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Background Cardiac resynchronization therapy (CRT) restores ventricular synchrony and induces left ventricular (LV) reverse remodeling in patients with heart failure (HF) and dyssynchrony. However, 30% of treated patients are non-responders despite all efforts. Cardiac magnetic resonance imaging (CMR) can be used to quantify regional contributions to stroke volume (SV) as potential CRT predictors. The aim of this study was to determine if LV longitudinal (SVlong%), lateral (SVlat%), and septal (SVsept%) contributions to SV differ from healthy controls and investigate if these parameters can predict CRT response. Methods Sixty-five patients (19 women, 67 ± 9 years) with symptomatic HF (LVEF ≤ 35%) and broadened QRS (≥ 120 ms) underwent CMR. SVlong% was calculated as the volume encompassed by the atrioventricular plane displacement (AVPD) from end diastole (ED) to end systole (ES) divided by total SV. SVlat%, and SVsept% were calculated as the volume encompassed by radial contraction from ED to ES. Twenty age- and sex-matched healthy volunteers were used as controls. The regional measures were compared to outcome response defined as ≥ 15% decrease in echocardiographic LV end-systolic volume (LVESV) from pre- to 6-months post CRT (delta, Δ). Results AVPD and SVlong% were lower in patients compared to controls (8.3 ± 3.2 mm vs 15.3 ± 1.6 mm, P P sept% was lower (0 ± 15% vs 10 ± 4%, P lat% in the patient group (42 ± 16% vs 29 ± 7%, P long% (P = 0.87), SVlat% (P = 0.09), nor SVsept% (P = 0.65). In patients with septal net motion towards the right ventricle (n = 28) ΔLVESV was − 18 ± 22% and with septal net motion towards the LV (n = 37) ΔLVESV was − 19 ± 23% (P = 0.96). Conclusions Longitudinal function, expressed as AVPD and longitudinal contribution to SV, is decreased in patients with HF scheduled for CRT. A larger lateral contribution to SV compensates for the abnormal septal systolic net movement. However, LV reverse remodeling could not be predicted by these regional contributors to SV.

Non-invasive quantification of pressure-volume (PV) loops from brachial pressure and cardiovascular magnetic resonance is a validated method but its application has been limited to resting heart rates. The aim of this study was to improve the previous method and validate it against invasive left-ventricular pressure measurements in an experimental porcine model, and further apply it to 16 healthy humans at rest and during dobutamine stress. In addition, the improved method calculates the arterial elastance which provides the computation of the ratio of effective arterial (Ea) to maximal ventricular elastance (Emax) representing the ventricular-arterial coupling. In the porcine model, the differences between the improved non-invasively derived PV loops and invasively measured PV loops were for stroke work (mean ± SD) 0.00 ± 0.03 J, ventricular efficiency −1.1 ± 0.4%, and contractility 1.1 ± 0.1 mmHg/ml. In human subjects during dobutamine stress, stroke work increased from 1.3 ± 0.3 to 1.7 ± 0.4 J, ventricular efficiency from 71 ± 4 to 82 ± 4%, contractility from 1.3 ± 0.2 to 2.3 ± 0.6 mmHg/ml, and the ratio of arterial to ventricular elastance decreased from 0.96 to 0.56. The improved method for non-invasive PV loops constitutes a more robust diagnostic tool for cardiac disease states in a wider range of study cohorts at both rest and during stress. (Less)

Background Pressure–volume (PV) loops provide comprehensive information of cardiac function, but commonly implies an invasive procedure under general anesthesia. A novel technique has made it possible to non-invasively estimate PV loops with cardiac magnetic resonance (CMR) and brachial pressure which would enable good volume estimation of often anatomically complex ventricles without the need of anesthesia in most cases. In this study we aimed to compare how hemodynamic parameters derived from PV loops in patients with Fontan circulation differ to controls. Methods Patients with Fontan circulation (n = 17, median age 12 years, IQR 6–15) and healthy controls (n = 17, 14 years, IQR 13–22) were examined with CMR. Short axis balanced steady-state free-precession cine images covering the entire heart were acquired. PV loops were derived from left ventricular volumes in all timeframes and brachial blood pressure from cuff sphygmomanometry. Results Fontan patients had lower stroke work, ventricular mechanical efficiency and external power compared to controls. Fontan patients with dominant right ventricle had higher potential energy indexed to body surface area but lower contractility (Ees) compared to controls. Fontan patients had higher arterial elastance (Ea) and Ea/Ees ratio than controls. Contractility showed no correlation with ejection fraction (EF) in Fontan patients irrespective of ventricular morphology. No difference was seen in energy per ejected volume between Fontan patients and controls. Conclusions This non-invasive PV-loop method could be used in future studies to show the potential prognostic value of these measures and if changes in ventricular function over time can be detected earlier by this method compared to changes in ventricular volumes and EF. In contrast to patients with acquired heart failure, Fontan patients had similar energy per ejected volume as controls which suggests similar ventricular oxygen consumption to deliver the same volume in Fontan patients as in controls.

INTRODUCTION Both echocardiography and CMR imaging are used to quantify longitudinal function. Inter-method variability for mitral (MAPSE) and tricuspid (TAPSE) annular plane systolic excursion, and variability between directly measured MAPSE and TAPSE and as based on atrioventricular plane displacement (AVPD) analysis by CMR, are, however, not known. This study, therefore, assessed inter-method variability and variability between annular plane systolic excursion and AVPD-based values in a healthy adult population. METHODS Echocardiography and CMR were performed in 111 adults (35 [32-38] years). Method comparisons were assessed with Deming regression, Bland-Altman analysis and coefficient of variation. Observer reproducibility was assessed by the concordance correlation coefficient. RESULTS Echocardiography and semi-automatic CMR agreed on MAPSE (17 ± 2 mm vs. 17 ± 2 mm, p = 0.1) and TAPSE (25 ± 3 mm vs. 25 ± 3 mm, p = 0.5), correlated highly between methods (fitted-slope 1.22 [95% CI 1.07-1.38] and 1.12 [95% CI 0.95-1.29]) and showed low bias (0.42 [95% CI - 2.05 to 2.88] and - 0.18 [95% CI - 4.78 to 4.43]). Intra-/inter-observer reproducibility was high for both methods for both MAPSE (echocardiography 0.96/0.86; CMR 0.87/0.85) and TAPSE (echocardiography 0.96/0.95; CMR 0.97/0.96). MAPSE (16 ± 2 mm vs. 17 ± 2 mm; p

The aim of this study was to investigate if there was an association between infarct size (IS) measured by cardiac magnetic resonance (CMR) and echocardiographic global longitudinal strain (GLS) in the early stage of acute myocardial infarction in patients with preserved left ventricular ejection fraction (LVEF). Patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention were assessed with CMR and transthoracic echocardiogram within 1 week of hospital admission. Two-dimensional speckle tracking was performed using a semi-automatic algorithm (EchoPac, GE Healthcare). Longitudinal strain curves were generated in a 17-segment model covering the entire left ventricular myocardium. GLS was calculated automatically. LVEF was measured by auto-LVEF in EchoPac. IS was measured by late gadolinium enhancement CMR in short-axis views covering the left ventricle. The study population consisted of 49 patients (age 60.4 ± 9.7 years; 92% male). The study population had preserved echocardiographic LVEF with a mean of 45.8 ± 8.7%. For each percent increase of IS, we found an impairment in GLS by 1.59% (95% CI 0.57–2.61), P = 0.02, after adjustment for sex, age and LVEF. No significant association between IS and echocardiographic LVEF was found: −0.25 (95% CI: −0.61 to 0.11), P = 0.51. At the segmental level, the strongest association between IS and longitudinal strain was found in the apical part of the LV: impairment of 1.69% (95% CI: 1.14–2.23), P < 0.001, for each percent increase in IS. In conclusion, GLS was significantly associated with IS in the early stage of acute myocardial infarction in patients with preserved LVEF, and this association was strongest in the apical part of the LV. No association between IS and LVEF was found.

