Impact of right ventricular volume and function evaluated using cardiovascular magnetic resonance imaging on outcomes after surgical ventricular reconstruction

Impact of right ventricular volume and function evaluated using cardiovascular magnetic resonance... Abstract OBJECTIVES This study aimed to evaluate whether cardiac magnetic resonance imaging (MRI)-derived right ventricular (RV) assessment can facilitate risk stratification among patients with ischaemic cardiomyopathy who underwent surgical ventricular reconstruction (SVR). METHODS We retrospectively analysed 53 patients who underwent SVR. The patients were preoperatively evaluated using cardiac MRI. Cine-MRI was acquired for left ventricular (LV) and RV volume. Gadolinium-enhanced MRI was performed to evaluate LV scarring. The mid-term (median, 58 months) risk factors of all-cause mortality and major adverse cardiac events were analysed. RESULTS A significant reduction in LV end-diastolic and end-systolic volume index and an increase in LV ejection fraction were observed early after SVR. RV end-diastolic volume index (RVEDVI) and RV end-systolic volume index (RVESVI) decreased after SVR (preoperative versus postoperative: RVEDVI, 71 ± 24 vs 62 ± 17 ml/m2, P = 0.006; RVESVI, 44 ± 26 vs 37 ± 16 ml/m2, P = 0.033), but RV ejection fraction did not change (preoperative versus postoperative: RV ejection fraction 40.8±14.6 vs 42.0±11.0%, P = 0.067). At follow-up, 25 deaths and 31 major adverse cardiac events occurred. After adjustment for age, creatinine level and preoperative mitral regurgitation grade, the Cox-hazard model indicated that RVEDVI [P = 0.006, hazard ratio (HR) 1.03, 95% confidence interval (CI) 1.01–1.05] and RVESVI [P = 0.007, HR 1.02, 95% CI 1.01–1.04] were significant predictors for all-cause mortality. As for major adverse cardiac events, RVEDVI (P = 0.007, HR 1.03, 95% CI 1.01–1.05), RVESVI (P = 0.002, HR 1.03, 95% CI 1.01–1.04) and RV ejection fraction (P = 0.018, HR 0.97, 95% CI 0.94–0.99) were significant. CONCLUSIONS RV parameters were more sensitive than LV parameters for predicting worse outcomes following SVR. Preoperative assessment of RV volume and function using cardiac MRI may improve the risk stratification of SVR. Cardiac magnetic resonance imaging, Surgical ventricular reconstruction, Right ventricular function INTRODUCTION Surgical left ventricular (LV) reconstruction was developed to restore a more physiological shape to the spherical LV and improve the contractile performance of stretched remote myocardial muscles. Surgical ventricular reconstruction (SVR) clearly modifies LV reverse remodelling in patients with ischaemic heart failure. Several studies have reported the efficacy and benefit of SVR in improving heart failure symptoms and mechanical dyssynchrony [1, 2]. However, the Surgical Treatment for Ischaemic Heart Failure (STICH) randomized trial [3] and its substudies, which showed several parameters associated with a worse outcome after SVR in addition to coronary artery bypass grafting (CABG) [4, 5], emphasize the importance of patient selection for SVR. Most of these studies focused on the assessment of LV parameters. Little attention has been devoted to investigate the impact of reduced right ventricular (RV) function on outcomes in patients who underwent SVR. The cardiovascular system is a closed loop; thus, failure of the LV leads to the malfunction of the RV [6]. RV systolic dysfunction has been found to be a strong and independent predictor of worse outcomes in heart failure patients. Many of these heart failure patients with ischaemic cardiomyopathy (ICM) and reduced LV ejection fraction (LVEF), including those who underwent SVR, have concomitant RV systolic dysfunction. Thus, the significance of RV function is being increasingly recognized in SVR patients [7–9]. Although different modalities can be used for imaging of the RV, accurate measurement of RV volume and function using echocardiography or radionuclide technique is challenging because of the complex geometry of the RV. In recent years, cardiac magnetic resonance imaging (MRI) has emerged as the gold standard technique for the quantification of RV function with high accuracy and reproducibility. The objective of this study was to evaluate whether cardiac MRI-derived RV assessment can facilitate risk stratification among patients with ICM who underwent SVR concomitant with CABG. MATERIALS AND METHODS Patients and study design In this retrospective study, we performed a nonrandomized review of patients who underwent SVR for ICM and preoperative cardiac MRI. A total of 63 consecutive patients underwent SVR for ICM between March 2004 and December 2016. Among them, 54 patients underwent preoperative cardiac MRI. One patient was excluded due to poor image quality. Finally, 53 patients were included in the analysis. Preoperative clinical data included the patient’s age, sex, height, weight, serum creatinine, calculated body surface area (BSA) and preoperative New York Heart Association (NYHA) functional class; presence of preoperative atrial fibrillation, diabetes mellitus, hypertension, haemodialysis, hyperlipidaemia, cerebral vascular disease and peripheral vascular disease; and the need for a preoperative intra-aortic balloon pump (Table 1). Echocardiographic studies were performed within 2 weeks before the surgery, and LV dimensions and valvular functions were assessed. The grades of mitral regurgitation (MR), as well as those of tricuspid regurgitation, were quantified as numerical variables as follows: 0, none; 1+, mild; 2+, moderate; 3+, moderately severe; and 4+, severe. Tricuspid regurgitation peak pressure gradient was determined using the modified Bernoulli equation {4 × (tricuspid regurgitation peak velocity)}2. Table 1: Preoperative characteristics Variables All patients Age (years) 64 ± 10 Male 43 (81) BSA (m2) 1.6 ± 0.2 Serum createnine level (mg/dl) 1.1 (0.9, 1.6) NYHA class  ≤2 21 (40)  3 21 (40)  4 11 (21) Hypertension 33 (62) Hyperlipidaemia 30 (57) Diabetes mellitus 20 (38) Haemodialysis 7 (13) PVD 8 (15) CVD 13 (25) Coronary artery disease  1-vessel disease 6 (11)  2-vessel disease 7 (13)  3-vessel disease 40 (75) Atrial fibrillation 5 (9) Mitral regurgitation grade  ≤1 22 (42)  2 16 (30)  3 10 (19)  4 5 (9) Tricuspid regurgitation grade  ≤1 40 (75)  2 10 (19)  3/4 3 (6) TRPG (mmHg) 33 ± 18 Variables All patients Age (years) 64 ± 10 Male 43 (81) BSA (m2) 1.6 ± 0.2 Serum createnine level (mg/dl) 1.1 (0.9, 1.6) NYHA class  ≤2 21 (40)  3 21 (40)  4 11 (21) Hypertension 33 (62) Hyperlipidaemia 30 (57) Diabetes mellitus 20 (38) Haemodialysis 7 (13) PVD 8 (15) CVD 13 (25) Coronary artery disease  1-vessel disease 6 (11)  2-vessel disease 7 (13)  3-vessel disease 40 (75) Atrial fibrillation 5 (9) Mitral regurgitation grade  ≤1 22 (42)  2 16 (30)  3 10 (19)  4 5 (9) Tricuspid regurgitation grade  ≤1 40 (75)  2 10 (19)  3/4 3 (6) TRPG (mmHg) 33 ± 18 Data are presented as numbers (percentage) or mean ± SD. Serum creatinine level is presented in median and interquartile range. BSA: body surface area; CVD: cerebral vascular disease; NYHA: New York Heart Association; PVD: peripheral vascular disease; TRPG: tricuspid regurgitation pressure gradient. Table 1: Preoperative characteristics Variables All patients Age (years) 64 ± 10 Male 43 (81) BSA (m2) 1.6 ± 0.2 Serum createnine level (mg/dl) 1.1 (0.9, 1.6) NYHA class  ≤2 21 (40)  3 21 (40)  4 11 (21) Hypertension 33 (62) Hyperlipidaemia 30 (57) Diabetes mellitus 20 (38) Haemodialysis 7 (13) PVD 8 (15) CVD 13 (25) Coronary artery disease  1-vessel disease 6 (11)  2-vessel disease 7 (13)  3-vessel disease 40 (75) Atrial fibrillation 5 (9) Mitral regurgitation grade  ≤1 22 (42)  2 16 (30)  3 10 (19)  4 5 (9) Tricuspid regurgitation grade  ≤1 40 (75)  2 10 (19)  3/4 3 (6) TRPG (mmHg) 33 ± 18 Variables All patients Age (years) 64 ± 10 Male 43 (81) BSA (m2) 1.6 ± 0.2 Serum createnine level (mg/dl) 1.1 (0.9, 1.6) NYHA class  ≤2 21 (40)  3 21 (40)  4 11 (21) Hypertension 33 (62) Hyperlipidaemia 30 (57) Diabetes mellitus 20 (38) Haemodialysis 7 (13) PVD 8 (15) CVD 13 (25) Coronary artery disease  1-vessel disease 6 (11)  2-vessel disease 7 (13)  3-vessel disease 40 (75) Atrial fibrillation 5 (9) Mitral regurgitation grade  ≤1 22 (42)  2 16 (30)  3 10 (19)  4 5 (9) Tricuspid regurgitation grade  ≤1 40 (75)  2 10 (19)  3/4 3 (6) TRPG (mmHg) 33 ± 18 Data are presented as numbers (percentage) or mean ± SD. Serum creatinine level is presented in median and interquartile range. BSA: body surface area; CVD: cerebral vascular disease; NYHA: New York Heart Association; PVD: peripheral vascular disease; TRPG: tricuspid regurgitation pressure gradient. All patients received optimized medical regimens, including beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers and diuretics. This study was approved by the institutional ethics committee, and the committee waived the need for individual informed consent. Magnetic resonance imaging protocol and image analysis A standardized cardiac MRI protocol was performed using a 1.5-T scanner (Gilloscan; Philips Medical Systems, Eindhoven, the Netherlands), as described previously [5]. Briefly, steady-state free precession cine images were acquired in multiple short-axis views (9–12 slices at 10-mm intervals throughout the entire left and right ventricles). Using the segment inversion recovery technique in identical planes, delayed enhanced images were obtained at matching cine-image slice locations 10–15 min after the intravenous administration of gadolinium-diethylenetriamine pentaacetic acid (0.2 ml/kg). All short-axis cine-MRI data were analysed using a commercial postprocessing workstation (View Forum; Philips). The LV and RV volumes and LVEF and RV ejection fraction (RVEF) were calculated by manually outlining the LV and RV endocardial borders on the end-diastolic and end-systolic frames. Thus, the LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), RV end-diastolic volume index (RVEDVI) and RV end-systolic volume index (RVESVI) were initially obtained. Subsequently, the LVEF and RVEF were determined as the ratios of (LVEDV − LVESV) to LVEDV and (RVEDV − RVESV) to RVEDV. The LV end-systolic volume index (LVESVI), RVESVI, LV end-diastolic volume index (LVEDVI) and RVEDVI were calculated according to the BSA, as LVESV/BSA, LVEDV/BSA, RVESV/BSA and RVEDV/BSA, respectively. The presence of myocardial infarction was analysed using delayed enhanced images. A hyper-enhanced area was defined as a region with a signal intensity threshold of >3 SD and 2–3 SD above the remote normal myocardium. The percentage of the hyper-enhanced area was assessed for each of the 16 standard LV myocardial segments. The apex segment was excluded from this analysis because visualization and calculation of the hyper-enhanced area in this segment are difficult and inaccurate. An LV segment with myocardial infarction was defined as an LV segment with >25% enhancement. The percentage of hyper-enhancement in the entire LV area (% HE) was also calculated. MRI studies were performed within 2 weeks before the surgery and 2–3 weeks after the surgery. Operative management Our most preferred SVR procedure was the endocardial linear infarct exclusion technique (ELIET), which