Heart failure represents a primary cause of morbidity and mortality in older people and despite significant therapeutic advances, it is still characterized by important unmet needs, thus remaining a challenging field of clinical research. The recent PARADIGM-HF trial compared the novel compound LCZ696, a combination of the angiotensin receptor blocker valsartan and the neprilysin inhibitor sacubitril, versus the angiotensin-converting enzyme inhibitor enalapril in 8,442 patients with symptomatic chronic systolic heart failure. LCZ696 led to a 20% reduction in the rate of death or hospitalization for heart failure and a 16% reduction in the rate of all-cause death compared to enalapril at 3.5 years of follow-up. Despite those impressive results, the clinical application of this novel agent that requires the substitution of a cornerstone of current heart failure therapy, the angiotensin-converting enzyme inhibitors, should follow careful steps as imposed by the study design, the recruited population and the outcome in specific patient subgroups. Further insights into the effects of LCZ696 will be provided by the ongoing PARAGON-HF trial in patients with diastolic heart failure. Heart failure (HF) represents a main cause of morbidity and mortality and the first reason for hospital admission in older people . The impThe incidence of HF keeps rising owing mainly to the aging of the population and the effective management of formerly lethal conditions, such as acute coronary syndromes. This is followed by an increasing trend in HF hospitalizations along with an enormous economic burden that also keeps growing ,4. In adProspective comparison of Angiotensin Receptor neprilysin inhibitors with Angiotensin converting enzyme inhibitors to Determine Impact on Global Mortality and morbidity in Heart Failure’  trial applied an innovative approach to the introduction of new HF therapies. Instead of adding the new agent on top of standard care, an approach followed by the majority of previous HF clinical trials [The recently published ‘l trials . In addiThe new compound with the code name LCZ696 (400 mg daily), a combination of the ARB valsartan and the neprilysin inhibitor sacubitril, was compared with the ACEi enalapril (20 mg daily) in 8,442 patients with symptomatic chronic HFrEF and increased levels of natriuretic peptides . At 3.5 If one takes a better look at the design of the PARADIGM-HF trial, it seems that the clinical application of LCZ696 needs to follow careful steps. First, the study was preceded by a single-blinded run-in phase, during which about 10% of patients dropped out mainly due to adverse events or abnormal laboratory results . AlthougAccording to the trial’s subgroup analyses, LCZ696 was ‘less’ beneficial in ACEi-naïve patients, while LCZ696 led to a higher incidence of symptomatic hypotension compared to enalapril, which, however, did not result in a higher treatment discontinuation ,6,8. ThoThe results reported by the PARADIGM-HF trial investigators are indeed impressive and introduce a paradigm shift in the treatment of chronic HFrEF. However, the clinical application of the novel agent LCZ696 will definitely require a new paradigm for many HF patients. Further to PARADIGM-HF, the ongoing PARAGON-HF trial addresses the effects of LCZ696 on patients with HFpEF, a condition characterized by a total lack of evidence-based therapies, as stressed earlier, thus leading to high expectations for another major paradigm shift in HF.


LV performance is coupled to loading conditions (i.e. preload and afterload) and myocardial contractility . Therefore load-independence is an important means to isolate and study LV contractility in preclinical studies of cardiovascular pharmaceuticals and devices (3). Precise and rapid assessment of LV pressure is achieved with high fidelity catheter-based pressure transducers but measurements of LV volume are more difficult and less reliable. Thus far, MRI has not demonstrated sufficient spatiotemporal resolution to measure beat-to-beat changes of the pressure-volume (PV) loop to measure left ventricular (LV) elasticity or preload-recruitable stroke work (PRSW). Our aim was to develop a real-time (rtMRI) approach to measure PV and Frank-Starling relationships in a preclinical model of heart disease under normal and stressed physiologic conditions.The University of Pennsylvania IACUC approved all experiments. Yorkshire swine (n = 8) were anesthetized and instrumented with expandable vascular occluders placed at the inferior (20 mm) and superior (24 mm) vena cavae and transiently inflated during simultaneous rtMRI and intraventricular pressure measurement. Images were reconstructed with non-Cartesian parallel SENSE and >10 k frames were segmented in < 5 min with semi-automatic active contours.The relationship between Te, Tr and ejection fraction is shown Figure . We founRtMRI can accurately assess LV volumes, elasticity and PRSW at baseline and elevated inotropic state, providing non-invasive into the Frank-Starling relationship of the intact heart.The authors gratefully acknowledge support from the National Institutes of Health through awards K99HL108157 and R01HL63904.


