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ObjectivesTo compare variability of echocardiographic and cardiovascular magnetic resonance (CMR) measured left ventricular (LV) function parameters and their relationship to cancer therapeutics-related cardiac dysfunction (CTRCD).MethodsWe prospectively recruited 60 participants (age: 49.8±11.6 years), 30 women with human epidermal growth factor receptor 2-positive breast cancer (15 with CTRCD and 15 without CTRCD) and 30 healthy volunteers. Patients were treated with anthracyclines and trastuzumab. Participants underwent three serial CMR (1.5T) and echocardiography studies at ~3-month intervals. Cine-CMR for LV ejection fraction (LVEF), myocardial tagging for global longitudinal strain (GLS) and global circumferential strain (GCS), two-dimensional (2D) echocardiography for strain and LVEF and three-dimensional (3D) echocardiography for LVEF measurements were obtained. Temporal, interobserver and intraobserver variability were calculated as the coefficient of variation and as the SE of the measurement (SEM). Minimal detected difference (MDD) was defined as 2xSEM.ResultsPatients with CTRCD demonstrated larger mean temporal changes in all parameters compared with those without: 2D-LVEF: 4.6% versus 2.8%; 3D-LVEF: 5.2% vs 2.3%; CMR-LVEF: 6.6% versus 2.7%; 2D-GLS: 1.9% versus 0.7%, 2D-GCS: 2.5% versus 2.2%; CMR-GCS: 2.7% versus 1.6%; and CMR-GLS: 2.1% versus 1.4%, with overlap in 95% CI for 2D-LVEF, 2D-GCS, CMR-GLS and CMR-GCS. The respective mean temporal variability/MDD in healthy volunteers were 3.3%/6.5%, 1.8%/3.7%, 2.2%/4.4%, 0.8%/1.5%, 1.9%/3.7%, 1.8%/3.6% and 1.4%/2.8%. Although the mean temporal variability in healthy volunteers was lower than the mean temporal changes in CTRCD, at the individual level, 2D-GLS, 3D-LVEF and CMR-LVEF had the least overlap. 2D-GLS and CMR-LVEF had the lowest interobserver/intraobserver variabilities.ConclusionTemporal changes in 3D-LVEF, 2D-GLS and CMR LVEF in patients with CTRCD had the least overlap with the variability in healthy volunteers; however, 2D-GLS appears to be the most suitable for clinical application in individual patients.

Regional variability of longitudinal strain (LS) has been previously described with echocardiography in patients with cardiac amyloidosis (CA), however, the reason for this variability is not completely evident. We sought to describe regional patterns in LS using feature-tracking software applied to cardiovascular magnetic resonance (CMR) cine images in patients with CA, hypertrophic cardiomyopathy (HCM), and Anderson-Fabry's disease (AFD) and to relate these patterns to the distribution of late gadolinium enhancement (LGE). Patients with CA (n = 45) were compared to LV mass indexed matched patients with HCM (n = 19) and AFD (n = 19). Peak systolic LS measurements were obtained using Velocity Vector Imaging (VVI) software on CMR cine images. A relative regional LS ratio (RRSR) was calculated as the ratio of the average of the apical segmental LS divided by the sum of the average basal and mid-ventricular segmental LS. LGE was quantified for the basal, mid, and apical segments using a threshold of 5SD above remote myocardium. A regional LGE ratio was calculated similar to RRSR. Patients with CA had significantly had worse global LS (−15.7 ± 4.6%) than those with HCM (−18.0 ± 4.6%, p = 0.046) and AFD (−21.9 ± 5.1%, p < 0.001). The RRSR was higher in patients with CA (1.00 ± 0.31) than in AFD (0.79 ± 0.24; p = 0.018) but not HCM (0.84 ± 0.32; p = 0.114). In CA, a regional difference in LGE burden was noted, with lower LGE in the apex (31.5 ± 19.1%) compared to the mid (38.2 ± 19.0%) and basal (53.7 ± 22.7%; p < 0.001 for both) segments. The regional LGE ratio was not significantly different between patients with CA (0.33 ± 0.15) and AFD (0.47 ± 0.58; p = 0.14) but lower compared to those with HCM (0.72 ± 0.43; p < 0.0001). LGE percentage showed a significant impact on LS (p < 0.0001), with a 0.9% decrease in absolute LS for every 10% increase in LGE percentage. The presence of marked “relative apical sparing” of LS along with a significant reduction in global LS seen in patients with CA on CMR cine analysis may provide an additional tool to differentiate CA from other cause of LVH. The concomitant presence of a base to apex gradient in quantitative LGE burden suggests that the regional strain gradient may be at least partially explained by the burden of amyloid deposition and fibrosis.

