomyocyte‐specific Deletion of AMP‐activated Protein Kinase Exacerbates Right Ventricular Dysfunction in Pulmonary Hypertension

Right ventricular (RV) dysfunction dictates survival in aged-related left –heart failure and pulmonary hypertension (PH), yet RV remodeling is poorly understood and no RV directed therapies exist. Our group previously reported that metformin, an AMP-activated protein kinase (AMPK) activator, protects against PH-induced RV dysfunction, yet the mechanisms of metformin-mediated protection are unclear. The objective of this study was to elucidate the role of cardiac AMPK in PH-RV dysfunction and whether AMPK is required for the cardioprotective effects of metformin. We used Cre-Lox recombination techniques to delete AMPKα2 temporally and selectively from cardiomyocytes before placing male and female AMPK deleted (KO) and wild type (WT) C57Bl6 mice in a hypobaric hypoxia (HH) chamber (~17,000ft) for 4 weeks with and without metformin (200mg/kg/day). HH exposure induced cardiopulmonary remodeling as evidenced by higher lung and RV weights as well as lower RV fractional area change, pulmonary acceleration time (PAT), stroke volume (SV) and cardiac output (CO). HH-induced cardiopulmonary remodeling was exacerbated in males compared to females, consistent with previous reports of sex differences in this model. Deletion of AMPK resulted in higher RV weights normalized to TL (RV/TL) even in control conditions, with male KO AMPK mice undergoing significantly worse RV remodeling in response to HH than females. Interestingly, deletion of cardiac-specific AMPK also impacts lung remodeling. AMPK KO male and female mice demonstrated higher lung weights than WT in control mice and AMPK KO exacerbated lung remodeling in HH. Together, we suggest that AMPK is critical in the RV and PH-RHF. Ongoing work will determine if cardiac-specific AMPK is required for metformin-mediated protection in PH-RHF.

Abstract 13549: GP130 Signaling Promotes Right Ventricular Dysfunction in Pulmonary Arterial Hypertension via Microtubules

Introduction: Pulmonary arterial hypertension (PAH) is a lethal pulmonary arterial vasculopathy that results in right ventricle dysfunction (RVD). We showed that microtubule-mediated junctophilin-2 (MT-JPH2 pathway) downregulation promotes t-tubule disruption and RVD; however, the upstream regulators of this pathway are unknown. GP130 signaling via its downstream mediator, STAT3 promotes microtubule remodeling in neonatal cardiomyocytes. However, the relationship between GP130 signaling and the MT-JPH2 pathway in RVD are unknown. Methods: Immunoblots of RV extracts were probed for the GP130 and the MT-JPH2 pathways in MCT rats treated with a GP130 antagonist (2 weeks after MCT injection). Quantitative mass spectrometry analyzed the microtubule associated protein (MAP) fraction of RV extracts. Echocardiography and invasive closed-chest right heart catheterization quantified RV function and pulmonary vascular disease. Pulmonary vasculature remodeling was assessed by H&E histology. Finally, the relationship between the GP130 agonist, interleukin (IL)-6, and RVD in PAH patients was examined. Results: GP130 antagonist treatment blunted RV STAT3 activation, normalized the MT-JPH2 pathway, and restored t-tubule architecture. Hierarchical cluster analysis and principal component analysis of 2842 proteins identified using mass spectrometry revealed normalization of the MAP-fraction with GP130 antagonist treatment. These molecular changes manifested as improved RV function, improved RV-pulmonary artery coupling, blunted RV hypertrophy, and improved survival despite no differences in pulmonary vascular disease severity. In PAH patients, higher IL-6 levels were associated with higher N-terminal pro-brain natriuretic peptide and lower RV fractional area change despite no differences in pulmonary vascular disease burden. Conclusions: Small molecular inhibition of GP130 enhances RV function, and improves survival in MCT PAH via modulation of the MT-JPH2 pathway.

