Right atrial and ventricular echocardiographic strain analysis predicts requirement for right ventricular support after left ventricular assist device implantation

Right atrial and ventricular echocardiographic strain analysis predicts requirement for right... Abstract Aims The need for right ventricular assist device (RVAD) support after left ventricular assist device (LVAD) therapy is associated with increased morbidity and mortality. We used 2D echocardiographic strain analysis to assess right atrial (RA) and right ventricular (RV) mechanics and predict the need for RV mechanical support after LVAD implantation. Methods and results Seventy advanced chronic heart failure (ACHF) patients [59 male, age 47 ± 12 years, 79% dilated cardiomyopathy, left ventricular ejection fraction 23 ± 10%] received continuous-flow LVAD as a bridge to transplantation over an 18 month period. A retrospective analysis of RV and RA strain and right heart dyssynchrony was performed comparing those requiring RVAD (20%, n = 14) with those who did not (non-RVAD 80%, n = 56). One-year survival was significantly lower in the RVAD group (50% vs. 79%; P < 0.03). Independent predictors of RVAD support were: low peak RA longitudinal strain (RALS) [odds ratio (OR) 2.5, 95% confidence interval (95% CI) 1.37–2.0; P = 0.03], low RV free-wall longitudinal strain (RVFWLS) (OR 1.3, 95% CI 1.03–2.3; P = 0.04), and degree of intra-RV dyssynchrony (DRVFW-IVS, OR 1.3, 95% CI 1.02–1.3; P = 0.04). Conclusion In LVAD recipients needing RVAD support, there was lower RALS and RVFWLS in addition to greater RV free-wall mechanical delay. We conclude that RA and RV strain and dyssynchrony analysis have the potential to add incremental value to the pre-VAD-implantation assessment made using conventional echo measurements. right atrial strain , right ventricular strain , ventricular assist device , heart failure Introduction Left ventricular assist device (LVAD) implantation improves prognosis in patients with advanced chronic heart failure (ACHF) and is used as a bridge to transplantation or as destination therapy.1 The incidence of right ventricular failure (RVF) after LVAD implantation has decreased with the new-generation rotary devices.2 However, mortality and morbidity associated with severe RVF remain high.3 Outcomes may improve if high-risk patients are electively implanted with biventricular assist devices (BiVAD) at first surgery.4 However, current risk-prediction models have low sensitivity and specificity for identifying patients who would benefit from this approach.3,5 Strain analysis by two-dimensional speckle-tracking echocardiography (2DSTE) is a new method of studying right ventricular (RV) function.6–8 Studies suggest that reduced RV longitudinal strain is associated with a high risk of RVF9,10 and that reduced right atrial (RA) strain correlates with decreased myocardial reserve and less favourable outcomes.11,12 In this study, we used a combination of RA and RV longitudinal strain from 2DSTE to predict the need for right ventricular assist device (RVAD) in patients undergoing LVAD implantation. We also compared the prognostic value of RH 2DSTE with conventional echocardiographic parameters of RH performance. Methods We analysed data from patients who underwent continuous-flow LVAD implant at our centre within an 18 month period. Haemodynamic measurements were obtained during RH catheterization. Cardiac output (CO) and RV stroke volume (RVSV) were estimated by the Fick technique. The endpoint was development of post-operative RV failure requiring RVAD implantation within 30 days. Patients were divided into two groups: RVAD and non-RVAD, and comparisons were made for echo parameters including strain, strain rate (SR), and dyssynchrony. Echocardiography Echocardiograms were acquired and processed using commercially available systems (Vivid 7 and EchoPac; GE Vingmed Ultrasound AS, Amersham, UK) within 48 h prior to LVAD implantation. Digital loops of three cardiac cycles’ length were recorded with additional RV-focused apical 4-chamber (A4CH) views13,14 ensuring frame rate 55–80 fps. Analysis was performed by a single operator who had not been involved in image acquisition and who was blinded to subjects’ clinical details. Longitudinal strain and SR analyses were performed for the RA, RV, RV free wall (RVFW), interventricular septum (IVS), LV, and LV free wall (LVFW) (Figures 1–3). Pulmonary and aortic valve opening and closure times were identified and marked on the relevant image frames (Figures 1–3). Figure 1 View largeDownload slide Right ventricular (RV) myocardial strain (upper left and right) and strain rate (lower left and right) curves in a non-RVAD (left) and an RVAD (right) patient. The RVAD patient shows RV dyssynchrony and prolonged duration of global RV (white dotted curve) myocardial shortening, beyond pulmonary valve closure (yellow arrow). Longitudinal SRs also reached its peak value earlier in systole (white arrow). Figure 1 View largeDownload slide Right ventricular (RV) myocardial strain (upper left and right) and strain rate (lower left and right) curves in a non-RVAD (left) and an RVAD (right) patient. The RVAD patient shows RV dyssynchrony and prolonged duration of global RV (white dotted curve) myocardial shortening, beyond pulmonary valve closure (yellow arrow). Longitudinal SRs also reached its peak value earlier in systole (white arrow). Figure 2 View largeDownload slide RV free-wall (RVFW), septal, and LV free-wall (LVFW) strain curves from a RVAD patient. The dotted white lines in each curve represent the average strain for the RVFW, septum, and LVFW, respectively. The yellow arrows represent the time to longitudinal peak strain). Figure 2 View largeDownload slide RV free-wall (RVFW), septal, and LV free-wall (LVFW) strain curves from a RVAD patient. The dotted white lines in each curve represent the average strain for the RVFW, septum, and LVFW, respectively. The yellow arrows represent the time to longitudinal peak strain). Figure 3 View largeDownload slide Right atrial (RA) strain and strain rate curves from the right heart focused apical 4-chamber view in a non-RVAD (left) and a RVAD (right) patient. The white dotted curves represent the average strain and strain rate curves. Figure 3 View largeDownload slide Right atrial (RA) strain and strain rate curves from the right heart focused apical 4-chamber view in a non-RVAD (left) and a RVAD (right) patient. The white dotted curves represent the average strain and strain rate curves. The optimal RH image was selected and the endocardial border was traced manually on the end-diastolic frame. The region of interest (ROI) was adjusted to fit with RV wall thickness. The same was done for the left heart (LH) images. ROIs were subdivided into six standard segments for the RA, RV and LV, and three slices (basal, mid-ventricle, and apical) for the RVFW, IVS, and LVFW (Figures 1–3). Accuracy of automated tracking of cardiac contours through the cardiac cycle was assessed visually and corrected by manual adjustment as required. Subsequently, the software generated both segmental and mean strain and SR curves for each ROI (Figures 1–3). Time to ventricular longitudinal peak strain (RV global, RV free wall, septal, LVFW, and LV global, Figures 1 and 2) and time to RA or LA global longitudinal peak SR (Figure 3) were estimated from the S and SR curves. As a reference point, we used the onset of the QRS complex (for ventricular strain or SR) or the P wave (for atrial strain or SR) on the corresponding ECG. Each parameter is expressed as a proportion of the R-R interval. The terms systolic and diastolic in the atrial analysis refer to ventricular systole and diastole. To determine the degree of RV mechanical dyssynchrony prior to LVAD implantation, we examined the RV free wall mechanical delay in relation to both the IVS and the LVFW (Figure 2). Statistical analysis Analyses were performed using SPSS 12.0 software (SPSS Inc., Chicago, IL, USA). Continuous variables were expressed as mean ± standard deviation (SD). Categorical variables were expressed as frequencies or percentages. A two-tailed P-value <0.05 was considered a significant difference. The Student’s t-test and χ2 tests were used for between-group data comparisons. Univariable logistic regression was performed to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs) for the outcome ‘RVAD implantation’. This was followed by a multiple regression analysis of the detected univariate predictors in a forward stepwise fashion. The predictive values were obtained by determining the area under receiver operating characteristic (ROC) curves. Ethics approval The study has NHI ethics approval, and patients gave informed consent for data collection and use for this study. The study followed the principles of the Declaration of Helsinki for medical research. Results A total of 70 LVAD recipients were included in the study (47 ± 12 years, 59 male, left ventricular ejection fraction (LVEF): 23 ± 10%, ischaemic LV dysfunction: 23%, non-ischaemic dilated cardiomyopathy (DCM) 77%, NYHA functional Class III or IV). All participants were in sinus rhythm. Severe RVF requiring RVAD support developed in 14 (20%) patients within 72 h of LVAD implantation. One-year survival was 73% (51 patients). The 1-year mortality rates were 50% (7/14) and 21% (12/56) in the RVAD and non-RVAD groups, respectively (P = 0.03). Baseline characteristics Pre-LVAD implantation characteristics are shown in Table 1. There were no significant differences between the RVAD and non-RVAD groups in LVEF, cardiac index, RV stroke work index (RVSWI), and afterload parameters. RVAD patients had higher right ventricular end-diastolic pressure (RVEDP, 25 ± 6 mmHg vs. 16 ± 7; P = 0.008) and mean right atrial pressure (mRAP, 25 ± 5 mmHg vs. 15 ± 7; P = 0.01). No differences were shown in baseline RV or LV function indices between ischaemic and non-ischaemic HF patients (Table 2). Table 1 Patient characteristics, selected laboratory, and invasively measured haemodynamic data before LVAD implantation in RVAD and non-RVAD patients Baseline characteristics RVAD Non-RVAD P-value Clinical data  Age (years) 45 ± 11 48 ± 12 0.9  Male gender (n, %) 9 (64%) 50 (89%) 0.03  BSA (m2) 1.9 ± 0.2 2.3 ± 0.3 0.4  Ischaemic cause (n, %) 3 (21%) 13 (23%) 0.1  INTERMACS (n, %) 0.03   Class I 8 (57%) 16 (28%)   Class II 2 (14%) 16 (28%)   Class III 4 (29%) 22 (44%)  QRS (ms) 132 ± 33 128 ± 32 0.8  CRT (n, %) 3 (21%) 15 (27%) 0.5  Inotropic support (n, %) 12 (87%) 47 (84%) 0.3  Intra-aortic balloon pump preop. (n, %) 4 (28%) 7 (13%) 0.04  Mechanical ventilation preop. (n, %) 8 (38%) 10 (20%) 0.05 Laboratory data  Na (mmol/L) 135 ± 4 134 ± 4 0.4  UREA (mmol/L) 10 ± 6 9.4 ± 4 0.3  CREA (μmol/L) 124 ± 53 105 ± 32 0.01  Total bilirubin (μmol/L) 43 ± 20 22 ± 12 0.001  BNP (pg/mL) 1320 ± 1122 1361 ± 1058 0.2 Left heart functional parameters  LV ejection fraction (Simpson’s biplane, %) 22 ± 9 26 ± 11 0.2  LV myocardial performance index (TDI) 0.37 ± 0.21 0.40 ± 0.13 0.1  Cardiac index (L/min/m2) 1.8 ± 0.4 1.9 ± 0.5 0.3  Mitral valve regurgitation ≥moderate (n, %) 4 (19%) 7 (14%) 0.5  Pericardial effusion (n, %) 2 (10%) 5 (10%) 0.8 Right heart haemodynamic data  Mean right atrial pressure (mmHg) 25 ± 5 15 ± 7 0.01  RV end-diastolic pressure (mmHg) 25 ± 6 16 ± 7 0.008  Mean pulmonary artery pressure (mmHg) 32 ± 8 37 ± 12 0.1  Pulmonary vascular resistance index (WU/m2) 1.5 ± 1 1.9 ± 1.6 0.3  RV stroke work index (gm.m/m2/beat) 5.1 ± 3.3 5.9 ± 3.6 0.3 Baseline characteristics RVAD Non-RVAD P-value Clinical data  Age (years) 45 ± 11 48 ± 12 0.9  Male gender (n, %) 9 (64%) 50 (89%) 0.03  BSA (m2) 1.9 ± 0.2 2.3 ± 0.3 0.4  Ischaemic cause (n, %) 3 (21%) 13 (23%) 0.1  INTERMACS (n, %) 0.03   Class I 8 (57%) 16 (28%)   Class II 2 (14%) 16 (28%)   Class III 4 (29%) 22 (44%)  QRS (ms) 132 ± 33 128 ± 32 0.8  CRT (n, %) 3 (21%) 15 (27%) 0.5  Inotropic support (n, %) 12 (87%) 47 (84%) 0.3  Intra-aortic balloon pump preop. (n, %) 4 (28%) 7 (13%) 0.04  Mechanical ventilation preop. (n, %) 8 (38%) 10 (20%) 0.05 Laboratory data  Na (mmol/L) 135 ± 4 134 ± 4 0.4  UREA (mmol/L) 10 ± 6 9.4 ± 4 0.3  CREA (μmol/L) 124 ± 53 105 ± 32 0.01  Total bilirubin (μmol/L) 43 ± 20 22 ± 12 0.001  BNP (pg/mL) 1320 ± 1122 1361 ± 1058 0.2 Left heart functional parameters  LV ejection fraction (Simpson’s biplane, %) 22 ± 9 26 ± 11 0.2  LV myocardial performance index (TDI) 0.37 ± 0.21 0.40 ± 0.13 0.1  Cardiac index (L/min/m2) 1.8 ± 0.4 1.9 ± 0.5 0.3  Mitral valve regurgitation ≥moderate (n, %) 4 (19%) 7 (14%) 0.5  Pericardial effusion (n, %) 2 (10%) 5 (10%) 0.8 Right heart haemodynamic data  Mean right atrial pressure (mmHg) 25 ± 5 15 ± 7 0.01  RV end-diastolic pressure (mmHg) 25 ± 6 16 ± 7 0.008  Mean pulmonary artery pressure (mmHg) 32 ± 8 37 ± 12 0.1  Pulmonary vascular resistance index (WU/m2) 1.5 ± 1 1.9 ± 1.6 0.3  RV stroke work index (gm.m/m2/beat) 5.1 ± 3.3 5.9 ± 3.6 0.3 BSA, body surface area; CRT, cardiac resynchronization therapy; INTERMACS, Interagency Registry for Mechanically Assisted Circulatory Support; LV, left ventricular; preop., preoperatively; RV, right ventricular; TDI, tissue doppler imaging. Table 1 Patient characteristics, selected laboratory, and invasively measured haemodynamic data before LVAD implantation in RVAD and non-RVAD patients Baseline characteristics RVAD Non-RVAD P-value Clinical data  Age (years) 45 ± 11 48 ± 12 0.9  Male gender (n, %) 9 (64%) 50 (89%) 0.03  BSA (m2) 1.9 ± 0.2 2.3 ± 0.3 0.4  Ischaemic cause (n, %) 3 (21%) 13 (23%) 0.1  INTERMACS (n, %) 0.03   Class I 8 (57%) 16 (28%)   Class II 2 (14%) 16 (28%)   Class III 4 (29%) 22 (44%)  QRS (ms) 132 ± 33 128 ± 32 0.8  CRT (n, %) 3 (21%) 15 (27%) 0.5  Inotropic support (n, %) 12 (87%) 47 (84%) 0.3  Intra-aortic balloon pump preop. (n, %) 4 (28%) 7 (13%) 0.04  Mechanical ventilation preop. (n, %) 8 (38%) 10 (20%) 0.05 Laboratory data  Na (mmol/L) 135 ± 4 134 ± 4 0.4  UREA (mmol/L) 10 ± 6 9.4 ± 4 0.3  CREA (μmol/L) 124 ± 53 105 ± 32 0.01  Total bilirubin (μmol/L) 43 ± 20 22 ± 12 0.001  BNP (pg/mL) 1320 ± 1122 