Abstract Background and aims Anthracyclines can cause cancer therapy-related cardiac dysfunction (CTRCD). We aimed to assess whether statins prevent decline in left ventricular ejection fraction (LVEF) in anthracycline-treated patients at increased risk for CTRCD. Methods In this multicenter double-blinded, placebo-controlled trial, patients with cancer at increased risk of anthracycline-related CTRCD (per ASCO guidelines) were randomly assigned to atorvastatin 40 mg or placebo once-daily. Cardiovascular magnetic resonance (CMR) imaging was performed before and within 4 weeks after anthracyclines. Blood biomarkers were measured at every cycle. The primary outcome was post-anthracycline LVEF, adjusted for baseline. CTRCD was defined as a fall in LVEF by >10% to <53%. Secondary endpoints included left ventricular (LV) volumes, CTRCD, CMR tissue characterization, high sensitivity troponin I (hsTnI), and B-type natriuretic peptide (BNP). Results We randomized 112 patients (56.9 ± 13.6 years, 87 female, and 73 with breast cancer): 54 to atorvastatin and 58 to placebo. Post-anthracycline CMR was performed 22 (13–27) days from last anthracycline dose. Post-anthracycline LVEF did not differ between the atorvastatin and placebo groups (57.3 ± 5.8% and 55.9 ± 7.4%, respectively) when adjusted for baseline LVEF (P = 0.34). There were no significant between-group differences in post-anthracycline LV end-diastolic (P = 0.20) or end-systolic volume (P = 0.12), CMR myocardial edema and/or fibrosis (P = 0.06–0.47), or peak hsTnI (P ≥ 0.99) and BNP (P = 0.23). CTRCD incidence was similar (4% versus 4%, P ≥ 0.99). There was no difference in adverse events. Conclusions In patients at increased risk of CTRCD, primary prevention with atorvastatin during anthracycline therapy did not ameliorate early LVEF decline, LV remodeling, CTRCD, change in serum cardiac biomarkers, or CMR myocardial tissue changes. Trial registration NCT03186404. Graphical Abstract Graphical Abstract Summary of study enrollment, assessments, and outcomes. Randomized patients had cardiovascular magnetic resonance imaging (CMR) pre- and 72 (63–122) days post-anthracycline initiation / 22 (13–27) days post last dose of anthracycline. The stethoscopes and blood tubes reflect repeated clinical and biomarker assessment after every anthracycline cycle.

Background Cardiac involvement is common and is the leading cause of mortality in Fabry disease (FD). We explored the association between cardiovascular magnetic resonance (CMR) myocardial strain, T1 mapping, late gadolinium enhancement (LGE) and left ventricular hypertrophy (LVH) in patients with FD. Methods In this prospective study, 38 FD patients (45.0 ± 14.5 years, 37% male) and 8 healthy controls (40.1 ± 13.7 years, 63% male) underwent 3 T CMR including cine balanced steady-state free precession (bSSFP), LGE and modified Look-Locker Inversion recovery (MOLLI) T1 mapping. Global longitudinal (GLS) and circumferential (GCS) strain and base-to-apex longitudinal strain (LS) and circumferential strain (CS) gradients were derived from cine bSSFP images using feature tracking analysis. Results Among FD patients, 8 had LVH (FD LVH+, 21%) and 17 had LGE (FD LGE+, 45%). Nineteen FD patients (50%) had neither LVH nor LGE (FD LVH- LGE-). None of the healthy controls had LVH or LGE. FD patients and healthy controls did not differ significantly with respect to GLS (− 15.3 ± 3.5% vs. − 16.3 ± 1.5%, p  = 0.45), GCS (− 19.4 ± 3.0% vs. -19.5 ± 2.9%, p  = 0.84) or base-to-apex LS gradient (7.5 ± 3.8% vs. 9.3 ± 3.5%, p  = 0.24). FD patients had significantly lower base-to-apex CS gradient (2.1 ± 3.7% vs. 6.5 ± 2.2%, p  = 0.002) and native T1 (1170.2 ± 37.5 ms vs. 1239.0 ± 18.0 ms, p  < 0.001). Base-to-apex CS gradient differentiated FD LVH- LGE- patients from healthy controls (OR 0.42, 95% CI: 0.20 to 0.86, p  = 0.019), even after controlling for native T1 (OR 0.24, 95% CI: 0.06 to 0.99, p  = 0.049). In a nested logistic regression model with native T1, model fit was significantly improved by the addition of base-to-apex CS gradient (χ 2 (df = 1) = 11.04, p  < 0.001). Intra- and inter-observer agreement were moderate to good for myocardial strain parameters: GLS (ICC 0.849 and 0.774, respectively), GCS (ICC 0.831 and 0.833, respectively), and base-to-apex CS gradient (ICC 0.737 and 0.613, respectively). Conclusions CMR reproducibly identifies myocardial strain abnormalities in FD. Loss of base-to-apex CS gradient may be an early marker of cardiac involvement in FD, with independent and incremental value beyond native T1.