Comparison of Outcomes in Adults With Ventricular Septal Defect Closed Earlier in Life Versus Those in Whom the Defect Was Never Closed

Ventricular septal defects (VSDs) have recently demonstrated poorer functional outcome with disrupted ventricular contractility during exercise in young patients. It is not known whether this will change with age. Therefore, echocardiography was performed in older patients with congenital VSDs, either surgically closed or unrepaired and all without Eisenmenger physiology, to compare functional outcomes with healthy peers. Transthoracic echocardiography was performed at rest and during supine bicycle exercise, with tissue velocity Doppler for assessment of primary end points: isovolumetric acceleration and systolic velocities. In total, 30 surgically closed VSDs (51 ± 8 years) with 30 healthy controls (52 ± 9 years) and 30 unrepaired VSDs (55 ± 12 years) with 30 matched controls (55 ± 10 years) were included. Surgical patients displayed lower right ventricular (RV) systolic and early diastolic-filling velocities compared with controls, p <0.01, lower tricuspid annular plane systolic excursion (17.8 ± 5 vs 22.7 ± 3mm, p <0.01) and lower fractional area change (37.8 ± 6 vs 46.4% ± 7%, p <0.01). Unrepaired VSDs also had lower RV fractional area change than matched controls (39.9 ± 7 vs 48.4% ± 7%, p <0.01). Both patient groups had more tricuspid regurgitation and larger RV outflow tract dimensions than controls, p <0.01. During exercise, isovolumetric acceleration and systolic velocities were lower in both patient groups compared with controls, with the difference increasing with workload level. In conclusion, adults in their mid-50s with surgically closed or unrepaired VSDs have abnormal RV function at rest, with even more pronounced differences during exercise. These results suggest that a VSD, whether repaired early or considered hemodynamically insignificant, is not a benign lesion and continuous follow-up of adults is warranted.

Association of pulmonary hypertension and right ventricular function with exercise capacity in heart failure.

AimRelationships of pulmonary artery systolic pressure (PASP) and right ventricular (RV) dysfunction with exercise capacity are understudied. To assess the relationship of PASP and RV function with functional capacity and ventilatory efficiency in heart failure (HF) with a wide range of left ventricular ejection fraction (LVEF).Methods and resultsFive hundred thirty‐two consecutive HF patients referred for cardiopulmonary exercise testing [percent predicted peak VO2 (ppVO2), VE/VCO2 slope] and echocardiography [LVEF, PASP, and RV fractional area change (RVFAC)] were studied. Associations of PASP and RVFAC with ppVO2 and VE/VCO2 slope were assessed by multivariable linear regression and restricted cubic splines. Associations with composite of death, heart transplant, and LV assist device (median 3.9 year follow‐up) was assessed using multivariable Cox proportional hazard models.Mean age was 56 ± 14 years and mean LVEF was 35 ± 15%. Mean PASP was 34 ± 12 mmHg, RVFAC was 41 ± 13%, ppVO2 was 60 ± 21%, and VE/VCO2 slope was 35 ± 12. After adjusting for demographics, co‐morbidities, LVEF, mitral regurgitation severity, and left atrial volume index, higher PASP was associated with worse ppVO2 (P = 0.004) and was more robust in patients with LVEF ≥45% vs. <45% (P interaction = 0.006). Lower RVFAC was associated with both worse ppVO2 (P = 0.002) and higher VE/VCO2 slope (P = 0.002). Higher PASP and lower RVFAC were both associated with heightened risk of composite endpoint (HR 1.07 per 5 mmHg increase, P = 0.03; HR 1.17 per 5% decrease, P <0.001, respectively).ConclusionsIn HF across wide range of LVEF, greater PASP and worse RV function predict worse functional capacity and greater respiratory inefficiency, independent of LV structure and function.

P371 Right ventricle end-systolic remodeling index in patients with atrial septal defect and severe pulmonary arterial hypertension