Patients with repaired tetralogy of Fallot (TOF) frequently have right bundle branch block. However, the contribution of cardiac dyssynchrony to dysfunction remains controversial. To better understand this phenomenon and ultimately study therapies, we developed a method to quantify left (LV), right (RV) and inter-ventricular cardiac dyssynchrony using standard cine CMR.30 patients with repaired TOF  and 17 healthy controls  underwent cine CMR. Patients were imaged twice to assess inter-test reproducibility. Circumferential strain vs time curves were generated with a custom feature tracking algorithm for 12 LV and 12 RV segments in 4-7 slices encompassing the ventricles. For each segment, the temporal offset (TO) of the strain curve relative to a global reference curve derived from the controls was calculated and expressed as a percent of the cardiac cycle. The intra-ventricular dyssynchrony index (DI) for each ventricle was computed as the standard deviation (SD) of the TOs (more dyssynchrony increases the SD). The inter-ventricular DI was calculated as the difference in median RV and median LV TOs. Regional dyssynchrony was quantified in 3 LV  and 3 RV  regions using median TOs.Compared to controls, patients with repaired TOF had a greater LV, RV and inter-ventricular DI Figure . The grePatients with repaired TOF suffer from left, right and inter-ventricular cardiac dyssynchrony which can all be quantified from standard cine CMR with good inter-test reproducibility. Future studies need to determine whether these patients may benefit from resynchronization therapy.This work was supported by a National Institutes of Health (NIH) Director's Early Independence Award (1DP5OD012132-01), and NIH grant number KL2 RR033171 from the National Center for Research Resources and the National Center for Advancing Translational Sciences. The content is solely the responsibility of the authors and does not necessarily represent the official views of NIH.


This report describes a patient presenting with a narrow complex tachycardia in the context of prior myocardial infarction and impaired ventricular function. Electrophysiological studies confirmed ventricular tachycardia and activation and entrainment mapping demonstrated a critical isthmus within an area of scar involving the His-Purkinje system accounting for the narrow QRS morphology. This very rare case shares some similarities with upper septal ventricular tachycardia seen in patients with structurally normal hearts, but to our knowledge has not been seen previously in patients with ischemic heart disease. Introduction Monomorphic ventricular tachycardia (VT) is commonly seen in patients with prior myocardial infarction and impaired left ventricular systolic function. In most cases of ischemic VT the QRS morphology during tachycardia is broad, as ventricular activation emerges from a critical isthmus of slow conduction and spreads away from the exit site passively without involvement of the specialized conduction tissue of the His-Purkinje system (HPS) . In a miA 62 year old man, with a history of remote inferior wall myocardial infarction, coronary artery bypass surgery and a dual chamber implantable cardioverter defibrillator (ICD) presented with multiple shocks related to recurrent ventricular tachycardia with a cycle length (CL) of 340 ms despite anti-arrhythmic drug therapy with sotalol. Coronary angiography revealed a chronic total occlusion of the right coronary artery, with moderate atheroma in the left coronary artery. An electrophysiology study was performed using the VelocityTM 3D mapping system , a hexapolar catheter at the bundle of His, a decapolar catheter at the right ventricular apex and a roving irrigated-tip mapping catheter . A 12-lead electrocardiogram (ECG) in sinus rhythm showed Q waves in V1-3, a QRS duration of 102ms and T wave inversion in the inferolateral leads .Baseline sinus intervals revealed an atrio-His (AH) and His-ventricular (HV) intervals of 132 and 45ms respectively . Anterograde testing demonstrated smooth, decremental atrioventricular nodal conduction with no jump in the AH interval. Retrograde testing demonstrated decremental midline VA conduction. A narrow complex tachycardia (CL 340ms) was induced easily (and reproducibly) with programmed stimulation with a single extrastimulus from the right ventricle, with a QRS morphology which was very similar, but not identical, to the QRS morphology during sinus rhythm and a normal axis . During His-synchronous ventricular premature beats did not advance the subsequent His signal, it was not possible to entrain the tachycardia from the atria, and the tachycardia cycle length did not increase with the development of catheter induced right bundle branch block. Activation mapping localized the earliest ventricular signal to the base of the left ventricle approximately 2 cm below the His catheter within the border zone of a large area of scar on the inferior left ventricular wall . A mid-dRadiofrequency energy was delivered at this site with termination of the tachycardia after 16 seconds. No Purkinje potential was recorded at this site either during tachycardia or during sinus rhythm. The tachycardia was non-inducible with programmed stimulation subsequently. The patient made an uneventful recovery and remains well 6 months later with no recurrence of ventricular tachycardia.We have described a patient with ischemic heart disease presenting with VT with a narrow QRS morphology in whom the successful ablation target at the posterior basal septum revealed a low amplitude, mid-diastolic signal and no Purkinje potential. The QRS morphology during tachycardia was almost identical