Background Infarct evolution rate and response to acute reperfusion therapy may differ between patients, which is important to consider for accurate management and treatment of patients with ST-elevation myocardial infarction (STEMI). The aim of this study was therefore to investigate the association of infarct size and myocardial salvage with gender, smoking status, presence of diabetes or history of hypertension in a cohort of STEMI-patients. Methods Patients (n = 301) with first-time STEMI from the three recent multi-center trials (CHILL-MI, MITOCARE and SOCCER) underwent cardiac magnetic resonance (CMR) imaging to determine myocardium at risk (MaR) and infarct size (IS). Myocardial salvage index (MSI) was calculated as MSI = 1-IS/MaR. Pain to balloon time, culprit vessel, trial treatments, age, TIMI grade flow and collateral flow by Rentrop grading were included as explanatory variables in the statistical model. Results Women (n = 66) had significantly smaller MaR (mean difference: 5.0 ± 1.5% of left ventricle (LV), p

Intracardiac hemodynamic forces have been proposed to influence remodeling and be a marker of ventricular dysfunction. We aimed to quantify the hemodynamic forces in patients with repaired tetralogy of Fallot (rToF) to further understand the pathophysiological mechanisms as this could be a potential marker for pulmonary valve replacement (PVR) in these patients. Patients with rToF and pulmonary regurgitation (PR) > 20% ( n = 18) and healthy control subjects ( n = 15) underwent MRI, including four-dimensional flow. A subset of patients ( n = 8) underwent PVR and MRI after surgery. Time-resolved hemodynamic forces were quantified using 4D-flow data and indexed to ventricular volume. Patients had higher systolic and diastolic left ventricular (LV) hemodynamic forces compared with control subjects in the lateral-septal/LV outflow tract ( P = 0.011 and P = 0.0031) and inferior-anterior ( P < 0.0001 and P < 0.0001) directions, which are forces not aligned with blood flow. Forces did not change after PVR. Patients had higher RV diastolic forces compared with control subjects in the diaphragm-right ventricular (RV) outflow tract (RVOT; P < 0.001) and apical-basal ( P = 0.0017) directions. After PVR, RV systolic forces in the diaphragm-RVOT direction decreased ( P = 0.039) to lower levels than in control subjects ( P = 0.0064). RV diastolic forces decreased in all directions ( P = 0.0078, P = 0.0078, and P = 0.039) but were still higher than in control subjects in the diaphragm-RVOT direction ( P = 0.046). In conclusion, patients with rToF and PR had LV hemodynamic forces less aligned with intraventricular blood flow compared with control subjects and higher diastolic RV forces along the regurgitant flow direction in the RVOT and that of tricuspid inflow. Remaining force differences in the LV and RV after PVR suggest that biventricular pumping does not normalize after surgery. NEW & NOTEWORTHY Biventricular hemodynamic forces in patients with repaired tetralogy of Fallot and pulmonary regurgitation were quantified for the first time. Left ventricular hemodynamic forces were less aligned to the main blood flow direction in patients compared with control subjects. Higher right ventricular forces were seen along the pulmonary regurgitant and tricuspid inflow directions. Differences in forces versus control subjects remain after pulmonary valve replacement, suggesting that altered biventricular pumping does not normalize after surgery.

Patients with heart failure with left ventricular (LV) dyssynchrony often do not respond to cardiac resynchronization therapy (CRT), indicating that the pathophysiology is insufficiently understood. Intracardiac hemodynamic forces computed from four-dimensional (4-D) flow MRI have been proposed as a new measure of cardiac function. We therefore aimed to investigate how hemodynamic forces are altered in LV dyssynchrony. Thirty-one patients with heart failure and LV dyssynchrony and 39 control subjects underwent cardiac MRI with the acquisition of 4-D flow. Hemodynamic forces were computed using Navier-Stokes equations and integrated over the manually delineated LV volume. The ratio between transverse (lateral-septal and inferior-anterior) and longitudinal (apical-basal) forces was calculated for systole and diastole separately and compared with QRS duration, aortic valve opening delay, global longitudinal strain, and ejection fraction (EF). Patients exhibited hemodynamic force patterns that were significantly altered compared with control subjects, including loss of longitudinal forces in diastole (force ratio, control subjects vs. patients: 0.32 vs. 0.90, P < 0.0001) and increased transverse force magnitudes. The systolic force ratio was correlated with global longitudinal strain and EF ( P < 0.01). The diastolic force ratio separated patients from control subjects (area under the curve: 0.98, P < 0.0001) but was not correlated to other dyssynchrony measures ( P > 0.05 for all). Hemodynamic forces by 4-D flow represent a new approach to the quantification of LV dyssynchrony. Diastolic force patterns separate healthy from diseased ventricles. Different force patterns in patients indicate the possible use of force analysis for risk stratification and CRT implantation guidance. NEW & NOTEWORTHY In this report, we demonstrate that patients with heart failure with left ventricular dyssynchrony exhibit significantly altered hemodynamic forces compared with normal. Force patterns in patients mechanistically reflect left ventricular dysfunction on the organ level, largely independent of traditional dyssynchrony measures. Force analysis may help clinical decision making and could potentially be used to improve therapy outcomes.

To assess (1) global longitudinal strain (GLS) by feature tracking cardiac magnetic resonance (CMR) in the sub-acute and chronic phases after ST-elevation infarction (STEMI) and compare to GLS in healthy controls, and (2) the evolution of GLS and regional longitudinal strain (RLS) over time, and their relationship to infarct location and size. Seventy-seven patients from the CHILL-MI-trial (NCT01379261) who underwent CMR 2–6 days and 6 months after STEMI and 27 healthy controls were included for comparison. Steady state free precession (SSFP) long-axis cine images were obtained for GLS and RLS, and late gadolinium enhancement (LGE) images were obtained for infarct size quantifications. GLS was impaired in the sub-acute (− 11.8 ± 3.0%) and chronic phases (− 14.3 ± 2.9%) compared to normal GLS in controls (− 18.4 ± 2.4%; p 2 = 0.2; chronic: r2 = 0.2, p

Background Atrioventricular plane displacement (AVPD) reflects longitudinal left ventricular (LV) systolic function, and wall thickening (WT) regional radial LV function. The temporal evolution of these measures after STEMI with CMR has not been evaluated. We aimed to investigate how AVPD and WT are affected globally and regionally from the sub-acute to the chronic phase after ST-elevation myocardial infarction (STEMI). Methods Healthy volunteers without cardiovascular disease and medication (controls, n = 20) and patients from the CHILL-MI study (NCT01379261) prospectively underwent magnetic resonance imaging (MRI) 2–6 days and 6 months after STEMI (n = 77). CHILL-MI randomized STEMI-patients to cooling therapy initiated before reperfusion or standard of care. AVPD was measured at six points in three long axis cine images and wall thickening in short axis cine images. Infarction was quantified using late gadolinium enhancement (LGE) and used to define infarct and remote segments. Results There were no difference in AVPD either at acute or chronic phase (p = 0.90 and p = 0.40) or WT (p = 0.85 and p = 0.99) between patients randomized to cooling therapy and standard of care. Therefore, the results are presented for the pooled cohort. Global AVPD was decreased in both the sub-acute (12 ± 2 mm, p Conclusion AVPD was a global rather than regional marker of cardiac function in this STEMI study and this may explain the prognostic importance of local measurements of mitral annular plane systolic excursion (MAPSE). The decrease in WT in remote myocardium even in the chronic phase needs to be taken into consideration when combining functional measurements with infarct quantification for diagnosis of post-ischemic stunning and hibernation.

