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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)

To evaluate the association between impaired left ventricular (LV) longitudinal function and LV underfilling in patients with pulmonary arterial hypertension (PAH). Thirty-nine patients with PAH and 18 age and sex-matched healthy controls were included. LV volume and left atrial volume (LAV) were delineated in short-axis cardiac magnetic resonance (CMR) cine images. LV longitudinal function was assessed from atrio-ventricular plane displacement (AVPD) and global longitudinal strain (GLS) was assessed using feature tracking in three long-axis views. LV filling was assessed by LAV and by pulmonary artery wedge pressure (PAWP) using right heart catheterisation. Patients had a smaller LAV, LV volume and stroke volume as well as a lower LV-AVPD and LV-GLS than controls. PAWP was 6 [IQR 5––9] mmHg in patients. LV ejection fraction did not differ between groups. LV stroke volume correlated with LV-AVPD (r = 0.445, p = .001), LV-GLS (r = − 0.549, p

Timing and indication for pulmonary valve replacement (PVR) in patients with repaired Tetralogy of Fallot (rToF) and pulmonary regurgitation (PR) are uncertain. To improve understanding of pumping mechanics, we investigated atrioventricular coupling before and after surgical PVR. Cardiovascular magnetic resonance was performed in patients ( n = 12) with rToF and PR > 35% before and after PVR and in healthy controls ( n = 15). Atrioventricular plane displacement (AVPD), global longitudinal peak systolic strain (GLS), atrial and ventricular volumes, and caval blood flows were analyzed. Right ventricular (RV) AVPD and RV free wall GLS were lower in patients before PVR compared with controls ( P < 0.0001; P < 0.01) and decreased after PVR ( P < 0.0001 for both). Left ventricular AVPD was lower in patients before PVR compared with controls ( P < 0.05) and decreased after PVR ( P < 0.01). Left ventricular GLS did not differ between patients and controls ( P > 0.05). Right atrial reservoir volume and RV stroke volume generated by AVPD correlated in controls ( r = 0.93; P < 0.0001) and patients before PVR ( r = 0.88; P < 0.001) but not after PVR. In conclusion, there is a clear atrioventricular coupling in patients before PVR that is lost after PVR, possibly because of loss of pericardial integrity. Impaired atrioventricular coupling complicates assessment of ventricular function after surgery using measurements of longitudinal function. Changes in atrioventricular coupling seen in patients with rToF may be energetically unfavorable, and long-term effects of surgery on atrioventricular coupling is therefore of interest. Also, AVPD and GLS cannot be used interchangeably to assess longitudinal function in rToF. NEW & NOTEWORTHY There is a clear atrioventricular coupling in patients with Tetralogy of Fallot (ToF) and pulmonary regurgitation before surgical pulmonary valve replacement (PVR) that is lost after operation, possibly because of loss of pericardial integrity. The impaired atrioventricular coupling complicates assessment of ventricular function after surgery when using measurements of longitudinal function. Left ventricular atrioventricular plane displacement (AVPD) found differences between patients and controls and changes after PVR that longitudinal strain could not detect. This indicates that AVPD and strain cannot be used interchangeably to assess longitudinal function in repaired ToF.

Acute myocardial infarction (AMI) can progress to heart failure, which has a poor prognosis. Normally, 60% of stroke volume (SV) is attributed to the longitudinal ventricular shortening and lengthening evident in the atrioventricular plane displacement (AVPD) during the cardiac cycle, but there is no information on how the relationship changes between SV and AVPD before and after AMI. Therefore, the aim of this study was to determine how SV depends on AVPD before and after AMI in two swine models. Serial cardiac magnetic resonance imaging was carried out before and 1–2 h after AMI in a microembolization model ( n = 12) and an ischemia-reperfusion model ( n = 14). A subset of pigs ( n = 7) were additionally imaged at 24 h and at 7 days. Cine and late gadolinium enhancement images were analyzed for cardiac function, AVPD measurements and infarct size estimation, respectively. AVPD decreased ( P < 0.05) in all myocardial regions after AMI, with a concomitant SV decrease ( P < 0.001). The ischemia-reperfusion model affected SV to a higher degree and had a larger AVPD decrease than the microembolization model (−29 ± 14% vs. −15 ± 18%; P < 0.05). Wall thickening decreased in infarcted areas ( P < 0.001), and A-wave AVPD remained unchanged ( P = 0.93) whereas E-wave AVPD decreased ( P < 0.001) after AMI. We conclude that AVPD is coupled to SV independent of infarct type but likely to a greater degree in ischemia-reperfusion infarcts compared with microembolization infarcts. AMI reduces diastolic early filling AVPD but not AVPD from atrial contraction. These findings shed light on the physiological significance of atrioventricular plane motion when assessing acute and subacute myocardial infarction. NEW & NOTEWORTHY The link between cardiac longitudinal motion, measured as atrioventricular plane displacement (AVPD), and stroke volume (SV) is investigated in swine after acute myocardial infarction (AMI). This cardiac magnetic resonance study demonstrates a close coupling between AVPD and SV before and after AMI in an experimental setting and demonstrates that this connection is present in ischemia-reperfusion and microembolization infarcts, acutely and during the first week. Furthermore, AVPD is equally and persistently depressed in infarcted and remote myocardium after AMI.