1361 ± 1058 0.2 Left heart functional parameters  LV ejection fraction (Simpson’s biplane, %) 22 ± 9 26 ± 11 0.2  LV myocardial performance index (TDI) 0.37 ± 0.21 0.40 ± 0.13 0.1  Cardiac index (L/min/m2) 1.8 ± 0.4 1.9 ± 0.5 0.3  Mitral valve regurgitation ≥moderate (n, %) 4 (19%) 7 (14%) 0.5  Pericardial effusion (n, %) 2 (10%) 5 (10%) 0.8 Right heart haemodynamic data  Mean right atrial pressure (mmHg) 25 ± 5 15 ± 7 0.01  RV end-diastolic pressure (mmHg) 25 ± 6 16 ± 7 0.008  Mean pulmonary artery pressure (mmHg) 32 ± 8 37 ± 12 0.1  Pulmonary vascular resistance index (WU/m2) 1.5 ± 1 1.9 ± 1.6 0.3  RV stroke work index (gm.m/m2/beat) 5.1 ± 3.3 5.9 ± 3.6 0.3 Baseline characteristics RVAD Non-RVAD P-value Clinical data  Age (years) 45 ± 11 48 ± 12 0.9  Male gender (n, %) 9 (64%) 50 (89%) 0.03  BSA (m2) 1.9 ± 0.2 2.3 ± 0.3 0.4  Ischaemic cause (n, %) 3 (21%) 13 (23%) 0.1  INTERMACS (n, %) 0.03   Class I 8 (57%) 16 (28%)   Class II 2 (14%) 16 (28%)   Class III 4 (29%) 22 (44%)  QRS (ms) 132 ± 33 128 ± 32 0.8  CRT (n, %) 3 (21%) 15 (27%) 0.5  Inotropic support (n, %) 12 (87%) 47 (84%) 0.3  Intra-aortic balloon pump preop. (n, %) 4 (28%) 7 (13%) 0.04  Mechanical ventilation preop. (n, %) 8 (38%) 10 (20%) 0.05 Laboratory data  Na (mmol/L) 135 ± 4 134 ± 4 0.4  UREA (mmol/L) 10 ± 6 9.4 ± 4 0.3  CREA (μmol/L) 124 ± 53 105 ± 32 0.01  Total bilirubin (μmol/L) 43 ± 20 22 ± 12 0.001  BNP (pg/mL) 1320 ± 1122 1361 ± 1058 0.2 Left heart functional parameters  LV ejection fraction (Simpson’s biplane, %) 22 ± 9 26 ± 11 0.2  LV myocardial performance index (TDI) 0.37 ± 0.21 0.40 ± 0.13 0.1  Cardiac index (L/min/m2) 1.8 ± 0.4 1.9 ± 0.5 0.3  Mitral valve regurgitation ≥moderate (n, %) 4 (19%) 7 (14%) 0.5  Pericardial effusion (n, %) 2 (10%) 5 (10%) 0.8 Right heart haemodynamic data  Mean right atrial pressure (mmHg) 25 ± 5 15 ± 7 0.01  RV end-diastolic pressure (mmHg) 25 ± 6 16 ± 7 0.008  Mean pulmonary artery pressure (mmHg) 32 ± 8 37 ± 12 0.1  Pulmonary vascular resistance index (WU/m2) 1.5 ± 1 1.9 ± 1.6 0.3  RV stroke work index (gm.m/m2/beat) 5.1 ± 3.3 5.9 ± 3.6 0.3 BSA, body surface area; CRT, cardiac resynchronization therapy; INTERMACS, Interagency Registry for Mechanically Assisted Circulatory Support; LV, left ventricular; preop., preoperatively; RV, right ventricular; TDI, tissue doppler imaging. Table 2 Baseline RV and LV function according to heart failure aetiology HF substrate RVSWI (gm.m/m2/beat) TAPSE (mm) LVEF (%) MAPSE (mm) Ischaemic 4.5 ± 2.4 12 ± 4.3 25 ± 9.8 9 ± 2.6 Non-ischaemic 6.5 ± 4.5 13 ± 4 22 ± 10 9.1 ± 2.8 P-value 0.2 0.2 0.3 0.9 HF substrate RVSWI (gm.m/m2/beat) TAPSE (mm) LVEF (%) MAPSE (mm) Ischaemic 4.5 ± 2.4 12 ± 4.3 25 ± 9.8 9 ± 2.6 Non-ischaemic 6.5 ± 4.5 13 ± 4 22 ± 10 9.1 ± 2.8 P-value 0.2 0.2 0.3 0.9 LVEF, left ventricular ejection fraction; MAPSE, mitral annular systolic plane excursion; RVSWI, RV stroke work index; TAPSE, tricuspid annular plane systolic excursion. Table 2 Baseline RV and LV function according to heart failure aetiology HF substrate RVSWI (gm.m/m2/beat) TAPSE (mm) LVEF (%) MAPSE (mm) Ischaemic 4.5 ± 2.4 12 ± 4.3 25 ± 9.8 9 ± 2.6 Non-ischaemic 6.5 ± 4.5 13 ± 4 22 ± 10 9.1 ± 2.8 P-value 0.2 0.2 0.3 0.9 HF substrate RVSWI (gm.m/m2/beat) TAPSE (mm) LVEF (%) MAPSE (mm) Ischaemic 4.5 ± 2.4 12 ± 4.3 25 ± 9.8 9 ± 2.6 Non-ischaemic 6.5 ± 4.5 13 ± 4 22 ± 10 9.1 ± 2.8 P-value 0.2 0.2 0.3 0.9 LVEF, left ventricular ejection fraction; MAPSE, mitral annular systolic plane excursion; RVSWI, RV stroke work index; TAPSE, tricuspid annular plane systolic excursion. Baseline echocardiographic parameters Echocardiographic parameters for the RH are shown in Table 3. There were no significant differences between the groups for parameters reflecting RV contractility, diastolic function and remodelling, including fractional change area (RVFCA), tricuspid annular plane systolic excursion (TAPSE), and RV myocardial (RVMPI performance index). However, RVAD recipients had significantly larger RA areas, lower RA fractional area change (RAFCA), and lower RA emptying fraction. No statistically significant differences between the two groups were found for LA and LV parameters. Table 3 Baseline right heart conventional echocardiographic parameters RH echocardiographic parameters RVAD Non-RVAD P-value RA function  RA end-diastolic area (cm2) 30 ± 12 21 ± 8 0.001  RA end-systolic area (cm2) 36 ± 11 25 ± 8 0.02  RA FAC (%) 22 ± 13 32 ± 12 0.04  RA emptying fraction (%) 21 ± 15 35 ± 16 0.04 RV dimensions  RV basal diameter (mm) 43 ± 9 45 ± 9 0.3  RV mid-cavity diameter (mm) 34 ± 10 36 ± 7 0.5  RV longitudinal dimension (mm) 75 ± 16 79 ± 13 0.3  RV wall thickness (cm) 0.5 ± 0.2 0.45 ± 0.1 0.7  LV eccentricity index 1.12 ± 0.15 0.96 ± 0.12 0.07 RV systolic function  TAPSE (mm) 12 ± 4 13 ± 4 0.1  Lateral St′ (m/s) 0.95 ± 0.1 0.98 ± 0.1 0.6  RV myocardial performance index 0.46 ± 0.1 0.44 ± 0.08 0.5  RV FAC (%) 29 ± 13 30 ± 12 0.7  RV ejection time (ms) 230 ± 38 231 ± 49 0.9  RV outflow acceleration time (ms) 93 ± 29 88 ± 22 0.4 RV diastolic function  Et (m/s) 0.87 ± 0.2 0.84 ± 0.2 0.3  At (m/s) 0.75 ± 0.2 0.74 ± 0.2 0.2  Et/At 1.2 ± 0.3 1.1 ± 0.1 0.7  Et wave deceleration time (ms) 178 ± 90 148 ± 56 0.1  Et/Et′ 7.5 ± 1.2 7.2 ± 1.5 0.4 Haemodynamic surrogates  TR jet estimated RVSP (mmHg) 43 ± 14 40 ± 16 0.7  PR estimated RVDP (mmHg) 10 ± 5 8 ± 5 0.4  Tricuspid valve regurgitation (TR) ≥ moderate (n, %) 4 (19%) 9 (18%) 0.3  Pulmonary valve regurgitation (PR) > mild (n, %) 1 (5%) 2 (5%) 0.6 RH echocardiographic parameters RVAD Non-RVAD P-value RA function  RA end-diastolic area (cm2) 30 ± 12 21 ± 8 0.001  RA end-systolic area (cm2) 36 ± 11 25 ± 8 0.02  RA FAC (%) 22 ± 13 32 ± 12 0.04  RA emptying fraction (%) 21 ± 15 35 ± 16 0.04 RV dimensions  RV basal diameter (mm) 43 ± 9 45 ± 9 0.3  RV mid-cavity diameter (mm) 34 ± 10 36 ± 7 0.5  RV longitudinal dimension (mm) 75 ± 16 79 ± 13 0.3  RV wall thickness (cm) 0.5 ± 0.2 0.45 ± 0.1 0.7  LV eccentricity index 1.12 ± 0.15 0.96 ± 0.12 0.07 RV systolic function  TAPSE (mm) 12 ± 4 13 ± 4 0.1  Lateral St′ (m/s) 0.95 ± 0.1 0.98 ± 0.1 0.6  RV myocardial performance index 0.46 ± 0.1 0.44 ± 0.08 0.5  RV FAC (%) 29 ± 13 30 ± 12 0.7  RV ejection time (ms) 230 ± 38 231 ± 49 0.9  RV outflow acceleration time (ms) 93 ± 29 88 ± 22 0.4 RV diastolic function  Et (m/s) 0.87 ± 0.2 0.84 ± 0.2 0.3  At (m/s) 0.75 ± 0.2 0.74 ± 0.2 0.2  Et/At 1.2 ± 0.3 1.1 ± 0.1 0.7  Et wave deceleration time (ms) 178 ± 90 148 ± 56 0.1  Et/Et′ 7.5 ± 1.2 7.2 ± 1.5 0.4 Haemodynamic surrogates  TR jet estimated RVSP (mmHg) 43 ± 14 40 ± 16 0.7  PR estimated RVDP (mmHg) 10 ± 5 8 ± 5 0.4  Tricuspid valve regurgitation (TR) ≥ moderate (n, %) 4 (19%) 9 (18%) 0.3  Pulmonary valve regurgitation (PR) > mild (n, %) 1 (5%) 2 (5%) 0.6 At, tricuspid annular late diastolic velocity on TDI; Et, TDI tricuspid annular early diastolic velocity; FAC, fractional area change; LV, left ventricular; PR, pulmonary valve regurgitation; RA, right atrial; RV, right ventricular; RVDP, RV diastolic pressure; RVSP, RV systolic pressure; TAPSE, tricuspid annular plane systolic excursion; St′, tricuspid annular systolic velocity on TDI; TR, tricuspid valve regurgitation. Table 3 Baseline right heart conventional echocardiographic parameters RH echocardiographic parameters RVAD Non-RVAD P-value RA function  RA end-diastolic area (cm2) 30 ± 12 21 ± 8 0.001  RA end-systolic area (cm2) 36 ± 11 25 ± 8 0.02  RA FAC (%) 22 ± 13 32 ± 12 0.04  RA emptying fraction (%) 21 ± 15 35 ± 16 0.04 RV dimensions  RV basal diameter (mm) 43 ± 9 45 ± 9 0.3  RV mid-cavity diameter (mm) 34 ± 10 36 ± 7 0.5  RV longitudinal dimension (mm) 75 ± 16 79 ± 13 0.3  RV wall thickness (cm) 0.5 ± 0.2 0.45 ± 0.1 0.7  LV eccentricity index 1.12 ± 0.15 0.96 ± 0.12 0.07 RV systolic function  TAPSE (mm) 12 ± 4 13 ± 4 0.1  Lateral St′ (m/s) 0.95 ± 0.1 0.98 ± 0.1 0.6  RV myocardial performance index 0.46 ± 0.1 0.44 ± 0.08 0.5  RV FAC (%) 29 ± 13 30 ± 12 0.7  RV ejection time (ms) 230 ± 38 231 ± 49 0.9  RV outflow acceleration time (ms) 93 ± 29 88 ± 22 0.4 RV diastolic function  Et (m/s) 0.87 ± 0.2 0.84 ± 0.2 0.3  At (m/s) 0.75 ± 0.2 0.74 ± 0.2 0.2  Et/At 1.2 ± 0.3 1.1 ± 0.1 0.7  Et wave deceleration time (ms) 178 ± 90 148 ± 56 0.1  Et/Et′ 7.5 ± 1.2 7.2 ± 1.5 0.4 Haemodynamic surrogates  TR jet estimated RVSP (mmHg) 43 ± 14 40 ± 16 0.7  PR estimated RVDP (mmHg) 10 ± 5 8 ± 5 0.4  Tricuspid valve regurgitation (TR) ≥ moderate (n, %) 4 (19%) 9 (18%) 0.3  Pulmonary valve regurgitation (PR) > mild (n, %) 1 (5%) 2 (5%) 0.6 RH echocardiographic parameters RVAD Non-RVAD P-value RA function  RA end-diastolic area (cm2) 30 ± 12 21 ± 8 0.001  RA end-systolic area (cm2) 36 ± 11 25 ± 8 0.02  RA FAC (%) 22 ± 13 32 ± 12 0.04  RA emptying fraction (%) 21 ± 15 35 ± 16 0.04 RV dimensions  RV basal diameter (mm) 43 ± 9 45 ± 9 0.3  RV mid-cavity diameter (mm) 34 ± 10 36 ± 7 0.5  RV longitudinal dimension (mm) 75 ± 16 79 ± 13 0.3  RV wall thickness (cm) 0.5 ± 0.2 0.45 ± 0.1 0.7  LV eccentricity index 1.12 ± 0.15 0.96 ± 0.12 0.07 RV systolic function  TAPSE (mm) 12 ± 4 13 ± 4 0.1  Lateral St′ (m/s) 0.95 ± 0.1 0.98 ± 0.1 0.6  RV myocardial performance index 0.46 ± 0.1 0.44 ± 0.08 0.5  RV FAC (%) 29 ± 13 30 ± 12 0.7  RV ejection time (ms) 230 ± 38 231 ± 49 0.9  RV outflow acceleration time (ms) 93 ± 29 88 ± 22 0.4 RV diastolic function  Et (m/s) 0.87 ± 0.2 0.84 ± 0.2 0.3  At (m/s) 0.75 ± 0.2 0.74 ± 0.2 0.2  Et/At 1.2 ± 0.3 1.1 ± 0.1 0.7  Et wave deceleration time (ms) 178 ± 90 148 ± 56 0.1  Et/Et′ 7.5 ± 1.2 7.2 ± 1.5 0.4 Haemodynamic surrogates  TR jet estimated RVSP (mmHg) 43 ± 14 40 ± 16 0.7  PR estimated RVDP (mmHg) 10 ± 5 8 ± 5 0.4  Tricuspid valve regurgitation (TR) ≥ moderate (n, %) 4 (19%) 9 (18%) 0.3  Pulmonary valve regurgitation (PR) > mild (n, %) 1 (5%) 2 (5%) 0.6 At, tricuspid annular late diastolic velocity on TDI; Et, TDI tricuspid annular early diastolic velocity; FAC, fractional area change; LV, left ventricular; PR, pulmonary valve regurgitation; RA, right atrial; RV, right ventricular; RVDP, RV diastolic pressure; RVSP, RV systolic pressure; TAPSE, tricuspid annular plane systolic excursion; St′, tricuspid annular systolic velocity on TDI; TR, tricuspid valve regurgitation. Atrial strain and strain rate results from STE RA strain parameters are shown in Table 4. The RVAD group had significantly lower pre-operative RA peak strain (11 ± 1% vs. 33 ± 8%; P = 0.004), longer time to peak strain (0.49 ± 0.05 vs. 0.58 ± 0.02; P = 0.05), and lower RA late diastolic SR (0.51 ± 0.5 s−1 vs. 0.62 ± 0.46 s−1, P = 0.04). No significant differences were noted for the LA STE parameters. Table 4 Right atrial (RA) strain and strain rate (SR) parameters RA strain parameters RVAD Non-RVAD P-value Peak strain (%) 11 ± 1 33 ± 8 0.004 Time to peak strain/R-R 0.58 ± 0.02 0.49 ± 0.05 0.05 Peak systolica SR (s−1) 0.71 ± 0.36 0.73 ± 0.38 0.9 Peak early diastolicb strain (s−1) 0.66 ± 0.22 0.68 ± 0.15 0.5 Peak late diastolic SR (s−1) 0.51 ± 0.50 0.62 ± 0.46 0.04 RA strain parameters RVAD Non-RVAD P-value Peak strain (%) 11 ± 1 33 ± 8 0.004 Time to peak strain/R-R 0.58 ± 0.02 0.49 ± 0.05 0.05 Peak systolica SR (s−1) 0.71 ± 0.36 0.73 ± 0.38 0.9 Peak early diastolicb strain (s−1) 0.66 ± 0.22 0.68 ± 0.15 0.5 Peak late diastolic SR (s−1) 0.51 ± 0.50 0.62 ± 0.46 0.04 a Systolic refers to ventricular systole. b Diastolic refers to ventricular diastole. Table 4 Right atrial (RA) strain and strain rate (SR) parameters RA strain parameters RVAD Non-RVAD P-value Peak strain (%) 11 ± 1 33 ± 8 0.004 Time to peak strain/R-R 0.58 ± 0.02 0.49 ± 0.05 0.05 Peak systolica SR (s−1) 0.71 ± 0.36 0.73 ± 0.38 0.9 Peak early diastolicb strain (s−1) 0.66 ± 0.22 0.68 ± 0.15 0.5 Peak late diastolic SR (s−1) 0.51 ± 0.50 0.62 ± 0.46 0.04 RA strain parameters RVAD Non-RVAD P-value Peak strain (%) 11 ± 1 33 ± 8 0.004 Time to peak strain/R-R 0.58 ± 0.02 0.49 ± 0.05 0.05 Peak systolica SR (s−1) 0.71 ± 0.36 0.73 ± 0.38 0.9 Peak early diastolicb strain (s−1) 0.66 ± 0.22 0.68 ± 0.15 0.5 Peak late diastolic SR (s−1) 0.51 ± 0.50 0.62 ± 0.46 0.04 a Systolic refers to ventricular systole. b Diastolic refers to ventricular diastole. Ventricular strain and strain rate results from STE RV strain and SR parameters are shown in Table 5. RV global longitudinal peak strain was lower in the RVAD group than in the non-RVAD patients (8.0 ± 2.8% vs. 9.2 ± 4.5%, P = 0.02), as was RVFW peak strain (8.6% ± 2.7 vs. 11.8% ± 6.2, P = 0.01). RVFW longitudinal peak systolic SR was also significantly lower in the RVAD group and occurred earlier during the cardiac cycle. Table 5 Systolic ventricular strain and strain rate (SR) analysis Ventricular strain parameters RVAD Non-RVAD P-value Peak systolic strain (%) RV global 8.0 ± 2.8 9.2 ± 4.5 0.02 RV free wall 8.6 ± 2.7 11.8 ± 6.2 0.01 Septal 7.9 ± 4.4 8.6 ± 6.0 0.4 Time to peak systolic strain/R-R (%) RV global 56 ± 19 46 ± 17 0.04 (Myocardial shortening duration) RV free wall 57 ± 10 45 ± 20 0.03 Septal 55 ± 17 54 ± 18 0.9 Peak systolic SR (s−1) RV global 0.61 ± 0.32 0.62 ± 0.24 0.1 RV free wall 0.84 ± 0.47 1.10 ± 0.30 0.04 Septal 0.58 ± 0.29 0.65 ± 0.29 0.9 Time to peak systolic SR/R-R RV global 0.22 ± 0.05 0.32 ± 0.01 0.04 RV free wall 0.17 ± 0.01 0.28 ± 0.01 0.03 Septal 0.34 ± 0.19 0.28 ± 0.12 0.2 Peak early diastolic SR (s−1) RV global 0.62 ± 0.44 0.61 ± 0.39 0.2 RV free wall 0.97 ± 0.47 1.05 ± 0.66 0.1 Septal 0.52 ± 0.39 0.62 ± 0.40 0.8 Peak late diastolic SR (s−1) RV global 0.38 ± 0.21 0.51 ± 0.42 0.01 RV free wall 0.53 ± 0.50 0.73 ± 0.60 0.04 Septal 0.32 ± 0.30 0.32 ± 0.23 0.09 Post-PVC RV myocardial shortening (n, %) RV global 17(81%) 34(70%) 0.04 RV free wall 17(81%) 34(70%) 0.04 Septal 18(86%) 40(82%) 0.5 Ventricular strain parameters RVAD Non-RVAD P-value Peak systolic strain (%) RV global 8.0 ± 2.8 9.2 ± 4.5 0.02 RV free wall 8.6 ± 2.7 11.8 ± 6.2 0.01 Septal 7.9 ± 4.4 8.6 ± 6.0 0.4 Time to peak systolic strain/R-R (%) RV global 56 ± 19 46 ± 17 0.04 (Myocardial shortening duration) RV free wall 57 ± 10 45 ± 20 0.03 Septal 55 ± 17 54 ± 18 0.9 Peak systolic SR (s−1) RV global 0.61 ± 0.32 0.62 ± 0.24 0.1 RV free wall 0.84 ± 0.47 1.10 ± 0.30 0.04 Septal 0.58 ± 0.29 0.65 ± 0.29 0.9 