Background Anteroseptal ST elevation myocardial infarction (STEMI) is traditionally defined on the electrocardiogram (ECG) by ST elevation (STE) in leads V1-V3, with or without involvement of lead V4. It is commonly taught that such infarcts affect the basal anteroseptal myocardial segment. While there are suggestions in the literature that Q waves limited to V1-V4 represent predominantly apical infarction, none have evaluated anteroseptal ST elevation territories. We compared the distribution of the myocardium at risk (MaR) in STEMI patients presenting with STE limited to V1-V4 and those with more extensive STE (V1-V6). Methods We identified patients in the MITOCARE study presenting with a first acute STEMI and new STE in at least two contiguous anterior leads from V1 to V6. Patients underwent cardiac magnetic resonance (CMR) imaging three to five days after acute infarction. Results Thirty-two patients met inclusion criteria. In patients with STE in V1-V4 (n = 20), myocardium at risk (MaR) > 50% was seen in 0%, 85%, 75%, 100%, and 90% in the basal anteroseptal, mid anteroseptal, apical anterior, apical septal segments, and apex, respectively. The group with STE in V1-V6 (n = 12), MaR > 50% was seen in 8%, 83%, 83%, 92%, and 83% of the same segments. Conclusions Patients with acute STEMI and STE in leads V1-V4, exhibit MaR in predominantly apical territories and rarely in the basal anteroseptum. We found no evidence to support existence of isolated basal anteroseptal or septal STEMI. “Anteroapical” infarction is a more precise description than “anteroseptal” infarction for acute STEMI patients exhibiting STE in V1-V4.

Objective. We aim to determine the correlation between ST-segment changes in leads V4–V6 and the extent of myocardial injury by cardiac magnetic resonance (CMR) in patients with inferior ST elevation (STE) myocardial infarction (iSTEMI). Design. Admission electrocardiogram and CMR data from the MITOCARE trial were used. Differences in mean myocardium at risk, infarct size, ejection fraction and myocardial segment involvement by CMR were compared in patients with first iSTEMI with STE, ST depression (STD) or no ST changes (NST) in V4–V6. Myocardial segment involvement was further evaluated by comparing proportion of patients in each group with ≥25% and ≥50% segment involvement. Results. Fifty-four patients were included. Patients with STE (n = 22) and STD (n = 16) in V4–V6 had significantly lower ejection fraction compared to NST (n = 16) (48% vs 48% vs 54%, p = .02). STE showed more apical, apical lateral and mid-inferolateral involvement but less basal inferior involvement than NST. STD exhibited greater basal inferoseptal involvement compared to STE. There were more patients with STE that had ≥25% and ≥50% apical lateral involvement compared with STD and NST groups. Patients with STD were more likely to have ≥25% and ≥50% basal inferoseptal involvement compared with STE and NST groups.Conclusion. Our study suggests that in iSTEMI, ST changes in the precordial leads V4–V6 correlates with greater myocardial injury and distribution of myocardium at risk.

The aim of our study was to examine the pathophysiology of ST depression (STD) in leads V1–V3 in the setting of inferior ST elevation myocardial infarction (iSTEMI) through the perspective of cardiac magnetic resonance (CMR). Methods: Differences in myocardial area at risk (MaR), infarct size, ejection fraction and myocardial segment involvement by CMR were compared in MITOCARE trial patients with first iSTEMI with ST elevation (STE), STD or no ST changes (NST) in V1–V3. The frontal plane projection of the inferior wall MaR in relationship to the anterior/posterior chest wall was calculated and compared between groups. Results: Fifty-six patients were included. Patients with STD (n = 38) and STE (n = 5) in V1–V3 had significantly larger mean MaR compared to NST (n = 13; 32 ± 7%LV, 36 ± 10%LV and 26 ± 6%LV, respectively; p = 0.01). STD in leads V1–V3 was associated with more apical inferior and mid inferoseptal involvement and had a larger mean frontal plane projection of MaR compared with NST (24 ± 6%LV vs. 20 ± 6%LV, p = 0.04). Conclusion: STD in V1–V3 in iSTEMI is associated with larger MaR, more extension into the inferoseptal segments and likely results from greater frontal plane projection of the MaR, leading to reciprocal changes on the electrocardiogram.

Background: Regional ventricular pumping mechanisms in patients with volume-loaded right ventricles (RV) are altered, but the cause is unknown. The aim was to determine whether these changes in ventricular pumping mechanisms are influenced by the RV dilatation itself or the aetiology behind it. Methods: Seventeen patients with atrial septal defects (ASD) and 10 healthy controls underwent cardiovascular magnetic resonance (CMR) at rest and during dobutamine/atropine stress. Sixteen patients underwent transcutaneous ASD closure. Follow-up CMR at rest was performed the following day. Thirty patients with RV overload due to pulmonary regurgitation (PR) underwent CMR at rest. Cine images were used to measure left ventricular (LV) and RV volumes as well as septal, longitudinal and lateral contributions to LV and RV stroke volume (SV). Results: At rest, septal contribution to LVSV was lower in ASD patients than controls (-1% versus 7%, P

Introduction: The myocardium at risk (MaR) represents the quantitative ischemic area destined to myocardial infarction (MI) if no reperfusion therapy is initiated. Different ECG scores for MaR have been developed, but there is no consensus as to which should be preferred. Objective: Comparisons of ECG scores and Cardiac Magnetic Resonance (CMR) for determining MaR. Methods: MaR was determined by 3 different ECG scores, and by CMR in ST-segment elevation MI (STEMI) patients from the MITOCARE cardioprotection trial. The Aldrich score (AL) is based on the number of leads with ST-elevation for anterior MI and the sum of ST-segment elevation for inferior MI on the admission ECG. The van Hellemond score (VH) considers both the ischemic and infarcted component of the MaR by adding the AL and the QRS score, which is an estimate of final infarct size. The Hasche score is based on the maximal possible infarct size determined from the QRS score on the baseline ECG. Results: Ninety-eight patients (85% male, mean age 61. years) met STEMI criteria on their admission ECG and underwent CMR within 3-5. days after STEMI. Mean MaR by CMR was 41.2. ±. 10.2 and 30.3. ±. 7.2 for anterior and inferior infarcts, respectively. For both anterior and inferior infarcts the Aldrich (18.2. ±. 5.1 and 18.6. ±. 6.0) and Hasche (25.3. ±. 9.8 and 26.4. ±. 8.8) scores significantly underestimated MaR compared to MaR measured by CMR. In contrast, MaR by the van Hellemond score (37.0. ±. 14.2 and 31.7. ±. 12.8) was comparable to CMR. Conclusion: We tested the performance of the electrocardiographic estimation of myocardium area at risk by Aldrich, Hasche and van Hellemond ECG scores in comparison to MaR measured by CMR in STEMI patients. MaR by the van Hellemond score and CMR were comparable, while Aldrich and Hasche underestimated MaR.