Introduction We investigated if uptake pattern on myocardial perfusion SPECT (MPS) in patients with left bundle branch block (LBBB) is related to myocardial fibrosis, myocardial wall motion, and electrocardiography (ECG) characteristics. Methods Twenty-three patients (9 women) with LBBB, examined with MPS and cardiac magnetic resonance (CMR), were included. Tracer uptake on MPS was classified by visual interpretation as typical LBBB pattern (Defect+, n = 13) or not (Defect−, n = 10) and quantitatively. CMR images were evaluated for wall thickness and for myocardial wall motion both by visual assessment and by regional myocardial radial strain from feature tracking, and for presence and location of myocardial fibrosis. ECGs were analyzed regarding QRS duration and the presence of strict criteria for LBBB. Results Wall thickness was slightly lower in the septum compared to the lateral wall in Defect+ patients (5.6 ± 1.1 vs 6.0 ± 1.3 mm, P = 0.03) but not in Defect− patients (5.6 ± 1.0 vs 5.6 ± 0.9 mm, P = 0.84). Defect+ patients showed a larger proportion of dyskinetic segments in the septum and hyperkinetic segments in the lateral wall compared to Defect− patients (P = 0.006 and P = 0.004, respectively). Decreased myocardial radial strain was associated with decreased tracer uptake by MPS (R = 0.37, P Conclusion The heterogeneous regional tracer uptake in some patients with LBBB is related to underlying regional myocardial dyskinesia, wall thickening, and wall thickness rather than stress-induced ischemia, myocardial fibrosis, or specific ECG characteristics.

Background Patients with pulmonary arterial hypertension (PAH) exhibit high mortality, partially related to right heart failure. Right ventricular (RV) volumes and ejection fraction (EF) can be measured accurately with cardiac magnetic resonance (CMR), but EF is a crude measure of cardiac function. Additional methods for risk assessment and prognosis are of value. Stroke volume (SV) is generated by longitudinal, lateral and septal myocardial contraction. Longitudinal contribution to SV (SVlong%) generated from the atrioventricular displacement (AVPD) is the major contributor to SV in both the left ventricle (LV) and RV. AVPD in both sides and LVSVlong% are lower in patients with PAH compared to controls. However, it is unknown if altered AVPD or regional contributions to SV are prognostic in patients with PAH. The aim of this study was therefore to evaluate if AVPD, longitudinal, lateral or septal contribution to LVSV and RVSV are associated with death or lung transplantation in patients with PAH. Purpose To evaluate if biventricular AVPD, and regional contributions to SV are associated with outcome in patients with PAH. Methods Seventy-one patients with PAH and 20 sex and age-matched healthy controls underwent CMR. Endocardial and epicardial borders and RV insertion points were defined in end diastole and end systole in cine short-axis stacks to compute biventricular volumes, SVlat% and SVsept%. Eight atrioventricular points were defined in end diastole and end systole in 2-, 3- and 4-chamber cine long-axis views, for computation of AVPD and SVlong%. Cut-off values for survival analysis were defined as above or below mean ± 2 standard deviations from the healthy controls. Outcome was defined as death or lung-transplantation. Results Median follow-up time was 3.6 [IQR 3.7] years. AVPD, SVlong%, SVlat% in both ventricles and SVsept% were altered in PAH compared to controls. Transplantation-free survival was lower with values below cut-off for LV-AVPD (hazard ratio (HR)=2.1, 95% CI: 1.2–3.9, p=0.02) and RV-AVPD (HR=9.8, 95% CI: 4.6–21.1, p=0.005) (fig 1). In cox regression analysis, decreased LV-AVPD and RV-AVPD inferred lower transplantation-free survival (LV: HR=1.16 per mm decrease, p=0.007; RV: HR=1.11 per mm decrease, p=0.01) (table 1). LVEF, RVEF, LV-SVlong%, RV-SVlong%, LV-SVlat%, RV-SVlat% or SVsept% did not affect outcome (table 1). Conclusions Decreased left and right AVDP were associated with decreased transplantation-free survival in patients with PAH. There were no associations between ejection fraction, longitudinal, lateral or septal contribution to stroke volume. Funding Acknowledgement Type of funding sources: Public hospital(s). Main funding source(s): Skåne University Hospital, Region of Skåne Southern Healthcare Region of Sweden