was described previously [5, 10, 11]. The other SVR procedures performed included the Dor and the septal anterior ventricular exclusion (SAVE) procedures. The choice of procedure depended on the SVR location, extent of the infarction and preference of the attending surgeons. The SVR locations were anterior region in 26 cases, anterior and inferior regions in 11 cases, anterior and lateral regions in 4 cases, inferior regions in 7 cases and lateral regions in 5 cases. A total of 51 patients who had significant coronary artery disease (>50% luminal stenosis of at least 1 principal coronary artery) underwent CABG to achieve complete revascularization, including the left or right internal mammary artery (IMA) to LAD, to preserve the septal branches. Mitral repair was performed in 25 patients with more than 2+ MR using a complete semi-rigid ring (Carpentier-Edwards Physio Ring I in 18 patients, Physio Ring II in 6 patients; Edwards Lifesciences) and a partial semi-rigid band (CG future annuloplasty band; Medtronic) in 1 patient. Papillary muscle relocation was added in 14 patients. The indication to perform this procedure was a coaptation depth of >5 mm. Mitral valve replacement was indicated in 5 patients with an extremely tethered mitral valve or mitral stenosis. Tricuspid repair was performed in 9 patients with more than 2+ tricuspid regurgitation and/or 1+ regurgitation with an annular diameter >21 mm/m2. Follow-up data collection Postoperative clinical data, including postoperative complications and mortality, were obtained from patient’s medical records, outpatient clinic or contact with the patient’s physician, the patients or their relatives through a mailed questionnaire or telephone interviews from January 2017 to August 2017. Their last follow-up date was within this period or at their mortality. Our primary end point was all-cause mortality at any postoperative point within the study period. The cause of death was obtained, and deaths associated with refractory heart failure, arrhythmia, fatal myocardial infarction and any sudden deaths were considered to be due to cardiac causes. Noncardiovascular death included cancer, infectious diseases, such as pneumonia and sepsis, cerebrovascular complication, trauma and suicide. The secondary end point was major adverse cardiac events (MACEs) at any postoperative point within the study period. MACEs were defined as all-cause mortality, nonfatal infarction, ventricular tachycardia/fibrillation and symptomatic congestive heart failure requiring hospitalization. We could not get any information on the 1 patient who dropped out. The last known survival time of the patient was at his 6 months of follow-up. So the follow-up was completed in 98% of patients; the median follow-up period was 58 months (range 0.1–151 months). Statistical analysis Categorical variables are presented as frequencies and percentages. Continuous data are expressed as mean ± SD or median with ranges. A simple linear regression analysis was used to model the relationships between continuous variables. Correlations between variables were assessed with Pearson’s product-moment correlation coefficient. Paired t-test was used to compare the mean difference between baseline and postoperative measurements. Survival and event rates were estimated using Kaplan–Meier curves. The index date was the date of the operation. The primary end point was all-cause mortality (n = 25), and the secondary end point was MACE (n = 31). The independent prognostic effect of MRI-derived LV and RV parameters (preoperative LVEDVI, LVESVI, LVEF, RVEDVI, RVESVI, RVEF, total hyperenhancement area and number of segments with hyperenhancement area >25%) was evaluated using the Cox proportional hazards model. Age, creatinine level and preoperative MR grade were included in the multivariable analysis along with 1 LV or RV parameter per model. Proportional hazards assumption was confirmed with complementary log–log plots, and no violations were detected. Hazard ratio (HR) and 95% confidence interval (CI) were calculated. A P-value of <0.05 was considered statistically significant. Statistical analysis was performed using IBM SPSS Statistics (IBM Corp. Released 2012, IBM SPSS Statistics for Mac, Version 21.0; IBM Corp., Armonk, NY, USA). RESULTS Patient characteristics The preoperative and operative characteristics of patients are listed in Tables 1 and 2. The mean age was 64.1 ± 9.6 years, and 43 (81%) patients were men. Sixty percent of the patients had an NYHA functional class of 3 or 4. Comorbidities included hypertension in 33 (62%) patients, diabetes mellitus in 20 (38%) patients, cerebral vascular disease in 13 (25%) patients, haemodialysis in 7 (13%) patients and peripheral vascular disease in 8 (15%) patients. Table 2: Operative characteristics Variables All patients CABG 51 (96)  No. of distal anastomoses/patient 2.8 ± 1.5  No. of IMA graft/patient 1.2 ± 0.7 SVR  Dor 6 (11)  SAVE 3 (6)  ELIET 44 (83) Location of SVR  Anterior 41 (77)  Inferior 18 (34)  Lateral 9 (17) MAP 25 (47) MVR 5 (9) Relocation of PMs 14 (26) TAP 9 (17) AVR 2 (4) CPB time (min) 227 ± 72 ACC time (min) 149 ± 59 Variables All patients CABG 51 (96)  No. of distal anastomoses/patient 2.8 ± 1.5  No. of IMA graft/patient 1.2 ± 0.7 SVR  Dor 6 (11)  SAVE 3 (6)  ELIET 44 (83) Location of SVR  Anterior 41 (77)  Inferior 18 (34)  Lateral 9 (17) MAP 25 (47) MVR 5 (9) Relocation of PMs 14 (26) TAP 9 (17) AVR 2 (4) CPB time (min) 227 ± 72 ACC time (min) 149 ± 59 Data are presented as numbers (percentage) or mean ± SD. ACC: aortic cross-clamp; AVR: aortic valve replacement; CABG: coronary artery bypass grafting; CPB: cardiopulmonary bypass; ELIET: endocardial linear infarct exclusion technique; IMA: internal mammary artery; MAP: mitral annuloplasty; MVR: mitral valve replacement; PMs: papillary muscles; SAVE: septal anterior ventricular exclusion; SVR: surgical ventricular reconstruction; TAP: tricuspid annuloplasty. Table 2: Operative characteristics Variables All patients CABG 51 (96)  No. of distal anastomoses/patient 2.8 ± 1.5  No. of IMA graft/patient 1.2 ± 0.7 SVR  Dor 6 (11)  SAVE 3 (6)  ELIET 44 (83) Location of SVR  Anterior 41 (77)  Inferior 18 (34)  Lateral 9 (17) MAP 25 (47) MVR 5 (9) Relocation of PMs 14 (26) TAP 9 (17) AVR 2 (4) CPB time (min) 227 ± 72 ACC time (min) 149 ± 59 Variables All patients CABG 51 (96)  No. of distal anastomoses/patient 2.8 ± 1.5  No. of IMA graft/patient 1.2 ± 0.7 SVR  Dor 6 (11)  SAVE 3 (6)  ELIET 44 (83) Location of SVR  Anterior 41 (77)  Inferior 18 (34)  Lateral 9 (17) MAP 25 (47) MVR 5 (9) Relocation of PMs 14 (26) TAP 9 (17) AVR 2 (4) CPB time (min) 227 ± 72 ACC time (min) 149 ± 59 Data are presented as numbers (percentage) or mean ± SD. ACC: aortic cross-clamp; AVR: aortic valve replacement; CABG: coronary artery bypass grafting; CPB: cardiopulmonary bypass; ELIET: endocardial linear infarct exclusion technique; IMA: internal mammary artery; MAP: mitral annuloplasty; MVR: mitral valve replacement; PMs: papillary muscles; SAVE: septal anterior ventricular exclusion; SVR: surgical ventricular reconstruction; TAP: tricuspid annuloplasty. Magnetic resonance imaging results The MRI results are listed in Table 3. Using cine-MRI, the mean (±SD) baseline RVEDVI and RVESVI were 71 ± 24 ml/m2 (range 30–149) and 44 ± 26 ml/m2 (range 13–131), respectively. The mean RVEF was 40.8% ± 14.6% (range 11.7–65.2%). Seventeen patients (32%) exhibited RVEF of <35%. A significant correlation was found between preoperative LVEF and RVEF (Fig. 1A) We could also observe positive relationships between preoperative LVEDVI and RVEDVI, and LVESVI and RVESVI (Fig. 1B and C). Table 3: Magnetic resonance imaging findings Variables All patients Cine MRI  LVEDVI (ml/m2) 157 ± 42  LVESVI (ml/m2) 126 ± 43  LVEF (%) 21.6 ± 8.6  RVEDVI (ml/m2) 71 ± 24  RVESVI (ml/m2) 44 ± 26  RVEF (%) 40.8 ± 14.6 Gadolinium-enhanced MRI  Total HE area (%) 31 ± 12  Number of HE > 25% 8.3 ± 2.7 Variables All patients Cine MRI  LVEDVI (ml/m2) 157 ± 42  LVESVI (ml/m2) 126 ± 43  LVEF (%) 21.6 ± 8.6  RVEDVI (ml/m2) 71 ± 24  RVESVI (ml/m2) 44 ± 26  RVEF (%) 40.8 ± 14.6 Gadolinium-enhanced MRI  Total HE area (%) 31 ± 12  Number of HE > 25% 8.3 ± 2.7 Data are presented as mean ± SD. HE: hyperenhancement; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MRI: magnetic resonance imaging; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Table 3: Magnetic resonance imaging findings Variables All patients Cine MRI  LVEDVI (ml/m2) 157 ± 42  LVESVI (ml/m2) 126 ± 43  LVEF (%) 21.6 ± 8.6  RVEDVI (ml/m2) 71 ± 24  RVESVI (ml/m2) 44 ± 26  RVEF (%) 40.8 ± 14.6 Gadolinium-enhanced MRI  Total HE area (%) 31 ± 12  Number of HE > 25% 8.3 ± 2.7 Variables All patients Cine MRI  LVEDVI (ml/m2) 157 ± 42  LVESVI (ml/m2) 126 ± 43  LVEF (%) 21.6 ± 8.6  RVEDVI (ml/m2) 71 ± 24  RVESVI (ml/m2) 44 ± 26  RVEF (%) 40.8 ± 14.6 Gadolinium-enhanced MRI  Total HE area (%) 31 ± 12  Number of HE > 25% 8.3 ± 2.7 Data are presented as mean ± SD. HE: hyperenhancement; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MRI: magnetic resonance imaging; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Figure 1: View largeDownload slide Scatter plot graphs showing significant linear correlations between the LVEF and RVEF (A), the LVEDVI and the RVEDVI (B), the LVESVI and RVESVI (C). LVEF: left ventricular ejection fraction; LVEDVI: left ventricular end-diastolic volume index; LVESVI: left ventricular end-systolic volume index; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI, right ventricular end-systolic volume index. Figure 1: View largeDownload slide Scatter plot graphs showing significant linear correlations between the LVEF and RVEF (A), the LVEDVI and the RVEDVI (B), the LVESVI and RVESVI (C). LVEF: left ventricular ejection fraction; LVEDVI: left ventricular end-diastolic volume index; LVESVI: left ventricular end-systolic volume index; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI, right ventricular end-systolic volume index. A total of 45 patients underwent evaluation of LV and RV volumes using a cardiovascular MRI early after SVR; however, postoperative MRI could not be examined in 8 patients: five of them suffered from in-hospital death, 2 patients were transferred to a local hospital before the examination and 1 patient was discharged from the hospital before the examination during our early experiences (in 2004). A significant reduction in LVEDVI and LVESVI and an increase in LVEF were observed early after SVR (postoperative LVEDVI, 115 ± 32 ml/m2, vs preoperative, P < 0.001; postoperative LVESVI, 85 ± 32 ml/m2, vs preoperative, P < 0.001; postoperative LVEF, 27.8 ± 9.1%, vs preoperative, P < 0.001). RVEDVI and RVESVI significantly decreased after SVR (postoperative RVEDVI, 62 ± 17 ml/m2, vs preoperative, P = 0.006; postoperative RVESVI, 37 ± 16 ml/m2, vs preoperative, P = 0.033); however, RVEF (postoperative RVEF, 42.0 ± 11.0%, vs preoperative, P = 0.067) did not change (Fig. 2A–C). Figure 2: View largeDownload slide Postoperative changes in the LVEF and the RVEF (A), the LVEDVI and the RVEDVI (B), and the LVESVI and the RVESVI (C). Markers show the average obtained at preoperative and early postoperative periods. Error bars represent standard errors. †P < 0.001 