SummaryPurpose Patients with complex congenital heart disease may need to be converted to a Fontan circulation with systemic venous return surgically connected to the pulmonary circulation. These patients frequently form aortopulmonary collaterals (APC), that is arterial inflows to the pulmonary artery vascular tree. The aim of this study was to develop a method to calculate the effect of APC on the pulmonary flow distribution based on magnetic resonance imaging (MRI) measurements and computational fluid dynamics simulations in order to enable prediction of interventional outcomes in Fontan patients. Methods Patient-specific models of 11 patients were constructed in a 3D-design software based on MRI segmentations. APC flow was quantified as the difference between pulmonary venous flow and pulmonary artery flow, measured by MRI. A method was developed to include the modulating effect of the APC flow by calculating the patient-specific relative pulmonary vascular resistance. Simulations, including interventions with a Y-graft replacement and a stent dilatation, were validated against MRI results. Results The bias between simulated and MRI-measured fraction of blood to the left lung was 2·9 ± 5·3%. Including the effects of the APC flow in the simulation (n = 6) reduced simulation error from 9·8 ± 7·0% to 5·2 ± 6·3%. Preliminary findings in two patients show that the effect of surgical and catheter interventions could be predicted using the demonstrated methods. Conclusions The work demonstrates a novel method to include APC flow in predictive simulations of Fontan hemodynamics. APC flow was found to have a significant contribution to the pulmonary flow distribution in Fontan patients.

PURPOSE: To develop and assess a technique for self-gated fetal cardiac cine magnetic resonance imaging (MRI) using tiny golden angle radial sampling combined with iGRASP (iterative Golden-angle RAdial Sparse Parallel) for accelerated acquisition based on parallel imaging and compressed sensing.MATERIALS AND METHODS: Fetal cardiac data were acquired from five volunteers in gestational week 29-37 at 1.5T using tiny golden angles for eddy currents reduction. The acquired multicoil radial projections were input to a principal component analysis-based compression stage. The cardiac self-gating (CSG) signal for cardiac gating was extracted from the acquired radial projections and the iGRASP reconstruction procedure was applied. In all acquisitions, a total of 4000 radial spokes were acquired within a breath-hold of less than 15 seconds using a balanced steady-state free precession pulse sequence. The images were qualitatively compared by two independent observers (on a scale of 1-4) to a single midventricular cine image from metric optimized gating (MOG) and real-time acquisitions.RESULTS: For iGRASP and MOG images, good overall image quality (2.8 ± 0.4 and 2.6 ± 1.3, respectively, for observer 1; 3.6 ± 0.5 and 3.4 ± 0.9, respectively, for observer 2) and cardiac diagnostic quality (3.8 ± 0.4 and 3.4 ± 0.9, respectively, for observer 1; 3.6 ± 0.5 and 3.6 ± 0.9, respectively, for observer 2) were obtained, with visualized myocardial thickening over the cardiac cycle and well-defined myocardial borders to ventricular lumen and liver/lung tissue. For iGRASP, MOG, and real time, left ventricular lumen diameter (14.1 ± 2.2 mm, 14.2 ± 1.9 mm, 14.7 ± 1.1 mm, respectively) and wall thickness (2.7 ± 0.3 mm, 2.6 ± 0.3 mm, 3.0 ± 0.4, respectively) showed agreement and no statistically significant difference was found (all P > 0.05). Images with iGRASP tended to have higher overall image quality scores compared with MOG and particularly real-time images, albeit not statistically significant in this feasibility study (P > 0.99 and P = 0.12, respectively).CONCLUSION: Fetal cardiac cine MRI can be performed with iGRASP using tiny golden angles and CSG. Comparison with other fetal cardiac cine MRI methods showed that the proposed method produces high-quality fetal cardiac reconstructions.LEVEL OF EVIDENCE: 2 J. Magn. Reson. Imaging 2017. (Less)

Background: Pressure-volume (PV) loops provide a wealth of information on cardiac function but are not readily available in clinical routine or in clinical trials. This study aimed to develop and validate a noninvasive method to compute individualized left ventricular PV loops. Methods: The proposed method is based on time-varying elastance, with experimentally optimized model parameters from a training set (n=5 pigs), yielding individualized PV loops. Model inputs are left ventricular volume curves from cardiovascular magnetic resonance imaging and brachial pressure. The method was experimentally validated in a separate set (n=9 pig experiments) using invasive pressure measurements and cardiovascular magnetic resonance images and subsequently applied to human healthy controls (n=13) and patients with heart failure (n=28). Results: There was a moderate-to-excellent agreement between in vivo-measured and model-calculated stroke work (intraclass correlation coefficient, 0.93; bias, −0.02±0.03 J), mechanical potential energy (intraclass correlation coefficient, 0.57; bias, −0.04±0.03 J), and ventricular efficiency (intraclass correlation coefficient, 0.84; bias, 3.5±2.1%). The model yielded lower ventricular efficiency ( P P P P Conclusions: We have developed the first experimentally validated, noninvasive method to compute left ventricular PV loops and associated quantitative measures. The proposed method shows significant agreement with in vivo-derived measurements and could support clinical decision-making and provide surrogate end points in clinical heart failure trials.

Cardiovascular disease is the leading cause of death in the western world. With the application of theoretical physics to the clinic, a variety of imaging technologies are available to the physician for diagnosing and accurately quantifying disease progression. These tools can influence how therapies are applied and impact patient outcome. Radiographic methods based on x-rays are used for diagnosis (Computed Tomography) and therapy (catheterization suite). Nuclear medicine with Single Photon Emission Tomography (SPECT) and Positron Emission Tomography (PET) are routinely used for detecting irreversible and reversible ischemic injury. Ultrasound echocardiography is also routinely used for visualizing contractile function and quantifying blood velocities. Cardiac Magnetic Resonant Imaging allows for a one-stop-shop evaluation of the cardiovascular system including function, tissue perfusion and viability and well as edema visualization, extracellular volume imaging, iron overload, etc. The emergence of new technologies for acquiring data with existing techniques, such as sparse undersampling, and radically new approaches, such as Optical Coherence Tomography and Near Infrared Spectroscopy, open uncharted domains and promise even better diagnostics in the future.

Introduction: Four-dimensional (4D) flow magnetic resonance imaging (MRI) enables kinetic energy (KE) quantification of intraventricular blood flow. In this study we aimed to quantify the KE in in patients with univentricular heart and to assess the change in the KE after different types of interventions. Methods: 4D flow MRI was acquired in patients with Fontan circulation (n=12; median age 12, range 3-29 years) and in healthy volunteers (n =8; median age 26, range 23-36 years). MRI was repeated after transcatheter embolization of significant aortopulmonary collaterals (APC; n = 1), after stenting of left pulmonary artery (n=1) and after surgical replacement of hepatic flow tunnel with a Y graft due to significant central pulmonary artery stenosis with secondary formation of arteriovenous (AV) fistulas in the right lung (n= 1). Intraventricular KE was calculated throughout the cardiac cycle and indexed to stroke volume (SV). Results: The systole/diastole ratio of KE in Fontan patients was similar to the ratio of the controls' left ventricle (LV) or right ventricle (RV) depending on the ventricular morphology (Cohens kappa =1.0). Peak systolic KE/SV did not differ in patients compared to the LV in controls (0.016 ± 0.006 mJ/ml vs 0.020 ±0.004 mJ/ml, p= 0.09). Peak diastolic KE/SV in Fontan patients was lower than in the LV of the control group (0.028 ±0.010 vs 0.057± 0.011 mJ/ml, p (Less)

AIMS: Myocardial salvage, determined by cardiac magnetic resonance imaging (CMR), is used as end point in cardioprotection trials. To calculate myocardial salvage, infarct size is related to myocardium at risk (MaR), which can be assessed by T2-short tau inversion recovery (T2-STIR) and contrast-enhanced steady-state free precession magnetic resonance imaging (CE-SSFP). We aimed to determine how T2-STIR and CE-SSFP perform in determining MaR when applied in multicentre, multi-vendor settings.METHODS AND RESULTS: A total of 215 patients from 17 centres were included after percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction. CMR was performed within 1-8 days. These patients participated in the MITOCARE or CHILL-MI cardioprotection trials. Additionally, 8 patients from a previous study, imaged 1 day post-CMR, were included. Late gadolinium enhancement, T2-STIR, and CE-SSFP images were acquired on 1.5T MR scanners (Philips, Siemens, or GE). In 65% of the patients, T2-STIR was of diagnostic quality compared with 97% for CE-SSFP. In diagnostic quality images, there was no difference in MaR by T2-STIR and CE-SSFP (bias: 0.02 ± 6%, P = 0.96, r(2) = 0.71, P < 0.001), or between treatment and control arms. No change in size or quality of MaR nor ability to identify culprit artery was seen over the first week after the acute event (P = 0.44).CONCLUSION: In diagnostic quality images, T2-STIR and CE-SSFP provide similar estimates of MaR, were constant over the first week, and were not affected by treatment. CE-SSFP had a higher degree of diagnostic quality images compared with T2 imaging for sequences from two out of three vendors. Therefore, CE-SSFP is currently more suitable for implementation in multicentre, multi-vendor clinical trials. (Less)

To present and validate a new method for 4D flow quantification of vortex-ring mixing during early, rapid filling of the left ventricle (LV) as a potential index of diastolic dysfunction and heart failure.