Time to peak systolic SR/R-R RV global 0.22 ± 0.05 0.32 ± 0.01 0.04 RV free wall 0.17 ± 0.01 0.28 ± 0.01 0.03 Septal 0.34 ± 0.19 0.28 ± 0.12 0.2 Peak early diastolic SR (s−1) RV global 0.62 ± 0.44 0.61 ± 0.39 0.2 RV free wall 0.97 ± 0.47 1.05 ± 0.66 0.1 Septal 0.52 ± 0.39 0.62 ± 0.40 0.8 Peak late diastolic SR (s−1) RV global 0.38 ± 0.21 0.51 ± 0.42 0.01 RV free wall 0.53 ± 0.50 0.73 ± 0.60 0.04 Septal 0.32 ± 0.30 0.32 ± 0.23 0.09 Post-PVC RV myocardial shortening (n, %) RV global 17(81%) 34(70%) 0.04 RV free wall 17(81%) 34(70%) 0.04 Septal 18(86%) 40(82%) 0.5 PVC, pulmonary valve closure. Table 5 Systolic ventricular strain and strain rate (SR) analysis Ventricular strain parameters RVAD Non-RVAD P-value Peak systolic strain (%) RV global 8.0 ± 2.8 9.2 ± 4.5 0.02 RV free wall 8.6 ± 2.7 11.8 ± 6.2 0.01 Septal 7.9 ± 4.4 8.6 ± 6.0 0.4 Time to peak systolic strain/R-R (%) RV global 56 ± 19 46 ± 17 0.04 (Myocardial shortening duration) RV free wall 57 ± 10 45 ± 20 0.03 Septal 55 ± 17 54 ± 18 0.9 Peak systolic SR (s−1) RV global 0.61 ± 0.32 0.62 ± 0.24 0.1 RV free wall 0.84 ± 0.47 1.10 ± 0.30 0.04 Septal 0.58 ± 0.29 0.65 ± 0.29 0.9 Time to peak systolic SR/R-R RV global 0.22 ± 0.05 0.32 ± 0.01 0.04 RV free wall 0.17 ± 0.01 0.28 ± 0.01 0.03 Septal 0.34 ± 0.19 0.28 ± 0.12 0.2 Peak early diastolic SR (s−1) RV global 0.62 ± 0.44 0.61 ± 0.39 0.2 RV free wall 0.97 ± 0.47 1.05 ± 0.66 0.1 Septal 0.52 ± 0.39 0.62 ± 0.40 0.8 Peak late diastolic SR (s−1) RV global 0.38 ± 0.21 0.51 ± 0.42 0.01 RV free wall 0.53 ± 0.50 0.73 ± 0.60 0.04 Septal 0.32 ± 0.30 0.32 ± 0.23 0.09 Post-PVC RV myocardial shortening (n, %) RV global 17(81%) 34(70%) 0.04 RV free wall 17(81%) 34(70%) 0.04 Septal 18(86%) 40(82%) 0.5 Ventricular strain parameters RVAD Non-RVAD P-value Peak systolic strain (%) RV global 8.0 ± 2.8 9.2 ± 4.5 0.02 RV free wall 8.6 ± 2.7 11.8 ± 6.2 0.01 Septal 7.9 ± 4.4 8.6 ± 6.0 0.4 Time to peak systolic strain/R-R (%) RV global 56 ± 19 46 ± 17 0.04 (Myocardial shortening duration) RV free wall 57 ± 10 45 ± 20 0.03 Septal 55 ± 17 54 ± 18 0.9 Peak systolic SR (s−1) RV global 0.61 ± 0.32 0.62 ± 0.24 0.1 RV free wall 0.84 ± 0.47 1.10 ± 0.30 0.04 Septal 0.58 ± 0.29 0.65 ± 0.29 0.9 Time to peak systolic SR/R-R RV global 0.22 ± 0.05 0.32 ± 0.01 0.04 RV free wall 0.17 ± 0.01 0.28 ± 0.01 0.03 Septal 0.34 ± 0.19 0.28 ± 0.12 0.2 Peak early diastolic SR (s−1) RV global 0.62 ± 0.44 0.61 ± 0.39 0.2 RV free wall 0.97 ± 0.47 1.05 ± 0.66 0.1 Septal 0.52 ± 0.39 0.62 ± 0.40 0.8 Peak late diastolic SR (s−1) RV global 0.38 ± 0.21 0.51 ± 0.42 0.01 RV free wall 0.53 ± 0.50 0.73 ± 0.60 0.04 Septal 0.32 ± 0.30 0.32 ± 0.23 0.09 Post-PVC RV myocardial shortening (n, %) RV global 17(81%) 34(70%) 0.04 RV free wall 17(81%) 34(70%) 0.04 Septal 18(86%) 40(82%) 0.5 PVC, pulmonary valve closure. Global and free-wall RV myocardial shortening (time to longitudinal peak strain/R-R) was significantly longer for the RVAD patients (RV global: 56 ± %19 vs. 46± 17%; P < 0.04 and RVFW: 57 ± 10% vs. 45 ± 20%; P < 0.03). This group showed continuation of RVFW myocardial shortening beyond the time of pulmonary valve closure (PVC) (n = 17, 81% vs. n = 34, 70%, P = 0.04). Finally, lower global and free-wall RV late diastolic strain rates were observed in the RVAD group. No significant differences were noted between the two groups for the LV strain and SR parameters. RV mechanical dyssynchrony Analysis of RVFW mechanical delay in relation to both the IVS and the LVFW showed that the RVAD group showed a greater degree of both intra-RV and interventricular dyssynchrony preoperatively (Table 6). Table 6 Ventricular dyssynchrony parameters Dyssynchrony parameters RVAD Non-RVAD P-value Intra-RV dyssynchrony, DRVFW-IVS (RV free wall to septal peak strain time difference, ms) 117 ± 92 53 ± 38 0.03 Intra-LV dyssychrony, DLVFW-IVS (LV free wall to septal peak strain time difference, ms) 109 ± 51 69 ± 48 0.05 Interventricular dyssynchrony, DRVFW-LVFW (RV free wall to LV free-wall peak strain time difference, ms) 116 ± 75 78 ± 40 0.03 Dyssynchrony parameters RVAD Non-RVAD P-value Intra-RV dyssynchrony, DRVFW-IVS (RV free wall to septal peak strain time difference, ms) 117 ± 92 53 ± 38 0.03 Intra-LV dyssychrony, DLVFW-IVS (LV free wall to septal peak strain time difference, ms) 109 ± 51 69 ± 48 0.05 Interventricular dyssynchrony, DRVFW-LVFW (RV free wall to LV free-wall peak strain time difference, ms) 116 ± 75 78 ± 40 0.03 Table 6 Ventricular dyssynchrony parameters Dyssynchrony parameters RVAD Non-RVAD P-value Intra-RV dyssynchrony, DRVFW-IVS (RV free wall to septal peak strain time difference, ms) 117 ± 92 53 ± 38 0.03 Intra-LV dyssychrony, DLVFW-IVS (LV free wall to septal peak strain time difference, ms) 109 ± 51 69 ± 48 0.05 Interventricular dyssynchrony, DRVFW-LVFW (RV free wall to LV free-wall peak strain time difference, ms) 116 ± 75 78 ± 40 0.03 Dyssynchrony parameters RVAD Non-RVAD P-value Intra-RV dyssynchrony, DRVFW-IVS (RV free wall to septal peak strain time difference, ms) 117 ± 92 53 ± 38 0.03 Intra-LV dyssychrony, DLVFW-IVS (LV free wall to septal peak strain time difference, ms) 109 ± 51 69 ± 48 0.05 Interventricular dyssynchrony, DRVFW-LVFW (RV free wall to LV free-wall peak strain time difference, ms) 116 ± 75 78 ± 40 0.03 Correlations of RA and RV strain with invasively determined haemodynamic parameters RA strain correlates relatively strongly with RVEDP (r = −0.57, P < 0.01), moderately with RVSWI (r = 0.39, P = 0.02) and mRAP (−0.39, P = 0.02) and weakly with RA end-systolic area (0.31, P = 0.03). RV strain correlates moderately with RVSWI (r = −0.35, P = 0.03), mRAP (r = −0.39, P = 0.01) and weekly with RA area (r = 0.3, P = 0.04). Table 7 shows the relationship between invasively determined indices of pulmonary hypertension (PH), HF substrate, and post-operative RVAD need. MRAP was significantly higher in the RVAD than in the non-RVAD patients for both ischaemic and non-ischaemic HF. There were no significant differences between the two groups for the majority of pre-LVAD PH indices. However, in the ischaemic HF group, RVAD patients had higher PVR 6 months post-LVAD. Table 7 Pre- and post-LVAD pulmonary arterial hypertension indices according heart failure aetiology Pre-LVAD Post-LVAD sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) Ischaemic (n = 15) RVAD (n = 4) 46 ± 15 30 ± 10 28 ± 10 3.1 ± 2 45 ± 4 32 ± 2 14 ± 10 3 ± 1.8 Non-RVAD (n = 11) 50 ± 15 34 ± 11 17 ± 8 3.4 ± 1.5 30 ± 11 20 ± 8 7 ± 2 1.5 ± 1 P-value 0.8 0.7 0.01 0.9 0.08 0.07 0.2 0.007 Non-ischaemic (n = 55) RVAD (n = 10) 57 ± 19 39 ± 12 24 ± 9 2.9 ± 1 31 ± 6 19 ± 4 7 ± 4 1.4 ± 1 Non-RVAD (n = 45) 48 ± 15 34 ± 10 15 ± 7 3.4 ± 2 31 ± 11 20 ± 9 8 ± 6 1.5 ± 1 P-value 0.1 0.1 0.01 0.9 0.9 0.6 0.6 0.5 Pre-LVAD Post-LVAD sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) Ischaemic (n = 15) RVAD (n = 4) 46 ± 15 30 ± 10 28 ± 10 3.1 ± 2 45 ± 4 32 ± 2 14 ± 10 3 ± 1.8 Non-RVAD (n = 11) 50 ± 15 34 ± 11 17 ± 8 3.4 ± 1.5 30 ± 11 20 ± 8 7 ± 2 1.5 ± 1 P-value 0.8 0.7 0.01 0.9 0.08 0.07 0.2 0.007 Non-ischaemic (n = 55) RVAD (n = 10) 57 ± 19 39 ± 12 24 ± 9 2.9 ± 1 31 ± 6 19 ± 4 7 ± 4 1.4 ± 1 Non-RVAD (n = 45) 48 ± 15 34 ± 10 15 ± 7 3.4 ± 2 31 ± 11 20 ± 9 8 ± 6 1.5 ± 1 P-value 0.1 0.1 0.01 0.9 0.9 0.6 0.6 0.5 mPAP, mean pulmonary artery pressure; mRAP, mean right atrial pressure; PVR, pulmonary vascular resistance; SPAP, systolic pulmonary artery pressure. Table 7 Pre- and post-LVAD pulmonary arterial hypertension indices according heart failure aetiology Pre-LVAD Post-LVAD sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) Ischaemic (n = 15) RVAD (n = 4) 46 ± 15 30 ± 10 28 ± 10 3.1 ± 2 45 ± 4 32 ± 2 14 ± 10 3 ± 1.8 Non-RVAD (n = 11) 50 ± 15 34 ± 11 17 ± 8 3.4 ± 1.5 30 ± 11 20 ± 8 7 ± 2 1.5 ± 1 P-value 0.8 0.7 0.01 0.9 0.08 0.07 0.2 0.007 Non-ischaemic (n = 55) RVAD (n = 10) 57 ± 19 39 ± 12 24 ± 9 2.9 ± 1 31 ± 6 19 ± 4 7 ± 4 1.4 ± 1 Non-RVAD (n = 45) 48 ± 15 34 ± 10 15 ± 7 3.4 ± 2 31 ± 11 20 ± 9 8 ± 6 1.5 ± 1 P-value 0.1 0.1 0.01 0.9 0.9 0.6 0.6 0.5 Pre-LVAD Post-LVAD sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) Ischaemic (n = 15) RVAD (n = 4) 46 ± 15 30 ± 10 28 ± 10 3.1 ± 2 45 ± 4 32 ± 2 14 ± 10 3 ± 1.8 Non-RVAD (n = 11) 50 ± 15 34 ± 11 17 ± 8 3.4 ± 1.5 30 ± 11 20 ± 8 7 ± 2 1.5 ± 1 P-value 0.8 0.7 0.01 0.9 0.08 0.07 0.2 0.007 Non-ischaemic (n = 55) RVAD (n = 10) 57 ± 19 39 ± 12 24 ± 9 2.9 ± 1 31 ± 6 19 ± 4 7 ± 4 1.4 ± 1 Non-RVAD (n = 45) 48 ± 15 34 ± 10 15 ± 7 3.4 ± 2 31 ± 11 20 ± 9 8 ± 6 1.5 ± 1 P-value 0.1 0.1 0.01 0.9 0.9 0.6 0.6 0.5 mPAP, mean pulmonary artery pressure; mRAP, mean right atrial pressure; PVR, pulmonary vascular resistance; SPAP, systolic pulmonary artery pressure. Univariate predictors of post-operative RVAD implantation These are shown in Table 8. The single most powerful predictor was RA longitudinal peak strain (RALS) (OR 2.5 95% CI 1.8–2.6, P = 0.01). Other significant predictors were greater RA end-systolic area and lower RA emptying fraction. RV strain and SR indices shown to be univariate predictors were: lower global and free-wall peak strain, longer time from QRS onset to global/free-wall peak strain, lower free-wall systolic SR, greater global and free-wall late diastolic SR, increased intra-RV mechanical dyssynchrony, and longer duration of myocardial shortening. Table 8 Univariate predictors of RVAD support Baseline variables OR 95% confidence interval P-value Conventional echo parameters  RA end-systolic area (echo) 0.29 0.11–0.74 0.03  RA emptying fraction (echo) 0.95 0.92–0.99 0.03 RA speckle-tracking variables  RA peak strain 2.51 1.84–2.61 0.01 RV free-wall (RVFW) speckle-tracking parameters  RVFW peak strain 1.39 1.25–1.99 0.02  Time to RVFW strain 1.05 1.03–1.17 0.03  RVFW systolic strain rate 1.04 1.02–2.35 0.05  Time to RVFW systolic strain rate 1.35 1.03–2.24 0.03  RVFW late diastolic strain rate 1.60 1.24–1.61 0.03 RV global (RVG) speckle-tracking parameters  RVG peak strain 1.02 1.01–1.23 0.04  Time to RVG peak strain 1.02 1.01–1.05 0.03  RVG peak systolic strain rate 1.56 0.93–9.76 0.1  Time to RVG peak systolic rate 1.07 1.01–1.15 0.03  RV global late diastolic strain rate 1.62 1.09–4.25 0.04 RV dyssynchrony assessment (speckle-tracking)  RVFW myocardial shortening duration 1.82 1.02–4.94 0.03  Intra-RV dyssynchrony 1.21 1.10–1.23 0.01 Baseline variables OR 95% confidence interval P-value Conventional echo parameters  RA end-systolic area (echo) 0.29 0.11–0.74 0.03  RA emptying fraction (echo) 0.95 0.92–0.99 0.03 RA speckle-tracking variables  RA peak strain 2.51 1.84–2.61 0.01 RV free-wall (RVFW) speckle-tracking parameters  RVFW peak strain 1.39 1.25–1.99 0.02  Time to RVFW strain 1.05 1.03–1.17 0.03  RVFW systolic strain rate 1.04 1.02–2.35 0.05  Time to RVFW systolic strain rate 1.35 1.03–2.24 0.03  RVFW late diastolic strain rate 1.60 1.24–1.61 0.03 RV global (RVG) speckle-tracking parameters  RVG peak strain 1.02 1.01–1.23 0.04  Time to RVG peak strain 1.02 1.01–1.05 0.03  RVG peak systolic strain rate 1.56 0.93–9.76 0.1  Time to RVG peak systolic rate 1.07 1.01–1.15 0.03  RV global late diastolic strain rate 1.62 1.09–4.25 0.04 RV dyssynchrony assessment (speckle-tracking)  RVFW myocardial shortening duration 1.82 1.02–4.94 0.03  Intra-RV dyssynchrony 1.21 1.10–1.23 0.01 Table 8 Univariate predictors of RVAD support Baseline variables OR 95% confidence interval P-value Conventional echo parameters  RA end-systolic area (echo) 0.29 0.11–0.74 0.03  RA emptying fraction (echo) 0.95 0.92–0.99 0.03 RA speckle-tracking variables  RA peak strain 2.51 1.84–2.61 0.01 RV free-wall (RVFW) speckle-tracking parameters  RVFW peak strain 1.39 1.25–1.99 0.02  Time to RVFW strain 1.05 1.03–1.17 0.03  RVFW systolic strain rate 1.04 1.02–2.35 0.05  Time to RVFW systolic strain rate 1.35 1.03–2.24 0.03  RVFW late diastolic strain rate 1.60 1.24–1.61 0.03 RV global (RVG) speckle-tracking parameters  RVG peak strain 1.02 1.01–1.23 0.04  Time to RVG peak strain 1.02 1.01–1.05 0.03  RVG peak systolic strain rate 1.56 0.93–9.76 0.1  Time to RVG peak systolic rate 1.07 1.01–1.15 0.03  RV global late diastolic strain rate 1.62 1.09–4.25 0.04 RV dyssynchrony assessment (speckle-tracking)  RVFW myocardial shortening duration 1.82 1.02–4.94 0.03  Intra-RV dyssynchrony 1.21 1.10–1.23 0.01 Baseline variables OR 95% confidence interval P-value Conventional echo parameters  RA end-systolic area (echo) 0.29 0.11–0.74 0.03  RA emptying fraction (echo) 0.95 0.92–0.99 0.03 RA speckle-tracking variables  RA peak strain 2.51 1.84–2.61 0.01 RV free-wall (RVFW) speckle-tracking parameters  RVFW peak strain 1.39 1.25–1.99 0.02  Time to RVFW strain 1.05 1.03–1.17 0.03  RVFW systolic strain rate 1.04 1.02–2.35 0.05  Time to RVFW systolic strain rate 1.35 1.03–2.24 0.03  RVFW late diastolic strain rate 1.60 1.24–1.61 0.03 RV global (RVG) speckle-tracking parameters  RVG peak strain 1.02 1.01–1.23 0.04  Time to RVG peak strain 1.02 1.01–1.05 0.03  RVG peak systolic strain rate 1.56 0.93–9.76 0.1  Time to RVG peak systolic rate 1.07 1.01–1.15 0.03  RV global late diastolic strain rate 1.62 1.09–4.25 0.04 RV dyssynchrony assessment (speckle-tracking)  RVFW myocardial shortening duration 1.82 1.02–4.94 0.03  Intra-RV dyssynchrony 1.21 1.10–1.23 0.01 Independent predictors of RVAD support by multiple regression analysis The results of multiple regression analysis are shown in Figure 4. Three independent predictors were identified from the STE parameters: RALS (OR 2.5, 95% CI 1.37–2; P = 0.03), RVFW longitudinal peak strain (OR 1.3, 95% CI 1.03–2.3; P = 0.04) and intra-RV longitudinal dyssynchrony (OR 1.3, 95% CI 1.02–1.3; P = 0.04). Figure 4 View largeDownload slide Independent predictors of RVAD implantation during LVAD support and ROC curve analysis. RAS, RA peak strain; RVD, intra-RV dyssynchrony (DRVFW-IVS); RVFWS, free-wall RV peak strain. Figure 4 View largeDownload slide Independent predictors of RVAD implantation during LVAD support and ROC curve analysis. RAS, RA peak strain; RVD, intra-RV dyssynchrony (DRVFW-IVS); RVFWS, free-wall RV peak strain. 