COOL AMI EU pilot was a multi-center, randomized controlled trial to assess feasibility and safety of rapid intravascular therapeutic hypothermia (TH) in conscious patients with anterior ST-elevation myocardial infarction (STEMI) undergoing primary PCI (PPCI). We report the effect of hypothermia upon microvascular obstruction (MVO).Conscious patients with anterior STEMI and symptom duration6 h were recruited and randomized to PPCI + TH or PPCI alone. TH was induced using the ZOLL® Proteus™ intravascular temperature management system and rapid infusion of 1 L of cold normal saline, with a target temperature of 32 °C. MVO was measured by cardiac magnetic resonance (CMR) at 4 to 6 days post-MI. MVO larger than 3.9% of LV was considered as extensive MVO.50 patients were randomized; mean age was 58 years, and 86% were men. At reperfusion, mean intravascular temperature for the TH group was 33.6 ± 1 °C. The presence of MVO was high and not different in both groups (74% vs. 77%, p = 0.79). The proportion of patients with extensive MVO was 11% in the TH group and 23% in the control group (OR 0.4 95%CI 0.07-2.35, p = 0.30). Patients with extensive MVO showed reduced EF at 4-6 days (34% versus 43%, p = 0.01). The percentage of patients with EF35% at 30 days was 6% in the TH group versus 24% in the control group (p = 0.19).In the COOL-AMI Pilot Trial, the presence of MVO in both test groups was high and extensive MVO was related with reduced LVEF. The efficacy of therapeutic hypothermia (TH) in MVO reduction should be tested in a pivotal trial.

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

Investigate ventricular and atrial remodeling following atrial septal defect (ASD) closure and examine if pulmonary-to-systemic flow ratio (QP/QS) and right ventricular (RV) volume predict improvement, determined as percentage of predicted oxygen uptake (VO2%). Long-term cardiovascular magnetic resonance (CMR) data on atrial and ventricular remodeling after ASD-closure is limited and treatment effect on exercise capacity is debated. Sixteen patients undergoing transcatheter ASD closure and 16 age and sexmatched controls were studied. CMR was performed before treatment, the day after and 3 and 12 months later. Exercise test with gas analysis was performed before and 12 months after treatment. QP/QS decreased from 2.1 ± 0.5 to 1.4 ± 0.3 at day 1 and 1.1 ± 0.1 at 3 and 12 months. Left ventricular (LV) volumes increased and normalized on day 1 whereas left atrial volumes were unchanged. RV and right atrial volumes decreased the first 3 months. LV and RV volumes had not equalized at 12 months (RV/LV ratio 1.2 ± 0.1, P

Summary Purpose Patients with pulmonary arterial hypertension (PAH) due to systemic sclerosis (SSc) have high mortality. Left ventricular (LV) peak global longitudinal strain (GLS) is decreased in SSc. It is unknown whether low GLS is due to SSc or PAH. Therefore, our primary aim was to evaluate both LV and right ventricular free wall GLS (RVFW GLS) in SSc, with and without PAH, using cardiac magnetic resonance with feature tracking. Secondary aim was to relate GLS to invasive mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR). Methods Thirty‐eight patients with SSc, 19 patients with SSc‐PAH and 19 healthy controls for comparison, were included. Endocardial and epicardial borders were delineated in cine images (short‐axis stack and three long‐axis views) for volumetric and strain calculations. Results Systemic sclerosis‐PAH had lower LV and RVFW GLS than SSc (LV: P = 0·01, RV: P

Background Evaluation of cardiac resynchronization therapy (CRT) often includes New York Heart Association (NYHA) classification, and echocardiography. However, these measures have limitations. Perfusion gradients from ventilation/perfusion single-photon emission computed tomography (V/P SPECT) are related to left-heart filling pressures and have been validated against invasive right-heart catheterization. The aim was to assess if changes in perfusion gradients are associated with improvements in heart failure (HF) symptoms after CRT, and if they correlate with currently used diagnostic methods in the follow-up of patients with HF after receiving CRT. Methods and results Nineteen patients underwent V/P SPECT, echocardiography, NYHA classification, and the quality-of-life scoring system “Minnesota living with HF” (MLWHF), before and after CRT. CRT caused improvement in perfusion gradients from V/P SPECT which were associated with improvements in NYHA classification (P = .0456), whereas improvements in end-systolic volume (LVESV) from echocardiography were not. After receiving CRT, the proportion of patients who improved was lower using LVESV (n = 7/19, 37%) than perfusion gradients (n = 13/19, 68%). Neither change in perfusion gradients nor LVESV was associated with changes in MLWHF (P = 1.0, respectively). Conclusions Measurement of perfusion gradients from V/P SPECT is a promising quantitative user-independent surrogate measure of left-sided filling pressure in the assessment of CRT response in patients with HF.