to that seen during sinus rhythm except for a subtle change in the polarity of limb lead I and V4. This suggests that the majority of ventricular activation occurred via the His-Purkinje system with a small degree of fusion accounting for the subtle differences between tachycardia and sinus rhythm. In fact subtle alternans in the cycle length was noted occasionally during tachycardia and was associated with beat to beat variation in the presence of the small S wave in limb lead I .Ventricular tachycardia with a relatively narrow QRS morphology is well recognized in patients with idiopathic fascicular VT of which there are three main types: (1) left posterior fascicular VT with RBBB and superior axis, (2) left anterior fascicular VT with RBBB and inferior axis and 3) the very rare upper septal VT with a normal QRS morphology and normal axis  the very. FirstlyIn patients with structural heart disease involvement of the His-Purkinje system during ventricular tachycardia is uncommon, but well recognized . Lopera Hayashi et al. described 4 patients with prior myocardial infarction in whom VT involving the His-Purkinje system was observed . In all Sakamoto et al. described a patient with previous inferior myocardial infarction in whom a relatively narrow complex tachycardia (QRSd 120ms) was induced which was similar but not identical to the QRS morphology in sinus rhythm . In thisThe clinical significance of this case is that VT with HPS involvement  should occasionally be considered in the differential diagnosis of a narrow complex tachycardia. In our patient VA dissociation was observed facilitating the recognition of VT, although 1:1 VA association would certainly be possible if retrograde VA conduction were sufficiently rapid. The differential diagnosis of a narrow complex tachycardia with VA dissociation includes junctional tachycardia with retrograde block, AV nodal reentry tachycardia (AVNRT) with upper common pathway block, orthodromic AV reentry tachycardia (AVRT) associated with a nodofascicular accessory pathway as the retrograde limb of the circuit and upper septal fascicular VT. Differential pacing during tachycardia and the location of the successful ablation site excluded all of the above possibilities however, leaving VT with HPS involvement as the best explanation for our findings.We cannot be certain of the precise mechanism of this tachycardia, however reentry is likely given that the tachycardia was easily and reproducibly initiated with programmed stimulation from the ventricle, the tachycardia could be reproducibly entrained, and there was a mid-diastolic signal at the successful ablation site suggesting a critical isthmus involving, or close to, the HPS in the region of the posterior basal LV septum. Activation mapping identified a localized focal area of earliest activation suggesting that micro-reentry was the likely mechanism. We assume that the narrow QRS morphology and nearly identical morphology to sinus rhythm is due to the involvement of the proximal HPS with balanced anterograde activation of all the main branches of the HPS. The proposed mechanism of this tachycardia is shown in In summary we have described a patient with scar-related ischemic VT with a narrow QRS morphology with a mechanism different to that normally seen in this context. The presence of a mid-diastolic potential and the absence of a pre-systolic Purkinje potential is unusual and the nearly identical QRS morphology to sinus rhythm is very unusual for VT and might lead to an erroneous diagnosis of supraventricular tachycardia unless alert to the possibility of this rare form of scar-related VT.


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.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.Patients with heart failure (p = 0.048), but lower when indexing to EDV . No difference was seen in diastolic average KE  even when indexing to EDV . In patients, a smaller fraction of diastolic average KE was observed inside the vortex ring compared to controls . Three distinctive KE time curves were seen in patients which were markedly different from findings in controls, and with a moderate agreement between KE time curve patterns and degree of diastolic dysfunction (Cohen’s kappa = 0.49), but unrelated to NYHA classification (p = 0.12), or 6-minute walk test (p = 0.72).The systolic average KE was higher in patients compared to controls (2.2 ± 1.4 mJ vs 1.6 ± 0.6 mJ, Patients with heart failure exhibit higher systolic average KE compared to controls, suggesting altered intracardiac blood flow. The different KE time curves seen in patients may represent a conceptually new approach for heart failure classification. Heart failure (HF) is a common disease  with higBlood flow patterns in the left ventricle (LV) are closely connected to the shape and motion of the myocardium, valves and great vessels, and may therefore be a sensitive marker of cardiac function and dysfunction, including HF . KineticFurthermore, one of the most prominent features of LV blood flow is the formation of a vortex ring downstream from the mitral valve during early rapid filling , 9. ReceTherefore, the aim of this study was to quantify LV KE in patients with moderate and severe heart failure. Furthermore, we aimed to investigate the relationship between KE and diastolic vortex ring formation, as well as cardiac dyssynchrony and current clinical measures of HF.The regional ethics committee in Lund, Sweden, approved the study and all subjects provided written informed consent. We prospectively included 29 patients with NYHA class I-IV heart failure, and 12 healthy controls. Patient inclusion criteria were LV ejection fraction (EF) < 40 % and optimal heart failure medication. Exclusion criteria were severe renal failure (GFR < 30 ml/min), unstable angina pectoris or acute myocardial infarction within 30 days prior to inclusion, chronic atrial fibrillation, significant valvular disease, or pregnancy. Ischemic etiology to heart failure was defined prior to cardiovascular magnetic resonance (CMR), by history of previous angina and detection of cardiac-specific Troponin, and previous percutaneous coronary intervention (PCI) or coronary artery bypass-graft (CABG). No history of previous angina, PCI, or CABG resulted in the diagnosis dilated cardiomyopathy (DCM). Controls were free from medication and had no history of cardiovascular or systemic disease. Population characteristics are shown in Table Eight out of 12 controls (67 %) and 21/29 patients (72 %) underwent CMR at 1.5 T. A 32-channel cardiac coil was used at 1.5 T and a 6-channel cardiac coil was used on 3 T. For all subjects, balanced steady-state free precession (bSSFP) cine images were acquired in standardized short-axis and long-axis views, and three-dimensional, time-resolved phase contrast images (4D flow) were acquired covering the entire heart. Patients underwent a clinical CMR exam for viability assessment and determination of regional and global LV function.4D flow: A segmented gradient echo sequence, 2 views per segment, with retrospective ECG triggering and a SENSE parallel imaging factor of 2 was used as previously described [escribed . 4D flowescribed , 13. Theescribed ; 2) the escribed , 12, 13.LV volumetrics and KE analysis: The LV was defined by manually drawing the contours of the blood volume in short-axis slices over the entire cardiac cycle in cine images acquired with retrospective ECG triggering . Left ventricular mass (LVM), end-diastolic volume (EDV), and end-systolic volume (ESV) were measured by manual delineation of endocardial and epicardial borders of the LV. The papillary muscles were excluded in LVM measurements. Stroke volume (SV) was defined as EDV-ESV. The peak emptying rate  and peak filling rate  were acquired from the time-resolved short-axis delineations of the LV. The delineations were transferred to the 4D data set and KE was calculated as the sum of ½mv2 for each voxel [3 [ch voxel , where mvoxel [3 ) and v iKinetic energy terminology was defined as follows: “KE time curve” = the amount of KE inside the LV for each time step over the entire cardiac cycle; “Systolic average KE” = average of KE for all systolic time steps; “Diastolic average KE” = average of KE for all diastolic time steps.Vortex ring size and vortex KE: In order to delineate the vortex ring formed from blood flowing into the LV during diastole [diastole , 9, Lagrdiastole  and validiastole . ParticlTerminology for vortex KE was defined as follows: “KE inside vortex” = average of KE in all voxels inside the diastolic vortex; “KE outside vortex” = average of KE in all voxels outside the diastolic vortex.Viability analysis: ECG-triggered late gadolinium enhancement (LGE) imaging was performed with a 3D inversion recovery (IR) gradient echo (GRE) sequence in mid-diastole. Images were acquired in short-axis slices covering the entire LV, and in long-axis views. LGE imaging was performed 10–20 min after intravenous administration of 0.2 mmol/kg gadolinium-based CMR contrast agent . Typical scanning parameters were: TE 1.3 ms, effective repetition time every heartbeat, 5 slices per breath-hold, flip angle 15°, slice thickness 8 mm, no slice gap, and in-plane resolution 1.5x1.5 mm. Inversion time was chosen to optimally null the myocardium. LGE was quantified using a semi-automatic weighted algorithm with manual corrections as previously described [escribed .Diastolic function: Diastolic function in patients was assessed using the following measures by CMR: early and atrial mitral inflow ratios (E/A), mitral E-wave deceleration time (MDT), E-wave peak velocity, velocity of the LV myocardium in early diastole (mean E’), E/E’, maximum left atrial volume normalized to BSA, and pulmonary venous flow profile [ profile . E, A, aDyskinesia: Dyskinesia was assessed in patients using CMR. Dyskinesia was visually assessed based on the presence of septal segments with dyskinesia, from 0 segments = no dyskinesia, to 1–4 septal segments = dyskinesia.All image analysis and visualization was performed using Segment 1.9  . ComputaU test, Pearson’s correlation analysis, comparisons between KE time curve pattern groups using Kruskal-Wallis test, and agreement of rating of diastolic dysfunction using Cohen’s kappa. The variability in the KE time curve patterns was assessed using the coefficient of variation [p-value <0.05 were considered statistically significant. For entry into the regression models, p < 0.10 was used, and for removal p > 0.15.Continuous variables are presented as mean ± SD unless otherwise stated. The following statistical analyses were performed using GraphPad Prism 6.04, : Comparisons between patients and controls using Mann–Whitney ariation  calculatCharacteristics and LV volumes for patients and controls are presented in Table p = 0.13). For systolic average KE, a statistically significant difference was seen  . Indexing KE to SV showed that patients had higher values compared to controls both for systolic average KE/SV  and diastolic average KE/SV  . When indexed to EDV, patients showed lower systolic average KE , but no difference in diastolic average KE  .There was no statistically significant difference in diastolic average KE between patients with heart failure and controls  to be determinants of diastolic average KE Table  and tempp = 0.89). Furthermore, Kruskal-Wallis