2D echo and speckle-tracking to predict RVAD support ROC curves were drawn and the areas under the curves (AUC) calculated (Figure 4). The strongest predictor was peak RA systolic strain (AUC 0.913), followed by intra-RV longitudinal dyssynchrony (AUC 0.845) and RV free-wall peak systolic strain (AUC 0.623). A value ≤10.5% predicted RVAD implantation with a sensitivity of 94% and specificity of 65%. Discussion To our knowledge, this is the first study to combine RA and RV STE to assess their value as predictors of the need for RVAD after LVAD implantation. Multivariable modelling identified pre-operative RALS, free-wall RV longitudinal peak strain (RVLS) and longitudinal intra-RV dyssynchrony (DRVFW-IVS) as independent predictors, stronger than conventional parameters including TAPSE, RVFCA, or tissue doppler imaging (TDI) S′.14 RA strain and SR analysis Patients in the RVAD group had lower pre-operative RALS suggesting a state of reduced RA compliance.15,16 RALS was the strongest independent predictor of RVAD implantation and was more sensitive than other echocardiographic parameters. RVAD patients also showed greater RA remodelling, indicated by larger RA area index.12 These findings may be associated with the significantly higher mean RAP and RVEDP noted in the RVAD group.15 RALS has been shown to reflect RVSWI, RV filling pressure, and pulmonary artery pressure and may be a useful parameter to include in the pre-operative assessment of LVAD candidates.11,15 RVAD patients also had lower RA late diastolic SR, an index of reduced RA pump functional capacity. At early stages of ventricular dysfunction, atrial contractility is increased to compensate for reduced early diastolic filling due to high RVEDP.7,16 However, in more advanced stages of ventricular dysfunction, atrial contractile capacity decreases compromising ventricular filling and output.16 Therefore, RA strain and SR parameters may reflect more advanced stages of compromised RV myocardial performance in the RVAD patients. Longitudinal RV peak systolic strain and strain rate analysis RVAD patients had lower pre-operative global and free-wall RVLS, along with lower, earlier-peaking RV longitudinal SR. Free-wall RVLS was an independent echocardiographic predictor of RVAD support. Our findings demonstrate pre-operative differences in RV functional reserve between the two groups, not demonstrated by invasively measured RVSWI or conventional echocardiographic parameters. Free-wall RVLS was a stronger predictor of RVAD support than global RVLS, consistent with published findings correlating RVSWI and free-wall RVLS.17 Global RVLS also includes septal strain18; thus it is not a ‘pure’ measure of RV mechanics. The RVAD group showed a greater degree of RV mechanical dyssynchrony. There was a greater delay in mechanical activation of the RVFW in relation to the IVS (DRVFW-IVS) and LVFW (DRVFW-LVFW). DRVFW-IVS was amongst the independent predictors of RVAD support. Our results agree with previous studies associating RV mechanical delay with RV dilatation and systolic dysfunction.19–21 The combination of increased free-wall RV mechanical delay and lower RVLS may indicate more advanced stages of intrinsic RV dysfunction. The RVAD group had higher pre-operative RVEDP. Increased pressure or volume loading results in higher ventricular wall tension and prolonged myocardial shortening,22,23 leading to ineffective, disco-ordinate RV contractility, especially after RV preload increases with the LVAD support.24 As a result, the RV fails to maintain adequate output and additional mechanical support is needed. Finally, we showed that RV myocardial shortening continued after PVC in a greater proportion of the RVAD patients. RV myocardial shortening after PVC does not contribute to RV ejection; it reflects increased RV dyssynchrony and impaired myocardial performance.23 Clinical implications Our study demonstrates potential value of RA and RV STE for preoperatively identifying LVAD candidates who may require additional RVAD support. To date, suggested RVF risk indices have focused on markers which reflect the consequences of RV dysfunction rather than intrinsic RV functional capacity.24,25 Our data suggest that incorporating RH STE into pre-operative assessment may allow better planning for biventricular mechanical support or implantation of a total artificial heart, hence leading to improved outcomes.9 Previous studies have shown the incremental prognostic value of reduced RVLS when added to conventional RVF risk factors.9,26 In our study, RALS, free-wall RVLS and DRVFW-IVS were the independent echocardiographic predictors of severe RVF requiring RVAD support. The most powerful predictor was RALS. However, the prognostic significance of these parameters needs to be evaluated prospectively in order to formulate a more sensitive, specific and fully descriptive index to guide peri-operative management. Study limitations Our study is subject to several limitations. First of all, it reflects the practice of a single institution in the UK where LVAD implantation is used as a bridge to transplantation or myocardial recovery but not as destination therapy. Ideally, a multi-centre study and hence a larger cohort of LVAD recipients is needed to validate and further develop these results. In this study, we analysed only longitudinal strain and SR and not circumferential or radial strain. This was felt to be valid considering that RV function depends mainly on longitudinal fibres with free-wall contraction generating 80% of the RVSV.27,28 At the time of analysis, there was no available software specifically for analysis of STE of the RH, so we used LV software with relevant adjustments. This method has been shown to be feasible in previously published studies with acceptable reproducibility.26 Conclusion In conclusion, our study has shown RA and RV strain analysis by STE to be more sensitive than conventional echocardiography for predicting the need for RVAD support after LVAD implantation. The most powerful predictor was RALS, but free-wall RVLS and DRVFW-IVS were also significant. An index combining these parameters with haemodynamic and clinical risk factors of post-LVAD implantation RVF could help to differentiate those AHF patients who will benefit from early BiVAD or artificial heart from those who are more suitable for long-term therapy with an LVAD. Conflict of interest: None declared. References 1 Trivedi JR , Cheng A , Singh R , Williams ML , Slaughter MS. Survival on the heart transplant waiting list: impact of continuous flow left ventricular assist device as bridge to transplant . Ann Thorac Surg 2014 ; 98 : 830 – 4 . Google Scholar CrossRef Search ADS PubMed 2 Kormos RL , Teuteberg JJ , Pagani FD , Russell SD , John R , Miller LW et al. Right ventricular failure in patients with the HeartMate II continuous-flow left ventricular assist device: incidence, risk factors, and effect on outcomes . J Thorac Cardiovasc Surg 2010 ; 139 : 1316 – 24 . Google Scholar CrossRef Search ADS PubMed 3 John R , Lee S , Eckman P , Liao K. Right ventricular failure-a continuing problem in patients with left ventricular assist device support . J Cardiovasc Transl Res 2010 ; 3 : 604 – 11 Google Scholar CrossRef Search ADS PubMed 4 Fitzpatrick JR 3rd , Frederick JR , Hiesinger W , Hsu VM , McCormick RC , Kozin ED et al. Early planned institution of biventricular mechanical circulatory support results in improved outcomes compared with delayed conversion of a left ventricular assist device to a biventricular assist device . J Thorac Cardiovasc Surg 2009 ; 137 : 971 – 7 . Google Scholar CrossRef Search ADS PubMed 5 Fitzpatrick JR 3rd , Frederick JR , Hsu VM , Kozin ED , O'Hara ML , Howell E et al. Risk score derived from pre-operative data analysis predicts the need for biventricular mechanical circulatory support . J Heart Lung Transplant 2008 ; 27 : 1286 – 92 . Google Scholar CrossRef Search ADS PubMed 6 Cameli M , Lisi M , Righini FM , Focardi M , Lunghetti S , Bernazzali S et al. Speckle tracking echocardiography as a new technique to evaluate right ventricular function in patients with left ventricular assist device therapy . J Heart Lung Transplant 2013 ; 32 : 424 – 30 . Google Scholar CrossRef Search ADS PubMed 7 Meris A , Faletra F , Conca C , Klersy C , Regoli F , Klimusina J et al. Timing and magnitude of regional right ventricular function: a speckle tracking-derived strain study of normal subjects and patients with right ventricular dysfunction . J Am Soc Echocardiogr 2010 ; 23 : 823 – 31 . 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Google Scholar CrossRef Search ADS PubMed 11 Padeletti M , Cameli M , Lisi M , Zacà V , Tsioulpas C , Bernazzali S et al. Right atrial speckle tracking analysis as a novel noninvasive method for pulmonary hemodynamics assessment in patients with chronic systolic heart failure . Echocardiography 2011 ; 28 : 658 – 6 . Google Scholar CrossRef Search ADS PubMed 12 D’Andrea A , Scarafile R , Riegler L , Salerno G , Gravino R , Cocchia R et al. Right atrial size and deformation in patients with dilated cardiomyopathy undergoing cardiac resynchronization therapy . Eur J Heart Fail 2009 ; 11 : 1169 – 77 . Google Scholar CrossRef Search ADS PubMed 13 Lang RM , Badano LP , Mor-Avi V , Afilalo J , Armstrong A , Ernande L et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging . Eur Heart J Cardiovasc Imaging 2015 ; 16 : 233 – 70 . Google Scholar CrossRef Search ADS PubMed 14 Rudski LG1 , Lai WW , Afilalo J , Hua L , Handschumacher MD , Chandrasekaran K et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography . J Am Soc Echocardiogr 2010 ; 23 : 685 – 713 . Google Scholar CrossRef Search ADS PubMed 15 Teixeira R , Monteiro R , Garcia J , Baptista R , Ribeiro M , Cardim N et al. The relationship between tricuspid regurgitation severity and right atrial mechanics: a speckle tracking echocardiography study . Int J Cardiovasc Imaging 2015 ; 31 : 1125 – 35 . Google Scholar CrossRef Search ADS PubMed 16 Leischik R , Littwitz H , Dworrak B , Garg P , Zhu M , Sahn DJ et al. Echocardiographic evaluation of left atrial mechanics: function, history, novel techniques, advantages, and pitfalls . Biomed Res Int 2015 ; 2015 : 765921. Google Scholar CrossRef Search ADS PubMed 17 Cameli M , Lisi M , Righini FM , Tsioulpas C , Bernazzali S , Maccherini M et al. Right ventricular longitudinal strain correlates well with right ventricular stroke work index in patients with advanced heart failure referred for heart transplantation . J Card Fail 2012 ; 18 : 208 – 15 . Google Scholar CrossRef Search ADS PubMed 18 Fine NM , Chen L , Bastiansen PM , Frantz RP , Pellikka PA , Oh JK et al. Reference values for right ventricular strain in patients without cardiopulmonary disease: a prospective evaluation and meta-analysis . Echocardiography 2015 ; 32 : 787 – 96 . Google Scholar CrossRef Search ADS PubMed 19 Esmaeilzadeh M , Poorzand H , Maleki M , Sadeghpour A , Parsaee M. Evaluation of longitudinal right ventricular mechanical dyssynchrony before and early after cardiac resynchronization therapy: a strain imaging study . J Tehran Heart Cent 2011 ; 6 : 24 – 30 . Google Scholar PubMed 20 Chow PC , Liang XC , Lam WW , Cheung EW , Wong KT , Cheung YF. Mechanical right ventricular dyssynchrony in patients after atrial switch operation for transposition of the great arteries . Am J Cardiol 2008 ; 101 : 874 – 8 . Google Scholar CrossRef Search ADS PubMed 21 Tops LF , Prakasa K , Tandri H , Dalal D , Jain R , Dimaano VL et al. Revalence and pathophysiologic attributes of ventricular dyssynchrony in arrhythmogenic right ventricular dysplasia/cardiomyopathy . J Am Coll Cardiol 2009 ; 54 : 445. Google Scholar CrossRef Search ADS PubMed 22 Schuster P , Faerestrand S , Ohm OJ. Color Doppler tissue velocity imaging can disclose systolic left ventricular asynchrony independent of the QRS morphology in patients with severe heart failure . Pacing Clin Electrophysiol 2004 ; 27 : 460 – 7 . Google Scholar CrossRef Search ADS PubMed 23 Marcus JT , Gan CT , Zwanenburg JJ , Boonstra A , Allaart CP , Götte MJ et al. Interventricular mechanical asynchrony in pulmonary arterial hypertension: left-to-right delay in peak shortening is related to right ventricular overload and left ventricular underfilling . J Am Coll Cardiol 2008 ; 51 : 750 – 7 . Google Scholar CrossRef Search ADS PubMed 24 Kerckhoffs RC , Bovendeerd PH , Kotte JC , Prinzen FW , Smits K , Arts T. Homogeneity of cardiac contraction despite physiological asynchrony of depolarization: a model study . Ann Biomed Eng 2003 ; 31 : 536 – 47 . Google Scholar CrossRef Search ADS PubMed 25 Matthews JC , Koelling TM , Pagani FD , Aaronson KD. The right ventricular failure risk score a pre-operative tool for assessing the risk of right ventricular failure in left ventricular assist device candidates . J Am Coll Cardiol 2008 ; 51 : 2163 – 72 . Google Scholar CrossRef Search ADS PubMed 26 Fukuda Y , Tanaka H , Sugiyama D , Ryo K , Onishi T , Fukuya H et al. Utility of right ventricular free wall speckle-tracking strain for evaluation of right ventricular performance in patients with pulmonary hypertension . J Am Soc Echocardiogr 2011 ; 24 : 1101 – 8 . Google Scholar CrossRef Search ADS PubMed 27 Carlsson M , Ugander M , Heiberg E , Arheden H. The quantitative relationship between longitudinal and radial function in left, right, and total heart pumping in humans . Am J Physiol Heart Circ Physiol 2007 ; 293 : H636 – 44 . Google Scholar CrossRef Search ADS PubMed 28 Padeletti M , Cameli M , Lisi M , Malandrino A , Zacà V , Mondillo S. Reference values of right atrial longitudinal strain imaging by two-dimensional speckle tracking . Echocardiography 2012 ; 29 : 147 – 52 . Google Scholar CrossRef Search ADS PubMed Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Heart Journal – Cardiovascular Imaging Oxford University Press

Right atrial and ventricular echocardiographic strain analysis predicts requirement for right ventricular support after left ventricular assist device implantation

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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com.