Reduced ventricular longitudinal shortening measured by atrioventricular plane displacement (AVPD) and global longitudinal strain (GLS) are prognostic markers in heart disease. This study aims to determine if AVPD and GLS with cardiovascular magnetic resonance (CMR) are independent predictors of cardiovascular (CV) and all-cause death also in heart failure with reduced ejection fraction (HFrEF). Patients (n = 287) were examined with CMR and AVPD, GLS, ventricular volumes, myocardial fibrosis/scar were measured. Follow-up was 5 years with cause of death retrieved from a national registry. Forty CV and 60 all-cause deaths occurred and CV non-survivors had a lower AVPD (6.4 ± 2.0 vs 8.0 ± 2.4 mm, p

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

Key Points Question Does fetal cardiovascular magnetic resonance improve prenatal diagnosis of complex congenital heart defects when fetal echocardiography is insufficient? Findings In this cohort study of 31 fetuses referred for fetal cardiovascular magnetic resonance imaging, additional clinically useful information regarding cardiovascular anatomy and function was obtained in 84% of referred cases, covering a wide spectrum of congenital heart defects. This information affected choice of mode of delivery, planning of early postnatal care, and parental counseling. Meaning These findings suggest that fetal cardiovascular magnetic resonance imaging can add important diagnostic information and affect clinical decision-making and parental counseling., This cohort study assesses the clinical utility of fetal cardiovascular magnetic resonance imaging when fetal echocardiography could not visualize all relevant anatomy., Importance Prenatal diagnosis of complex congenital heart defects reduces mortality and morbidity in affected infants. However, fetal echocardiography can be limited by poor acoustic windows, and there is a need for improved diagnostic methods. Objective To assess the clinical utility of fetal cardiovascular magnetic resonance imaging in cases in which fetal echocardiography could not visualize all relevant anatomy. Design, Setting, and Participants This cohort study was conducted between January 20, 2017, and June 29, 2020, at Skåne University Hospital (Lund, Sweden), a tertiary center for pediatric cardiology and thoracic surgery. Participants were fetuses referred for fetal cardiovascular magnetic resonance examination by a pediatric cardiologist after an inconclusive echocardiograph. Exposures Fetal cardiovascular magnetic resonance examination requested by the patient’s pediatric cardiologist. Main Outcomes and Measures Any change in patient management because of diagnostic information gained from fetal cardiovascular magnetic resonance imaging. Results A total of 31 fetuses underwent cardiovascular magnetic resonance examination at a median gestational age of 36 weeks (range, 31-39 weeks). Overall, fetal cardiovascular magnetic resonance imaging had clinical utility, affecting patient management and/or parental counseling in 26 cases (84%). For aortic arch anatomy including signs of coarctation (20 fetuses), fetal cardiovascular magnetic resonance imaging added diagnostic information in 16 cases (80%). For assessment of univentricular vs biventricular outcome in borderline left ventricle, unbalanced atrioventricular septal defect, and pulmonary atresia with intact ventricular septum (15 fetuses), fetal cardiovascular magnetic resonance imaging visualized intracardiac anatomy and ventricular function, allowing assessment of outcome in 13 cases (87%). In 4 fetuses with hypoplastic left heart syndrome, fetal cardiovascular magnetic resonance imaging helped delivery planning in 3 cases (75%). Finally, fetal cardiovascular magnetic resonance imaging provided valuable information for parental counseling in 21 cases (68%). Conclusions and Relevance In this cohort study, fetal cardiovascular magnetic resonance imaging added clinically useful information to what was available from echocardiography. These findings suggest that fetal CMR has the potential to affect clinical decision-making in challenging cases of congenital heart defects with inconclusive data from echocardiography. Fetal cardiovascular magnetic resonance imaging showed an association with clinical decision-making, including mode of delivery and early postnatal care, as well as with parental counseling.