versus preoperative, ‡P < 0.01 versus preoperative and ¶P < 0.05 versus preoperative. EDVI: end-diastolic volume index; EF: ejection fraction; ESVI: end-systolic volume index; LV: left ventricular; postop: postoperative; preop: preoperative; RV: right ventricular. Figure 2: View largeDownload slide Postoperative changes in the LVEF and the RVEF (A), the LVEDVI and the RVEDVI (B), and the LVESVI and the RVESVI (C). Markers show the average obtained at preoperative and early postoperative periods. Error bars represent standard errors. †P < 0.001 versus preoperative, ‡P < 0.01 versus preoperative and ¶P < 0.05 versus preoperative. EDVI: end-diastolic volume index; EF: ejection fraction; ESVI: end-systolic volume index; LV: left ventricular; postop: postoperative; preop: preoperative; RV: right ventricular. All-cause mortality and major adverse cardiac event Postoperative in-hospital death occurred in 5 patients (4 due to cardiac causes and 1 due to acute limb ischaemia). During follow-up, 20 patients died, including 8 due to cardiac conditions (4, heart failure; and 4, sudden death) and 12 due to noncardiac conditions (3, pneumonia; 2, cerebral bleeding; 2, cancer; 3, sepsis; 1, suicide; and 1, trauma). The 5- and 10-year rates of freedom from all-cause mortality were 64 ± 7% and 41 ± 8%, respectively (Fig. 3). Unadjusted proportional hazards estimates showed that both preoperative LVEDVI and LVESVI, as well as RVEDVI, RVESVI and RVEF, were associated with increasing mortality. However, after adjusting for age, creatinine level and preoperative MR grade, only RVEDVI (P = 0.006; HR 1.03; 95% CI 1.01–1.05) and RVESVI (P = 0.007; HR 1.02; 95% CI 1.01–1.04) were shown to have a prognostic value in predicting long-term mortality (Table 4). Table 4: Unadjusted and adjusted Cox analyses for all-cause mortality Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.10 (1.05–1.17) <0.001 Preoperative creatinine level (mg/dl) 1.36 (1.18–1.58) <0.001 Preoperative MR grade 1.46 (1.04–2.04) 0.028 Preoperative LVEDVI (ml/m2) 1.02 (1.01–1.02) 0.002 1.01 (1.00–1.02) 0.156 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.005 1.01 (1.00–1.02) 0.168 Preoperative LVEF (%) 0.97 (0.92–1.02) 0.195 0.98 (0.93–1.03) 0.425 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.04) 0.016 1.03 (1.01–1.05) 0.006 Preoperative RVESVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.02 (1.01–1.04) 0.007 Preoperative RVEF (%) 0.97 (0.95–1.00) 0.024 0.99 (0.95–1.01) 0.128 Total HE area (%) 1.00 (0.97–1.05) 0.720 1.02 (0.98–1.06) 0.398 Number of HE >25% 1.11 (0.92–1.32) 0.276 1.18 (0.98–1.41) 0.080 Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.10 (1.05–1.17) <0.001 Preoperative creatinine level (mg/dl) 1.36 (1.18–1.58) <0.001 Preoperative MR grade 1.46 (1.04–2.04) 0.028 Preoperative LVEDVI (ml/m2) 1.02 (1.01–1.02) 0.002 1.01 (1.00–1.02) 0.156 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.005 1.01 (1.00–1.02) 0.168 Preoperative LVEF (%) 0.97 (0.92–1.02) 0.195 0.98 (0.93–1.03) 0.425 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.04) 0.016 1.03 (1.01–1.05) 0.006 Preoperative RVESVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.02 (1.01–1.04) 0.007 Preoperative RVEF (%) 0.97 (0.95–1.00) 0.024 0.99 (0.95–1.01) 0.128 Total HE area (%) 1.00 (0.97–1.05) 0.720 1.02 (0.98–1.06) 0.398 Number of HE >25% 1.11 (0.92–1.32) 0.276 1.18 (0.98–1.41) 0.080 a Each variable was adjusted for age, creatinine level and preoperative MR grade. CI: confidence interval; HE: hyperenhancement; HR: hazard ratio; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MR: mitral regurgitation; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Table 4: Unadjusted and adjusted Cox analyses for all-cause mortality Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.10 (1.05–1.17) <0.001 Preoperative creatinine level (mg/dl) 1.36 (1.18–1.58) <0.001 Preoperative MR grade 1.46 (1.04–2.04) 0.028 Preoperative LVEDVI (ml/m2) 1.02 (1.01–1.02) 0.002 1.01 (1.00–1.02) 0.156 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.005 1.01 (1.00–1.02) 0.168 Preoperative LVEF (%) 0.97 (0.92–1.02) 0.195 0.98 (0.93–1.03) 0.425 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.04) 0.016 1.03 (1.01–1.05) 0.006 Preoperative RVESVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.02 (1.01–1.04) 0.007 Preoperative RVEF (%) 0.97 (0.95–1.00) 0.024 0.99 (0.95–1.01) 0.128 Total HE area (%) 1.00 (0.97–1.05) 0.720 1.02 (0.98–1.06) 0.398 Number of HE >25% 1.11 (0.92–1.32) 0.276 1.18 (0.98–1.41) 0.080 Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.10 (1.05–1.17) <0.001 Preoperative creatinine level (mg/dl) 1.36 (1.18–1.58) <0.001 Preoperative MR grade 1.46 (1.04–2.04) 0.028 Preoperative LVEDVI (ml/m2) 1.02 (1.01–1.02) 0.002 1.01 (1.00–1.02) 0.156 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.005 1.01 (1.00–1.02) 0.168 Preoperative LVEF (%) 0.97 (0.92–1.02) 0.195 0.98 (0.93–1.03) 0.425 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.04) 0.016 1.03 (1.01–1.05) 0.006 Preoperative RVESVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.02 (1.01–1.04) 0.007 Preoperative RVEF (%) 0.97 (0.95–1.00) 0.024 0.99 (0.95–1.01) 0.128 Total HE area (%) 1.00 (0.97–1.05) 0.720 1.02 (0.98–1.06) 0.398 Number of HE >25% 1.11 (0.92–1.32) 0.276 1.18 (0.98–1.41) 0.080 a Each variable was adjusted for age, creatinine level and preoperative MR grade. CI: confidence interval; HE: hyperenhancement; HR: hazard ratio; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MR: mitral regurgitation; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Figure 3: View largeDownload slide Kaplan–Meier curves for all-cause mortality (A) and MACE (B) in all patients. MACE: major adverse cardiac event. Figure 3: View largeDownload slide Kaplan–Meier curves for all-cause mortality (A) and MACE (B) in all patients. MACE: major adverse cardiac event. A total of 31 patients developed MACE. The 5- and 10-year rates of freedom from MACE were 48 ± 7% and 33 ± 8%, respectively (Fig. 3). Adjusted proportional hazards estimates showed that RVEDVI (P = 0.007; HR 1.03; 95% CI 1.01–1.05), RVESVI (P = 0.002; HR 1.03; 95% CI 1.01–1.04) and RVEF (P = 0.018; HR 0.97; 95% CI 0.94–0.99) had significant relationships with long-term occurrences of MACE (Table 5). Table 5: Unadjusted and adjusted Cox analyses for MACE Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.06 (1.02–1.11) 0.005 Preoperative creatinine level (mg/dl) 1.44 (1.23–1.69) <0.001 Preoperative MR grade 1.69 (1.24–2.31) 0.001 Preoperative LVEDVI (ml/m2) 1.01 (1.01–1.02) 0.001 1.01 (1.00–1.02) 0.082 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.002 1.01 (1.00–1.02) 0.076 Preoperative LVEF (%) 0.96 (0.91–1.01) 0.084 0.97 (0.92–1.02) 0.221 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.03 (1.01–1.05) 0.007 Preoperative RVESVI (ml/m2) 1.02 (1.01–1.03) 0.003 1.03 (1.01–1.04) 0.002 Preoperative RVEF (%) 0.96 (0.94–0.98) 0.001 0.97 (0.94–0.99) 0.018 Total HE area (%) 1.02 (0.98–1.05) 0.369 1.02 (0.99–1.06) 0.279 Number of HE >25% 1.15 (0.98–1.35) 0.089 1.18 (0.99–1.39) 0.058 Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.06 (1.02–1.11) 0.005 Preoperative creatinine level (mg/dl) 1.44 (1.23–1.69) <0.001 Preoperative MR grade 1.69 (1.24–2.31) 0.001 Preoperative LVEDVI (ml/m2) 1.01 (1.01–1.02) 0.001 1.01 (1.00–1.02) 0.082 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.002 1.01 (1.00–1.02) 0.076 Preoperative LVEF (%) 0.96 (0.91–1.01) 0.084 0.97 (0.92–1.02) 0.221 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.03 (1.01–1.05) 0.007 Preoperative RVESVI (ml/m2) 1.02 (1.01–1.03) 0.003 1.03 (1.01–1.04) 0.002 Preoperative RVEF (%) 0.96 (0.94–0.98) 0.001 0.97 (0.94–0.99) 0.018 Total HE area (%) 1.02 (0.98–1.05) 0.369 1.02 (0.99–1.06) 0.279 Number of HE >25% 1.15 (0.98–1.35) 0.089 1.18 (0.99–1.39) 0.058 a Each variable was adjusted for age, creatinine level and preoperative MR grade. CI: confidence interval; HE: hyperenhancement; HR: hazard ratio; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MACE: major adverse cardiac event; MR: mitral regurgitation; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Table 5: Unadjusted and adjusted Cox analyses for MACE Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.06 (1.02–1.11) 0.005 Preoperative creatinine level (mg/dl) 1.44 (1.23–1.69) <0.001 Preoperative MR grade 1.69 (1.24–2.31) 0.001 Preoperative LVEDVI (ml/m2) 1.01 (1.01–1.02) 0.001 1.01 (1.00–1.02) 0.082 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.002 1.01 (1.00–1.02) 0.076 Preoperative LVEF (%) 0.96 (0.91–1.01) 0.084 0.97 (0.92–1.02) 0.221 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.03 (1.01–1.05) 0.007 Preoperative RVESVI (ml/m2) 1.02 (1.01–1.03) 0.003 1.03 (1.01–1.04) 0.002 Preoperative RVEF (%) 0.96 (0.94–0.98) 0.001 0.97 (0.94–0.99) 0.018 Total HE area (%) 1.02 (0.98–1.05) 0.369 1.02 (0.99–1.06) 0.279 Number of HE >25% 1.15 (0.98–1.35) 0.089 1.18 (0.99–1.39) 0.058 Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.06 (1.02–1.11) 0.005 Preoperative creatinine level (mg/dl) 1.44 (1.23–1.69) <0.001 Preoperative MR grade 1.69 (1.24–2.31) 0.001 Preoperative LVEDVI (ml/m2) 1.01 (1.01–1.02) 0.001 1.01 (1.00–1.02) 0.082 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.002 1.01 (1.00–1.02) 0.076 Preoperative LVEF (%) 0.96 (0.91–1.01) 0.084 0.97 (0.92–1.02) 0.221 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.03 (1.01–1.05) 0.007 Preoperative RVESVI (ml/m2) 1.02 (1.01–1.03) 0.003 1.03 (1.01–1.04) 0.002 Preoperative RVEF (%) 0.96 (0.94–0.98) 0.001 0.97 (0.94–0.99) 0.018 Total HE area (%) 1.02 (0.98–1.05) 0.369 1.02 (0.99–1.06) 0.279 Number of HE >25% 1.15 (0.98–1.35) 0.089 1.18 (0.99–1.39) 0.058 a Each variable was adjusted for age, creatinine level and preoperative MR grade. CI: confidence interval; HE: hyperenhancement; HR: hazard ratio; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MACE: major adverse cardiac event; MR: mitral regurgitation; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. DISCUSSION The 3 main findings of this study were as follows: first, RV function and volume measured by cardiovascular MRI strongly correlated with LV function and volume in patients with ICM. Second, although LVEF significantly improved immediately after SVR, RVEF did not change. Third, preoperative RV function and volume were more sensitive predictors of mortality and MACE than LV parameters after SVR. This study confirmed the importance of preoperative evaluation of RV function and volume as a risk stratification tool among patients who have undergone SVR. The RV is functionally different from the LV. The RV is very compliant and tolerates a large increase in preload, without a corresponding increase in RV end-diastolic and right atrial pressures. Furthermore, increase in RV preload improves myocardial contraction on the basis of the Frank–Starling mechanism. Beyond the physiological range, excessive RV volume loading can compress the LV and impair global ventricular function through the mechanism of ventricular interdependence. On the other hand, compared with the LV, the RV demonstrates heightened sensitivity to afterload change and is at risk for acute and chronic RV failure [6]. Patients with LV dysfunction also have RV dysfunction with considerable