test showed no difference in diastolic average KE between patients with 0, 2, 3, or 4 dyskinetic septal segments (p = 0.76).Seventeen out of 29 patients had at least 2 dyskinetic septal segments . In patients with septal dyskinesia, there was no difference in diastolic average KE compared to patients without dyskinesia . Percentage of scarred LV myocardium (%scar) did not contribute further to the model . The majority of total KE was found within the vortex ring in healthy controls . Analysis of diastasis only (excluding E-wave and A-wave) revealed similar correlations . Since KE = ½mv2, this means that in patients, the change in KE inside the vortex can be explained to a higher degree by the change in velocity squared than by change in volume. However, in controls, the change in KE is about equally explained by change in volume and by change in velocity squared.Controls presented similar appearance of KE time curve patterns as previously described ; a peak 2) and coincide with the early diastolic filling (corresponding to E-wave) and atrial contraction (corresponding to A-wave), three main KE time curves in heart failure patients were discerned: 1) lower KE during early diastolic filling (corresponding to E-wave) compared to atrial contraction (corresponding to A-wave); 2) higher KE during the E-wave compared to during the A-wave; and 3) partial or complete fusion of the KE peaks during early diastolic filling and atrial contraction.Patterns in the appearance of the diastolic part of the KE time curves were identified. Since the early and late diastolic KE peaks depend mainly on velocity (½mvTime curve pattern 1: 10 out of 29 patients (34 %)  Fig. . Within Time curve pattern 2: 4 out of 29 patients (14 %)  . 11 out of 15 patients in pattern 3 were in the same heart rate range as pattern 1. %) Fig. , panel dNone of the patients were classified as having normal KE time curve pattern. There was a moderate correlation between KE time curve pattern and degree of diastolic dysfunction by CMR .p < 0.0001) meaning that the KE time curves in patients were more flat compared to controls, who have distinct peaks in the KE time curves.The coefficient of variability of the KE time curve patterns was lower in patients compared to controls . In time curve pattern 2, only one patient underwent 6-minute walk test (6MWT). Mann–Whitney U test showed no statistically significant difference in 6MWT between patients in time curve pattern 1 and time curve pattern 3 .Median NYHA classification in time curve pattern 1, 2, and 3 were NYHA II, III, and III, respectively. Kruskal-Wallis test showed no statistically significant difference in NYHA classification between the three KE time curve patterns  on ECG and were under consideration for cardiac resynchronization therapy, and the dyssynchrony was expected to affect KE. Interestingly, regional wall motion in terms of presence or absence of septal dyskinesia had no impact on KE in this study.. [Altered energy levels during systole was interpreted as due to abnormal flow conditions, and may contribute to increased remodeling of the heart through convective deceleration and associated pressure increase, thereby contributing to the downward spiral into advanced stages of heart failure. Abnormal flow conditions in heart failure was also discussed by Zajac et al.  who founThe KE time curve patterns in heart failure were unrelated to NYHA classification. These results highlights the issue of heart failure as a clinical diagnosis, since the degree of cardiac function impairment is poorly reflected in terms of subjectively assessed physical performance. This study shows that the mean KE in IHD can be partially explained by heart size expressed as EDV, but not by the amount of scarred LV myocardium. Thus, larger LV volume gives higher KE. This is exemplified in the patient exhibiting the highest mean KE in our study (9.1 mJ); this patient has an extremely large LV EDV of almost 750 ml.There was only a moderate strength of agreement between KE time curve pattern and degree of diastolic dysfunction by CMR (Cohen’s kappa = 0.41) and no clear correlation between KE time curve pattern and NYHA classification or 6MWT. This indicates that KE time curves differ from established measures of cardiac function and as such constitute a conceptually new approach to the assessment of heart failure through the study of intracardiac flow.All patients in this study were included during stable, compensated disease. Thus, it is not known whether the same findings could be seen in acutely decompensated states of heart failure or in isolated diastolic heart failure. Much is yet to be elucidated about the transition from normal myocardial function to heart failure, as well as for the transition from isolated diastolic heart failure to combined diastolic and systolic heart failure.This study lacks invasive pressure measurements and therefore the cardiac load conditions are unknown. Echocardiography scanning ranged between 1 and 184 days before or after CMR (in one patient >6 years after CMR). Therefore comparison between the modalities would be misleading, and was therefore not performed. This study was also not designed to compare the two modalities. The patients included in this study were older than the controls and since metabolism has been shown to decrease with age , this coThis study shows that patients with heart failure can be divided into three kinetic energy (KE) time curve patterns, all qualitatively altered compared to controls. The KE time curves do not correlate with NYHA classification or 6-minute walk test, and may therefore constitute a conceptually new method to quantify heart failure.