Objectives This study aimed to investigate whether an overestimation of infarct size on cardiac magnetic resonance (CMR) versus triphenyltetrazolium chloride (TTC) exists acutely and whether it remains after 7 days in an experimental pig model and to elucidate possible mechanisms. Background Overestimation of infarct size (IS) on late gadolinium enhancement CMR early after acute myocardial infarction has been debated. Methods Pigs were subjected to 40 min of left anterior descending artery occlusion and 6 h (n = 9) or 7 days (n = 9) reperfusion. IS by in vivo and ex vivo CMR was compared with TTC staining. Extracellular volume (ECV) was obtained from biopsies using technetium 99m diethylenetriamine pentaacetic acid (99mTc-DTPA) and light microscopy. TTC slices were rescanned on CMR enabling slice-by-slice comparison. Results IS did not differ between in vivo and ex vivo CMR (p = 0.77). IS was overestimated by 27.3% with ex vivo CMR compared with TTC (p = 0.008) acutely with no significant difference at 7 days (p = 0.39). Slice-by-slice comparison showed similar results. A significant decrease in ECV was seen in biopsies of myocardium at risk (MaR) close to the infarct (sometimes referred to as the peri-infarction zone) over 7 days (48.3 ± 4.4% vs. 29.2 ± 2.4%; p = 0.0025). The ECV differed between biopsies of MaR close to the infarct and the rest of the salvaged MaR acutely (48.3 ± 4.4% vs. 32.4 ± 3.2%; p = 0.013) but not at 7 days (29.2 ± 2.4% vs 25.7 ± 1.4%; p = 0.23). Conclusions CMR overestimates IS compared with TTC acutely but not at 7 days. This difference may be explained by higher ECV in MaR closest to the infarct acutely that decreases during 7 days to the same level as the rest of the salvaged MaR. The increased ECV in the MaR closest to the infarct day 1 could be due to severe edema or an admixture of infarcted and salvaged myocardium (partial volume) or both. Nonetheless, this could not be reproduced at 7 days. These results have implications for timing of magnetic resonance infarct imaging early after acute myocardial infarction.

Atrial fibrosis can be estimated noninvasively by magnetic resonance imaging (MRI) using late gadolinium enhancement (LGE), but diastolic dysfunction is clinically assessed by transthoracic echocardiography (TTE), and rarely by MRI. This study aimed to evaluate well‐established diastolic parameters using MRI, and validate them with TTE and left ventricular (LV) filling pressures, and to study the relationship between left atrial (LA) remodeling and parameters of diastolic function. The study retrospectively included 105 patients (53 ± 16 years, 39 females) who underwent 3D LGE MRI between 2012 and 2016. Medical charts were reviewed for the echocardiographic diastolic parameters E, A, and e′ by TTE, and pressure catheterizations. E and A were measured from in‐plane phase‐contrast cardiac MRI images, and e′ by feature‐tracking, and validated with TTE. Interobserver and intraobserver variability was examined. Furthermore, LA volumes, function, and atrial LGE was correlated with diastolic parameters. Evaluation of e′ in MRI had strong agreement with TTE (r = 0.75, P

Background Cardiovascular magnetic resonance (CMR) can be used to calculate myocardial extracellular volume fraction (ECV) by relating the longitudinal relaxation rate in blood and myocardium before and after contrast-injection to hematocrit (Hct) in blood. Hematocrit is known to vary with body posture, which could affect the calculations of ECV. The aim of this study was to test the hypothesis that there is a significant increase in calculated ECV values if the Hct is sampled after the CMR examination in supine position compared to when the patient arrives at the MR department. Methods Forty-three consecutive patients including various pathologies as well as normal findings were included in the study. Venous blood samples were drawn upon arrival to the MR department and directly after the examination with the patient remaining in supine position. A Modified Look-Locker Inversion recovery (MOLLI) protocol was used to acquire mid-ventricular short-axis images before and after contrast injection from which motion-corrected T1 maps were derived and ECV was calculated. Results Hematocrit decreased from 44.0 ± 3.7% before to 40.6 ± 4.0% after the CMR examination (p

Background: Anterolateral myocardial infarction (MI) is traditionally defined on the electrocardiogram by ST-elevation (STE) in I, aVL, and the precordial leads. Traditional literature holds STE in lead aVL to be associated with occlusion proximal to the first diagonal branch of the left anterior descending coronary artery. However, concomitant ischemia of the inferior myocardium may theoretically lead to attenuation of STE in aVL. We compared segmental distribution of myocardial area at risk (MaR) in patients with and without STE in aVL. Methods: We identified patients in the MITOCARE study presenting with a first acute MI and new STE in two contiguous anterior leads from V1 to V6, with or without aVL STE. Patients underwent cardiac magnetic resonance imaging 3-5 days after acute infarction for quantitative assessment of MaR. Results: A total of 32 patients met inclusion criteria; 13 patients with and 19 without STE in lead aVL. MaR > 20% at the basal anterior segment was seen in 54% of patients with aVL STE, and 11% of those without (p = 0.011). MaR > 20% at the apical inferior segment was seen in 62% and 95% of patients with and without aVL STE, respectively (p = 0.029). The total MaR was not different between groups (44% ± 10% and 39% ± 8.3% respectively, p = 0.15). Conclusion: Patients with anterior STEMI and concomitant STE in aVL have less MaR in the apical inferior segment and more MaR in the basal anterior segment.

BACKGROUND: In traditional literature, it appears that "anteroseptal" MIs with Q waves in V1-V3 involve basal anteroseptal segments although studies have questioned this belief.METHODS: We studied patients with first acute anterior Q-wave (>30ms) MI. All underwent late gadolinium enhancement (LGE) cardiac magnetic resonance imaging (MRI).RESULTS: Those with Q waves in V1-V2 (n=7) evidenced LGE >50% in 0%, 43%, 43%, 57%, and 29% of the basal anteroseptal, mid anteroseptal, apical anterior, apical septal segments, and apex, respectively. Patients with Q waves in V1-V3 (n=14), evidenced involvement was 14%, 43%, 43%, 50%, and 7% of the same respective segments. In those with extensive anterior Q waves (n=7), involvement was 0%, 71%, 57%, 86%, and 86%.CONCLUSIONS: Q-wave MI in V1-V2/V3 primarily involves mid- and apical anterior and anteroseptal segments rather than basal segments. Data do not support existence of isolated basal anteroseptal or septal infarction. "Anteroapical infarction" is a more appropriate term than "anteroseptal infarction."