Background Hemodynamic force analysis has been proposed as a noninvasive marker of cardiac function. In a recent study, longitudinal (apical-to-basal) hemodynamic forces were derived from anatomical MRI images and found decreased in heart failure with preserved ejection fraction (HFpEF) patients compared to controls, indicating a potential use for prognostication and testing of therapeutic response. This issue has not been investigated using the reference method of measurement. Purpose To investigate whether intraventricular hemodynamic forces computed using gold-standard cardiac magnetic resonance flow maps can reproducibly differentiate between healthy controls and HFpEF patients. Methods 4D flow data were acquired in 59 subjects through cardiac magnetic resonance imaging using a 1.5T scanner (Siemens Healthcare, Erlangen, Germany). Hemodynamic forces within the LV were computed across the cardiac cycle using the Navier-Stokes equation to find the global pressure gradient, which was then integrated over the LV volume to produce the instantaneous hemodynamic force (unit: Newton) and subsequently normalized to ventricular volume, resulting in a force-volume index (N/l). Average longitudinal forces (root mean square, FRMS) were quantified over the entire cardiac cycle, with and without volume normalization. Results We studied 33 healthy subjects, 14 patients with HFpEF, 6 patients with HFmEF and 6 patients with HFrEF. Groups were similar with regards to sex, cardiac output, heart rate, systolic and diastolic blood pressure, and body surface area. Volume-normalized FRMS did not differ between controls and HFpEF (0.86±0.19 vs. 0.75±0.19 N/l, p=0.08) while lower values were found in HFmEF (0.60±0.19 N/l, p=0.004) and HFrEF (0.38±0.15 N/l, p Conclusions Hemodynamic forces computed from reference standard 4D flow CMR data do not differentiate between healthy controls and HFpEF patients regardless of whether volume normalization is used or not. Our findings do not support a role for hemodynamic forces in HFpEF assessment. Figure 1. (A) Volume-normalized hemodynamic forces over the entire cardiac cycle (lines: average values, shaded area: ±1SD for HFpEF), and (B) variation of volume-normalized average force, FRMS, with left ventricular ejection fraction (LVEF). (C), (D): When indexing to LV volume was not performed, the differences between groups was attenuated, and no correlation was seen between EF and FRMS. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Swedish Heart and Lung Foundation, Region of Scania

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 Oxygen (O2) treatment has been a cornerstone in the treatment of patients with myocardial infarction. Recent studies, however, state that supplemental O2 therapy may have no effect or harmful effects in these patients. The aim of this study was thus to evaluate the effect of O2 therapy in patients with ST Elevation Myocardial Infarction (STEMI) based on the culprit vessel; Left Anterior Descending Artery (LAD) or Non-LAD. Methods This was a two-center, investigator-initiated, single-blind, parallel-group, randomized controlled trial at the Skåne university hospital, Sweden. A simple computer-generated randomization was used. Patients were either randomized to standard care with O2 therapy (10 l/min) or air until the end of the primary percutaneous coronary intervention. The patients underwent a Cardiac Magnetic Resonance Imaging (CMRI) days 2–6. The main outcome measures were Myocardium at Risk (MaR), Infarct Size (IS) and Myocardial Salvage Index (MSI) as measured by CMRI, and median high-sensitive troponin T (hs-cTnT). Results A total of 229 patients were assessed for eligibility, and 160 of them were randomized to the oxygen or air arm. Because of primarily technical problems with the CMRI, 95 patients were included in the final analyses; 46 in the oxygen arm and 49 in the air arm. There were no significant differences between patients with LAD and Non-LAD as culprit vessel with regard to their allocation (oxygen or air) with regards to MSI, MaR, IS and hs-cTnT. Conclusion The results indicate that the location of the culprit vessel has probably no effect on the role of supplemental oxygen therapy in STEMI patients. Trial registration Swedish Medical Products Agency (EudraCT No. 2011–001452-11) and ClinicalTrials.gov Identifier (NCT01423929).

Background ECG changes after revascularization predicts improved outcome for patients with ST‐elevation myocardial infarction (STEMI). Worst lead residual (WLR) ST deviation and resolution of worst lead ST elevation (rST elevation) are simple measures that can be obtained early after PCI. The objective of the current study was to investigate whether simple ECG measures, obtained one hour following PCI, could predict cardiac magnetic resonance (CMR)‐derived myocardial salvage index (MSI), infarct size (IS), and microvascular obstruction (MVO) in patients with STEMI included in the MITOCARE trial. Methods The MITOCARE trial included 165 patients with a first‐time STEMI presenting within six hours of symptom onset. The current analysis included patients that had an ECG recorded at baseline and one hour after PCI and underwent CMR imaging after 3–5 days. Independent core laboratories determined WLR ST deviation, rST elevation, and the CMR variables (MSI, IS, and MVO). Results 83 patients with a mean age of 61 years were included. 83.1% were males and 41% had anterior infarctions. In logistic regression models, WLR ST deviation was a statistically significant predictor of IS (OR 2.2, 95% CI 1.3–3.8) and MVO (OR 2.8, 95% CI 1.5–5.2), but not of MSI (OR 0.8, 95% CI 0.5–1.2). rST elevation showed a trend toward a significant association with IS (OR 0.3, 95% CI 0.1–1.0), but not with the other CMR variables. Conclusion WLR ST deviation one hour after PCI was a predictor of IS and MVO. WLR ST deviation, a measure easily obtained from ECGs following PCI, may provide important prognostic information in patients with STEMI. publishedVersion