Abstract Background Outcome of patients with atrial septal defect (ASD) and severe pulmonary arterial hypertension (PAH) relates to right ventricular (RV) function. Magnetic resonance imaging (MRI) remains the gold standard for evaluating the RV function but it is not used routinely. We investigated the relationship between MRI and multiple echocardiography parameters, including the Right Ventricle End-Systolic Remodeling Index (RVESRI), a new prognostic marker in patients with PAH. Methods 23 patients with ASD and severe PAH (median age 49y.o.[39-59], Sp0 2 92% [90-95], WHO functional class II or III, mean pulmonary artery pressure 51mmHg [40-59]) were included between 2014 and 2018. All patients underwent MRI and echocardiography assessment. Echocardiographic measurements of RV remodeling and function included TAPSE, RV fractional area change (RVFAC), peak systolic velocity of the tricuspid valve (S’TV), right atrial (RA) area, RV strain, Systolic to diastolic ratio, eccentricity index and RVESRI, defined by septum length divided by lateral wall length (Figure 1). Pericardial effusion was noted. Results Median RV ejection fraction (EF) evaluated with MRI was 46 % [34-59]. RV dysfunction (RVEF &amp;lt; 45%) was observed in 43% of patients. Median RVFAC and RVESRI were 29.6%[23-34] and 1.6[1.4-1.7] respectively. By spearman correlation, RVFAC and RVESRI were significantly correlated to RVEF (Rho 0.62, p &amp;lt; 0.007 and Rho -0.51,p &amp;lt; 0.02 respectively). By linear regression, RVFAC and RVESRI were also correlated to RVEF (R 2 =0.36, p &amp;lt; 0.003 and R 2 =0.34, p &amp;lt; 0.08). Pericardial effusion was associated with RV dysfunction (p&amp;lt; 0.008) and a lower RVFAC (p &amp;lt; 0.01). TAPSE, S’TV and RV strain were not correlated with RVEF. Conclusion RVFAC, RVESRI and pericardial effusion were markers of RV dysfunction in patients with ASD and severe PAH. RVESRI appears as a simple and reliable parameter for follow-up. Its prognostic value in patients with CHD remains to be demonstrated.

Right ventricular end-systolic remodelling index in patients with atrial septal defect and severe pulmonary arterial hypertension

Outcome of patients with atrial septal defect (ASD) and severe pulmonary arterial hypertension (PAH) relates to right ventricular (RV) function. Magnetic resonance imaging (MRI) remains the gold standard for evaluating the RV function but it is not used routinely. We investigated the relationship between MRI and multiple echocardiography parameters, including the Right Ventricle End-Systolic Remodelling Index (RVESRI), a new prognostic marker in patients with PAH. A total of 23 patients with ASD and severe PAH (median age 49 y.o. [39–59], Sp0 2 92% [90–95], WHO functional class II or III, mean pulmonary artery pressure 51 mmHg [40–59]) were included between 2014 and 2018. All patients underwent MRI and echocardiography assessment. Echocardiographic measurements of RV remodelling and function included TAPSE, RV fractional area change (RVFAC), peak systolic velocity of the tricuspid valve (S’TV), right atrial (RA) area, RV strain, Systolic to diastolic ratio, eccentricity index and RVESRI, defined by septum length divided by lateral wall length. Pericardial effusion was noted. Median RV ejection fraction (EF) evaluated with MRI was 46% [34–59]. RV dysfunction (RVEF < 45%) was observed in 43% of patients. Median RVFAC and RVESRI were 29.6%[23–34] and 1.6[1.4–1.7] respectively. By spearman correlation, RVFAC and RVESRI were significantly correlated to RVEF (Rho 0.62, P < 0.007 and Rho −0.51, P < 0.02 respectively). By linear regression, RVFAC and RVESRI were also correlated to RVEF (R 2 = 0.36, P < 0.003 and R 2 = 0.34, P < 0.08). Pericardial effusion was associated with RV dysfunction ( P < 0.008) and a lower RVFAC ( P < 0.01). TAPSE, S’TV and RV strain were not correlated with RVEF. RVFAC, RVESRI and pericardial effusion were markers of RV dysfunction in patients with ASD and severe PAH. RVESRI appears as a simple and reliable parameter for follow-up. Its prognostic value in patients with CHD remains to be demonstrated.

Right ventricular strain rate during exercise accurately identifies male athletes with right ventricular arrhythmias.