Sixty percent of stroke volume (SV) is generated by atrioventricular plane displacement (AVPD) in a healthy left ventricle (LV). The aims were to determine the effect of ST-elevation myocardial infarction (STEMI) on AVPD and contribution of AVPD to SV and to study the relationship between AVPD and infarct size (IS) and location. Patients from CHILL-MI and MITOCARE studies with cardiovascular magnetic resonance within a week of STEMI (n = 177, 59 ± 11 years) and healthy controls (n = 20, 62 ± 11 years) were included. Left ventricular volumes were quantified in short-axis images. AVPD was measured in six locations in long-axis images. Longitudinal contribution to SV was calculated as AVPD multiplied by the short-axis epicardial area. Patients (IS 17 ± 10% of LV) had decreased ejection fraction (48 ± 8%) compared to controls (60 ± 5%, P2=0·06) but no differences in global AVPD linked to infarct location. Decrease in global and regional AVPD occur even in remote myocardium within 1 week of STEMI. Global AVPD decrease is independent of MI location, and MI size has only minor effect. Longitudinal pumping is slightly lower compared to controls but remains to be the main component to SV even after STEMI. These results highlight the difficulty in determining infarct location and size from longitudinal measures of LV function.

We thank Guaricci et al for their interest in our study1 to find a late gadolinium enhancement (LGE) cardiovascular magnetic resonance characteristic as a predictor of implantable cardioverter defibrillator therapy. Below, we have addressed the concerns raised about certain technical aspects of the study. Guaricci et al state that acquisition of LGE using different schemes (2-dimensional [2D] and 3D acquisition) in the current study1 should be considered a limitation. In this context, Guaricci et al discuss the result from a previous validation study2 from our group, and refer to the use of 8 SD from remote myocardium for infarct quantification as a problem. This previous validation study from 20132 included 2D phase sensitive inversion recovery (PSIR) and 3D-IR in patients with …

AIM: Longitudinal ventricular contraction is a parameter of cardiac performance with predictive power. Right ventricular (RV) longitudinal function is impaired in patients with free pulmonary regurgitation (PR) following corrective surgery for Tetralogy of Fallot (TOF). It remains unclear whether this is a consequence of the surgical repair, or whether it is inherent to PR. The aim of this study was to assess the relationship between longitudinal, lateral and septal pumping in a porcine model of isolated PR.METHODS: Piglets were divided into a control (n = 8) group and a treatment (n = 12) group, which received a stent in the pulmonary valve orifice, inducing PR. After 2-3 months, animals were subjected to cardiac magnetic resonance imaging. A subset of animals (n = 6) then underwent percutaneous pulmonary valve replacement (PPVR) with follow-up 1 month later. Longitudinal, lateral and septal contributions to stroke volume (SV) were quantified by measuring volumetric displacements from end-diastole to end-systole in the cardiac short axis and long axis.RESULTS: PR resulted in a lower longitudinal contribution to RV stroke volume, compared to controls (60.0 ± 2.6% vs. 73.6 ± 3.8%; P = 0.012). Furthermore, a compensatory increase in septal contribution to RVSV was observed (11.0 ± 1.6% vs. -3.1 ± 1.5%; P < 0.0001). The left ventricle (LV) showed counter-regulation with an increased longitudinal LVSV. Changes in RV longitudinal function were reversed by PPVR.CONCLUSION: These findings suggest that PR contributes to decreased RV longitudinal function in the absence of scarring from cardiac surgery. Measurement of longitudinal RVSV may aid risk stratification and timing for interventional correction of PR in TOF patients.

Objectives Indications for pulmonary valve replacement (PVR) in patients with pulmonary regurgitation (PR) after repaired tetralogy of Fallot (rToF) are debated. We aimed to compare right (RV) and left ventricular (LV) kinetic energy (KE) measured by 4D-flow magnetic resonance imaging (MRI) in patients to controls, to further understand the pathophysiological effects of PR. Methods Fifteen patients with rToF with PR > 20% and 14 controls underwent MRI. Ventricular volumes and KE were quantified from cine MRI and 4D-flow, respectively. Lagrangian coherent structures were used to discriminate KE in the PR. Restrictive RV physiology was defined as end-diastolic forward flow. Results LV systolic peak KE was lower in rToF, 2.8 ± 1.1 mJ, compared to healthy volunteers, 4.8 ± 1.1 mJ, p < 0.0001. RV diastolic peak KE was higher in rToF (7.7 ± 4.3 mJ vs 3.1 ± 1.3 mJ, p = 0.0001) and the difference most pronounced in patients with non-restrictive RV physiology. KE was primarily located in the PR volume at the time of diastolic peak KE, 64 ± 17%. Conclusion This is the first study showing disturbed KE in patients with rToF and PR, in both the RV and LV. The role of KE as a potential early marker of ventricular dysfunction to guide intervention needs to be addressed in future studies. Key Points • Kinetic energy (KE) reflects ventricular performance • KE is a potential marker of ventricular dysfunction in Fallot patients • KE is disturbed in both ventricles in patients with tetralogy of Fallot • KE contributes to the understanding of the pathophysiology of pulmonary regurgitation • Lagrangian coherent structures enable differentiation of ventricular inflows Electronic supplementary material The online version of this article (10.1007/s00330-018-5385-3) contains supplementary material, which is available to authorized users.

Background— Late gadolinium enhancement (LGE) border zone on cardiac magnetic resonance imaging has been proposed as an independent predictor of ventricular arrhythmias. The purpose was to determine whether size and heterogeneity of LGE predict appropriate implantable cardioverter defibrillator (ICD) therapy in ischemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NICM) patients and to evaluate 4 LGE border-zone algorithms. Methods and Results— ICM and NICM patients who underwent LGE cardiac magnetic resonance imaging prior to ICD implantation were retrospectively included. Two semiautomatic algorithms, expectation maximization, weighted intensity, a priori information and a weighted border zone algorithm, were compared with a modified full-width half-maximum and a 2-3SD threshold-based algorithm (2-3SD). Hazard ratios were calculated per 1% increase in LGE. A total of 74 ICM and 34 NICM were followed for 63 months (1–140) and 52 months (0–133), respectively. ICM patients had 27 appropriate ICD events, and NICM patients had 7 ICD events. In ICM patients with primary prophylactic ICD, LGE border zone predicted ICD therapy in univariable and multivariable analysis measured by the expectation maximization, weighted intensity, a priori information, weighted border zone, and modified full-width half-maximum algorithms (hazard ratios 1.23, 1.22, and 1.05, respectively; P P Conclusions— Appropriate ICD therapy can be predicted in ICM patients with primary prevention ICD by quantifying the LGE border zone. In NICM patients, total LGE but not LGE border zone had predictive value for ICD therapy. However, the algorithms used affects the predictive value of these measures.