Background Investigation of the myocardial strain characteristics of the left ventricular non-compaction (LVNC) phenotype with cardiovascular magnetic resonance (CMR) feature tracking. Methods CMR cine balanced steady-state free precession data sets of 59 retrospectively identified LVNC phenotype patients (40 years, IQR: 28–50 years; 51% male) and 36 healthy subjects (39 years, IQR: 30–47 years; 44% male) were evaluated for LV volumes, systolic function and mass. Hypertrabeculation in patients and healthy subjects was evaluated against established CMR diagnostic criteria. Global circumferential strain (GCS), global radial strain (GRS) and global longitudinal strain (GLS) were evaluated with feature-tracking software. Subgroup analyses were performed in patients ( n  = 25) and healthy subjects ( n  = 34) with normal LV volumetrics, and with healthy subjects ( n  = 18) meeting at least one LVNC diagnostic criteria. Results All LVNC phenotype patients, as well as a significant proportion of healthy subjects, met morphology-based CMR diagnostic criteria: non-compacted (NC): compacted myocardial diameter ratio > 2.3 (100% vs. 19.4%), NC mass > 20% (100% vs. 44.4%) and > 25% (100% vs. 13.9%), and NC mass indexed to body surface area > 15 g/m 2 (100% vs. 41.7%). LVNC phenotype patients demonstrated reduced GRS (26.4% vs. 37.1%; p  < 0.001), GCS (− 16.5% vs. -20.5%; p  < 0.001) and GLS (− 14.6% vs. -17.1%; p  < 0.001) compared to healthy subjects, with statistically significant differences persisting on subgroup comparisons of LVNC phenotype patients with healthy subjects meeting diagnostic criteria. GCS also demonstrated independent and incremental diagnostic value beyond each of the morphology-based CMR diagnostic criteria. Conclusions LVNC phenotype patients demonstrate impaired strain by CMR feature tracking, also present on comparison of subjects with normal LV volumetrics meeting diagnostic criteria. The high proportion of healthy subjects meeting morphology-based CMR diagnostic criteria emphasizes the important potential complementary diagnostic value of strain in differentiating LVNC from physiologic hypertrabeculation.

Purpose The aim of this study was to evaluate diagnostic performance of non-contrast-enhanced 2D quiescent-interval single-shot (QISS) and 3D turbo spin-echo (TSE)-based subtraction magnetic resonance angiography (MRA) in the assessment of peripheral arteries in patients with critical limb ischemia (CLI). Materials and methods Nineteen consecutive patients (74 % male, 72.8 ± 9.9 years) with CLI underwent 2D QISS and 3D TSE-based subtraction MRA at 1.5 T. Axial-overlapping QISS MRA (3 mm/2 mm; 1 × 1 mm 2 ) covered from the toes to the aortic bifurcation while coronal 3D TSE-based subtraction MRA (1.3 × 1.2 × 1.3 mm 3 ) was restricted to the calf only. MRA data sets (two readers) were evaluated for stenosis (≥50 %) and image quality. Results were compared with digital subtraction angiography (DSA). Results Two hundred and sixty-seven (267) segments were available for MRA-DSA comparison, with a prevalence of stenosis ≥50 % of 41.9 %. QISS MRA was rated as good to excellent in 79.5–96.0 % of segments without any nondiagnostic segments; 89.8–96.1 % of segments in 3D TSE-based subtraction MRA were rated as nondiagnostic or poor. QISS MRA sensitivities and specificities (segmental) were 92 % and 95 %, respectively, for reader one and 81–97 % for reader two. Due to poor image quality of 3D TSE-based subtraction MRA, diagnostic performance measures were not calculated. Conclusion QISS MRA demonstrates excellent diagnostic performance and higher robustness than 3D TSE-based subtraction MRA in the challenging patient population with CLI. Key Points • QISS MRA allows reliable diagnosis of peripheral artery stenosis in critical limb ischemia. • Robustness of TSE-based subtraction MRA is limited in critical limb ischemia. • QISS MRA allows robust therapy planning in PAD patients with resting leg pain.