Athletes with right ventricular (RV) arrhythmias, even in the absence of desmosomal mutations, may have subtle RV abnormalities which can be unmasked by deformation imaging. As exercise places a disproportionate stress on the right ventricle, evaluation of cardiac function and deformation during exercise might improve diagnostic performance. We performed bicycle stress echocardiography in 17 apparently healthy endurance athletes (EAs), 12 non-athletic controls (NAs), and 17 athletes with RV arrhythmias without desmosomal mutations (EI-ARVCs) and compared biventricular function at rest and during low (25% of upright peak power) and moderate intensity (60%). At rest, we observed no differences in left ventricular (LV) or RV function between groups. During exercise, however, the increase in RV fractional area change (RVFAC), RV free wall strain (RVFWSL), and strain rate (RVFWSRL) were significantly attenuated in EI-ARVCs as compared to EAs and NAs. At moderate exercise intensity, EI-ARVCs had a lower RVFAC, RVFWSL, and RVFWSRL (all P < 0.01) compared to the control groups. Exercise-related increases in LV ejection fraction, strain, and strain rate were also attenuated in EI-ARVCs (P < 0.05 for interaction). Exercise but not resting parameters identified EI-ARVCs and RVFWSRL with a cut-off value of >-2.35 at moderate exercise intensity had the greatest accuracy to detect EI-ARVCs (area under the curve 0.95). Exercise deformation imaging holds promise as a non-invasive diagnostic tool to identify intrinsic RV dysfunction concealed at rest. Strain rate appears to be the most accurate parameter and should be incorporated in future, prospective studies to identify subclinical disease in an early stage.

Right ventricle end-systolic remodeling index in patients with atrial septal defect and severe pulmonary arterial hypertension

Outcome of patients with atrial septal defect (ASD) and severe pulmonary arterial hypertension (PAH) relates to right ventricular (RV) function. Magnetic resonance imaging (MRI) remains the gold standard for evaluating the RV function but it is not used routinely. We investigated the relationship between MRI and multiple echocardiography parameters, including the Right Ventricle End-Systolic Remodeling Index (RVESRI), a new prognostic marker in patients with PAH. Twenty-three patients with ASD and severe PAH (median age 49 year old [39-59], Sp02 92% [90–95], WHO functional class II or III, mean pulmonary artery pressure 51 mmHg [40–59]) were included between 2014 and 2018. All patients underwent MRI and echocardiography assessment. Echocardiographic measurements of RV remodeling and function included TAPSE, RV fractional area change (RVFAC), peak systolic velocity of the tricuspid valve (S’TV), right atrial (RA) area, RV strain, Systolic to diastolic ratio, eccentricity index and RVESRI, defined by septum length divided by lateral wall length ( Fig. 1 ). Pericardial effusion was noted. Median RV ejection fraction (EF) evaluated with MRI was 46% [34–59]. RV dysfunction (RVEF < 45%) was observed in 43% of patients. Median RVFAC and RVESRI were 29.6%[23–34] and 1.6[1.4–1.7] respectively. By spearman correlation, RVFAC and RVESRI were significantly correlated to RVEF (Rho 0.62, P < 0.007 and Rho − 0.51, P < 0.02 respectively). By linear regression, RVFAC and RVESRI were also correlated to RVEF (R2 = 0.36, P < 0.003 and R2 = 0.34, P < 0.08). Pericardial effusion was associated with RV dysfunction ( P < 0.008) and a lower RVFAC ( P < 0.01). TAPSE, S’TV and RV strain were not correlated with RVEF. RVFAC, RVESRI and pericardial effusion were markers of RV dysfunction in patients with ASD and severe PAH. RVESRI appears as a simple and reliable parameter for follow-up. Its prognostic value in patients with CHD remains to be demonstrated.

The impact of a hyperdynamic left ventricle on right ventricular function measurements in preterm infants with a patent ductus arteriosus

Background and aimsRight ventricular (RV) functional assessment in premature infants includes basal longitudinal strain (RV BLS), RV systolic tissue Doppler velocity (RV s′), tricuspid annular plane systolic excursion (TAPSE) and...

A meta-analysis for echocardiographic assessment of right ventricular structure and function in ARVC.

IntroductionArrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited pathology that can increase the risk of sudden death. Current task force criteria for echocardiographic diagnosis do not include new, regional assessment tools which may be relevant in a phenotypically diverse disease. We adopted a systematic review and meta-analysis approach to highlight echocardiographic indices that differentiated ARVC patients and healthy controls.MethodsData was extracted and analysed from prospective trials that employed a case–control design meeting strict inclusion and exclusion as well as a priori quality criteria. Structural indices included proximal RV outflow tract (RVOT1) and RV diastolic area (RVDarea). Functional indices included RV fractional area change (RVFAC), tricuspid annular systolic excursion (TAPSE), peak systolic and early diastolic myocardial velocities (S′ and E′, respectively) and myocardial strain.ResultsPatients with ARVC had larger RVOT1 (mean ± s.d.; 34 vs 28 mm, P < 0.001) and RVDarea (23 vs 18 cm2, P < 0.001) compared with healthy controls. ARVC patients also had lower RVFAC (38 vs 46%, P < 0.001), TAPSE (17 vs 23 mm, P < 0.001), S′ (9 vs 12 cm/s, P < 0.001), E′ (9 vs 13 cm/s, P < 0.001) and myocardial strain (−17 vs −30%, P < 0.001).ConclusionThe data from this meta-analysis support current task force criteria for the diagnosis of ARVC. In addition, other RV measures that reflect the complex geometry and function in ARVC clearly differentiated between ARVC and healthy controls and may provide additional diagnostic and management value. We recommend that future working groups consider this data when proposing new/revised criteria for the echocardiographic diagnosis of ARVC.

Pre-Liver Transplant Transthoracic Echocardiogram Findings and 6-Month Post-Transplant Outcomes: A Case-Control Analysis.

BACKGROUND Cardiopulmonary (CP) outcomes remain a leading cause of morbidity and mortality following liver transplantation (LT). The optimal CP risk stratification of LT candidates remains unclear. The aim of this study was to evaluate the association of pre-LT transthoracic echocardiogram (TTE) findings and 6-month post-LT outcomes. MATERIAL AND METHODS This retrospective review analyzed adults who underwent LT, comparing those who died within 6 months of LT (cases; n=38) with age- and sex-matched patients who survived >6 months (controls; n=38). Cases were categorized by cause of death (COD) defined as either a primary CP process (n=20) or a non-CP process (n=18). Data were analyzed using logistic regression and survival analysis was performed using Kaplan-Meier curves. RESULTS There was a higher odds of death within 6 months of LT with ≥ mild mitral regurgitation (OR 3.44, p=0.03) or an incomplete assessment of right ventricular systolic function (RVSF) (OR 24, p=0.004). On subgroup analysis, these findings only persisted in patients with a CP COD. Patients with CP COD were older (61 vs. 54.5, p=0.04), had longer intervals between TTE and LT (122 vs. 29 days, p=0.05), less complete assessments of RVSF (p=0.009), and lower RV fractional area change (p=0.04) compared to patients with non-CP COD. CONCLUSIONS Multiple TTE parameters were associated with patients who died within 6 months of LT, and in particular patients with a CP COD. Our findings suggest that pre-LT TTEs can convey useful CP risk stratification information and emphasizes the importance of adequately assessing these parameters prior to LT.

Echocardiographic assessment of right ventricular functions in patients with proximal right coronary artery chronic total occlusion.

To assess right ventricular functions by echocardiography in patients with proximal right coronary artery (RCA) CTO and correlating it with clinical and angiographic variables. We studied 60 consecutive patients with CTO of the proximal RCA and no other significant lesions in the left coronary system. Echocardiography was performed in order to measure left ventricular (LV) dimensions, LVEF, RV end diastolic area (RVEDA), RV end systolic area (RVESA), RV fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), Doppler myocardial performance index (MPI), trans-tricuspid E and A waves, E/A ratio, S', e' and a'. Grades of coronary collaterals was assessed. Doppler MPI showed negative correlation with TAPSE (r=-0.8997, p<0.0001) and RVFAC (r=-0.928, p<0.0001). Positive correlation with trans-tricuspid E/A ratio (r=0.893, p<0.0001) and E/e' ratio (r=0.783, p<0.0001). Patients with no evidence of MI had more well-developed (grade 3) coronary collaterals (83.8 vs. 17.4%). Patients with evidence of MI had lower RVFAC 38.13±5.39 versus 45.08±4.99% (p<0.0001), lower TAPSE 20.17±3.85 versus 25.35±3.46mm (p<0.0001), higher MPI 0.4±0.08 versus 0.31±0.05 (p<0.0001), higher trans-tricuspid E/A ratio 1.79±0.38 versus 1.13±0.36 (p<0.0001) and E/e' ratio 5.23±1.02 versus 3.61±0.88 (p<0.0001). Patients with poorly developed collaterals had lower TAPSE and RVFAC and a higher MPI (p<0.0001 for each). Patients with proximal RCA CTOs and evidence of inferior wall MI have significant impairment of RV functions in addition to poorly developed coronary collaterals. Those with proximal RCA CTOs and well-developed coronary collaterals have better RV functions.