Background Acute myocardial infarct (AMI) size depicted by late gadolinium enhancement cardiovascular magnetic resonance (CMR) is increasingly used as an efficacy endpoint in randomized trials comparing AMI therapies. Infarct size is quantified using manual planimetry (MANUAL), visual scoring (VISUAL), or automated techniques using signal-intensity thresholding (AUTO). Although AUTO is considered the most reproducible, prior studies did not account for the subjective determination of endocardial/epicardial borders, which all methods require. For MANUAL and VISUAL, prior studies did not address how to treat intermediate signal intensities due to partial volume. Methods To assess sources of variability, AMI size was measured in 30 patients and 12 controls by 3 core-laboratories using 8 methods, each separated by more than 2 months time (n = 720 evaluations). The methods were: (1,2) AUTOSegment, AUTOFWHM (using Segment software or the full-width-at-half-maximum algorithm, respectively); (3,4) AUTO-UCSegment, AUTO-UCFWHM (user correction for endocardial border pixels, no-reflow, etc.); (5) MANUAL; (6) MANUAL-ISI (adjustment for intermediate signal-intensities); (7) VISUAL; (8) VISUAL-ISI. Results Mean infarct size varied between 16.8% and 27.2% of LV mass depending on method. Even automated techniques with no user interaction for infarct borders resulted in significant within-patient variability given the need to subjectively trace endocardial/epicardial contours. The coefficient-of-variation (CV) was 10.6% and 14.6% for AUTOSegment and AUTOFWHM, respectively. For manual and visual categories, reproducibility was improved when intermediate signal-intensities were considered (MANUAL-ISI vs MANUAL: CV = 8.3% vs 14.4%; p = 0.03; VISUAL-ISI vs VISUAL: CV = 8.4% vs 10.9%; p = 0.01). For AUTO-UCSegment, MANUAL-ISI, and VISUAL-ISI (best technique in each category) within-patient variability due to the quantification method was less than 10% of total variability, and the required sample sizes for detecting a 5% absolute difference in infarct size were 62, 63, and 62 patients, respectively. Conclusion Among CMR core-laboratories, an important source of variability in infarct size quantification is the subjective delineation of endocardial/epicardial borders. When intermediate signal intensities are considered in manual planimetry and visual scoring, reproducibility and impact on sample size are similar to automated techniques.

Background Atrioventricular plane displacement (AVPD) is an indicator for systolic and diastolic function and accounts for 60% of the left ventricular, and 80% of the right ventricular stroke volume. AVPD is commonly measured clinically in echocardiography as mitral and tricuspid annular plane systolic excursion (MAPSE and TAPSE), but has not been applied widely in cardiovascular magnetic resonance (CMR). To date, there is no robust automatic algorithm available that allows the AVPD to be measured clinically in CMR with input in a single timeframe. This study aimed to develop, validate and provide a method that automatically tracks the left and right ventricular AVPD in CMR images, which can be used in the clinical setting or in applied cardiovascular research in multi-center studies. Methods The proposed algorithm is based on template tracking by normalized cross-correlation combined with a priori information by principal component analysis. The AVPD in each timeframe is calculated for the left and right ventricle separately using CMR long-axis cine images of the 2, 3, and 4-chamber views. The algorithm was developed using a training set (n = 40), and validated in a test set (n = 113) of healthy subjects, athletes, and patients after ST-elevation myocardial infarction from 10 centers. Validation was done using manual measurements in end diastole and end systole as reference standard. Additionally, AVPD, peak emptying velocity, peak filling velocity, and atrial contraction was validated in 20 subjects, where time-resolved manual measurements were used as reference standard. Inter-observer variability was analyzed in 20 subjects. Results In end systole, the difference between the algorithm and the reference standard in the left ventricle was (mean ± SD) -0.6 ± 1.9 mm (R = 0.79), and −0.8 ± 2.1 mm (R = 0.88) in the right ventricle. Inter-observer variability in end systole was −0.6 ± 0.7 mm (R = 0.95), and −0.5 ± 1.4 mm (R = 0.95) for the left and right ventricle, respectively. Validation of peak emptying velocity, peak filling velocity, and atrial contraction yielded lower accuracy than the displacement measures. Conclusions The proposed algorithm show good agreement and low bias with the reference standard, and with an agreement in parity with inter-observer variability. Thus, it can be used as an automatic method of tracking and measuring AVPD in CMR. Electronic supplementary material The online version of this article (doi:10.1186/s12880-017-0189-5) contains supplementary material, which is available to authorized users.

Intracardiac blood flow is driven by hemodynamic forces that are exchanged between the blood and myocardium. Previous studies have been limited to 2D measurements or investigated only left ventricular (LV) forces. Right ventricular (RV) forces and their mechanistic contribution to asymmetric redirection of flow in the RV have not been measured. We therefore aimed to quantify 3D hemodynamic forces in both ventricles in a cohort of healthy subjects, using magnetic resonance imaging 4D flow measurements. Twenty five controls, 14 elite endurance athletes, and 2 patients with LV dyssynchrony were included. 4D flow data were used as input for the Navier-Stokes equations to compute hemodynamic forces over the entire cardiac cycle. Hemodynamic forces were found in a qualitatively consistent pattern in all healthy subjects, with variations in amplitude. LV forces were mainly aligned along the apical-basal longitudinal axis, with an additional component aimed toward the aortic valve during systole. Conversely, RV forces were found in both longitudinal and short-axis planes, with a systolic force component driving a slingshot-like acceleration that explains the mechanism behind the redirection of blood flow toward the pulmonary valve. No differences were found between controls and athletes when indexing forces to ventricular volumes, indicating that cardiac force expenditures are tuned to accelerate blood similarly in small and large hearts. Patients’ forces differed from controls in both timing and amplitude. Normal cardiac pumping is associated with specific force patterns for both ventricles, and deviation from these forces may be a sensitive marker of ventricular dysfunction. Reference values are provided for future studies.NEW & NOTEWORTHY Biventricular hemodynamic forces were quantified for the first time in healthy controls and elite athletes (n = 39). Hemodynamic forces constitute a slingshot-like mechanism in the right ventricle, redirecting blood flow toward the pulmonary circulation. Force patterns were similar between healthy subjects and athletes, indicating potential utility as a cardiac function biomarker.

The study by Stokke et al. [(1)][1] notes that circumferential strain contributes more than twice as much as longitudinal strain to left ventricular ejection fraction, but previous research has shown that 60% of stroke volume is generated by left ventricular longitudinal function [(2)][2]. The

Background— Contrast-enhanced steady state free precession (CE-SSFP) and T2-weighted short tau inversion recovery (T2-STIR) have been clinically validated to estimate myocardium at risk (MaR) by cardiovascular magnetic resonance while using myocardial perfusion single-photon emission computed tomography as reference standard. Myocardial perfusion single-photon emission computed tomography has been used to describe the coronary perfusion territories during myocardial ischemia. Compared with myocardial perfusion single-photon emission computed tomography, cardiovascular magnetic resonance offers superior image quality and practical advantages. Therefore, the aim was to describe the main coronary perfusion territories using CE-SSFP and T2-STIR cardiovascular magnetic resonance data in patients after acute ST-segment–elevation myocardial infarction. Methods and Results— CE-SSFP and T2-STIR data from 2 recent multicenter trials, CHILL-MI and MITOCARE (n=215), were used to assess MaR. Angiography was used to determine culprit vessel. Of 215 patients, 39% had left anterior descending artery occlusion, 49% had right coronary artery occlusion, and 12% had left circumflex artery occlusion. Mean extent of MaR using CE-SSFP was 44±10% for left anterior descending artery, 31±7% for right coronary artery, and 30±9% for left circumflex artery. Using T2-STIR, MaR was 44±9% for left anterior descending artery, 30±8% for right coronary artery, and 30±12% for left circumflex artery. MaR was visualized in polar plots, and expected overlap was found between right coronary artery and left circumflex artery. Detailed regional data are presented for use in software algorithms as a priori information on the extent of MaR. Conclusions— For the first time, cardiovascular magnetic resonance has been used to show the main coronary perfusion territories using CE-SSFP and T2-STIR. The good agreement between CE-SSFP and T2-STIR from this study and myocardial perfusion single-photon emission computed tomography from previous studies indicates that these 3 methods depict MaR accurately in individual patients and at a group level. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifiers: NCT01379261 and NCT01374321.