Background To relate findings of qualitative evaluation of first-pass perfusion-CMR and anatomical evaluation on coronary angiography (CA) to the reference standard of quantitative perfusion, cardiac PET, in patients with suspected or known stable coronary artery disease (CAD). Methods and Results Forty-one patients referred for CA due to suspected stable CAD, prospectively performed adenosine stress/rest first-pass perfusion-CMR as well as 13N-NH3 PET on the same day, 4 ± 3 weeks before CA. Angiographers were blinded to PET and CMR results. Regional myocardial flow reserve (MFR) < 2.0 on PET was considered pathological. Vessel territories with stress-induced ischemia by CMR or vessels with stenosis needing revascularization had a significantly lower MFR compared to those with no regional stress-induced ischemia or vessels not needing revascularization (P < 0.001). In 4 of 123 vessel territories with stress-induced ischemia by CMR, PET showed a normal MFR. In addition, 12 of 123 vessels that underwent intervention showed normal MFR assessed by PET. Conclusion The limited performance of qualitative assessment of presence of stable CAD with CMR and CA, when related to quantitative 13N-NH3 cardiac PET, shows the need for fully quantitative assessment of myocardial perfusion and the use of invasive flow reserve measurements for CA, to confirm the need of elective revascularization.

Background: Total heart volume (THV) within the pericardium is not constant throughout the cardiac cycle and THV would intuitively be lowest at end systole. We have, however, observed a phase shift between ventricular outflow and atrial inflow which causes the minimum THV to occur before end systole. The aims were to explain the mechanism of the late-systolic net inflow to the heart and determine whether this net inflow is affected by increased cardiac output or systolic heart failure. Methods and Results: Healthy controls (n = 21) and patients with EF

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.

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.

Aims: Pre-capillary pulmonary hypertension (PHpre-cap) has a poor prognosis, especially when caused by pulmonary arterial hypertension (PAH) associated with systemic sclerosis (SSc-PAH). Whether cardiac magnetic resonance (CMR)-based quantification of atrial volumes in PHpre-cap is beneficial in risk assessment is unknown. The aims were to investigate if (i) atrial volumes using CMR are associated with death or lung transplantation in PHpre-cap, (ii) atrial volumes differ among four unmatched major PHpre-cap subgroups, and (iii) atrial volumes differ between SSc-PAH and idiopathic/familial PAH (IPAH/FPAH) when matched for pulmonary vascular resistance (PVR). Methods and results: Seventy-five PHpre-cap patients (57 ± 19 years, 53 female, 43 de novo) with CMR and right heart catheterization were retrospectively included. Short-axis stacks of cine images were analysed, and right and left atrial maximum (RAVmax and LAVmax) and minimum volume (RAVmin and LAVmin) were indexed for body surface area. Increased (mean + 2 SD) and reduced (mean – 2 SD) volumes were predefined from CMR normal values. Transplantation-free survival was lower in patients with increased RAVmax than in those with normal [hazard ratio (HR) = 2.1, 95% confidence interval (CI) 1.1–4.0] but did not differ between those with reduced LAVmax and normal (HR 2.0, 95% CI 0.8–5.1). RAVmax and RAVmin showed no differences among unmatched or matched groups (P = ns). When matched for PVR, LAVmax, LAVmin, and pulmonary artery wedge pressure were reduced in SSc-PAH compared with IPAH/FPAH (95% CI 0.3–21.4, 95% CI 0.8–19.6, and 95% CI 2–7, respectively). Conclusions: Patients with PHpre-cap and increased right atrial volume measured with CMR had worse clinical outcome. When matched for PVR, left atrial volume was lower in SSc-PAH than in IPAH/FPAH, consistent with left-sided underfilling, indicating a potential differentiator between the groups. (Less)