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Abstract

Abstract Aims The need for right ventricular assist device (RVAD) support after left ventricular assist device (LVAD) therapy is associated with increased morbidity and mortality. We used 2D echocardiographic strain analysis to assess right atrial (RA) and right ventricular (RV) mechanics and predict the need for RV mechanical support after LVAD implantation. Methods and results Seventy advanced chronic heart failure (ACHF) patients [59 male, age 47 ± 12 years, 79% dilated cardiomyopathy, left ventricular ejection fraction 23 ± 10%] received continuous-flow LVAD as a bridge to transplantation over an 18 month period. A retrospective analysis of RV and RA strain and right heart dyssynchrony was performed comparing those requiring RVAD (20%, n = 14) with those who did not (non-RVAD 80%, n = 56). One-year survival was significantly lower in the RVAD group (50% vs. 79%; P < 0.03). Independent predictors of RVAD support were: low peak RA longitudinal strain (RALS) [odds ratio (OR) 2.5, 95% confidence interval (95% CI) 1.37–2.0; P = 0.03], low RV free-wall longitudinal strain (RVFWLS) (OR 1.3, 95% CI 1.03–2.3; P = 0.04), and degree of intra-RV dyssynchrony (DRVFW-IVS, OR 1.3, 95% CI 1.02–1.3; P = 0.04). Conclusion In LVAD recipients needing RVAD support, there was lower RALS and RVFWLS in addition to greater RV free-wall mechanical delay. We conclude that RA and RV strain and dyssynchrony analysis have the potential to add incremental value to the pre-VAD-implantation assessment made using conventional echo measurements. right atrial strain , right ventricular strain , ventricular assist device , heart failure Introduction Left ventricular assist device (LVAD) implantation improves prognosis in patients with advanced chronic heart failure (ACHF) and is used as a bridge to transplantation or as destination therapy.1 The incidence of right ventricular failure (RVF) after LVAD implantation has decreased with the new-generation rotary devices.2 However, mortality and morbidity associated with severe RVF remain high.3 Outcomes may improve if high-risk patients are electively implanted with biventricular assist devices (BiVAD) at first surgery.4 However, current risk-prediction models have low sensitivity and specificity for identifying patients who would benefit from this approach.3,5 Strain analysis by two-dimensional speckle-tracking echocardiography (2DSTE) is a new method of studying right ventricular (RV) function.6–8 Studies suggest that reduced RV longitudinal strain is associated with a high risk of RVF9,10 and that reduced right atrial (RA) strain correlates with decreased myocardial reserve and less favourable outcomes.11,12 In this study, we used a combination of RA and RV longitudinal strain from 2DSTE to predict the need for right ventricular assist device (RVAD) in patients undergoing LVAD implantation. We also compared the prognostic value of RH 2DSTE with conventional echocardiographic parameters of RH performance. Methods We analysed data from patients who underwent continuous-flow LVAD implant at our centre within an 18 month period. Haemodynamic measurements were obtained during RH catheterization. Cardiac output (CO) and RV stroke volume (RVSV) were estimated by the Fick technique. The endpoint was development of post-operative RV failure requiring RVAD implantation within 30 days. Patients were divided into two groups: RVAD and non-RVAD, and comparisons were made for echo parameters including strain, strain rate (SR), and dyssynchrony. Echocardiography Echocardiograms were acquired and processed using commercially available systems (Vivid 7 and EchoPac; GE Vingmed Ultrasound AS, Amersham, UK) within 48 h prior to LVAD implantation. Digital loops of three cardiac cycles’ length were recorded with additional RV-focused apical 4-chamber (A4CH) views13,14 ensuring frame rate 55–80 fps. Analysis was performed by a single operator who had not been involved in image acquisition and who was blinded to subjects’ clinical details. Longitudinal strain and SR analyses were performed for the RA, RV, RV free wall (RVFW), interventricular septum (IVS), LV, and LV free wall (LVFW) (Figures 1–3). Pulmonary and aortic valve opening and closure times were identified and marked on the relevant image frames (Figures 1–3). Figure 1 View largeDownload slide Right ventricular (RV) myocardial strain (upper left and right) and strain rate (lower left and right) curves in a non-RVAD (left) and an RVAD (right) patient. The RVAD patient shows RV dyssynchrony and prolonged duration of global RV (white dotted curve) myocardial shortening, beyond pulmonary valve closure (yellow arrow). Longitudinal SRs also reached its peak value earlier in systole (white arrow). Figure 1 View largeDownload slide Right ventricular (RV) myocardial strain (upper left and right) and strain rate (lower left and right) curves in a non-RVAD (left) and an RVAD (right) patient. The RVAD patient shows RV dyssynchrony and prolonged duration of global RV (white dotted curve) myocardial shortening, beyond pulmonary valve closure (yellow arrow). Longitudinal SRs also reached its peak value earlier in systole (white arrow). Figure 2 View largeDownload slide RV free-wall (RVFW), septal, and LV free-wall (LVFW) strain curves from a RVAD patient. The dotted white lines in each curve represent the average strain for the RVFW, septum, and LVFW, respectively. The yellow arrows represent the time to longitudinal peak strain). Figure 2 View largeDownload slide RV free-wall (RVFW), septal, and LV free-wall (LVFW) strain curves from a RVAD patient. The dotted white lines in each curve represent the average strain for the RVFW, septum, and LVFW, respectively. The yellow arrows represent the time to longitudinal peak strain). Figure 3 View largeDownload slide Right atrial (RA) strain and strain rate curves from the right heart focused apical 4-chamber view in a non-RVAD (left) and a RVAD (right) patient. The white dotted curves represent the average strain and strain rate curves. Figure 3 View largeDownload slide Right atrial (RA) strain and strain rate curves from the right heart focused apical 4-chamber view in a non-RVAD (left) and a RVAD (right) patient. The white dotted curves represent the average strain and strain rate curves. The optimal RH image was selected and the endocardial border was traced manually on the end-diastolic frame. The region of interest (ROI) was adjusted to fit with RV wall thickness. The same was done for the left heart (LH) images. ROIs were subdivided into six standard segments for the RA, RV and LV, and three slices (basal, mid-ventricle, and apical) for the RVFW, IVS, and LVFW (Figures 1–3). Accuracy of automated tracking of cardiac contours through the cardiac cycle was assessed visually and corrected by manual adjustment as required. Subsequently, the software generated both segmental and mean strain and SR curves for each ROI (Figures 1–3). Time to ventricular longitudinal peak strain (RV global, RV free wall, septal, LVFW, and LV global, Figures 1 and 2) and time to RA or LA global longitudinal peak SR (Figure 3) were estimated from the S and SR curves. As a reference point, we used the onset of the QRS complex (for ventricular strain or SR) or the P wave (for atrial strain or SR) on the corresponding ECG. Each parameter is expressed as a proportion of the R-R interval. The terms systolic and diastolic in the atrial analysis refer to ventricular systole and diastole. To determine the degree of RV mechanical dyssynchrony prior to LVAD implantation, we examined the RV free wall mechanical delay in relation to both the IVS and the LVFW (Figure 2). Statistical analysis Analyses were performed using SPSS 12.0 software (SPSS Inc., Chicago, IL, USA). Continuous variables were expressed as mean ± standard deviation (SD). Categorical variables were expressed as frequencies or percentages. A two-tailed P-value <0.05 was considered a significant difference. The Student’s t-test and χ2 tests were used for between-group data comparisons. Univariable logistic regression was performed to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs) for the outcome ‘RVAD implantation’. This was followed by a multiple regression analysis of the detected univariate predictors in a forward stepwise fashion. The predictive values were obtained by determining the area under receiver operating characteristic (ROC) curves. Ethics approval The study has NHI ethics approval, and patients gave informed consent for data collection and use for this study. The study followed the principles of the Declaration of Helsinki for medical research. Results A total of 70 LVAD recipients were included in the study (47 ± 12 years, 59 male, left ventricular ejection fraction (LVEF): 23 ± 10%, ischaemic LV dysfunction: 23%, non-ischaemic dilated cardiomyopathy (DCM) 77%, NYHA functional Class III or IV). All participants were in sinus rhythm. Severe RVF requiring RVAD support developed in 14 (20%) patients within 72 h of LVAD implantation. One-year survival was 73% (51 patients). The 1-year mortality rates were 50% (7/14) and 21% (12/56) in the RVAD and non-RVAD groups, respectively (P = 0.03). Baseline characteristics Pre-LVAD implantation characteristics are shown in Table 1. There were no significant differences between the RVAD and non-RVAD groups in LVEF, cardiac index, RV stroke work index (RVSWI), and afterload parameters. RVAD patients had higher right ventricular end-diastolic pressure (RVEDP, 25 ± 6 mmHg vs. 16 ± 7; P = 0.008) and mean right atrial pressure (mRAP, 25 ± 5 mmHg vs. 15 ± 7; P = 0.01). No differences were shown in baseline RV or LV function indices between ischaemic and non-ischaemic HF patients (Table 2). Table 1 Patient characteristics, selected laboratory, and invasively measured haemodynamic data before LVAD implantation in RVAD and non-RVAD patients Baseline characteristics RVAD Non-RVAD P-value Clinical data  Age (years) 45 ± 11 48 ± 12 0.9  Male gender (n, %) 9 (64%) 50 (89%) 0.03  BSA (m2) 1.9 ± 0.2 2.3 ± 0.3 0.4  Ischaemic cause (n, %) 3 (21%) 13 (23%) 0.1  INTERMACS (n, %) 0.03   Class I 8 (57%) 16 (28%)   Class II 2 (14%) 16 (28%)   Class III 4 (29%) 22 (44%)  QRS (ms) 132 ± 33 128 ± 32 0.8  CRT (n, %) 3 (21%) 15 (27%) 0.5  Inotropic support (n, %) 12 (87%) 47 (84%) 0.3  Intra-aortic balloon pump preop. (n, %) 4 (28%) 7 (13%) 0.04  Mechanical ventilation preop. (n, %) 8 (38%) 10 (20%) 0.05 Laboratory data  Na (mmol/L) 135 ± 4 134 ± 4 0.4  UREA (mmol/L) 10 ± 6 9.4 ± 4 0.3  CREA (μmol/L) 124 ± 53 105 ± 32 0.01  Total bilirubin (μmol/L) 43 ± 20 22 ± 12 0.001  BNP (pg/mL) 1320 ± 1122 1361 ± 1058 0.2 Left heart functional parameters  LV ejection fraction (Simpson’s biplane, %) 22 ± 9 26 ± 11 0.2  LV myocardial performance index (TDI) 0.37 ± 0.21 0.40 ± 0.13 0.1  Cardiac index (L/min/m2) 1.8 ± 0.4 1.9 ± 0.5 0.3  Mitral valve regurgitation ≥moderate (n, %) 4 (19%) 7 (14%) 0.5  Pericardial effusion (n, %) 2 (10%) 5 (10%) 0.8 Right heart haemodynamic data  Mean right atrial pressure (mmHg) 25 ± 5 15 ± 7 0.01  RV end-diastolic pressure (mmHg) 25 ± 6 16 ± 7 0.008  Mean pulmonary artery pressure (mmHg) 32 ± 8 37 ± 12 0.1  Pulmonary vascular resistance index (WU/m2) 1.5 ± 1 1.9 ± 1.6 0.3  RV stroke work index (gm.m/m2/beat) 5.1 ± 3.3 5.9 ± 3.6 0.3 Baseline characteristics RVAD Non-RVAD P-value Clinical data  Age (years) 45 ± 11 48 ± 12 0.9  Male gender (n, %) 9 (64%) 50 (89%) 0.03  BSA (m2) 1.9 ± 0.2 2.3 ± 0.3 0.4  Ischaemic cause (n, %) 3 (21%) 13 (23%) 0.1  INTERMACS (n, %) 0.03   Class I 8 (57%) 16 (28%)   Class II 2 (14%) 16 (28%)   Class III 4 (29%) 22 (44%)  QRS (ms) 132 ± 33 128 ± 32 0.8  CRT (n, %) 3 (21%) 15 (27%) 0.5  Inotropic support (n, %) 12 (87%) 47 (84%) 0.3  Intra-aortic balloon pump preop. (n, %) 4 (28%) 7 (13%) 0.04  Mechanical ventilation preop. (n, %) 8 (38%) 10 (20%) 0.05 Laboratory data  Na (mmol/L) 135 ± 4 134 ± 4 0.4  UREA (mmol/L) 10 ± 6 9.4 ± 4 0.3  CREA (μmol/L) 124 ± 53 105 ± 32 0.01  Total bilirubin (μmol/L) 43 ± 20 22 ± 12 0.001  BNP (pg/mL) 1320 ± 1122 1361 ± 1058 0.2 Left heart functional parameters  LV ejection fraction (Simpson’s biplane, %) 22 ± 9 26 ± 11 0.2  LV myocardial performance index (TDI) 0.37 ± 0.21 0.40 ± 0.13 0.1  Cardiac index (L/min/m2) 1.8 ± 0.4 1.9 ± 0.5 0.3  Mitral valve regurgitation ≥moderate (n, %) 4 (19%) 7 (14%) 0.5  Pericardial effusion (n, %) 2 (10%) 5 (10%) 0.8 Right heart haemodynamic data  Mean right atrial pressure (mmHg) 25 ± 5 15 ± 7 0.01  RV end-diastolic pressure (mmHg) 25 ± 6 16 ± 7 0.008  Mean pulmonary artery pressure (mmHg) 32 ± 8 37 ± 12 0.1  Pulmonary vascular resistance index (WU/m2) 1.5 ± 1 1.9 ± 1.6 0.3  RV stroke work index (gm.m/m2/beat) 5.1 ± 3.3 5.9 ± 3.6 0.3 BSA, body surface area; CRT, cardiac resynchronization therapy; INTERMACS, Interagency Registry for Mechanically Assisted Circulatory Support; LV, left ventricular; preop., preoperatively; RV, right ventricular; TDI, tissue doppler imaging. Table 1 Patient characteristics, selected laboratory, and invasively measured haemodynamic data before LVAD implantation in RVAD and non-RVAD patients Baseline characteristics RVAD Non-RVAD P-value Clinical data  Age (years) 45 ± 11 48 ± 12 0.9  Male gender (n, %) 9 (64%) 50 (89%) 0.03  BSA (m2) 1.9 ± 0.2 2.3 ± 0.3 0.4  Ischaemic cause (n, %) 3 (21%) 13 (23%) 0.1  INTERMACS (n, %) 