frequency. Pouleur et al. [12] reported that RV systolic dysfunction, defined by RVEF of 35% or less, is present in approximately one-third of their patients with coronary artery disease and low LVEF. Sabe et al. [13] reported that the mean RVEF of their patient population was 43%, whereas the mean LVEF was 24%. Their findings were consistent with our present study, wherein 32% of our patients, whose LVEF was <40%, had RV systolic dysfunction. Under normal circumstances, the RV is connected in series with the LV through the pulmonary circulation. Therefore, systolic and diastolic dysfunction of the LV greatly impacts RV contractility. The pathophysiology of secondary RV dysfunction includes increased afterload attributable to secondary pulmonary hypertension, ventricular interdependence, disruption of the neurohormonal process or myocardial ischaemia secondary to reduced coronary perfusion pressure [6]. The degree of RV dysfunction is often in proportion to that of LV dysfunction. A significant correlation was found between LVEF and RVEF in patients with ICM in many previous studies as shown in our study. Several prior studies have documented the association between RV function and poor prognosis in different heart failure populations of ICM [13] or dilated cardiomyopathy [14], even in patients with preserved LVEF [15], with the use of various methods of assessment. The importance of RV function in patients undergoing cardiac surgery has also been recognized in several previous studies. In the retrospective studies of Pouleur et al. [12], preoperative RV systolic dysfunction strongly predicts cardiovascular death after CABG in patients with low LVEF. Only few studies have been conducted on the association between RV function and outcomes after SVR. Couperus et al. [8] investigated the prognostic value of the baseline systolic RV function for 30-day mortality of patients undergoing SVR. They measured multiple RV functional parameters using echocardiography. They showed that the coexistence of several impaired RV parameters per patient is strongly associated with 30-day mortality after SVR. Garatti et al. [7] reported that 5- and 8-year survival rates, as well as freedom from cardiac events, are significantly lower in patients with RV dysfunction. They concluded that RV dysfunction is an independent predictor of late outcome in heart failure patients following SVR. Kukulski et al. [9] analysed the baseline RV function of 866 patients in the STICH trial. They showed that LV remodelling expressed by LVEDV, LVESV and LVEF worsens progressively with increasing RV dysfunction. Furthermore, patients with moderate or severe RV dysfunction who underwent SVR concomitant with CABG have significantly worse outcomes compared with those who received CABG alone, although in patients with less than mild RV dysfunction, no significant difference in outcomes was found between patients with and without SVR. These results may emphasize the importance of preoperative RV function for predicting worse outcomes after SVR. These results were consistent with our findings that preoperative RV volume and RVEF were significant predictors of long-term mortality and MACE after SVR. Although SVR enhances LV systolic function, its impact on RV function is scarcely known. SVR reduces LV wall stress and improves contractile function and mechanical dyssynchrony of the left ventricle [1, 2]. However, SVR could impair LV diastolic properties, resulting in the elevation of LV filling pressure [16, 17]. We investigated the changes in RVEDVI, RVESVI and RVEF early after the SVR, and found that RVEF did not show significant improvement. RVEDVI and RVESVI decreased significantly, but the degree of volume reduction was smaller than that of the LV. Couperus et al. [16] investigated RV function at a 2-year follow-up after SVR and observed the simultaneous reduction of RV function despite the significant increase in LVEF. RV dysfunction at follow-up was not related to the follow-up of LV volume or LVEF. Nevertheless, patients with RV dysfunction at follow-up have worse NYHA functional class and reduced freedom from the composite end point of LV assist device implantation, heart transplantation and death. Only data of early changes in RV function were available; thus, we could not conclude whether the changes may reveal the impact of SVR on RV function or whether RV dysfunction may improve at 6 months or later following treatment, as reported by Merlo et al. [18]. In this study, preoperative RV function and volume were more sensitive variables for worse outcomes than LV parameters. Kukulski et al. [9] reported that severity of RV dysfunction is strongly associated with not only LV remodelling but also the grade of LV diastolic dysfunction and the grade of left atrial remodelling. In patients with coronary artery disease, RV infarction and the resulting scar per se, which could not be improved after revascularization or SVR, may cause RV dysfunction and affect the outcome. However, Meyer et al. [19] suggested that low RVEF is not associated with inferoposterior myocardial infarction, which may involve the RV. Ketikoglou et al. [20] found that although RV function is impaired early after RV infarction, it improved significantly at 3 months. These results suggest that in ICM patients with advanced heart failure, RV function impairment may primarily be a final pathway, as reflected systolic and diastolic dysfunction, rather than extensive biventricular structural damage. RV function may be used to evaluate LV status completely and could be a more sensitive parameter than any single LV parameter. Although several descriptive indicators of RV are quantified using standard 2-dimensional echocardiographic techniques, 2-dimensional echocardiography has several limitations, including the anatomical factor and the high variability of the scanning planes, which results in poor reproducibility. In this study, the RV volume and function were evaluated using cardiac MRI, which provides several advantages compared with echocardiography such as the highly accurate and reproducible measurement of ventricular volumes and the ability to overcome anatomical limitations [21]. Limitations Our study has several limitations. It was a retrospective study performed in a single institution. Therefore, it can be susceptible to various sources of bias. Patients with contraindications for MRI study, such as pacemaker or implantable cardioverter-defibrillator implantation (which applies to many ICM patients before operation), were excluded from our study. Moreover, the number of patients was small, and the study group was heterogeneous. The effect of SVR may have been modified by additional procedures, such as restrictive mitral annuloplasty, mitral valve replacement and tricuspid annuloplasty. The difference in SVR methods was another limitation of this study. We evaluated only MRI-derived RV function. Although cardiac MRI is the most accurate method to quantify RV volume and RVEF, these factors were highly load dependent. We examined RV volume and function at preoperative and early postoperative periods. Evaluation of changes in RV parameters over time should be performed in future studies. CONCLUSIONS In patients with ICM who underwent the SVR procedure, RV function and volume were more sensitive variables than LV parameters for predicting worse outcomes. An accurate preoperative assessment of RV volume and function using cardiovascular MRI may improve the risk stratification of SVR. Conflict of interest: none declared. REFERENCES 1 Athanasuleas CL , Buckberg GD , Stanley AW , Siler W , Dor V , Di Donato M. Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation . J Am Coll Cardiol 2004 ; 44 : 1439 – 45 . Google Scholar CrossRef Search ADS PubMed 2 Di Donato M , Toso A , Dor V , Sabatier M , Barletta G , Menicanti L et al. Surgical ventricular restoration improves mechanical intraventricular dyssynchrony in ischemic cardiomyopathy . Circulation 2004 ; 109 : 2536 – 43 . Google Scholar CrossRef Search ADS PubMed 3 Jones RH , Velazquez EJ , Michler RE , Sopko G , Oh JK , O'Connor CM et al. 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Predictors and prognostic significance of right ventricular ejection fraction in patients with ischemic cardiomyopathy . Circulation 2016 ; 134 : 656 – 65 . Google Scholar CrossRef Search ADS PubMed 14 Gulati A , Ismail TF , Jabbour A , Alpendurada F , Guha K , Ismail NA et al. The prevalence and prognostic significance of right ventricular systolic dysfunction in nonischemic dilated cardiomyopathy . Circulation 2013 ; 128 : 1623 – 33 . Google Scholar CrossRef Search ADS PubMed 15 Mohammed SF , Hussain I , AbouEzzeddine OF , Takahama H , Kwon S , Forfia P et al. Right ventricular function in heart failure with preserved ejection fraction. A community-based study . Circulation 2014 ; 130 : 2310 – 20 . Google Scholar CrossRef Search ADS PubMed 16 Couperus LE , Delgado V , van Vessem ME , Tops LF , Palmen M , Braun J et al. Right ventricular dysfunction after surgical left ventricular restoration: prevalence, risk factors and clinical implications . Eur J Cardiothorac Surg 2017 ; 52 : 1161 – 7 . Google Scholar CrossRef Search ADS PubMed 17 Tulner SA , Steendijk P , Klautz RJ , Bax JJ , Schalij MJ , van der Wall EE et al. Surgical ventricular restoration in patients with ischemic dilated cardiomyopathy: evaluation of systolic and diastolic ventricular function, wall stress, dyssynchrony, and mechanical efficiency by pressure-volume loops . J Thorac Cardiovasc Surg 2006 ; 132 : 610 – 20 . Google Scholar CrossRef Search ADS PubMed 18 Merlo M , Gobbo M , Stolfo D , Losurdo P , Ramani F , Barbati G et al. The prognostic impact of the evaluation of RV function in idiopathic DCM . J Am Coll Cardiol 2016 ; 9 : 1034 – 42 . Google Scholar CrossRef Search ADS 19 Meyer P , Filippatos GS , Ahmed MI , Iskandrian AE , Bittner V , Perry GJ et al. Effects of right ventricular ejection fraction on outcomes in chronic systolic heart failure . Circulation 2010 ; 121 : 252 – 8 . Google Scholar CrossRef Search ADS PubMed 20 Ketikoglou DG , Karvounis HI , Papadopoulos CE , Zaglavara TA , Efthimiadis GK , Parharidis GE et al. Echocardiographic evaluation of spontaneous recovery of right ventricular systolic and diastolic function in patients with acute right ventricular infarction associated with posterior wall left ventricular infarction . Am J Cardiol 2004 ; 93 : 911 – 13 . Google Scholar CrossRef Search ADS PubMed 21 Valsangiacomo Buechel ER , Mertens LL. Imaging the right heart: the use of integrated multimodality imaging . Eur Heart J 2012 ; 33 : 949 – 60 . Google Scholar CrossRef Search ADS PubMed © The Author(s) 2018. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved. 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 Journal of Cardio-Thoracic Surgery Oxford University Press

Impact of right ventricular volume and function evaluated using cardiovascular magnetic resonance imaging on outcomes after surgical ventricular reconstruction

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Oxford University Press
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© The Author(s) 2018. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.