Cardiovascular imaging is exponentially increasing in the diagnosis, risk stratification, and therapeutic management of patients with cardiovascular disease. The European Society of Cardiovascular Radiology (ESCR) is a non-profit scientific medical society dedicated to promoting and coordinating activities in cardiovascular imaging. The purpose of this paper, written by ESCR committees and Executive board members and approved by the ESCR Executive Board and Guidelines committee, is to codify a standardized approach to creating ESCR scientific documents. Indeed, consensus development methods must be adopted to ensure transparent decision-making that optimizes national and global health and reaches a certain scientific credibility. ESCR consensus documents developed based on a rigorous methodology will improve their scientific impact on the management of patients with cardiac involvement.Critical relevance statementThis document aims to codify the methodology for producing consensus documents of the ESCR. These ESCR indications will broaden the scientific quality and credibility of further publications and, consequently, the impact on the diagnostic management of patients with cardiac involvement.Key PointsCardiovascular imaging is exponentially increasing for diagnosis, risk stratification, and therapeutic management.The ESCR is committed to promoting cardiovascular imaging.A rigorous methodology for ESCR consensus documents will improve their scientific impact.

Background Stress cardiovascular magnetic resonance (CMR) to screen for silent myocardial ischaemia in asymptomatic high risk patients with type 2 diabetes mellitus (DM) has never been performed, and its effectiveness is unknown. Our aim was to determine the feasibility of a screening programme using stress CMR by obtaining preliminary data on the prevalence of silent ischaemia caused by obstructive coronary artery disease (CAD) and quantify myocardial perfusion in asymptomatic high risk patients with type 2 diabetes. Methods In this prospective cohort study, we recruited 63 asymptomatic DM patients (mean age 66 years ± 4.4 years; 77.8% male); with Framingham risk score ≥ 20% from 3 sites from June 2017 to August 2018. Normal volunteers were recruited to determine normal global myocardial perfusion reserve index (MPRI). Adenosine stress CMR and global MPRI was performed and measured in all subjects. Positive stress CMR cases were referred for catheter coronary angiography (CCA) with/without fractional flow reserve (FFR) measurements. Positive CCA was defined as an FFR ≤ 0.8 or coronary narrowing ≥ 70%. Patients were followed up for major adverse cardiovascular events. Prevalence is presented as patient numbers and percentage. Mann–Whitney U test was used to compare global MPRI between patients and normal volunteers. Results 13 patients had positive stress CMR with positive CCA (20.6% of patient population), while 9 patients with positive stress CMR examinations had a negative CCA. 5 patients (7.9%) had infarcts detected of which 2 patients had no stress perfusion defects. 12 patients had coronary artery stents inserted, whilst 1 patient declined stent placement. DM patients had lower global MPRI than normal volunteers (n = 7) (1.43 ± 0.27 vs 1.83 ± 0.31 respectively; p < 0.01). After a median follow-up of 653 days, there was no death, heart failure, acute coronary syndrome hospitalisation or stroke. Conclusion 20.6% of asymptomatic DM patients (with Framingham risk ≥ 20%) had silent obstructive CAD. Furthermore, asymptomatic patients have reduced global MPRI than normal volunteers. Trial Registration: ClinicalTrials.gov Registration Number: NCT03263728 on 28th August 2017; https://clinicaltrials.gov/ct2/show/NCT03263728 .