Introduced in 1977, transesophageal echocardiography (TEE) offered imaging through a new acoustic window sitting directly behind the heart, allowing improved evaluation of many cardiac conditions. Shortly thereafter, TEE was applied to the intraoperative environment, as investigators quickly recognized that continuous cardiac evaluation and monitoring during surgery, particularly cardiac operations, were now possible. Among the many applications for perioperative TEE, this review will focus on four recent advances: three-dimensional TEE imaging, continuous TEE monitoring in the intensive care unit, strain imaging, and assessment of diastolic ventricular function. Transesophageal echocardiography (TEE) was introduced in 19776 and offered imaging through a new acoustic window sitting directly behind the heart, allowing improved evaluation of many cardiac conditions. It was only a short time until TEE was applied to the intraoperative environment (in 1981)7, as investigators quickly recognized that continuous cardiac evaluation and monitoring during surgery, particularly cardiac operations, were now possible. Perioperative TEE guidelines were first established by the joint efforts of the American Society of Anesthesiologists and the Society of Cardiac Anesthesiologists in 19968. European guidelines for this procedure soon followed, and there have been multiple updates published in recent years as newer TEE technologies have been developed12. The recent technological advances have significantly improved the perioperative care of patients with complex cardiac pathophysiology and will continue to advance both diagnostic and prognostic abilities of physicians via ultrasonography.Clinical cardiac ultrasound, or echocardiography, is a technology that was pioneered in the post-World War II era with evolving naval sonar technology. Initial images consisted of the time-motion approach, displaying images along a single vector over time, or what we term today “M-mode” imaging1 . Over th13. For example, precise placement of percutaneous mitral valve edge-to-edge repair devices using 3D TEE alone has been described14. This live imaging is accomplished without the use of ionizing radiation or contrast dye, both of which are potentially harmful. The temporal resolution of imaging can be improved by decreasing the visual field or sector width or by gated acquisition . Though helpful for improved resolution, gated acquisition is more demanding from a clinical perspective because artifact-free images are impaired by patient movement (including cardiac translation during respiration), cardiac arrhythmias, and surgical electrocautery. As a result, higher-resolution imaging is generally limited to the intraoperative setting, when patients are anesthetized and mechanically ventilated, so that ventilation can be interrupted to provide a cardiac target that is not distorted by respiratory movements. The improved imaging has been particularly helpful in mitral valve repair15  echocardiography are demonstrated, including precise sizing of the aortic annulus for transcatheter aortic valve replacement (TAVR), evaluation of mitral valve repair, confirmation of left ventricular assist device (LVAD) inflow cannula position, and real-time guidance of wire and catheter insertion for percutaneous procedures such as mitral valvuloplasty. bpm, beats per minute; LA, left atrium; LV, left ventricle; LVOT, left ventricular outflow tract; PAT T, patient temperature; RV, right ventricle; TEE T, transesophageal echocardiography temperature.Click here for additional data file.Copyright: © 2016 Maxwell C et al.2016Data associated with the article are available under the terms of the Creative Commons Zero "No rights reserved" data waiver (CC0 1.0 Public domain dedication).20. An emerging technology is that of the “continuous TEE” using a disposable TEE probe, which can remain in the patient for up to 72 hours in the ICU. This has shown some promise as a useful diagnostic tool for tracheally intubated patients with complex pathophysiology. The use of continuous TEE has been demonstrated to help predict neurologic outcomes of patients following cardiac arrest which is treated with hypothermic cooling21. Additionally, following valve replacement, continuous TEE monitoring has been helpful in guiding management in patients with hemodynamic instability22. Continuous TEE monitoring is a fledgling technology and as such does not have extensive cost efficacy or outcome data associated with it. Nonetheless, its role in the management of critically ill patients may be expanded and should be better defined in coming years  is well establishedg years .Video 2Evaluation of hypotension in the intensive care unit (ICU) is aided by transesophageal echocardiography (TEE) to establish volume status, cardiac function, and the presence or absence of hemodynamically significant valvular stenosis or regurgitation. 2D, two-dimensional; BPM, beats per minute; LA, left atrium; LV, left ventricle; Pat. T, patient temperature; RV, right ventricle; TEE T, transesophageal echocardiography temperature.Click here for additional data file.Copyright: © 2016 Maxwell C et al.2016Data associated with the article are available under the terms of the Creative Commons Zero "No rights reserved" data waiver (CC0 1.0 Public domain dedication).0)/L0 where L = length at end-systole and L0 is the initial length at end-diastole, is a unit-less percentage change in myocardial deformation. Directly tracking myocardial compression and expansion throughout the cardiac cycle may offer a more load-independent measure of cardiac function. Strain essentially measures changes in sarcomere length over each cardiac cycle as opposed to percentage volume change in the left ventricular cavity, which is highly susceptible to loading, chronotropic, and inotropic states. This is