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1010-7940
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1873-734X
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10.1093/ejcts/ezy189
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Abstract

Abstract OBJECTIVES This study aimed to evaluate whether cardiac magnetic resonance imaging (MRI)-derived right ventricular (RV) assessment can facilitate risk stratification among patients with ischaemic cardiomyopathy who underwent surgical ventricular reconstruction (SVR). METHODS We retrospectively analysed 53 patients who underwent SVR. The patients were preoperatively evaluated using cardiac MRI. Cine-MRI was acquired for left ventricular (LV) and RV volume. Gadolinium-enhanced MRI was performed to evaluate LV scarring. The mid-term (median, 58 months) risk factors of all-cause mortality and major adverse cardiac events were analysed. RESULTS A significant reduction in LV end-diastolic and end-systolic volume index and an increase in LV ejection fraction were observed early after SVR. RV end-diastolic volume index (RVEDVI) and RV end-systolic volume index (RVESVI) decreased after SVR (preoperative versus postoperative: RVEDVI, 71 ± 24 vs 62 ± 17 ml/m2, P = 0.006; RVESVI, 44 ± 26 vs 37 ± 16 ml/m2, P = 0.033), but RV ejection fraction did not change (preoperative versus postoperative: RV ejection fraction 40.8±14.6 vs 42.0±11.0%, P = 0.067). At follow-up, 25 deaths and 31 major adverse cardiac events occurred. After adjustment for age, creatinine level and preoperative mitral regurgitation grade, the Cox-hazard model indicated that RVEDVI [P = 0.006, hazard ratio (HR) 1.03, 95% confidence interval (CI) 1.01–1.05] and RVESVI [P = 0.007, HR 1.02, 95% CI 1.01–1.04] were significant predictors for all-cause mortality. As for major adverse cardiac events, RVEDVI (P = 0.007, HR 1.03, 95% CI 1.01–1.05), RVESVI (P = 0.002, HR 1.03, 95% CI 1.01–1.04) and RV ejection fraction (P = 0.018, HR 0.97, 95% CI 0.94–0.99) were significant. CONCLUSIONS RV parameters were more sensitive than LV parameters for predicting worse outcomes following SVR. Preoperative assessment of RV volume and function using cardiac MRI may improve the risk stratification of SVR. Cardiac magnetic resonance imaging, Surgical ventricular reconstruction, Right ventricular function INTRODUCTION Surgical left ventricular (LV) reconstruction was developed to restore a more physiological shape to the spherical LV and improve the contractile performance of stretched remote myocardial muscles. Surgical ventricular reconstruction (SVR) clearly modifies LV reverse remodelling in patients with ischaemic heart failure. Several studies have reported the efficacy and benefit of SVR in improving heart failure symptoms and mechanical dyssynchrony [1, 2]. However, the Surgical Treatment for Ischaemic Heart Failure (STICH) randomized trial [3] and its substudies, which showed several parameters associated with a worse outcome after SVR in addition to coronary artery bypass grafting (CABG) [4, 5], emphasize the importance of patient selection for SVR. Most of these studies focused on the assessment of LV parameters. Little attention has been devoted to investigate the impact of reduced right ventricular (RV) function on outcomes in patients who underwent SVR. The cardiovascular system is a closed loop; thus, failure of the LV leads to the malfunction of the RV [6]. RV systolic dysfunction has been found to be a strong and independent predictor of worse outcomes in heart failure patients. Many of these heart failure patients with ischaemic cardiomyopathy (ICM) and reduced LV ejection fraction (LVEF), including those who underwent SVR, have concomitant RV systolic dysfunction. Thus, the significance of RV function is being increasingly recognized in SVR patients [7–9]. Although different modalities can be used for imaging of the RV, accurate measurement of RV volume and function using echocardiography or radionuclide technique is challenging because of the complex geometry of the RV. In recent years, cardiac magnetic resonance imaging (MRI) has emerged as the gold standard technique for the quantification of RV function with high accuracy and reproducibility. The objective of this study was to evaluate whether cardiac MRI-derived RV assessment can facilitate risk stratification among patients with ICM who underwent SVR concomitant with CABG. MATERIALS AND METHODS Patients and study design In this retrospective study, we performed a nonrandomized review of patients who underwent SVR for ICM and preoperative cardiac MRI. A total of 63 consecutive patients underwent SVR for ICM between March 2004 and December 2016. Among them, 54 patients underwent preoperative cardiac MRI. One patient was excluded due to poor image quality. Finally, 53 patients were included in the analysis. Preoperative clinical data included the patient’s age, sex, height, weight, serum creatinine, calculated body surface area (BSA) and preoperative New York Heart Association (NYHA) functional class; presence of preoperative atrial fibrillation, diabetes mellitus, hypertension, haemodialysis, hyperlipidaemia, cerebral vascular disease and peripheral vascular disease; and the need for a preoperative intra-aortic balloon pump (Table 1). Echocardiographic studies were performed within 2 weeks before the surgery, and LV dimensions and valvular functions were assessed. The grades of mitral regurgitation (MR), as well as those of tricuspid regurgitation, were quantified as numerical variables as follows: 0, none; 1+, mild; 2+, moderate; 3+, moderately severe; and 4+, severe. Tricuspid regurgitation peak pressure gradient was determined using the modified Bernoulli equation {4 × (tricuspid regurgitation peak velocity)}2. Table 1: Preoperative characteristics Variables All patients Age (years) 64 ± 10 Male 43 (81) BSA (m2) 1.6 ± 0.2 Serum createnine level (mg/dl) 1.1 (0.9, 1.6) NYHA class  ≤2 21 (40)  3 21 (40)  4 11 (21) Hypertension 33 (62) Hyperlipidaemia 30 (57) Diabetes mellitus 20 (38) Haemodialysis 7 (13) PVD 8 (15) CVD 13 (25) Coronary artery disease  1-vessel disease 6 (11)  2-vessel disease 7 (13)  3-vessel disease 40 (75) Atrial fibrillation 5 (9) Mitral regurgitation grade  ≤1 22 (42)  2 16 (30)  3 10 (19)  4 5 (9) Tricuspid regurgitation grade  ≤1 40 (75)  2 10 (19)  3/4 3 (6) TRPG (mmHg) 33 ± 18 Variables All patients Age (years) 64 ± 10 Male 43 (81) BSA (m2) 1.6 ± 0.2 Serum createnine level (mg/dl) 1.1 (0.9, 1.6) NYHA class  ≤2 21 (40)  3 21 (40)  4 11 (21) Hypertension 33 (62) Hyperlipidaemia 30 (57) Diabetes mellitus 20 (38) Haemodialysis 7 (13) PVD 8 (15) CVD 13 (25) Coronary artery disease  1-vessel disease 6 (11)  2-vessel disease 7 (13)  3-vessel disease 40 (75) Atrial fibrillation 5 (9) Mitral regurgitation grade  ≤1 22 (42)  2 16 (30)  3 10 (19)  4 5 (9) Tricuspid regurgitation grade  ≤1 40 (75)  2 10 (19)  3/4 3 (6) TRPG (mmHg) 33 ± 18 Data are presented as numbers (percentage) or mean ± SD. Serum creatinine level is presented in median and interquartile range. BSA: body surface area; CVD: cerebral vascular disease; NYHA: New York Heart Association; PVD: peripheral vascular disease; TRPG: tricuspid regurgitation pressure gradient. Table 1: Preoperative characteristics Variables All patients Age (years) 64 ± 10 Male 43 (81) BSA (m2) 1.6 ± 0.2 Serum createnine level (mg/dl) 1.1 (0.9, 1.6) NYHA class  ≤2 21 (40)  3 21 (40)  4 11 (21) Hypertension 33 (62) Hyperlipidaemia 30 (57) Diabetes mellitus 20 (38) Haemodialysis 7 (13) PVD 8 (15) CVD 13 (25) Coronary artery disease  1-vessel disease 6 (11)  2-vessel disease 7 (13)  3-vessel disease 40 (75) Atrial fibrillation 5 (9) Mitral regurgitation grade  ≤1 22 (42)  2 16 (30)  3 10 (19)  4 5 (9) Tricuspid regurgitation grade  ≤1 40 (75)  2 10 (19)  3/4 3 (6) TRPG (mmHg) 33 ± 18 Variables All patients Age (years) 64 ± 10 Male 43 (81) BSA (m2) 1.6 ± 0.2 Serum createnine level (mg/dl) 1.1 (0.9, 1.6) NYHA class  ≤2 21 (40)  3 21 (40)  4 11 (21) Hypertension 33 (62) Hyperlipidaemia 30 (57) Diabetes mellitus 20 (38) Haemodialysis 7 (13) PVD 8 (15) CVD 13 (25) Coronary artery disease  1-vessel disease 6 (11)  2-vessel disease 7 (13)  3-vessel disease 40 (75) Atrial fibrillation 5 (9) Mitral regurgitation grade  ≤1 22 (42)  2 16 (30)  3 10 (19)  4 5 (9) Tricuspid regurgitation grade  ≤1 40 (75)  2 10 (19)  3/4 3 (6) TRPG (mmHg) 33 ± 18 Data are presented as numbers (percentage) or mean ± SD. Serum creatinine level is presented in median and interquartile range. BSA: body surface area; CVD: cerebral vascular disease; NYHA: New York Heart Association; PVD: peripheral vascular disease; TRPG: tricuspid regurgitation pressure gradient. All patients received optimized medical regimens, including beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers and diuretics. This study was approved by the institutional ethics committee, and the committee waived the need for individual informed consent. Magnetic resonance imaging protocol and image analysis A standardized cardiac MRI protocol was performed using a 1.5-T scanner (Gilloscan; Philips Medical Systems, Eindhoven, the Netherlands), as described previously [5]. Briefly, steady-state free precession cine images were acquired in multiple short-axis views (9–12 slices at 10-mm intervals throughout the entire left and right ventricles). Using the segment inversion recovery technique in identical planes, delayed enhanced images were obtained at matching cine-image slice locations 10–15 min after the intravenous administration of gadolinium-diethylenetriamine pentaacetic acid (0.2 ml/kg). All short-axis cine-MRI data were analysed using a commercial postprocessing workstation (View Forum; Philips). The LV and RV volumes and LVEF and RV ejection fraction (RVEF) were calculated by manually outlining the LV and RV endocardial borders on the end-diastolic and end-systolic frames. Thus, the LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), RV end-diastolic volume index (RVEDVI) and RV end-systolic volume index (RVESVI) were initially obtained. Subsequently, the LVEF and RVEF were determined as the ratios of (LVEDV − LVESV) to LVEDV and (RVEDV − RVESV) to RVEDV. The LV end-systolic volume index (LVESVI), RVESVI, LV end-diastolic volume index (LVEDVI) and RVEDVI were calculated according to the BSA, as LVESV/BSA, LVEDV/BSA, RVESV/BSA and RVEDV/BSA, respectively. The presence of myocardial infarction was analysed using delayed enhanced images. A hyper-enhanced area was defined as a region with a signal intensity threshold of >3 SD and 2–3 SD above the remote normal myocardium. The percentage of the hyper-enhanced area was assessed for each of the 16 standard LV myocardial segments. The apex segment was excluded from this analysis because visualization