Background: Late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) using magnitude inversion recovery (IR) or phase sensitive inversion recovery (PSIR) has become clinical standard for assessment of myocardial infarction (MI). However, there is no clinical standard for quantification of MI even though multiple methods have been proposed. Simple thresholds have yielded varying results and advanced algorithms have only been validated in single center studies. Therefore, the aim of this study was to develop an automatic algorithm for MI quantification in IR and PSIR LGE images and to validate the new algorithm experimentally and compare it to expert delineations in multi-center, multi-vendor patient data.Methods: The new automatic algorithm, EWA (Expectation Maximization, weighted intensity, a priori information), was implemented using an intensity threshold by Expectation Maximization (EM) and a weighted summation to account for partial volume effects.The EWA algorithm was validated in-vivo against triphenyltetrazolium-chloride (TTC) staining (n = 7 pigs with paired IR and PSIR images) and against ex-vivo high resolution T1-weighted images (n = 23 IR and n = 13 PSIR images). The EWA algorithm was also compared to expert delineation in 124 patients from multi-center, multi-vendor clinical trials 2–6 days following first time ST-elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention (PCI) (n = 124 IR and n = 49 PSIR images).Results: Infarct size by the EWA algorithm in vivo in pigs showed a bias to ex-vivo TTC of −1 ± 4%LVM (R = 0.84) in IR and −2 ± 3%LVM (R = 0.92) in PSIR images and a bias to ex-vivo T1-weighted images of 0 ± 4%LVM (R = 0.94) in IR and 0 ± 5%LVM (R = 0.79) in PSIR images. In multi-center patient studies, infarct size by the EWA algorithm showed a bias to expert delineation of −2 ± 6 %LVM (R = 0.81) in IR images (n = 124) and 0 ± 5%LVM (R = 0.89) in PSIR images (n = 49).Conclusions: The EWA algorithm was validated experimentally and in patient data with a low bias in both IR and PSIR LGE images. Thus, the use of EM and a weighted intensity as in the EWA algorithm, may serve as a clinical standard for the quantification of myocardial infarction in LGE CMR images.Clinical trial registration: CHILL-MI: NCT01379261 . MITOCARE: NCT01374321 .

Background Cardiac magnetic resonance ( CMR ) can quantify myocardial infarct ( MI ) size and myocardium at risk (MaR), enabling assessment of myocardial salvage index ( MSI ). We assessed how MSI impacts the number of patients needed to reach statistical power in relation to MI size alone and levels of biochemical markers in clinical cardioprotection trials and how scan day affect sample size. Methods and Results Controls (n=90) from the recent CHILL ‐ MI and MITOCARE trials were included. MI size, MaR, and MSI were assessed from CMR . High‐sensitivity troponin T (hsTnT) and creatine kinase isoenzyme MB ( CKMB ) levels were assessed in CHILL ‐ MI patients (n=50). Utilizing distribution of these variables, 100 000 clinical trials were simulated for calculation of sample size required to reach sufficient power. For a treatment effect of 25% decrease in outcome variables, 50 patients were required in each arm using MSI compared to 93, 98, 120, 141, and 143 for MI size alone, hsTnT (area under the curve [ AUC ] and peak), and CKMB ( AUC and peak) in order to reach a power of 90%. If average CMR scan day between treatment and control arms differed by 1 day, sample size needs to be increased by 54% (77 vs 50) to avoid scan day bias masking a treatment effect of 25%. Conclusion Sample size in cardioprotection trials can be reduced 46% to 65% without compromising statistical power when using MSI by CMR as an outcome variable instead of MI size alone or biochemical markers. It is essential to ensure lack of bias in scan day between treatment and control arms to avoid compromising statistical power.

The laws of fluid dynamics govern vortex ring formation and precede cardiac development by billions of years, suggesting that diastolic vortex ring formation is instrumental in defining the shape of the heart. Using novel and validated magnetic resonance imaging measurements, we show that the healthy left ventricle moves in tandem with the expanding vortex ring, indicating that cardiac form and function is epigenetically optimized to accommodate vortex ring formation for volume pumping. Healthy hearts demonstrate a strong coupling between vortex and cardiac volumes (R2 = 0.83), but this optimized phenotype is lost in heart failure, suggesting restoration of normal vortex ring dynamics as a new and possibly important consideration for individualized heart failure treatment. Vortex ring volume was unrelated to early rapid filling (E-wave) velocity in patients and controls. Characteristics of vortex-wall interaction provide unique physiologic and mechanistic information about cardiac diastolic function that may be applied to guide the design and implantation of prosthetic valves and have potential clinical utility as therapeutic targets for tailored medicine or measures of cardiac health.

The kinetic energy (KE) of intracardiac blood may play an important role in cardiac function. The aims of the present study were to 1) quantify and investigate the determinants of KE, 2) compare the KE expenditure of intracardiac blood between athletes and control subjects, and 3) quantify the amount of KE inside and outside the diastolic vortex. Fourteen athletes and fourteen volunteers underwent cardiac MRI, including four-dimensional phase-contrast sequences. KE was quantified in four chambers, and energy expenditure was calculated by determining the mean KE/cardiac index. Left ventricular (LV) mass was an independent predictor of diastolic LVKE ( R2= 0.66, P < 0.001), whereas right ventricular (RV) end-diastolic volume was important for diastolic RVKE ( R2= 0.76, P < 0.001). The mean KE/cardiac index did not differ between groups (control subjects: 0.53 ± 0.14 mJ·l−1·min·m2and athletes: 0.56 ± 0.21 mJ·l−1·min·m2, P = 0.98). Mean LV diastolic vortex KE made up 70 ± 1% and 73 ± 2% of total LV diastolic KE in athletes and control subjects ( P = 0.18). In conclusion, the characteristics of the LV as a pressure pump and the RV as a volume pump are demonstrated as an association between LVKE and LV mass and between RVKE and end-diastolic volume. This also suggests different filling mechanisms where the LV is dependent on diastolic suction, whereas the RV fills with a basal movement of the atrioventricular plane over “stationary” blood. Both groups had similar energy expenditure for intracardiac blood flow, indicating similar pumping efficiency, likely explained by the lower heart rate that cancels the higher KE per heart beat in athletes. The majority of LVKE is found within the LV diastolic vortex, in contrast to earlier findings.

Background Measurement of intracardiac kinetic energy (KE) provides new insights into cardiac hemodynamics and may improve assessment and understanding of heart failure. We therefore aimed to investigate left ventricular (LV) KE time curves in patients with heart failure and in controls. Methods Patients with heart failure (n = 29, NYHA class I-IV) and controls (n = 12) underwent cardiovascular magnetic resonance (CMR) including 4D flow. The vortex-ring boundary was computed using Lagrangian coherent structures. The LV endocardium and vortex-ring were manually delineated and KE was calculated as ½mv2 of the blood within the whole LV and the vortex ring, respectively. Results The systolic average KE was higher in patients compared to controls (2.2 ± 1.4 mJ vs 1.6 ± 0.6 mJ, p = 0.048), but lower when indexing to EDV (6.3 ± 2.2 μJ/ml vs 8.0 ± 2.1 μJ/ml, p = 0.025). No difference was seen in diastolic average KE (3.2 ± 2.3 mJ vs 2.0 ± 0.8 mJ, p = 0.13) even when indexing to EDV (9.0 ± 4.4 μJ/ml vs 10.2 ± 3.3 μJ/ml, p = 0.41). In patients, a smaller fraction of diastolic average KE was observed inside the vortex ring compared to controls (72 ± 6 % vs 54 ± 9 %, p

Anteroseptal myocardial infarction (MI) is traditionally defined on the electrocardiogram (ECG) by ST elevations (STE) in leads V1-V3, with or without involvement of lead V4. While existing pedagogy depicts such MIs as affecting the basal anteroseptal myocardial segment, there are reports that the

ST changes in leads V4-V6 have been associated with more extensive coronary artery disease and worse outcomes in patients with inferior ST elevation myocardial infarction (iSTEMI). Correlation of electrocardiographic (ECG) findings to myocardial injury, assessed by cardiac magnetic resonance (CMR)