Right ventricular plasticity in a porcine model of chronic pulmonary hypertension

Purpose: Ventricular-arterial coupling is a measure of the relationship between ventricular contractility and afterload. In this study, we sought to determine the relationship between ventricular-arterial coupling and right ventricular (RV) adaptation to chronic pressure overload in a novel porcine model of progressive pulmonary hypertension (PH). Methods: Chronic PH was induced in pigs by ligation of the left pulmonary artery (PA) followed by five weekly injections of cyanoacrylate to progressively obstruct the right lower lobe arteries (PH group, n=10). At 6 weeks, 5 PH animals underwent a reperfusion of the left lung to durably decrease RV afterload, while other animals did not receive any treatment. Five sham-operated piglets were used as controls. RV function was assessed using echocardiography and pressure-volume loops analysis. RV gene expression of β-myosin heavy chain (β-MHC) and B-type natriuretic peptide (BNP) were quantified by reverse transcription polymerase chain reaction. Experimental design was approved by our Institutional Committee on Animal Welfare and the study followed the Principles of laboratory animal care. Results: At 6 weeks, compared to controls, the PH group had higher PA pressure (32±6 vs. 14±2 mmHg, p<0.01), RV end-diastolic area index (RVEDAI, 11.1±2.9 cm2 vs. 4.8±0.3 cm2, p<0.01), PA elastance (Ea, 0.90±0.45 vs. 0.29±0.06 ml/mmHg, p=0.01) and RV elastance (Ees, 0.53±0.14 vs. 0.34±0.06 ml/mmHg, p=0.01), and lower RV fractional area change (27±9% vs. 52±10%, p<0.01) (Table 1). The relationship between Ea and RV-PA coupling could be estimated through a curvilinear relationship (R2=0.90, p<0.01). RV-PA coupling was an important determinant of RVEDAI (R2=0.48, p<0.01), RVFAC (R2=0.84, p<0.01) and stroke volume index response to dobutamine (R2=0.56, p<0.01). Changes in RV-PA coupling were also strongly related to changes in stroke volume index response to dobutamine (R2=0.80, p<0.01). Ventricular-arterial coupling and RV mass index 6 weeks after PH surgical treatment were associated with down-regulation of β-MHC (R2=0.75, p<0.01 and R2=0.71, p<0.01 respectively) and BNP expression (R2=0.91, p<0.01 and R2=0.80, p<0.01) (Figure 1). Conclusions: A curvilinear relationship between pulmonary arterial elastance and RV-PA coupling suggests a faster transition towards uncoupling at the early stage of PH. Contractile protein expression and BNP expression are associated with ventricular mass and ventricular-arterial coupling in a porcine model of RV pressure overload.

Right ventricular longitudinal deformation parameters and exercise capacity

Chronic thromboembolic pulmonary hypertension (CTEPH) is a progressive disease characterized by increased pulmonary vascular resistance resulting in pulmonary hypertension and right heart failure. The six-minute walk test (6MWT) distance is associated with the prognosis of CTEPH patients. Speckle tracking echocardiography (STE) is a reliable method for determining ventricular function. The aim of this study was to assess and compare the right ventricular (RV) function of CTEPH patients according to their 6MWT distances. Forty-nine consecutive CTEPH patients (mean age, 50 ± 16years; 22male) who were referred to our center for pulmonary thromboendarterectomy (PTE) were included in the study. All patients underwent the 6MWT and right heart catheterization (RHC). Standard echocardiography and STE were performed on all patients before PTE. Patients were divided into two groups based on their 6MWT distance being less or more than 300m. Patients with a shorter 6MWT distance had a significantly larger RV, while they had a significantly lower RV fractional area change and higher myocardial performance index suggesting impaired RV function. Both RV basal-lateral strain and strain rate measures were significantly lower in patients with shorter 6MWT distances than those with longer 6MWT distances. Similarly, they had lower RV basal-septal, mid-lateral, and global strain measures. 6MWT distances were correlated with RV basal-lateral and mid-lateral strain measures (r = 0.349, p = 0.025 and r = 0.415, p = 0.008, respectively). Our data suggest that RV myocardial deformation parameters are associated with 6MWT distances. Determination of RV dysfunction by STE may be helpful in identifying patients with a poor prognosis.