and calculation of the hyper-enhanced area in this segment are difficult and inaccurate. An LV segment with myocardial infarction was defined as an LV segment with >25% enhancement. The percentage of hyper-enhancement in the entire LV area (% HE) was also calculated. MRI studies were performed within 2 weeks before the surgery and 2–3 weeks after the surgery. Operative management Our most preferred SVR procedure was the endocardial linear infarct exclusion technique (ELIET), which was described previously [5, 10, 11]. The other SVR procedures performed included the Dor and the septal anterior ventricular exclusion (SAVE) procedures. The choice of procedure depended on the SVR location, extent of the infarction and preference of the attending surgeons. The SVR locations were anterior region in 26 cases, anterior and inferior regions in 11 cases, anterior and lateral regions in 4 cases, inferior regions in 7 cases and lateral regions in 5 cases. A total of 51 patients who had significant coronary artery disease (>50% luminal stenosis of at least 1 principal coronary artery) underwent CABG to achieve complete revascularization, including the left or right internal mammary artery (IMA) to LAD, to preserve the septal branches. Mitral repair was performed in 25 patients with more than 2+ MR using a complete semi-rigid ring (Carpentier-Edwards Physio Ring I in 18 patients, Physio Ring II in 6 patients; Edwards Lifesciences) and a partial semi-rigid band (CG future annuloplasty band; Medtronic) in 1 patient. Papillary muscle relocation was added in 14 patients. The indication to perform this procedure was a coaptation depth of >5 mm. Mitral valve replacement was indicated in 5 patients with an extremely tethered mitral valve or mitral stenosis. Tricuspid repair was performed in 9 patients with more than 2+ tricuspid regurgitation and/or 1+ regurgitation with an annular diameter >21 mm/m2. Follow-up data collection Postoperative clinical data, including postoperative complications and mortality, were obtained from patient’s medical records, outpatient clinic or contact with the patient’s physician, the patients or their relatives through a mailed questionnaire or telephone interviews from January 2017 to August 2017. Their last follow-up date was within this period or at their mortality. Our primary end point was all-cause mortality at any postoperative point within the study period. The cause of death was obtained, and deaths associated with refractory heart failure, arrhythmia, fatal myocardial infarction and any sudden deaths were considered to be due to cardiac causes. Noncardiovascular death included cancer, infectious diseases, such as pneumonia and sepsis, cerebrovascular complication, trauma and suicide. The secondary end point was major adverse cardiac events (MACEs) at any postoperative point within the study period. MACEs were defined as all-cause mortality, nonfatal infarction, ventricular tachycardia/fibrillation and symptomatic congestive heart failure requiring hospitalization. We could not get any information on the 1 patient who dropped out. The last known survival time of the patient was at his 6 months of follow-up. So the follow-up was completed in 98% of patients; the median follow-up period was 58 months (range 0.1–151 months). Statistical analysis Categorical variables are presented as frequencies and percentages. Continuous data are expressed as mean ± SD or median with ranges. A simple linear regression analysis was used to model the relationships between continuous variables. Correlations between variables were assessed with Pearson’s product-moment correlation coefficient. Paired t-test was used to compare the mean difference between baseline and postoperative measurements. Survival and event rates were estimated using Kaplan–Meier curves. The index date was the date of the operation. The primary end point was all-cause mortality (n = 25), and the secondary end point was MACE (n = 31). The independent prognostic effect of MRI-derived LV and RV parameters (preoperative LVEDVI, LVESVI, LVEF, RVEDVI, RVESVI, RVEF, total hyperenhancement area and number of segments with hyperenhancement area >25%) was evaluated using the Cox proportional hazards model. Age, creatinine level and preoperative MR grade were included in the multivariable analysis along with 1 LV or RV parameter per model. Proportional hazards assumption was confirmed with complementary log–log plots, and no violations were detected. Hazard ratio (HR) and 95% confidence interval (CI) were calculated. A P-value of <0.05 was considered statistically significant. Statistical analysis was performed using IBM SPSS Statistics (IBM Corp. Released 2012, IBM SPSS Statistics for Mac, Version 21.0; IBM Corp., Armonk, NY, USA). RESULTS Patient characteristics The preoperative and operative characteristics of patients are listed in Tables 1 and 2. The mean age was 64.1 ± 9.6 years, and 43 (81%) patients were men. Sixty percent of the patients had an NYHA functional class of 3 or 4. Comorbidities included hypertension in 33 (62%) patients, diabetes mellitus in 20 (38%) patients, cerebral vascular disease in 13 (25%) patients, haemodialysis in 7 (13%) patients and peripheral vascular disease in 8 (15%) patients. Table 2: Operative characteristics Variables All patients CABG 51 (96)  No. of distal anastomoses/patient 2.8 ± 1.5  No. of IMA graft/patient 1.2 ± 0.7 SVR  Dor 6 (11)  SAVE 3 (6)  ELIET 44 (83) Location of SVR  Anterior 41 (77)  Inferior 18 (34)  Lateral 9 (17) MAP 25 (47) MVR 5 (9) Relocation of PMs 14 (26) TAP 9 (17) AVR 2 (4) CPB time (min) 227 ± 72 ACC time (min) 149 ± 59 Variables All patients CABG 51 (96)  No. of distal anastomoses/patient 2.8 ± 1.5  No. of IMA graft/patient 1.2 ± 0.7 SVR  Dor 6 (11)  SAVE 3 (6)  ELIET 44 (83) Location of SVR  Anterior 41 (77)  Inferior 18 (34)  Lateral 9 (17) MAP 25 (47) MVR 5 (9) Relocation of PMs 14 (26) TAP 9 (17) AVR 2 (4) CPB time (min) 227 ± 72 ACC time (min) 149 ± 59 Data are presented as numbers (percentage) or mean ± SD. ACC: aortic cross-clamp; AVR: aortic valve replacement; CABG: coronary artery bypass grafting; CPB: cardiopulmonary bypass; ELIET: endocardial linear infarct exclusion technique; IMA: internal mammary artery; MAP: mitral annuloplasty; MVR: mitral valve replacement; PMs: papillary muscles; SAVE: septal anterior ventricular exclusion; SVR: surgical ventricular reconstruction; TAP: tricuspid annuloplasty. Table 2: Operative characteristics Variables All patients CABG 51 (96)  No. of distal anastomoses/patient 2.8 ± 1.5  No. of IMA graft/patient 1.2 ± 0.7 SVR  Dor 6 (11)  SAVE 3 (6)  ELIET 44 (83) Location of SVR  Anterior 41 (77)  Inferior 18 (34)  Lateral 9 (17) MAP 25 (47) MVR 5 (9) Relocation of PMs 14 (26) TAP 9 (17) AVR 2 (4) CPB time (min) 227 ± 72 ACC time (min) 149 ± 59 Variables All patients CABG 51 (96)  No. of distal anastomoses/patient 2.8 ± 1.5  No. of IMA graft/patient 1.2 ± 0.7 SVR  Dor 6 (11)  SAVE 3 (6)  ELIET 44 (83) Location of SVR  Anterior 41 (77)  Inferior 18 (34)  Lateral 9 (17) MAP 25 (47) MVR 5 (9) Relocation of PMs 14 (26) TAP 9 (17) AVR 2 (4) CPB time (min) 227 ± 72 ACC time (min) 149 ± 59 Data are presented as numbers (percentage) or mean ± SD. ACC: aortic cross-clamp; AVR: aortic valve replacement; CABG: coronary artery bypass grafting; CPB: cardiopulmonary bypass; ELIET: endocardial linear infarct exclusion technique; IMA: internal mammary artery; MAP: mitral annuloplasty; MVR: mitral valve replacement; PMs: papillary muscles; SAVE: septal anterior ventricular exclusion; SVR: surgical ventricular reconstruction; TAP: tricuspid annuloplasty. Magnetic resonance imaging results The MRI results are listed in Table 3. Using cine-MRI, the mean (±SD) baseline RVEDVI and RVESVI were 71 ± 24 ml/m2 (range 30–149) and 44 ± 26 ml/m2 (range 13–131), respectively. The mean RVEF was 40.8% ± 14.6% (range 11.7–65.2%). Seventeen patients (32%) exhibited RVEF of <35%. A significant correlation was found between preoperative LVEF and RVEF (Fig. 1A) We could also observe positive relationships between preoperative LVEDVI and RVEDVI, and LVESVI and RVESVI (Fig. 1B and C). Table 3: Magnetic resonance imaging findings Variables All patients Cine MRI  LVEDVI (ml/m2) 157 ± 42  LVESVI (ml/m2) 126 ± 43  LVEF (%) 21.6 ± 8.6  RVEDVI (ml/m2) 71 ± 24  RVESVI (ml/m2) 44 ± 26  RVEF (%) 40.8 ± 14.6 Gadolinium-enhanced MRI  Total HE area (%) 31 ± 12  Number of HE > 25% 8.3 ± 2.7 Variables All patients Cine MRI  LVEDVI (ml/m2) 157 ± 42  LVESVI (ml/m2) 126 ± 43  LVEF (%) 21.6 ± 8.6  RVEDVI (ml/m2) 71 ± 24  RVESVI (ml/m2) 44 ± 26  RVEF (%) 40.8 ± 14.6 Gadolinium-enhanced MRI  Total HE area (%) 31 ± 12  Number of HE > 25% 8.3 ± 2.7 Data are presented as mean ± SD. HE: hyperenhancement; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MRI: magnetic resonance imaging; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Table 3: Magnetic resonance imaging findings Variables All patients Cine MRI  LVEDVI (ml/m2) 157 ± 42  LVESVI (ml/m2) 126 ± 43  LVEF (%) 21.6 ± 8.6  RVEDVI (ml/m2) 71 ± 24  RVESVI (ml/m2) 44 ± 26  RVEF (%) 40.8 ± 14.6 Gadolinium-enhanced MRI  Total HE area (%) 31 ± 12  Number of HE > 25% 8.3 ± 2.7 Variables All patients Cine MRI  LVEDVI (ml/m2) 157 ± 42  LVESVI (ml/m2) 126 ± 43  LVEF (%) 21.6 ± 8.6  RVEDVI (ml/m2) 71 ± 24  RVESVI (ml/m2) 44 ± 26  RVEF (%) 40.8 ± 14.6 Gadolinium-enhanced MRI  Total HE area (%) 31 ± 12  Number of HE > 25% 8.3 ± 2.7 Data are presented as mean ± SD. HE: hyperenhancement; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MRI: magnetic resonance imaging; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Figure 1: View largeDownload slide Scatter plot graphs showing significant linear correlations between the LVEF and RVEF (A), the LVEDVI and the RVEDVI (B), the LVESVI and RVESVI (C). LVEF: left ventricular ejection fraction; LVEDVI: left ventricular end-diastolic volume index; LVESVI: left ventricular end-systolic volume index; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI, right ventricular end-systolic volume index. Figure 1: View largeDownload slide Scatter plot graphs showing significant linear correlations between the LVEF and RVEF (A), the LVEDVI and the RVEDVI (B), the LVESVI and RVESVI (C). LVEF: left ventricular ejection fraction; LVEDVI: left ventricular end-diastolic volume index; LVESVI: left ventricular end-systolic volume index; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI, right ventricular end-systolic volume index. A total of 45 patients underwent evaluation of LV and RV volumes using a cardiovascular MRI early after SVR; however, postoperative MRI could not be examined in 8 patients: five of them suffered from in-hospital death, 2 patients were transferred to a local hospital before the