0.03   Class I 8 (57%) 16 (28%)   Class II 2 (14%) 16 (28%)   Class III 4 (29%) 22 (44%)  QRS (ms) 132 ± 33 128 ± 32 0.8  CRT (n, %) 3 (21%) 15 (27%) 0.5  Inotropic support (n, %) 12 (87%) 47 (84%) 0.3  Intra-aortic balloon pump preop. (n, %) 4 (28%) 7 (13%) 0.04  Mechanical ventilation preop. (n, %) 8 (38%) 10 (20%) 0.05 Laboratory data  Na (mmol/L) 135 ± 4 134 ± 4 0.4  UREA (mmol/L) 10 ± 6 9.4 ± 4 0.3  CREA (μmol/L) 124 ± 53 105 ± 32 0.01  Total bilirubin (μmol/L) 43 ± 20 22 ± 12 0.001  BNP (pg/mL) 1320 ± 1122 1361 ± 1058 0.2 Left heart functional parameters  LV ejection fraction (Simpson’s biplane, %) 22 ± 9 26 ± 11 0.2  LV myocardial performance index (TDI) 0.37 ± 0.21 0.40 ± 0.13 0.1  Cardiac index (L/min/m2) 1.8 ± 0.4 1.9 ± 0.5 0.3  Mitral valve regurgitation ≥moderate (n, %) 4 (19%) 7 (14%) 0.5  Pericardial effusion (n, %) 2 (10%) 5 (10%) 0.8 Right heart haemodynamic data  Mean right atrial pressure (mmHg) 25 ± 5 15 ± 7 0.01  RV end-diastolic pressure (mmHg) 25 ± 6 16 ± 7 0.008  Mean pulmonary artery pressure (mmHg) 32 ± 8 37 ± 12 0.1  Pulmonary vascular resistance index (WU/m2) 1.5 ± 1 1.9 ± 1.6 0.3  RV stroke work index (gm.m/m2/beat) 5.1 ± 3.3 5.9 ± 3.6 0.3 Baseline characteristics RVAD Non-RVAD P-value Clinical data  Age (years) 45 ± 11 48 ± 12 0.9  Male gender (n, %) 9 (64%) 50 (89%) 0.03  BSA (m2) 1.9 ± 0.2 2.3 ± 0.3 0.4  Ischaemic cause (n, %) 3 (21%) 13 (23%) 0.1  INTERMACS (n, %) 0.03   Class I 8 (57%) 16 (28%)   Class II 2 (14%) 16 (28%)   Class III 4 (29%) 22 (44%)  QRS (ms) 132 ± 33 128 ± 32 0.8  CRT (n, %) 3 (21%) 15 (27%) 0.5  Inotropic support (n, %) 12 (87%) 47 (84%) 0.3  Intra-aortic balloon pump preop. (n, %) 4 (28%) 7 (13%) 0.04  Mechanical ventilation preop. (n, %) 8 (38%) 10 (20%) 0.05 Laboratory data  Na (mmol/L) 135 ± 4 134 ± 4 0.4  UREA (mmol/L) 10 ± 6 9.4 ± 4 0.3  CREA (μmol/L) 124 ± 53 105 ± 32 0.01  Total bilirubin (μmol/L) 43 ± 20 22 ± 12 0.001  BNP (pg/mL) 1320 ± 1122 1361 ± 1058 0.2 Left heart functional parameters  LV ejection fraction (Simpson’s biplane, %) 22 ± 9 26 ± 11 0.2  LV myocardial performance index (TDI) 0.37 ± 0.21 0.40 ± 0.13 0.1  Cardiac index (L/min/m2) 1.8 ± 0.4 1.9 ± 0.5 0.3  Mitral valve regurgitation ≥moderate (n, %) 4 (19%) 7 (14%) 0.5  Pericardial effusion (n, %) 2 (10%) 5 (10%) 0.8 Right heart haemodynamic data  Mean right atrial pressure (mmHg) 25 ± 5 15 ± 7 0.01  RV end-diastolic pressure (mmHg) 25 ± 6 16 ± 7 0.008  Mean pulmonary artery pressure (mmHg) 32 ± 8 37 ± 12 0.1  Pulmonary vascular resistance index (WU/m2) 1.5 ± 1 1.9 ± 1.6 0.3  RV stroke work index (gm.m/m2/beat) 5.1 ± 3.3 5.9 ± 3.6 0.3 BSA, body surface area; CRT, cardiac resynchronization therapy; INTERMACS, Interagency Registry for Mechanically Assisted Circulatory Support; LV, left ventricular; preop., preoperatively; RV, right ventricular; TDI, tissue doppler imaging. Table 2 Baseline RV and LV function according to heart failure aetiology HF substrate RVSWI (gm.m/m2/beat) TAPSE (mm) LVEF (%) MAPSE (mm) Ischaemic 4.5 ± 2.4 12 ± 4.3 25 ± 9.8 9 ± 2.6 Non-ischaemic 6.5 ± 4.5 13 ± 4 22 ± 10 9.1 ± 2.8 P-value 0.2 0.2 0.3 0.9 HF substrate RVSWI (gm.m/m2/beat) TAPSE (mm) LVEF (%) MAPSE (mm) Ischaemic 4.5 ± 2.4 12 ± 4.3 25 ± 9.8 9 ± 2.6 Non-ischaemic 6.5 ± 4.5 13 ± 4 22 ± 10 9.1 ± 2.8 P-value 0.2 0.2 0.3 0.9 LVEF, left ventricular ejection fraction; MAPSE, mitral annular systolic plane excursion; RVSWI, RV stroke work index; TAPSE, tricuspid annular plane systolic excursion. Table 2 Baseline RV and LV function according to heart failure aetiology HF substrate RVSWI (gm.m/m2/beat) TAPSE (mm) LVEF (%) MAPSE (mm) Ischaemic 4.5 ± 2.4 12 ± 4.3 25 ± 9.8 9 ± 2.6 Non-ischaemic 6.5 ± 4.5 13 ± 4 22 ± 10 9.1 ± 2.8 P-value 0.2 0.2 0.3 0.9 HF substrate RVSWI (gm.m/m2/beat) TAPSE (mm) LVEF (%) MAPSE (mm) Ischaemic 4.5 ± 2.4 12 ± 4.3 25 ± 9.8 9 ± 2.6 Non-ischaemic 6.5 ± 4.5 13 ± 4 22 ± 10 9.1 ± 2.8 P-value 0.2 0.2 0.3 0.9 LVEF, left ventricular ejection fraction; MAPSE, mitral annular systolic plane excursion; RVSWI, RV stroke work index; TAPSE, tricuspid annular plane systolic excursion. Baseline echocardiographic parameters Echocardiographic parameters for the RH are shown in Table 3. There were no significant differences between the groups for parameters reflecting RV contractility, diastolic function and remodelling, including fractional change area (RVFCA), tricuspid annular plane systolic excursion (TAPSE), and RV myocardial (RVMPI performance index). However, RVAD recipients had significantly larger RA areas, lower RA fractional area change (RAFCA), and lower RA emptying fraction. No statistically significant differences between the two groups were found for LA and LV parameters. Table 3 Baseline right heart conventional echocardiographic parameters RH echocardiographic parameters RVAD Non-RVAD P-value RA function  RA end-diastolic area (cm2) 30 ± 12 21 ± 8 0.001  RA end-systolic area (cm2) 36 ± 11 25 ± 8 0.02  RA FAC (%) 22 ± 13 32 ± 12 0.04  RA emptying fraction (%) 21 ± 15 35 ± 16 0.04 RV dimensions  RV basal diameter (mm) 43 ± 9 45 ± 9 0.3  RV mid-cavity diameter (mm) 34 ± 10 36 ± 7 0.5  RV longitudinal dimension (mm) 75 ± 16 79 ± 13 0.3  RV wall thickness (cm) 0.5 ± 0.2 0.45 ± 0.1 0.7  LV eccentricity index 1.12 ± 0.15 0.96 ± 0.12 0.07 RV systolic function  TAPSE (mm) 12 ± 4 13 ± 4 0.1  Lateral St′ (m/s) 0.95 ± 0.1 0.98 ± 0.1 0.6  RV myocardial performance index 0.46 ± 0.1 0.44 ± 0.08 0.5  RV FAC (%) 29 ± 13 30 ± 12 0.7  RV ejection time (ms) 230 ± 38 231 ± 49 0.9  RV outflow acceleration time (ms) 93 ± 29 88 ± 22 0.4 RV diastolic function  Et (m/s) 0.87 ± 0.2 0.84 ± 0.2 0.3  At (m/s) 0.75 ± 0.2 0.74 ± 0.2 0.2  Et/At 1.2 ± 0.3 1.1 ± 0.1 0.7  Et wave deceleration time (ms) 178 ± 90 148 ± 56 0.1  Et/Et′ 7.5 ± 1.2 7.2 ± 1.5 0.4 Haemodynamic surrogates  TR jet estimated RVSP (mmHg) 43 ± 14 40 ± 16 0.7  PR estimated RVDP (mmHg) 10 ± 5 8 ± 5 0.4  Tricuspid valve regurgitation (TR) ≥ moderate (n, %) 4 (19%) 9 (18%) 0.3  Pulmonary valve regurgitation (PR) > mild (n, %) 1 (5%) 2 (5%) 0.6 RH echocardiographic parameters RVAD Non-RVAD P-value RA function  RA end-diastolic area (cm2) 30 ± 12 21 ± 8 0.001  RA end-systolic area (cm2) 36 ± 11 25 ± 8 0.02  RA FAC (%) 22 ± 13 32 ± 12 0.04  RA emptying fraction (%) 21 ± 15 35 ± 16 0.04 RV dimensions  RV basal diameter (mm) 43 ± 9 45 ± 9 0.3  RV mid-cavity diameter (mm) 34 ± 10 36 ± 7 0.5  RV longitudinal dimension (mm) 75 ± 16 79 ± 13 0.3  RV wall thickness (cm) 0.5 ± 0.2 0.45 ± 0.1 0.7  LV eccentricity index 1.12 ± 0.15 0.96 ± 0.12 0.07 RV systolic function  TAPSE (mm) 12 ± 4 13 ± 4 0.1  Lateral St′ (m/s) 0.95 ± 0.1 0.98 ± 0.1 0.6  RV myocardial performance index 0.46 ± 0.1 0.44 ± 0.08 0.5  RV FAC (%) 29 ± 13 30 ± 12 0.7  RV ejection time (ms) 230 ± 38 231 ± 49 0.9  RV outflow acceleration time (ms) 93 ± 29 88 ± 22 0.4 RV diastolic function  Et (m/s) 0.87 ± 0.2 0.84 ± 0.2 0.3  At (m/s) 0.75 ± 0.2 0.74 ± 0.2 0.2  Et/At 1.2 ± 0.3 1.1 ± 0.1 0.7  Et wave deceleration time (ms) 178 ± 90 148 ± 56 0.1  Et/Et′ 7.5 ± 1.2 7.2 ± 1.5 0.4 Haemodynamic surrogates  TR jet estimated RVSP (mmHg) 43 ± 14 40 ± 16 0.7  PR estimated RVDP (mmHg) 10 ± 5 8 ± 5 0.4  Tricuspid valve regurgitation (TR) ≥ moderate (n, %) 4 (19%) 9 (18%) 0.3  Pulmonary valve regurgitation (PR) > mild (n, %) 1 (5%) 2 (5%) 0.6 At, tricuspid annular late diastolic velocity on TDI; Et, TDI tricuspid annular early diastolic velocity; FAC, fractional area change; LV, left ventricular; PR, pulmonary valve regurgitation; RA, right atrial; RV, right ventricular; RVDP, RV diastolic pressure; RVSP, RV systolic pressure; TAPSE, tricuspid annular plane systolic excursion; St′, tricuspid annular systolic velocity on TDI; TR, tricuspid valve regurgitation. Table 3 Baseline right heart conventional echocardiographic parameters RH echocardiographic parameters RVAD Non-RVAD P-value RA function  RA end-diastolic area (cm2) 30 ± 12 21 ± 8 0.001  RA end-systolic area (cm2) 36 ± 11 25 ± 8 0.02  RA FAC (%) 22 ± 13 32 ± 12 0.04  RA emptying fraction (%) 21 ± 15 35 ± 16 0.04 RV dimensions  RV basal diameter (mm) 43 ± 9 45 ± 9 0.3  RV mid-cavity diameter (mm) 34 ± 10 36 ± 7 0.5  RV longitudinal dimension (mm) 75 ± 16 79 ± 13 0.3  RV wall thickness (cm) 0.5 ± 0.2 0.45 ± 0.1 0.7  LV eccentricity index 1.12 ± 0.15 0.96 ± 0.12 0.07 RV systolic function  TAPSE (mm) 12 ± 4 13 ± 4 0.1  Lateral St′ (m/s) 0.95 ± 0.1 0.98 ± 0.1 0.6  RV myocardial performance index 0.46 ± 0.1 0.44 ± 0.08 0.5  RV FAC (%) 29 ± 13 30 ± 12 0.7  RV ejection time (ms) 230 ± 38 231 ± 49 0.9  RV outflow acceleration time (ms) 93 ± 29 88 ± 22 0.4 RV diastolic function  Et (m/s) 0.87 ± 0.2 0.84 ± 0.2 0.3  At (m/s) 0.75 ± 0.2 0.74 ± 0.2 0.2  Et/At 1.2 ± 0.3 1.1 ± 0.1 0.7  Et wave deceleration time (ms) 178 ± 90 148 ± 56 0.1  Et/Et′ 7.5 ± 1.2 7.2 ± 1.5 0.4 Haemodynamic surrogates  TR jet estimated RVSP (mmHg) 43 ± 14 40 ± 16 0.7  PR estimated RVDP (mmHg) 10 ± 5 8 ± 5 0.4  Tricuspid valve regurgitation (TR) ≥ moderate (n, %) 4 (19%) 9 (18%) 0.3  Pulmonary valve regurgitation (PR) > mild (n, %) 1 (5%) 2 (5%) 0.6 RH echocardiographic parameters RVAD Non-RVAD P-value RA function  RA end-diastolic area (cm2) 30 ± 12 21 ± 8 0.001  RA end-systolic area (cm2) 36 ± 11 25 ± 8 0.02  RA FAC (%) 22 ± 13 32 ± 12 0.04  RA emptying fraction (%) 21 ± 15 35 ± 16 0.04 RV dimensions  RV basal diameter (mm) 43 ± 9 45 ± 9 0.3  RV mid-cavity diameter (mm) 34 ± 10 36 ± 7 0.5  RV longitudinal dimension (mm) 75 ± 16 79 ± 13 0.3  RV wall thickness (cm) 0.5 ± 0.2 0.45 ± 0.1 0.7  LV eccentricity index 1.12 ± 0.15 0.96 ± 0.12 0.07 RV systolic function  TAPSE (mm) 12 ± 4 13 ± 4 0.1  Lateral St′ (m/s) 0.95 ± 0.1 0.98 ± 0.1 0.6  RV myocardial performance index 0.46 ± 0.1 0.44 ± 0.08 0.5  RV FAC (%) 29 ± 13 30 ± 12 0.7  RV ejection time (ms) 230 ± 38 231 ± 49 0.9  RV outflow acceleration time (ms) 93 ± 29 88 ± 22 0.4 RV diastolic function  Et (m/s) 0.87 ± 0.2 0.84 ± 0.2 0.3  At (m/s) 0.75 ± 0.2 0.74 ± 0.2 0.2  Et/At 1.2 ± 0.3 1.1 ± 0.1 0.7  Et wave deceleration time (ms) 178 ± 90 148 ± 56 0.1  Et/Et′ 7.5 ± 1.2 7.2 ± 1.5 0.4 Haemodynamic surrogates  TR jet estimated RVSP (mmHg) 43 ± 14 40 ± 16 0.7  PR estimated RVDP (mmHg) 10 ± 5 8 ± 5 0.4  Tricuspid valve regurgitation (TR) ≥ moderate (n, %) 4 (19%) 9 (18%) 0.3  Pulmonary valve regurgitation (PR) > mild (n, %) 1 (5%) 2 (5%) 0.6 At, tricuspid annular late diastolic velocity on TDI; Et, TDI tricuspid annular early diastolic velocity; FAC, fractional area change; LV, left ventricular; PR, pulmonary valve regurgitation; RA, right atrial; RV, right ventricular; RVDP, RV diastolic pressure; RVSP, RV systolic pressure; TAPSE, tricuspid annular plane systolic excursion; St′, tricuspid annular systolic velocity on TDI; TR, tricuspid valve regurgitation. Atrial strain and strain rate results from STE RA strain parameters are shown in Table 4. The RVAD group had significantly lower pre-operative RA peak strain (11 ± 1% vs. 33 ± 8%; P = 0.004), longer time to peak strain (0.49 ± 0.05 vs. 0.58 ± 0.02; P = 0.05), and lower RA late diastolic SR (0.51 ± 0.5 s−1 vs. 0.62 ± 0.46 s−1, P = 0.04). No significant differences were noted for the LA STE parameters. Table 4 Right atrial (RA) strain and strain rate (SR) parameters RA strain parameters RVAD Non-RVAD P-value Peak strain (%) 11 ± 1 33 ± 8 0.004 Time to peak strain/R-R 0.58 ± 0.02 0.49 ± 0.05 0.05 Peak systolica SR (s−1) 0.71 ± 0.36 0.73 ± 0.38 0.9 Peak early diastolicb strain (s−1) 0.66 ± 0.22 0.68 ± 0.15 0.5 Peak late diastolic SR (s−1) 0.51 ± 0.50 0.62 ± 0.46 0.04 RA strain parameters RVAD Non-RVAD P-value Peak strain (%) 11 ± 1 33 ± 8 0.004 Time to peak strain/R-R 0.58 ± 0.02 0.49 ± 0.05 0.05 Peak systolica SR (s−1) 0.71 ± 0.36 0.73 ± 0.38 0.9 Peak early diastolicb strain (s−1) 0.66 ± 0.22 0.68 ± 0.15 0.5 Peak late diastolic SR (s−1) 0.51 ± 0.50 0.62 ± 0.46 0.04 a Systolic refers to ventricular systole. b Diastolic refers to ventricular diastole. Table 4 Right atrial (RA) strain and strain rate (SR) parameters RA strain parameters RVAD Non-RVAD P-value Peak strain (%) 11 ± 1 33 ± 8 0.004 Time to peak strain/R-R 0.58 ± 0.02 0.49 ± 0.05 0.05 Peak systolica SR (s−1) 0.71 ± 0.36 0.73 ± 0.38 0.9 Peak early diastolicb strain (s−1) 0.66 ± 0.22 0.68 ± 0.15 0.5 Peak late diastolic SR (s−1) 0.51 ± 0.50 0.62 ± 0.46 0.04 RA strain parameters RVAD Non-RVAD P-value Peak strain (%) 11 ± 1 33 ± 8 0.004 Time to peak strain/R-R 0.58 ± 0.02 0.49 ± 0.05 0.05 Peak systolica SR (s−1) 0.71 ± 0.36 0.73 ± 0.38 0.9 Peak early diastolicb strain (s−1) 0.66 ± 0.22 0.68 ± 0.15 0.5 Peak late diastolic SR (s−1) 0.51 ± 0.50 0.62 ± 0.46 0.04 a Systolic refers to ventricular systole. b Diastolic refers to ventricular diastole. Ventricular strain and strain rate results from STE RV strain and SR parameters are shown in Table 5. RV global longitudinal peak strain was lower in the RVAD group than in the non-RVAD patients (8.0 ± 2.8% vs. 9.2 ± 4.5%, P = 0.02), as was RVFW peak strain (8.6% ± 2.7 vs. 11.8% ± 6.2, P = 0.01). RVFW longitudinal peak systolic SR was also significantly lower in the RVAD group and occurred earlier during the cardiac cycle. Table 5 Systolic ventricular strain and strain rate (SR) analysis Ventricular strain parameters RVAD Non-RVAD P-value Peak systolic strain (%) RV global 8.0 ± 2.8 9.2 ± 4.5 0.02 RV free wall 8.6 ± 2.7 11.8 ± 6.2 0.01 Septal 7.9 ± 4.4 8.6 ± 6.0 0.4 Time to peak systolic strain/R-R (%) RV global 56 ± 19 46 ± 17 0.04 (Myocardial shortening duration) RV free