particularly pertinent during intraoperative imaging, where there are abrupt changes in the aforementioned variables. Strain rate, or strain over time, may offer an even more load-independent measure of intrinsic myocardial function23.One of the more recent, yet infrequently used, technologies in clinical practice is myocardial strain analysis. Strain (ε), defined as .32. Furthermore, specific therapies for diastolic heart failure are limited. Current guidelines promulgated by the American College of Cardiology and the American Heart Association recommend blood pressure control and diuretics in volume overloaded states, but note that there is little evidence to support additional therapies33.Diastology, or the study of cardiac diastolic function, has gained steam in the past decade. Historically, echocardiographic attention has been focused on the quantification of left ventricular systolic function. However, systolic dysfunction is not always the cause of heart failure: roughly 50% of patients with symptomatic heart failure have a preserved left ventricular ejection fraction34. With limited therapies available for diastolic heart failure, classification of diastolic dysfunction carries mostly a prognostic value rather than serving to guide treatment options. Similarly, intraoperative decision-making based on diastolic function classification in patients undergoing cardiac surgery has limited evidence to guide specific therapy.Comprehensive assessment of left ventricular diastolic function has included multiple quantitative echocardiographic measurements, including pulsed wave Doppler assessment of mitral and pulmonary venous inflow velocities, tissue Doppler assessment of mitral annular velocities, color M-mode assessment of mitral inflow propagation velocity, and a variety of other methods. Many studies have looked at different measurement variables in the quantification of diastolic function. Therefore, in 2009, the European Association of Echocardiography, in conjunction with the American Society of Echocardiography, published guidelines for the assessment, quantification, and grading of diastolic functionet al. proposed a relatively simple and effective algorithm for intraoperative TEE evaluation and classification of left ventricular diastolic function35. This algorithm incorporates the measure of mitral annular tissue velocity recorded from the lateral mitral annulus in early diastole (e′), with a value of more than 10 cm/s indicating normal diastolic function. Further stratification of left ventricular diastolic dysfunction for mitral tissue Doppler velocities of less than 10 cm/s uses the ratio of early mitral inflow velocities (E) to e′. Higher E/e′ ratios are indicative of worsening left ventricular diastolic function, as early mitral inflow velocities increase while annular velocities are reduced with later stages of diastolic dysfunction , also known as impaired relaxation, maintenance of sinus rhythm with an adequate diastolic filling time (slower heart rate) is favorable, owing to a longer time period for ventricular relaxation . Convers39, including hemodynamic manipulation, in improving outcomes in these patients. Given the conflicting evidence for the effects of inotropic drugs on diastolic function, it is understandable that many clinicians remain skeptical of current efforts to use TEE to assess diastolic function parameters in the perioperative environment.Those who criticize efforts to assess and classify left ventricular diastolic function cite the limited evidence for targeted therapiesWith the pace of improvement in TEE technologies that we have seen since its introduction, it is likely that further refinements and novel imaging modalities will continue to be introduced in coming years. Three-dimensional echocardiography has made the diagnosis of complex pathologies more accurate and is essential for guiding procedural interventions in real time. Improvements in real-time 3D resolution will facilitate high-quality imaging without the artifacts caused by arrhythmias and cardiac translation. Continuous TEE monitoring in the ICU has shown some early promise and in coming years may replace the pulmonary artery catheter for hemodynamic evaluation of unstable tracheally intubated patients.Speckle-tracking and strain analysis have now been incorporated into the management of patients with chronic heart failure, but the practical use of these methods in the perioperative setting has yet to be elucidated. Current challenges include the time-consuming nature of speckle-tracking methods, which are not conducive to measurement in a busy intraoperative setting, and the clinical utility of detecting subtle reductions in systolic function. There is some evidence that in patients with preserved ejection fractions, global longitudinal strain may have predictive value in the development of post-operative atrial fibrillation. Additional studies are needed to determine the relevance of these findings.Although assessment and classification of diastolic function have improved and offer valuable prognostic information, there is currently little evidence to suggest that this leads to interventions that improve clinical outcomes. Despite the many advances in perioperative TEE in the past few decades, we still have opportunities ahead to improve the use of this technology for our patients.The data referenced by this article are under copyright with the following copyright statement: Copyright: © 2016 Maxwell C et al.Data associated with the article are available under the terms of the Creative Commons Zero "No rights reserved" data waiver (CC0 1.0 Public domain dedication).Video 1,10.5256/f1000research.7169.d11545840F1000Research: Dataset 1.Video 2,10.5256/f1000research.7169.d11545941F1000Research: Dataset 2.Video 3,10.5256/f1000research.7169.d11546042F1000Research: Dataset 3.