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

Variation of the blood content of the pulmonary vascular bed during a heartbeat can be quantified by pulmonary blood volume variation (PBVV) using magnetic resonance imaging (MRI). The aim was to evaluate whether PBVV differs in patients with heart failure compared with healthy controls and investigate the mechanisms behind the PBVV. Forty-six patients and 10 controls underwent MRI. PBVV was calculated from blood flow measurements in the main pulmonary artery and a pulmonary vein, defined as the maximum difference in cumulative PBV over one heartbeat. PBVV was indexed to stroke volume (SV) in the main pulmonary artery (PBVVSV). Patients displayed higher PBVVSV than controls (58 ± 14 vs. 43 ± 7%, P < 0.001). The change in PBVVSV could be explained by left ventricular (LV) longitudinal contribution to SV ( R2 = 0.15, P = 0.02) and the phase shift between in- and outflow ( R2 = 0.31, P < 0.001) in patients. Both variables contributed to the multiple regression analysis model and predicted PBVVSV ( R2 = 0.38); however, the phase shift alone explained ~30% of the variation in PBVVSV. No correlation was found between PBVVSV and large vessel area. In conclusion, PBVVSV was higher in patients compared with controls. Approximately 40% of the variation of PBVVSV in patients can be explained by the LV longitudinal contribution to SV and the phase shift between pulmonary in- and outflow, where the phase shift alone accounts for ~30%. The remaining variation (60–70%) most likely occurs on a small vessel level. Future studies are needed to show the clinical added value of PBVVSV compared with right-heart catheterization. NEW & NOTEWORTHY This study shows that the pulmonary blood volume variation indexed to the stroke volume is higher in patients with heart failure compared with controls. The mechanisms behind this are lack of systolic suction from the left ventricular atrioventricular plane descent and increased phase shift between the in- and outflow to the pulmonary circulation (~40%), where the phase shift alone accounts for ~30%. The remaining variation (60–70%) is suggested to occur on a small vessel level.

Aims Improved risk stratification is of value for decision making in pulmonary arterial hypertension (PAH). Right heart catheterization combined with quantitative tricuspid regurgitation (TR) by cardiovascular magnetic resonance (CMR) may provide this. The aims were to study: (i) to what extent quantitative TR is associated with event‐free survival; (ii) how quantitative TR is related to known prognostic markers in PAH; and (iii) to what extent quantitative TR and right atrial pressure determine right atrial dilation. Methods and results Fifty patients (63 ± 17 years) with PAH referred for CMR were included. Volumes and pulmonary artery flow by CMR and pressure and vascular resistance by right heart catheterization were obtained. Composite outcome was lung transplantation or death. Four transplantations and 27 deaths occurred over a median of 2.7 years. A trend towards higher hazard ratio was shown for TR volume (TRV; 2.1, 95% CI 1.0–4.4) and TR fraction (TR%; 1.6, 95% CI 0.8–3.3) above median. TRV and TR% correlated with right ventricular (RV) end‐diastolic (TRV r = 0.50; TR% r = 0.39) and end‐systolic (TRV r = 0.35; TR% r = 0.30) volumes, pulmonary vascular resistance (TRV r = 0.28; TR% r = 0.43), N terminal pro brain natriuretic peptide (TRV r = 0.65; TR% r = 0.68), cardiac index (TRV r = −0.32; TR% r = −0.54), pulmonary artery stroke volume (TRV r = −0.32; TR% r = −0.58) and effective RV ejection fraction by pulmonary artery quantitative flow (TRV r = −0.56; TR% r = −0.69), but not RVEF. Both TR% and right atrial pressure determined right atrial volumes (r 2 = 0.38; r 2 = 0.48). Conclusions A clear trend towards worse outcome with larger TRV or TR% was shown; however, the number of events was insufficient for significant outcome differences. Prognostic value of quantitative TR should be investigated in a larger multicentre cohort. Effective RV ejection fraction may be considered an improved measure of RV function in PAH.

Background Many patients undergo percutaneous coronary intervention (PCI) without the use of non-invasive stress testing prior to treatment. The aim of this study was to determine the potential added value of guiding revascularization by quantitative assessment of myocardial perfusion prior to intervention. Methods and Results Thirty-three patients (10 females) with suspected or established CAD who had been referred for a clinical coronary angiography (CA) with possibility for PCI were included. Adenosine stress and rest 13N-NH3 PET, cardiac magnetic resonance (CMR), and cardiopulmonary exercise test were performed 4 ± 3 weeks before and 5 ± 1 months after CA. The angiographer was blinded to the PET and CMR results. Myocardial flow reserve (MFR) P = 0.9). However, vessel territories with regional MFR P = 0.003). Of the 14 patients not undergoing PCI, four had MFR Conclusion Assessment of quantitative myocardial perfusion prior to revascularization could lead to more appropriate use of CA when managing patients with stable CAD.