Abstract 19057: Functional Tricuspid Regurgitation is an Independent Predictor of Mortality and Morbidity in Patients with Aortic Stenosis Undergoing Valve Replacement

Background: In patients with severe aortic stenosis (AS), pulmonary hypertension (PHT) and right ventricular (RV) dysfunction are predictors of adverse events. PHT and RV dysfunction can lead to progressive functional tricuspid regurgitation (FTR), which has an under-appreciated yet potentially devastating course. We describe the impact of FTR in patients with severe AS undergoing aortic valve replacement (AVR). Methods: We identified consecutive patients with severe AS who underwent AVR in 2009 and 2010. We excluded those with concomitant mitral or tricuspid valve replacement, organic tricuspid valve pathology, and those without an available echocardiogram (echo) within 3 months of surgery. A panel of quantitative echo parameters was measured according to American Society of Echocardiography guidelines. Clinical variables were extracted from the Society of Thoracic Surgeons (STS) database. The outcomes of interest were postoperative STS-composite mortality or major morbidity, and all-cause mortality over a mean follow-up of 1.8 years. Results: Of 207 patients studied, 21 (10.1%) had moderate-to-severe FTR. Moderate-to-severe FTR was associated with higher pulmonary artery systolic pressure (58 vs. 38 mmHg, P&lt;0.001), worse RV myocardial performance index (0.57 vs. 0.42, P=0.003), lower RV fractional area change (38% vs. 47%, P=0.004), lower LVEF (48% vs. 58%, P=0.002), and higher left atrial volume index (56 vs. 42 cm2/m2, P&lt;0.001), but not with aortic valve area (0.71 vs. 0.71 cm 2 , P=0.82) or peak aortic velocity (4.3 vs. 4.4 m/s, P=0.62). Patients with FTR were more likely to suffer postoperative in-hospital mortality or major morbidity (48% vs. 23%, P=0.02) and long-term mortality (17% vs. 9%, P=0.004). When echo parameters were entered in a multivariable model, optimal predictors of all-cause mortality were: FTR (HR 3.46, 95% CI 1.26, 9.49) and restrictive diastolic filling (HR 3.07, 95% CI 1.16, 8.11). Results were similar when adjusted for clinical covariates including chronic lung disease. Conclusion: In the setting of AVR, moderate-to-severe FTR is an independent predictor of postoperative mortality and major morbidity. FTR is prevalent in AS patients with PHT and poor right or left ventricular function.

Regional Right Ventricular Strain Pattern in Patients with Acute Pulmonary Embolism

Right ventricular (RV) dysfunction is a frequent consequence of pulmonary embolism (PE) and a marker of increased risk. However, current qualitative methods assessing RV function are imprecise. We sought to determine whether RV strain analysis would have clinical utility in patients with PE compared with normal controls. We compared 75 acute PE subjects (mean age 54 ± 16) with 30 normal controls (mean age 50 ± 15). Regional RV longitudinal strain was assessed using offline speckle tracking software to obtain strain and strain rate data from the basal, mid, and apical free wall and septum. Global RV free wall and septal strain was significantly reduced in PE subjects (-14.17 (±5.96) vs -24.92 (±4.16), P < 0.0001; -14.99 (±5.55) vs -18.54 (±7.34), P = 0.0082). Regional RV strain was markedly reduced in PE subjects in all regions of the free wall and in the mid and basal septum (P < 0.05). Strain rates of PE subjects were significantly reduced in all segments of the RV free wall (P < 0.05). In 36 PE subjects with regional RV dysfunction ("McConnell sign"), strain in the apical free wall was significantly reduced in comparison to those without (-10.08 vs -13.51; P = 0.0420), in parallel with higher RV:LV ratios (1.30, ±1.01 vs 0.78, ±0.16; P = 0.0035) and lower RV fractional area change (32.06, ±14.42 vs 42.52, ±11.61; P = 0.0021). Regional RV longitudinal strain is altered in the free wall and mid and basal septum in subjects with acute PE. Strain rates are only reduced in the RV free wall.