examination and 1 patient was discharged from the hospital before the examination during our early experiences (in 2004). A significant reduction in LVEDVI and LVESVI and an increase in LVEF were observed early after SVR (postoperative LVEDVI, 115 ± 32 ml/m2, vs preoperative, P < 0.001; postoperative LVESVI, 85 ± 32 ml/m2, vs preoperative, P < 0.001; postoperative LVEF, 27.8 ± 9.1%, vs preoperative, P < 0.001). RVEDVI and RVESVI significantly decreased after SVR (postoperative RVEDVI, 62 ± 17 ml/m2, vs preoperative, P = 0.006; postoperative RVESVI, 37 ± 16 ml/m2, vs preoperative, P = 0.033); however, RVEF (postoperative RVEF, 42.0 ± 11.0%, vs preoperative, P = 0.067) did not change (Fig. 2A–C). Figure 2: View largeDownload slide Postoperative changes in the LVEF and the RVEF (A), the LVEDVI and the RVEDVI (B), and the LVESVI and the RVESVI (C). Markers show the average obtained at preoperative and early postoperative periods. Error bars represent standard errors. †P < 0.001 versus preoperative, ‡P < 0.01 versus preoperative and ¶P < 0.05 versus preoperative. EDVI: end-diastolic volume index; EF: ejection fraction; ESVI: end-systolic volume index; LV: left ventricular; postop: postoperative; preop: preoperative; RV: right ventricular. Figure 2: View largeDownload slide Postoperative changes in the LVEF and the RVEF (A), the LVEDVI and the RVEDVI (B), and the LVESVI and the RVESVI (C). Markers show the average obtained at preoperative and early postoperative periods. Error bars represent standard errors. †P < 0.001 versus preoperative, ‡P < 0.01 versus preoperative and ¶P < 0.05 versus preoperative. EDVI: end-diastolic volume index; EF: ejection fraction; ESVI: end-systolic volume index; LV: left ventricular; postop: postoperative; preop: preoperative; RV: right ventricular. All-cause mortality and major adverse cardiac event Postoperative in-hospital death occurred in 5 patients (4 due to cardiac causes and 1 due to acute limb ischaemia). During follow-up, 20 patients died, including 8 due to cardiac conditions (4, heart failure; and 4, sudden death) and 12 due to noncardiac conditions (3, pneumonia; 2, cerebral bleeding; 2, cancer; 3, sepsis; 1, suicide; and 1, trauma). The 5- and 10-year rates of freedom from all-cause mortality were 64 ± 7% and 41 ± 8%, respectively (Fig. 3). Unadjusted proportional hazards estimates showed that both preoperative LVEDVI and LVESVI, as well as RVEDVI, RVESVI and RVEF, were associated with increasing mortality. However, after adjusting for age, creatinine level and preoperative MR grade, only RVEDVI (P = 0.006; HR 1.03; 95% CI 1.01–1.05) and RVESVI (P = 0.007; HR 1.02; 95% CI 1.01–1.04) were shown to have a prognostic value in predicting long-term mortality (Table 4). Table 4: Unadjusted and adjusted Cox analyses for all-cause mortality Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.10 (1.05–1.17) <0.001 Preoperative creatinine level (mg/dl) 1.36 (1.18–1.58) <0.001 Preoperative MR grade 1.46 (1.04–2.04) 0.028 Preoperative LVEDVI (ml/m2) 1.02 (1.01–1.02) 0.002 1.01 (1.00–1.02) 0.156 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.005 1.01 (1.00–1.02) 0.168 Preoperative LVEF (%) 0.97 (0.92–1.02) 0.195 0.98 (0.93–1.03) 0.425 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.04) 0.016 1.03 (1.01–1.05) 0.006 Preoperative RVESVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.02 (1.01–1.04) 0.007 Preoperative RVEF (%) 0.97 (0.95–1.00) 0.024 0.99 (0.95–1.01) 0.128 Total HE area (%) 1.00 (0.97–1.05) 0.720 1.02 (0.98–1.06) 0.398 Number of HE >25% 1.11 (0.92–1.32) 0.276 1.18 (0.98–1.41) 0.080 Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.10 (1.05–1.17) <0.001 Preoperative creatinine level (mg/dl) 1.36 (1.18–1.58) <0.001 Preoperative MR grade 1.46 (1.04–2.04) 0.028 Preoperative LVEDVI (ml/m2) 1.02 (1.01–1.02) 0.002 1.01 (1.00–1.02) 0.156 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.005 1.01 (1.00–1.02) 0.168 Preoperative LVEF (%) 0.97 (0.92–1.02) 0.195 0.98 (0.93–1.03) 0.425 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.04) 0.016 1.03 (1.01–1.05) 0.006 Preoperative RVESVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.02 (1.01–1.04) 0.007 Preoperative RVEF (%) 0.97 (0.95–1.00) 0.024 0.99 (0.95–1.01) 0.128 Total HE area (%) 1.00 (0.97–1.05) 0.720 1.02 (0.98–1.06) 0.398 Number of HE >25% 1.11 (0.92–1.32) 0.276 1.18 (0.98–1.41) 0.080 a Each variable was adjusted for age, creatinine level and preoperative MR grade. CI: confidence interval; HE: hyperenhancement; HR: hazard ratio; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MR: mitral regurgitation; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Table 4: Unadjusted and adjusted Cox analyses for all-cause mortality Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.10 (1.05–1.17) <0.001 Preoperative creatinine level (mg/dl) 1.36 (1.18–1.58) <0.001 Preoperative MR grade 1.46 (1.04–2.04) 0.028 Preoperative LVEDVI (ml/m2) 1.02 (1.01–1.02) 0.002 1.01 (1.00–1.02) 0.156 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.005 1.01 (1.00–1.02) 0.168 Preoperative LVEF (%) 0.97 (0.92–1.02) 0.195 0.98 (0.93–1.03) 0.425 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.04) 0.016 1.03 (1.01–1.05) 0.006 Preoperative RVESVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.02 (1.01–1.04) 0.007 Preoperative RVEF (%) 0.97 (0.95–1.00) 0.024 0.99 (0.95–1.01) 0.128 Total HE area (%) 1.00 (0.97–1.05) 0.720 1.02 (0.98–1.06) 0.398 Number of HE >25% 1.11 (0.92–1.32) 0.276 1.18 (0.98–1.41) 0.080 Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.10 (1.05–1.17) <0.001 Preoperative creatinine level (mg/dl) 1.36 (1.18–1.58) <0.001 Preoperative MR grade 1.46 (1.04–2.04) 0.028 Preoperative LVEDVI (ml/m2) 1.02 (1.01–1.02) 0.002 1.01 (1.00–1.02) 0.156 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.005 1.01 (1.00–1.02) 0.168 Preoperative LVEF (%) 0.97 (0.92–1.02) 0.195 0.98 (0.93–1.03) 0.425 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.04) 0.016 1.03 (1.01–1.05) 0.006 Preoperative RVESVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.02 (1.01–1.04) 0.007 Preoperative RVEF (%) 0.97 (0.95–1.00) 0.024 0.99 (0.95–1.01) 0.128 Total HE area (%) 1.00 (0.97–1.05) 0.720 1.02 (0.98–1.06) 0.398 Number of HE >25% 1.11 (0.92–1.32) 0.276 1.18 (0.98–1.41) 0.080 a Each variable was adjusted for age, creatinine level and preoperative MR grade. CI: confidence interval; HE: hyperenhancement; HR: hazard ratio; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MR: mitral regurgitation; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Figure 3: View largeDownload slide Kaplan–Meier curves for all-cause mortality (A) and MACE (B) in all patients. MACE: major adverse cardiac event. Figure 3: View largeDownload slide Kaplan–Meier curves for all-cause mortality (A) and MACE (B) in all patients. MACE: major adverse cardiac event. A total of 31 patients developed MACE. The 5- and 10-year rates of freedom from MACE were 48 ± 7% and 33 ± 8%, respectively (Fig. 3). Adjusted proportional hazards estimates showed that RVEDVI (P = 0.007; HR 1.03; 95% CI 1.01–1.05), RVESVI (P = 0.002; HR 1.03; 95% CI 1.01–1.04) and RVEF (P = 0.018; HR 0.97; 95% CI 0.94–0.99) had significant relationships with long-term occurrences of MACE (Table 5). Table 5: Unadjusted and adjusted Cox analyses for MACE Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.06 (1.02–1.11) 0.005 Preoperative creatinine level (mg/dl) 1.44 (1.23–1.69) <0.001 Preoperative MR grade 1.69 (1.24–2.31) 0.001 Preoperative LVEDVI (ml/m2) 1.01 (1.01–1.02) 0.001 1.01 (1.00–1.02) 0.082 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.002 1.01 (1.00–1.02) 0.076 Preoperative LVEF (%) 0.96 (0.91–1.01) 0.084 0.97 (0.92–1.02) 0.221 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.03 (1.01–1.05) 0.007 Preoperative RVESVI (ml/m2) 1.02 (1.01–1.03) 0.003 1.03 (1.01–1.04) 0.002 Preoperative RVEF (%) 0.96 (0.94–0.98) 0.001 0.97 (0.94–0.99) 0.018 Total HE area (%) 1.02 (0.98–1.05) 0.369 1.02 (0.99–1.06) 0.279 Number of HE >25% 1.15 (0.98–1.35) 0.089 1.18 (0.99–1.39) 0.058 Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.06 (1.02–1.11) 0.005 Preoperative creatinine level (mg/dl) 1.44 (1.23–1.69) <0.001 Preoperative MR grade 1.69 (1.24–2.31) 0.001 Preoperative LVEDVI (ml/m2) 1.01 (1.01–1.02) 0.001 1.01 (1.00–1.02) 0.082 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.002 1.01 (1.00–1.02) 0.076 Preoperative LVEF (%) 0.96 (0.91–1.01) 0.084 0.97 (0.92–1.02) 0.221 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.03 (1.01–1.05) 0.007 Preoperative RVESVI (ml/m2) 1.02 (1.01–1.03) 0.003 1.03 (1.01–1.04) 0.002 Preoperative RVEF (%) 0.96 (0.94–0.98) 0.001 0.97 (0.94–0.99) 0.018 Total HE area (%) 1.02 (0.98–1.05) 0.369 1.02 (0.99–1.06) 0.279 Number of HE >25% 1.15 (0.98–1.35) 0.089 1.18 (0.99–1.39) 0.058 a Each variable was adjusted for age, creatinine level and preoperative MR grade. CI: confidence interval; HE: hyperenhancement; HR: hazard ratio; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MACE: major adverse cardiac event; MR: mitral regurgitation; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. Table 5: Unadjusted and adjusted Cox analyses for MACE Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.06 (1.02–1.11) 0.005 Preoperative creatinine level (mg/dl) 1.44 (1.23–1.69) <0.001 Preoperative MR grade 1.69 (1.24–2.31) 0.001 Preoperative LVEDVI (ml/m2) 1.01 (1.01–1.02) 0.001 1.01 (1.00–1.02) 0.082 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.002 1.01 (1.00–1.02) 0.076 Preoperative LVEF (%) 0.96 (0.91–1.01) 0.084 0.97 (0.92–1.02) 0.221 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.03 (1.01–1.05) 0.007 Preoperative RVESVI (ml/m2) 1.02 (1.01–1.03) 0.003 1.03 (1.01–1.04) 0.002 Preoperative RVEF (%) 0.96 (0.94–0.98) 0.001 0.97 (0.94–0.99) 0.018 Total HE area (%) 1.02 (0.98–1.05) 0.369 1.02 (0.99–1.06) 0.279 Number of HE >25% 1.15 (0.98–1.35) 0.089 1.18 (0.99–1.39) 0.058 Unadjusted Adjusteda Variables HR (95% CI) P-value HR (95% CI) P-value Age (years) 1.06 (1.02–1.11) 0.005 Preoperative creatinine level (mg/dl) 1.44 (1.23–1.69) <0.001 Preoperative MR grade 1.69 (1.24–2.31) 0.001 Preoperative LVEDVI (ml/m2) 1.01 (1.01–1.02) 0.001 1.01 (1.00–1.02) 0.082 Preoperative LVESVI (ml/m2) 1.01 (1.00–1.02) 0.002 1.01 (1.00–1.02) 0.076 Preoperative LVEF (%) 0.96 (0.91–1.01) 0.084 0.97 (0.92–1.02) 0.221 Preoperative RVEDVI (ml/m2) 1.02 (1.00–1.03) 0.012 1.03 (1.01–1.05) 0.007 Preoperative RVESVI (ml/m2) 1.02 (1.01–1.03) 0.003 1.03 (1.01–1.04) 0.002 Preoperative RVEF (%) 0.96 (0.94–0.98) 0.001 0.97 (0.94–0.99) 0.018 Total HE area (%) 1.02 (0.98–1.05) 0.369 1.02 (0.99–1.06) 0.279 Number of HE >25% 1.15 (0.98–1.35) 0.089 1.18 (0.99–1.39) 0.058 a Each variable was adjusted for age, creatinine level and preoperative MR grade. CI: confidence