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.

Background: The purpose of this study was to determine the effect of stress on left-to-right shunting in patients with atrial septal defect (ASD) and to investigate if the degree of shunting, cardiac output (CO), and right ventricular (RV) volumes are related to exercise capacity. Methods: Twenty-six patients with a secundum ASD and 16 healthy volunteers were studied with rest/stress cardiac magnetic resonance using 20 μg/kg/min dobutamine and 0.25-0.75 mg atropine to quantify CO, pulmonary to systemic flow ratio (QP/QS), and left ventricular (LV) and RV volumes. Peak oxygen uptake (VO2 peak) was determined on ergospirometry. Results: In patients with ASD the QP/QS decreased from 2.0 ± 0.2 at rest to 1.5 ± 0.1 (P < 0.001) during dobutamine stress (n = 20) and shunt volume per heartbeat decreased from 70 ± 9 to 38 ± 9 mL (P < 0.001). However, absolute shunt volume per minute was unchanged (5.1 ± 0.8 vs. 4.5 ± 1.0 L/min, P = 0.32) explained by a higher increase in systemic CO during stress (90 ± 11%) compared with pulmonary CO (43 ± 7%, P < 0.001). In ASD patients, VO2 peak correlated with aortic CO during stress (r = 0.77) and QP/QS at rest (r = -0.48) but not during stress (P = 0.09). VO2 peak did not correlate with RV volumes in patients. Conclusion: Pulmonary to systemic flow ratio and shunt volume per heartbeat decrease during stress in ASD patients. This may be explained by an enhanced LV diastolic function during stress and may have implications to detect disturbances in LV compliance in ASD patients. A high systemic CO during stress is a strong predictor of exercise capacity. (Less)

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."

The association of markers of myocardial injury and dysfunction with infarct size (IS) and ejection fraction (EF) are well documented. However, limited data are available on the newer high-sensitivity troponin assays and comparison with morphologic and functional assessment with cardiac magnetic resonance imaging. We aimed to examine the associations of high-sensitivity cardiac Troponin-T (hs-cTnT), creatine kinase MB iso-enzyme (CKMB), and N-terminal pro B-type Natriuretic Peptide (NT-proBNP) to IS and EF at 6 months. Blood samples from 119 ST-segment elevation myocardial infarction patients from the Rapid Endovascular Catheter Core Cooling Combined With Cold Saline solution as an Adjunct to Percutaneous Coronary Intervention for the Treatment of Acute Myocardial Infarction trial were collected at baseline, 6, 24, and 48 hours after admission. Cardiac magnetic resonance was performed at 4 ± 2 days and 6 months. The association of biomarker levels to IS and EF was tested with Pearson's correlation coefficients and linear regression models with bootstrap resampling. The correlation coefficient of biomarker to IS was (CKMB: r = 0.71); (NT-proBNP: r = 0.55); (hs-cTnT: r = 0.80); and for EF (CKMB: r = 0.57); (NT-proBNP: r = 0.48); and (peak hs-cTnT: r = 0.68). IS and EF at 4 ± 2 days had the strongest correlations with IS and EF at 6 months respectively (IS: r = 0.84) and (EF: r = 0.74). Receiver operating characteristic of peak hs-cTnT for predicting EF ≤40% at 6 months was 0.87 compared with 0.75 for early IS. Early EF was a negative predictor of late EF

Item does not contain fulltext INTRODUCTION: The relationship between left ventricular (LV) ejection fraction (EF) and LV myocardial scar can identify potentially reversible causes of LV dysfunction. Left bundle branch block (LBBB) alters the electrical and mechanical activation of the LV. We hypothesized that the relationship between LVEF and scar extent is different in LBBB compared to controls. METHODS: We compared the relationship between LVEF and scar burden between patients with LBBB and scar (n=83), and patients with chronic ischemic heart disease and scar but no electrocardiographic conduction abnormality (controls, n=90), who had undergone cardiovascular magnetic resonance (CMR) imaging at one of three centers. LVEF (%) was measured in CMR cine images. Scar burden was quantified by CMR late gadolinium enhancement (LGE) and expressed as % of LV mass (%LVM). Maximum possible LVEF (LVEFmax) was defined as the function describing the hypotenuse in the LVEF versus myocardial scar extent scatter plot. Dysfunction index was defined as LVEFmax derived from the control cohort minus the measured LVEF. RESULTS: Compared to controls with scar, LBBB with scar had a lower LVEF (median [interquartile range] 27 [19-38] vs 36 [25-50] %, p

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 …

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.

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.