wall 57 ± 10 45 ± 20 0.03 Septal 55 ± 17 54 ± 18 0.9 Peak systolic SR (s−1) RV global 0.61 ± 0.32 0.62 ± 0.24 0.1 RV free wall 0.84 ± 0.47 1.10 ± 0.30 0.04 Septal 0.58 ± 0.29 0.65 ± 0.29 0.9 Time to peak systolic SR/R-R RV global 0.22 ± 0.05 0.32 ± 0.01 0.04 RV free wall 0.17 ± 0.01 0.28 ± 0.01 0.03 Septal 0.34 ± 0.19 0.28 ± 0.12 0.2 Peak early diastolic SR (s−1) RV global 0.62 ± 0.44 0.61 ± 0.39 0.2 RV free wall 0.97 ± 0.47 1.05 ± 0.66 0.1 Septal 0.52 ± 0.39 0.62 ± 0.40 0.8 Peak late diastolic SR (s−1) RV global 0.38 ± 0.21 0.51 ± 0.42 0.01 RV free wall 0.53 ± 0.50 0.73 ± 0.60 0.04 Septal 0.32 ± 0.30 0.32 ± 0.23 0.09 Post-PVC RV myocardial shortening (n, %) RV global 17(81%) 34(70%) 0.04 RV free wall 17(81%) 34(70%) 0.04 Septal 18(86%) 40(82%) 0.5 Ventricular strain parameters RVAD Non-RVAD P-value Peak systolic strain (%) RV global 8.0 ± 2.8 9.2 ± 4.5 0.02 RV free wall 8.6 ± 2.7 11.8 ± 6.2 0.01 Septal 7.9 ± 4.4 8.6 ± 6.0 0.4 Time to peak systolic strain/R-R (%) RV global 56 ± 19 46 ± 17 0.04 (Myocardial shortening duration) RV free wall 57 ± 10 45 ± 20 0.03 Septal 55 ± 17 54 ± 18 0.9 Peak systolic SR (s−1) RV global 0.61 ± 0.32 0.62 ± 0.24 0.1 RV free wall 0.84 ± 0.47 1.10 ± 0.30 0.04 Septal 0.58 ± 0.29 0.65 ± 0.29 0.9 Time to peak systolic SR/R-R RV global 0.22 ± 0.05 0.32 ± 0.01 0.04 RV free wall 0.17 ± 0.01 0.28 ± 0.01 0.03 Septal 0.34 ± 0.19 0.28 ± 0.12 0.2 Peak early diastolic SR (s−1) RV global 0.62 ± 0.44 0.61 ± 0.39 0.2 RV free wall 0.97 ± 0.47 1.05 ± 0.66 0.1 Septal 0.52 ± 0.39 0.62 ± 0.40 0.8 Peak late diastolic SR (s−1) RV global 0.38 ± 0.21 0.51 ± 0.42 0.01 RV free wall 0.53 ± 0.50 0.73 ± 0.60 0.04 Septal 0.32 ± 0.30 0.32 ± 0.23 0.09 Post-PVC RV myocardial shortening (n, %) RV global 17(81%) 34(70%) 0.04 RV free wall 17(81%) 34(70%) 0.04 Septal 18(86%) 40(82%) 0.5 PVC, pulmonary valve closure. Table 5 Systolic ventricular strain and strain rate (SR) analysis Ventricular strain parameters RVAD Non-RVAD P-value Peak systolic strain (%) RV global 8.0 ± 2.8 9.2 ± 4.5 0.02 RV free wall 8.6 ± 2.7 11.8 ± 6.2 0.01 Septal 7.9 ± 4.4 8.6 ± 6.0 0.4 Time to peak systolic strain/R-R (%) RV global 56 ± 19 46 ± 17 0.04 (Myocardial shortening duration) RV free wall 57 ± 10 45 ± 20 0.03 Septal 55 ± 17 54 ± 18 0.9 Peak systolic SR (s−1) RV global 0.61 ± 0.32 0.62 ± 0.24 0.1 RV free wall 0.84 ± 0.47 1.10 ± 0.30 0.04 Septal 0.58 ± 0.29 0.65 ± 0.29 0.9 Time to peak systolic SR/R-R RV global 0.22 ± 0.05 0.32 ± 0.01 0.04 RV free wall 0.17 ± 0.01 0.28 ± 0.01 0.03 Septal 0.34 ± 0.19 0.28 ± 0.12 0.2 Peak early diastolic SR (s−1) RV global 0.62 ± 0.44 0.61 ± 0.39 0.2 RV free wall 0.97 ± 0.47 1.05 ± 0.66 0.1 Septal 0.52 ± 0.39 0.62 ± 0.40 0.8 Peak late diastolic SR (s−1) RV global 0.38 ± 0.21 0.51 ± 0.42 0.01 RV free wall 0.53 ± 0.50 0.73 ± 0.60 0.04 Septal 0.32 ± 0.30 0.32 ± 0.23 0.09 Post-PVC RV myocardial shortening (n, %) RV global 17(81%) 34(70%) 0.04 RV free wall 17(81%) 34(70%) 0.04 Septal 18(86%) 40(82%) 0.5 Ventricular strain parameters RVAD Non-RVAD P-value Peak systolic strain (%) RV global 8.0 ± 2.8 9.2 ± 4.5 0.02 RV free wall 8.6 ± 2.7 11.8 ± 6.2 0.01 Septal 7.9 ± 4.4 8.6 ± 6.0 0.4 Time to peak systolic strain/R-R (%) RV global 56 ± 19 46 ± 17 0.04 (Myocardial shortening duration) RV free wall 57 ± 10 45 ± 20 0.03 Septal 55 ± 17 54 ± 18 0.9 Peak systolic SR (s−1) RV global 0.61 ± 0.32 0.62 ± 0.24 0.1 RV free wall 0.84 ± 0.47 1.10 ± 0.30 0.04 Septal 0.58 ± 0.29 0.65 ± 0.29 0.9 Time to peak systolic SR/R-R RV global 0.22 ± 0.05 0.32 ± 0.01 0.04 RV free wall 0.17 ± 0.01 0.28 ± 0.01 0.03 Septal 0.34 ± 0.19 0.28 ± 0.12 0.2 Peak early diastolic SR (s−1) RV global 0.62 ± 0.44 0.61 ± 0.39 0.2 RV free wall 0.97 ± 0.47 1.05 ± 0.66 0.1 Septal 0.52 ± 0.39 0.62 ± 0.40 0.8 Peak late diastolic SR (s−1) RV global 0.38 ± 0.21 0.51 ± 0.42 0.01 RV free wall 0.53 ± 0.50 0.73 ± 0.60 0.04 Septal 0.32 ± 0.30 0.32 ± 0.23 0.09 Post-PVC RV myocardial shortening (n, %) RV global 17(81%) 34(70%) 0.04 RV free wall 17(81%) 34(70%) 0.04 Septal 18(86%) 40(82%) 0.5 PVC, pulmonary valve closure. Global and free-wall RV myocardial shortening (time to longitudinal peak strain/R-R) was significantly longer for the RVAD patients (RV global: 56 ± %19 vs. 46± 17%; P < 0.04 and RVFW: 57 ± 10% vs. 45 ± 20%; P < 0.03). This group showed continuation of RVFW myocardial shortening beyond the time of pulmonary valve closure (PVC) (n = 17, 81% vs. n = 34, 70%, P = 0.04). Finally, lower global and free-wall RV late diastolic strain rates were observed in the RVAD group. No significant differences were noted between the two groups for the LV strain and SR parameters. RV mechanical dyssynchrony Analysis of RVFW mechanical delay in relation to both the IVS and the LVFW showed that the RVAD group showed a greater degree of both intra-RV and interventricular dyssynchrony preoperatively (Table 6). Table 6 Ventricular dyssynchrony parameters Dyssynchrony parameters RVAD Non-RVAD P-value Intra-RV dyssynchrony, DRVFW-IVS (RV free wall to septal peak strain time difference, ms) 117 ± 92 53 ± 38 0.03 Intra-LV dyssychrony, DLVFW-IVS (LV free wall to septal peak strain time difference, ms) 109 ± 51 69 ± 48 0.05 Interventricular dyssynchrony, DRVFW-LVFW (RV free wall to LV free-wall peak strain time difference, ms) 116 ± 75 78 ± 40 0.03 Dyssynchrony parameters RVAD Non-RVAD P-value Intra-RV dyssynchrony, DRVFW-IVS (RV free wall to septal peak strain time difference, ms) 117 ± 92 53 ± 38 0.03 Intra-LV dyssychrony, DLVFW-IVS (LV free wall to septal peak strain time difference, ms) 109 ± 51 69 ± 48 0.05 Interventricular dyssynchrony, DRVFW-LVFW (RV free wall to LV free-wall peak strain time difference, ms) 116 ± 75 78 ± 40 0.03 Table 6 Ventricular dyssynchrony parameters Dyssynchrony parameters RVAD Non-RVAD P-value Intra-RV dyssynchrony, DRVFW-IVS (RV free wall to septal peak strain time difference, ms) 117 ± 92 53 ± 38 0.03 Intra-LV dyssychrony, DLVFW-IVS (LV free wall to septal peak strain time difference, ms) 109 ± 51 69 ± 48 0.05 Interventricular dyssynchrony, DRVFW-LVFW (RV free wall to LV free-wall peak strain time difference, ms) 116 ± 75 78 ± 40 0.03 Dyssynchrony parameters RVAD Non-RVAD P-value Intra-RV dyssynchrony, DRVFW-IVS (RV free wall to septal peak strain time difference, ms) 117 ± 92 53 ± 38 0.03 Intra-LV dyssychrony, DLVFW-IVS (LV free wall to septal peak strain time difference, ms) 109 ± 51 69 ± 48 0.05 Interventricular dyssynchrony, DRVFW-LVFW (RV free wall to LV free-wall peak strain time difference, ms) 116 ± 75 78 ± 40 0.03 Correlations of RA and RV strain with invasively determined haemodynamic parameters RA strain correlates relatively strongly with RVEDP (r = −0.57, P < 0.01), moderately with RVSWI (r = 0.39, P = 0.02) and mRAP (−0.39, P = 0.02) and weakly with RA end-systolic area (0.31, P = 0.03). RV strain correlates moderately with RVSWI (r = −0.35, P = 0.03), mRAP (r = −0.39, P = 0.01) and weekly with RA area (r = 0.3, P = 0.04). Table 7 shows the relationship between invasively determined indices of pulmonary hypertension (PH), HF substrate, and post-operative RVAD need. MRAP was significantly higher in the RVAD than in the non-RVAD patients for both ischaemic and non-ischaemic HF. There were no significant differences between the two groups for the majority of pre-LVAD PH indices. However, in the ischaemic HF group, RVAD patients had higher PVR 6 months post-LVAD. Table 7 Pre- and post-LVAD pulmonary arterial hypertension indices according heart failure aetiology Pre-LVAD Post-LVAD sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) Ischaemic (n = 15) RVAD (n = 4) 46 ± 15 30 ± 10 28 ± 10 3.1 ± 2 45 ± 4 32 ± 2 14 ± 10 3 ± 1.8 Non-RVAD (n = 11) 50 ± 15 34 ± 11 17 ± 8 3.4 ± 1.5 30 ± 11 20 ± 8 7 ± 2 1.5 ± 1 P-value 0.8 0.7 0.01 0.9 0.08 0.07 0.2 0.007 Non-ischaemic (n = 55) RVAD (n = 10) 57 ± 19 39 ± 12 24 ± 9 2.9 ± 1 31 ± 6 19 ± 4 7 ± 4 1.4 ± 1 Non-RVAD (n = 45) 48 ± 15 34 ± 10 15 ± 7 3.4 ± 2 31 ± 11 20 ± 9 8 ± 6 1.5 ± 1 P-value 0.1 0.1 0.01 0.9 0.9 0.6 0.6 0.5 Pre-LVAD Post-LVAD sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) Ischaemic (n = 15) RVAD (n = 4) 46 ± 15 30 ± 10 28 ± 10 3.1 ± 2 45 ± 4 32 ± 2 14 ± 10 3 ± 1.8 Non-RVAD (n = 11) 50 ± 15 34 ± 11 17 ± 8 3.4 ± 1.5 30 ± 11 20 ± 8 7 ± 2 1.5 ± 1 P-value 0.8 0.7 0.01 0.9 0.08 0.07 0.2 0.007 Non-ischaemic (n = 55) RVAD (n = 10) 57 ± 19 39 ± 12 24 ± 9 2.9 ± 1 31 ± 6 19 ± 4 7 ± 4 1.4 ± 1 Non-RVAD (n = 45) 48 ± 15 34 ± 10 15 ± 7 3.4 ± 2 31 ± 11 20 ± 9 8 ± 6 1.5 ± 1 P-value 0.1 0.1 0.01 0.9 0.9 0.6 0.6 0.5 mPAP, mean pulmonary artery pressure; mRAP, mean right atrial pressure; PVR, pulmonary vascular resistance; SPAP, systolic pulmonary artery pressure. Table 7 Pre- and post-LVAD pulmonary arterial hypertension indices according heart failure aetiology Pre-LVAD Post-LVAD sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) Ischaemic (n = 15) RVAD (n = 4) 46 ± 15 30 ± 10 28 ± 10 3.1 ± 2 45 ± 4 32 ± 2 14 ± 10 3 ± 1.8 Non-RVAD (n = 11) 50 ± 15 34 ± 11 17 ± 8 3.4 ± 1.5 30 ± 11 20 ± 8 7 ± 2 1.5 ± 1 P-value 0.8 0.7 0.01 0.9 0.08 0.07 0.2 0.007 Non-ischaemic (n = 55) RVAD (n = 10) 57 ± 19 39 ± 12 24 ± 9 2.9 ± 1 31 ± 6 19 ± 4 7 ± 4 1.4 ± 1 Non-RVAD (n = 45) 48 ± 15 34 ± 10 15 ± 7 3.4 ± 2 31 ± 11 20 ± 9 8 ± 6 1.5 ± 1 P-value 0.1 0.1 0.01 0.9 0.9 0.6 0.6 0.5 Pre-LVAD Post-LVAD sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) sPAP (mmHg) mPAP (mmHg) mRAP (mmHg) PVR (WU) Ischaemic (n = 15) RVAD (n = 4) 46 ± 15 30 ± 10 28 ± 10 3.1 ± 2 45 ± 4 32 ± 2 14 ± 10 3 ± 1.8 Non-RVAD (n = 11) 50 ± 15 34 ± 11 17 ± 8 3.4 ± 1.5 30 ± 11 20 ± 8 7 ± 2 1.5 ± 1 P-value 0.8 0.7 0.01 0.9 0.08 0.07 0.2 0.007 Non-ischaemic (n = 55) RVAD (n = 10) 57 ± 19 39 ± 12 24 ± 9 2.9 ± 1 31 ± 6 19 ± 4 7 ± 4 1.4 ± 1 Non-RVAD (n = 45) 48 ± 15 34 ± 10 15 ± 7 3.4 ± 2 31 ± 11 20 ± 9 8 ± 6 1.5 ± 1 P-value 0.1 0.1 0.01 0.9 0.9 0.6 0.6 0.5 mPAP, mean pulmonary artery pressure; mRAP, mean right atrial pressure; PVR, pulmonary vascular resistance; SPAP, systolic pulmonary artery pressure. Univariate predictors of post-operative RVAD implantation These are shown in Table 8. The single most powerful predictor was RA longitudinal peak strain (RALS) (OR 2.5 95% CI 1.8–2.6, P = 0.01). Other significant predictors were greater RA end-systolic area and lower RA emptying fraction. RV strain and SR indices shown to be univariate predictors were: lower global and free-wall peak strain, longer time from QRS onset to global/free-wall peak strain, lower free-wall systolic SR, greater global and free-wall late diastolic SR, increased intra-RV mechanical dyssynchrony, and longer duration of myocardial shortening. Table 8 Univariate predictors of RVAD support Baseline variables OR 95% confidence interval P-value Conventional echo parameters  RA end-systolic area (echo) 0.29 0.11–0.74 0.03  RA emptying fraction (echo) 0.95 0.92–0.99 0.03 RA speckle-tracking variables  RA peak strain 2.51 1.84–2.61 0.01 RV free-wall (RVFW) speckle-tracking parameters  RVFW peak strain 1.39 1.25–1.99 0.02  Time to RVFW strain 1.05 1.03–1.17 0.03  RVFW systolic strain rate 1.04 1.02–2.35 0.05  Time to RVFW systolic strain rate 1.35 1.03–2.24 0.03  RVFW late diastolic strain rate 1.60 1.24–1.61 0.03 RV global (RVG) speckle-tracking parameters  RVG peak strain 1.02 1.01–1.23 0.04  Time to RVG peak strain 1.02 1.01–1.05 0.03  RVG peak systolic strain rate 1.56 0.93–9.76 0.1  Time to RVG peak systolic rate 1.07 1.01–1.15 0.03  RV global late diastolic strain rate 1.62 1.09–4.25 0.04 RV dyssynchrony assessment (speckle-tracking)  RVFW myocardial shortening duration 1.82 1.02–4.94 0.03  Intra-RV dyssynchrony 1.21 1.10–1.23 0.01 Baseline variables OR 95% confidence interval P-value Conventional echo parameters  RA end-systolic area (echo) 0.29 0.11–0.74 0.03  RA emptying fraction (echo) 0.95 0.92–0.99 0.03 RA speckle-tracking variables  RA peak strain 2.51 1.84–2.61 0.01 RV free-wall (RVFW) speckle-tracking parameters  RVFW peak strain 1.39 1.25–1.99 0.02  Time to RVFW strain 1.05 1.03–1.17 0.03  RVFW systolic strain rate 1.04 1.02–2.35 0.05  Time to RVFW systolic strain rate 1.35 1.03–2.24 0.03  RVFW late diastolic strain rate 1.60 1.24–1.61 0.03 RV global (RVG) speckle-tracking parameters  RVG peak strain 1.02 1.01–1.23 0.04  Time to RVG peak strain 1.02 1.01–1.05 0.03  RVG peak systolic strain rate 1.56 0.93–9.76 0.1  Time to RVG peak systolic rate 1.07 1.01–1.15 0.03  RV global late diastolic strain rate 1.62 1.09–4.25 0.04 RV dyssynchrony assessment (speckle-tracking)  RVFW myocardial shortening duration 1.82 1.02–4.94 0.03  Intra-RV dyssynchrony 1.21 1.10–1.23 0.01 Table 8 Univariate predictors of RVAD support Baseline variables OR 95% confidence interval P-value Conventional echo parameters  RA end-systolic area (echo) 0.29 0.11–0.74 0.03  RA emptying fraction (echo) 0.95 0.92–0.99 0.03 RA speckle-tracking variables  RA peak strain 2.51 1.84–2.61 0.01 RV free-wall (RVFW) speckle-tracking parameters  RVFW peak strain 1.39 1.25–1.99 0.02  Time to RVFW strain 1.05 1.03–1.17 0.03  RVFW systolic strain rate 1.04 1.02–2.35 0.05  Time to RVFW systolic strain rate 1.35 1.03–2.24 0.03  RVFW late diastolic strain rate 1.60 1.24–1.61 0.03 RV global (RVG) speckle-tracking parameters  RVG peak strain 1.02 1.01–1.23 0.04  Time to RVG peak strain 1.02 1.01–1.05 0.03  RVG peak systolic strain rate 1.56 0.93–9.76 0.1  Time to RVG peak systolic rate 1.07 1.01–1.15 0.03  RV global late diastolic strain rate 1.62 1.09–4.25 0.04 RV dyssynchrony assessment (speckle-tracking)  RVFW myocardial shortening duration 1.82 1.02–4.94 0.03  Intra-RV dyssynchrony 1.21 1.10–1.23 0.01 Baseline variables OR 95% confidence interval P-value Conventional echo parameters  RA end-systolic area (echo) 0.29 0.11–0.74 0.03  RA emptying fraction (echo) 0.95 0.92–0.99 0.03 RA speckle-tracking variables  RA peak strain 2.51 1.84–2.61 0.01 RV free-wall (RVFW) speckle-tracking parameters  RVFW peak strain 1.39 1.25–1.99 0.02  Time to RVFW strain 1.05 1.03–1.17 0.03  RVFW systolic strain rate 1.04 1.02–2.35 0.05  Time to RVFW systolic strain rate 1.35 1.03–2.24 0.03  RVFW late diastolic strain rate 1.60 1.24–1.61 0.03 RV global (RVG) speckle-tracking parameters  RVG peak strain 1.02 1.01–1.23 0.04  Time to RVG peak strain 1.02 1.01–1.05 0.03  RVG peak systolic strain rate 1.56 0.93–9.76 0.1  Time to RVG peak systolic rate 1.07 1.01–1.15 0.03  RV global late diastolic strain rate 1.62 1.09–4.25 0.04 RV dyssynchrony assessment (speckle-tracking)  RVFW myocardial shortening duration 1.82 1.02–4.94 0.03  Intra-RV dyssynchrony 1.21 1.10–1.23 0.01 Independent predictors of RVAD support by multiple regression analysis The results of multiple regression analysis are shown in Figure 4. Three independent predictors were identified from the STE parameters: RALS (OR 2.5, 95% CI 1.37–2; P = 0.03), RVFW longitudinal peak strain (OR 1.3, 95% CI 1.03–2.3; P = 0.04) and intra-RV longitudinal dyssynchrony (OR 1.3, 95% CI 1.02–1.3; P = 0.04). Figure 4 View largeDownload slide Independent predictors of RVAD implantation during LVAD support and ROC curve analysis. RAS, RA peak strain; RVD, intra-RV dyssynchrony (DRVFW-IVS); RVFWS, free-wall RV peak strain. Figure 4 View largeDownload slide Independent predictors of RVAD implantation during LVAD support and ROC curve analysis. RAS, RA peak strain; RVD, intra-RV dyssynchrony (DRVFW-IVS); RVFWS, free-wall RV peak strain. 