interval; HE: hyperenhancement; HR: hazard ratio; LVEDVI: left ventricular end-diastolic volume index; LVEF: left ventricular ejection fraction; LVESVI: left ventricular end-systolic volume index; MACE: major adverse cardiac event; MR: mitral regurgitation; RVEDVI: right ventricular end-diastolic volume index; RVEF: right ventricular ejection fraction; RVESVI: right ventricular end-systolic volume index. DISCUSSION The 3 main findings of this study were as follows: first, RV function and volume measured by cardiovascular MRI strongly correlated with LV function and volume in patients with ICM. Second, although LVEF significantly improved immediately after SVR, RVEF did not change. Third, preoperative RV function and volume were more sensitive predictors of mortality and MACE than LV parameters after SVR. This study confirmed the importance of preoperative evaluation of RV function and volume as a risk stratification tool among patients who have undergone SVR. The RV is functionally different from the LV. The RV is very compliant and tolerates a large increase in preload, without a corresponding increase in RV end-diastolic and right atrial pressures. Furthermore, increase in RV preload improves myocardial contraction on the basis of the Frank–Starling mechanism. Beyond the physiological range, excessive RV volume loading can compress the LV and impair global ventricular function through the mechanism of ventricular interdependence. On the other hand, compared with the LV, the RV demonstrates heightened sensitivity to afterload change and is at risk for acute and chronic RV failure [6]. Patients with LV dysfunction also have RV dysfunction with considerable frequency. Pouleur et al. [12] reported that RV systolic dysfunction, defined by RVEF of 35% or less, is present in approximately one-third of their patients with coronary artery disease and low LVEF. Sabe et al. [13] reported that the mean RVEF of their patient population was 43%, whereas the mean LVEF was 24%. Their findings were consistent with our present study, wherein 32% of our patients, whose LVEF was <40%, had RV systolic dysfunction. Under normal circumstances, the RV is connected in series with the LV through the pulmonary circulation. Therefore, systolic and diastolic dysfunction of the LV greatly impacts RV contractility. The pathophysiology of secondary RV dysfunction includes increased afterload attributable to secondary pulmonary hypertension, ventricular interdependence, disruption of the neurohormonal process or myocardial ischaemia secondary to reduced coronary perfusion pressure [6]. The degree of RV dysfunction is often in proportion to that of LV dysfunction. A significant correlation was found between LVEF and RVEF in patients with ICM in many previous studies as shown in our study. Several prior studies have documented the association between RV function and poor prognosis in different heart failure populations of ICM [13] or dilated cardiomyopathy [14], even in patients with preserved LVEF [15], with the use of various methods of assessment. The importance of RV function in patients undergoing cardiac surgery has also been recognized in several previous studies. In the retrospective studies of Pouleur et al. [12], preoperative RV systolic dysfunction strongly predicts cardiovascular death after CABG in patients with low LVEF. Only few studies have been conducted on the association between RV function and outcomes after SVR. Couperus et al. [8] investigated the prognostic value of the baseline systolic RV function for 30-day mortality of patients undergoing SVR. They measured multiple RV functional parameters using echocardiography. They showed that the coexistence of several impaired RV parameters per patient is strongly associated with 30-day mortality after SVR. Garatti et al. [7] reported that 5- and 8-year survival rates, as well as freedom from cardiac events, are significantly lower in patients with RV dysfunction. They concluded that RV dysfunction is an independent predictor of late outcome in heart failure patients following SVR. Kukulski et al. [9] analysed the baseline RV function of 866 patients in the STICH trial. They showed that LV remodelling expressed by LVEDV, LVESV and LVEF worsens progressively with increasing RV dysfunction. Furthermore, patients with moderate or severe RV dysfunction who underwent SVR concomitant with CABG have significantly worse outcomes compared with those who received CABG alone, although in patients with less than mild RV dysfunction, no significant difference in outcomes was found between patients with and without SVR. These results may emphasize the importance of preoperative RV function for predicting worse outcomes after SVR. These results were consistent with our findings that preoperative RV volume and RVEF were significant predictors of long-term mortality and MACE after SVR. Although SVR enhances LV systolic function, its impact on RV function is scarcely known. SVR reduces LV wall stress and improves contractile function and mechanical dyssynchrony of the left ventricle [1, 2]. However, SVR could impair LV diastolic properties, resulting in the elevation of LV filling pressure [16, 17]. We investigated the changes in RVEDVI, RVESVI and RVEF early after the SVR, and found that RVEF did not show significant improvement. RVEDVI and RVESVI decreased significantly, but the degree of volume reduction was smaller than that of the LV. Couperus et al. [16] investigated RV function at a 2-year follow-up after SVR and observed the simultaneous reduction of RV function despite the significant increase in LVEF. RV dysfunction at follow-up was not related to the follow-up of LV volume or LVEF. Nevertheless, patients with RV dysfunction at follow-up have worse NYHA functional class and reduced freedom from the composite end point of LV assist device implantation, heart transplantation and death. Only data of early changes in RV function were available; thus, we could not conclude whether the changes may reveal the impact of SVR on RV function or whether RV dysfunction may improve at 6 months or later following treatment, as reported by Merlo et al. [18]. In this study, preoperative RV function and volume were more sensitive variables for worse outcomes than LV parameters. Kukulski et al. [9] reported that severity of RV dysfunction is strongly associated with not only LV remodelling but also the grade of LV diastolic dysfunction and the grade of left atrial remodelling. In patients with coronary artery disease, RV infarction and the resulting scar per se, which could not be improved after revascularization or SVR, may cause RV dysfunction and affect the outcome. However, Meyer et al. [19] suggested that low RVEF is not associated with inferoposterior myocardial infarction, which may involve the RV. Ketikoglou et al. [20] found that although RV function is impaired early after RV infarction, it improved significantly at 3 months. These results suggest that in ICM patients with advanced heart failure, RV function impairment may primarily be a final pathway, as reflected systolic and diastolic dysfunction, rather than extensive biventricular structural damage. RV function may be used to evaluate LV status completely and could be a more sensitive parameter than any single LV parameter. Although several descriptive indicators of RV are quantified using standard 2-dimensional echocardiographic techniques, 2-dimensional echocardiography has several limitations, including the anatomical factor and the high variability of the scanning planes, which results in poor reproducibility. In this study, the RV volume and function were evaluated using cardiac MRI, which provides several advantages compared with echocardiography such as the highly accurate and reproducible measurement of ventricular volumes and the ability to overcome anatomical limitations [21]. Limitations Our study has several limitations. It was a retrospective study performed in a single institution. Therefore, it can be susceptible to various sources of bias. Patients with contraindications for MRI study, such as pacemaker or implantable cardioverter-defibrillator implantation (which applies to many ICM patients before operation), were excluded from our study. Moreover, the number of patients was small, and the study group was heterogeneous. The effect of SVR may have been modified by additional procedures, such as restrictive mitral annuloplasty, mitral valve replacement and tricuspid annuloplasty. The difference in SVR methods was another limitation of this study. We evaluated only MRI-derived RV function. Although cardiac MRI is the most accurate method to quantify RV volume and RVEF, these factors were highly load dependent. We examined RV volume and function at preoperative and early postoperative periods. Evaluation of changes in RV parameters over time should be performed in future studies. CONCLUSIONS In patients with ICM who underwent the SVR procedure, RV function and volume were more sensitive variables than LV parameters for predicting worse outcomes. An accurate preoperative assessment of RV volume and function using cardiovascular MRI may improve the risk stratification of SVR. Conflict of interest: none declared. REFERENCES 1 Athanasuleas CL , Buckberg GD , Stanley AW , Siler W , Dor V , Di Donato M. Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation . J Am Coll Cardiol 2004 ; 44 : 1439 – 45 . Google Scholar CrossRef Search ADS PubMed 2 Di Donato M , Toso A , Dor V , Sabatier M , Barletta G , Menicanti L et al. Surgical ventricular restoration improves mechanical intraventricular dyssynchrony in ischemic cardiomyopathy . Circulation 2004 ; 109 : 2536 – 43 . Google Scholar CrossRef Search ADS PubMed 3 Jones RH , Velazquez EJ , Michler RE , Sopko G , Oh JK , O'Connor CM et al. 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Google Scholar CrossRef Search ADS PubMed 20 Ketikoglou DG , Karvounis HI , Papadopoulos CE , Zaglavara TA , Efthimiadis GK , Parharidis GE et al. Echocardiographic evaluation of spontaneous recovery of right ventricular systolic and diastolic function in patients with acute right ventricular infarction associated with posterior wall left ventricular infarction . Am J Cardiol 2004 ; 93 : 911 – 13 . Google Scholar CrossRef Search ADS PubMed 21 Valsangiacomo Buechel ER , Mertens LL. Imaging the right heart: the use of integrated multimodality imaging . Eur Heart J 2012 ; 33 : 949 – 60 . Google Scholar CrossRef Search ADS PubMed © The Author(s) 2018. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved. 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 Journal of Cardio-Thoracic SurgeryOxford University Press

Published: May 17, 2018

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