2D echo and speckle-tracking to predict RVAD support ROC curves were drawn and the areas under the curves (AUC) calculated (Figure 4). The strongest predictor was peak RA systolic strain (AUC 0.913), followed by intra-RV longitudinal dyssynchrony (AUC 0.845) and RV free-wall peak systolic strain (AUC 0.623). A value ≤10.5% predicted RVAD implantation with a sensitivity of 94% and specificity of 65%. Discussion To our knowledge, this is the first study to combine RA and RV STE to assess their value as predictors of the need for RVAD after LVAD implantation. Multivariable modelling identified pre-operative RALS, free-wall RV longitudinal peak strain (RVLS) and longitudinal intra-RV dyssynchrony (DRVFW-IVS) as independent predictors, stronger than conventional parameters including TAPSE, RVFCA, or tissue doppler imaging (TDI) S′.14 RA strain and SR analysis Patients in the RVAD group had lower pre-operative RALS suggesting a state of reduced RA compliance.15,16 RALS was the strongest independent predictor of RVAD implantation and was more sensitive than other echocardiographic parameters. RVAD patients also showed greater RA remodelling, indicated by larger RA area index.12 These findings may be associated with the significantly higher mean RAP and RVEDP noted in the RVAD group.15 RALS has been shown to reflect RVSWI, RV filling pressure, and pulmonary artery pressure and may be a useful parameter to include in the pre-operative assessment of LVAD candidates.11,15 RVAD patients also had lower RA late diastolic SR, an index of reduced RA pump functional capacity. At early stages of ventricular dysfunction, atrial contractility is increased to compensate for reduced early diastolic filling due to high RVEDP.7,16 However, in more advanced stages of ventricular dysfunction, atrial contractile capacity decreases compromising ventricular filling and output.16 Therefore, RA strain and SR parameters may reflect more advanced stages of compromised RV myocardial performance in the RVAD patients. Longitudinal RV peak systolic strain and strain rate analysis RVAD patients had lower pre-operative global and free-wall RVLS, along with lower, earlier-peaking RV longitudinal SR. Free-wall RVLS was an independent echocardiographic predictor of RVAD support. Our findings demonstrate pre-operative differences in RV functional reserve between the two groups, not demonstrated by invasively measured RVSWI or conventional echocardiographic parameters. Free-wall RVLS was a stronger predictor of RVAD support than global RVLS, consistent with published findings correlating RVSWI and free-wall RVLS.17 Global RVLS also includes septal strain18; thus it is not a ‘pure’ measure of RV mechanics. The RVAD group showed a greater degree of RV mechanical dyssynchrony. There was a greater delay in mechanical activation of the RVFW in relation to the IVS (DRVFW-IVS) and LVFW (DRVFW-LVFW). DRVFW-IVS was amongst the independent predictors of RVAD support. Our results agree with previous studies associating RV mechanical delay with RV dilatation and systolic dysfunction.19–21 The combination of increased free-wall RV mechanical delay and lower RVLS may indicate more advanced stages of intrinsic RV dysfunction. The RVAD group had higher pre-operative RVEDP. Increased pressure or volume loading results in higher ventricular wall tension and prolonged myocardial shortening,22,23 leading to ineffective, disco-ordinate RV contractility, especially after RV preload increases with the LVAD support.24 As a result, the RV fails to maintain adequate output and additional mechanical support is needed. Finally, we showed that RV myocardial shortening continued after PVC in a greater proportion of the RVAD patients. RV myocardial shortening after PVC does not contribute to RV ejection; it reflects increased RV dyssynchrony and impaired myocardial performance.23 Clinical implications Our study demonstrates potential value of RA and RV STE for preoperatively identifying LVAD candidates who may require additional RVAD support. To date, suggested RVF risk indices have focused on markers which reflect the consequences of RV dysfunction rather than intrinsic RV functional capacity.24,25 Our data suggest that incorporating RH STE into pre-operative assessment may allow better planning for biventricular mechanical support or implantation of a total artificial heart, hence leading to improved outcomes.9 Previous studies have shown the incremental prognostic value of reduced RVLS when added to conventional RVF risk factors.9,26 In our study, RALS, free-wall RVLS and DRVFW-IVS were the independent echocardiographic predictors of severe RVF requiring RVAD support. The most powerful predictor was RALS. However, the prognostic significance of these parameters needs to be evaluated prospectively in order to formulate a more sensitive, specific and fully descriptive index to guide peri-operative management. Study limitations Our study is subject to several limitations. First of all, it reflects the practice of a single institution in the UK where LVAD implantation is used as a bridge to transplantation or myocardial recovery but not as destination therapy. Ideally, a multi-centre study and hence a larger cohort of LVAD recipients is needed to validate and further develop these results. In this study, we analysed only longitudinal strain and SR and not circumferential or radial strain. This was felt to be valid considering that RV function depends mainly on longitudinal fibres with free-wall contraction generating 80% of the RVSV.27,28 At the time of analysis, there was no available software specifically for analysis of STE of the RH, so we used LV software with relevant adjustments. This method has been shown to be feasible in previously published studies with acceptable reproducibility.26 Conclusion In conclusion, our study has shown RA and RV strain analysis by STE to be more sensitive than conventional echocardiography for predicting the need for RVAD support after LVAD implantation. The most powerful predictor was RALS, but free-wall RVLS and DRVFW-IVS were also significant. An index combining these parameters with haemodynamic and clinical risk factors of post-LVAD implantation RVF could help to differentiate those AHF patients who will benefit from early BiVAD or artificial heart from those who are more suitable for long-term therapy with an LVAD. Conflict of interest: None declared. References 1 Trivedi JR , Cheng A , Singh R , Williams ML , Slaughter MS. Survival on the heart transplant waiting list: impact of continuous flow left ventricular assist device as bridge to transplant . Ann Thorac Surg 2014 ; 98 : 830 – 4 . Google Scholar CrossRef Search ADS PubMed 2 Kormos RL , Teuteberg JJ , Pagani FD , Russell SD , John R , Miller LW et al. Right ventricular failure in patients with the HeartMate II continuous-flow left ventricular assist device: incidence, risk factors, and effect on outcomes . J Thorac Cardiovasc Surg 2010 ; 139 : 1316 – 24 . Google Scholar CrossRef Search ADS PubMed 3 John R , Lee S , Eckman P , Liao K. Right ventricular failure-a continuing problem in patients with left ventricular assist device support . J Cardiovasc Transl Res 2010 ; 3 : 604 – 11 Google Scholar CrossRef Search ADS PubMed 4 Fitzpatrick JR 3rd , Frederick JR , Hiesinger W , Hsu VM , McCormick RC , Kozin ED et al. Early planned institution of biventricular mechanical circulatory support results in improved outcomes compared with delayed conversion of a left ventricular assist device to a biventricular assist device . J Thorac Cardiovasc Surg 2009 ; 137 : 971 – 7 . 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Google Scholar CrossRef Search ADS PubMed 17 Cameli M , Lisi M , Righini FM , Tsioulpas C , Bernazzali S , Maccherini M et al. Right ventricular longitudinal strain correlates well with right ventricular stroke work index in patients with advanced heart failure referred for heart transplantation . J Card Fail 2012 ; 18 : 208 – 15 . Google Scholar CrossRef Search ADS PubMed 18 Fine NM , Chen L , Bastiansen PM , Frantz RP , Pellikka PA , Oh JK et al. Reference values for right ventricular strain in patients without cardiopulmonary disease: a prospective evaluation and meta-analysis . Echocardiography 2015 ; 32 : 787 – 96 . Google Scholar CrossRef Search ADS PubMed 19 Esmaeilzadeh M , Poorzand H , Maleki M , Sadeghpour A , Parsaee M. Evaluation of longitudinal right ventricular mechanical dyssynchrony before and early after cardiac resynchronization therapy: a strain imaging study . J Tehran Heart Cent 2011 ; 6 : 24 – 30 . Google Scholar PubMed 20 Chow PC , Liang XC , Lam WW , Cheung EW , Wong KT , Cheung YF. Mechanical right ventricular dyssynchrony in patients after atrial switch operation for transposition of the great arteries . Am J Cardiol 2008 ; 101 : 874 – 8 . Google Scholar CrossRef Search ADS PubMed 21 Tops LF , Prakasa K , Tandri H , Dalal D , Jain R , Dimaano VL et al. Revalence and pathophysiologic attributes of ventricular dyssynchrony in arrhythmogenic right ventricular dysplasia/cardiomyopathy . J Am Coll Cardiol 2009 ; 54 : 445. Google Scholar CrossRef Search ADS PubMed 22 Schuster P , Faerestrand S , Ohm OJ. Color Doppler tissue velocity imaging can disclose systolic left ventricular asynchrony independent of the QRS morphology in patients with severe heart failure . Pacing Clin Electrophysiol 2004 ; 27 : 460 – 7 . Google Scholar CrossRef Search ADS PubMed 23 Marcus JT , Gan CT , Zwanenburg JJ , Boonstra A , Allaart CP , Götte MJ et al. Interventricular mechanical asynchrony in pulmonary arterial hypertension: left-to-right delay in peak shortening is related to right ventricular overload and left ventricular underfilling . J Am Coll Cardiol 2008 ; 51 : 750 – 7 . Google Scholar CrossRef Search ADS PubMed 24 Kerckhoffs RC , Bovendeerd PH , Kotte JC , Prinzen FW , Smits K , Arts T. Homogeneity of cardiac contraction despite physiological asynchrony of depolarization: a model study . Ann Biomed Eng 2003 ; 31 : 536 – 47 . Google Scholar CrossRef Search ADS PubMed 25 Matthews JC , Koelling TM , Pagani FD , Aaronson KD. The right ventricular failure risk score a pre-operative tool for assessing the risk of right ventricular failure in left ventricular assist device candidates . J Am Coll Cardiol 2008 ; 51 : 2163 – 72 . Google Scholar CrossRef Search ADS PubMed 26 Fukuda Y , Tanaka H , Sugiyama D , Ryo K , Onishi T , Fukuya H et al. Utility of right ventricular free wall speckle-tracking strain for evaluation of right ventricular performance in patients with pulmonary hypertension . J Am Soc Echocardiogr 2011 ; 24 : 1101 – 8 . Google Scholar CrossRef Search ADS PubMed 27 Carlsson M , Ugander M , Heiberg E , Arheden H. The quantitative relationship between longitudinal and radial function in left, right, and total heart pumping in humans . Am J Physiol Heart Circ Physiol 2007 ; 293 : H636 – 44 . Google Scholar CrossRef Search ADS PubMed 28 Padeletti M , Cameli M , Lisi M , Malandrino A , Zacà V , Mondillo S. Reference values of right atrial longitudinal strain imaging by two-dimensional speckle tracking . Echocardiography 2012 ; 29 : 147 – 52 . Google Scholar CrossRef Search ADS PubMed Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

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European Heart Journal – Cardiovascular ImagingOxford University Press

Published: Apr 13, 2018

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