The American Heart Association (AHA)/American College of Cardiology (ACC) guidelines for the classification of heart failure (HF) are descriptive but lack precise and objective measures which would assist in categorising such patients. Our aim was two fold, firstly to demonstrate quantitatively the progression of HF through each stage using a meta-analysis of existing left ventricular (LV) pressure-volume (PV) loop data and secondly use the LV PV loop data to create stage specific HF models.A literature search yielded 31 papers with PV data, representing over 200 patients in different stages of HF. The raw pressure and volume data were extracted from the papers using a digitising software package and the means were calculated. The data demonstrated that, as HF progressed, stroke volume (SV), ejection fraction (EF%) decreased while LV volumes increased. A 2-element lumped parameter model was employed to model the mean loops and the error was calculated between the loops, demonstrating close fit between the loops. The only parameter that was consistently and statistically different across all the stages was the elastance (Emax).For the first time, the authors have created a visual and quantitative representation of the AHA/ACC stages of LVSD-HF, from normal to end-stage. The study demonstrates that robust, load-independent and reproducible parameters, such as elastance, can be used to categorise and model HF, complementing the existing classification. The modelled PV loops establish previously unknown physiological parameters for each AHA/ACC stage of LVSD-HF, such as LV elastance and highlight that it this parameter alone, in lumped parameter models, that determines the severity of HF. Such information will enable cardiovascular modellers with an interest in HF, to create more accurate models of the heart as it fails. To model LV performance, quantitative data, such as pressure and volume, is vital to ensure that any model is an accurate representation of reality. As such, a computational model of the LV cannot be built on single parameters alone such as left ventricular end-diastolic volume (LVEDV), subjective symptoms such as dyspnoea, nor surrogate markers such as natriuretic peptides (NP's) but direct measures of the system being modelled, both anatomical e.g. volume and physiological e.g. pressure.Previous attempts to model the HF, and the effect of potential therapies, have applied hypothetical haemodynamic states according to symptomatic New York Heart Association (NYHA) class rather than actual patient data, from individuals or populations. The NYHA class, whilst useful clinically, correlates poorly with even non-invasive measures of LV performance In 2001, the joint American Heart Association (AHA)/American College of Cardiology (ACC) guidelines categorised for the first time HF and its progression in terms of pathophysiology see . This waThe authors wished to define quantitatively each AHA/ACC stage of HF and so for the first time define the risk and the onset and progression of left ventricular systolic dysfunction heart failure (LVSD-HF) according to objective changes in left ventricular physical properties represented by the left ventricular pressure-volume loops. The choice of the pressure-volume (PV) loop is based on its direct description of the performance of the LV in real-time and for reasons mentioned above, quantifying LVSD-HF by other parameters such as LV volume or symptoms is insufficient for modelling purposes.For this study, we concentrated on the chronic LVSD-HF population based on both pragmatic approach, and a more therapeutic consideration since only patients with LVSD-HF have interventions that are associated with significant impact on morbidity and mortality. There have been many studies looking at LV PV loops in patients with heart disease, but this is the first time they have all been collated, compared and modelling parameters derived. For comparision and completeness, a healthy normal group (stage O) was created also, not contained in the AHA/ACC guidelines,The methodology for PV loop acquisition has been described in detail previously An online literature search of Pubmed, Web of Knowledge, Medline and Google, using the search term “pressure volume loop” was conducted and the references were studied to check that they met criteria to be included in the final analysis see .Studies with complete LV PV loops in adult humans in English.(and) Studies representing any AHA/ACC stage including healthy normal subjects.(and) HF, if present, due to chronic LVSD-HF only.Diastolic HF or HFPEF.HF secondary to an uncommon cause such as Chagas' disease.An unclear past medical, symptom or drug history, meaning HF stage was vague.No pictorial representation of an entire loop, such as a diastolic limb only.Acquisition during experimental treatment only without a baseline measureOf the papers identified, 97 were potentially useable, but only 31 met the inclusion, and not the exclusion, criteria and so were included in the final analysis, accounting for 203 patients http://digitizer.sourceforge.net/) was then used to upload the graphical PV loop images from the original studies and convert them into numerical data, as seen in Engauge digitizing software , total peripheral resistance and systemic vascular compliance, the components of which are described below. The progression of LVSD-HF is thus expressed in terms of the evolution of these four parameters. Furthermore it is suggested that the values of the components that represent the systemic afterload might be used to determine appropriate boundary conditions for the modeller who is interested in using such representations for complex 3D models of the left ventricle, which still rely on a specific afterload for the LV to “push” against.http://www.cellml.org/tools/opencell) such models can be run and the input variables of E, R and C manipulated, for example, to model hypertension one could reduce the compliance and increase the resistance of the vasculature, whilst leaving the value of E unaltered. The resulting outputs of LV pressure and volume can be exported to a database, extracted from one cardiac cycle and then converted into a PV loop.A lumped parameter model represents complex systems such as the cardiovascular system as a hydro-electrical analogue. In particular, the Windkessel model (meaning “air chamber” in German) contains a two element afterload, a capacitor representing the elastic property of the large arteries which determines systemic vascular compliance (C) and a resistor representing the frictional loss in the smaller vessels e.g. arterioles which determine the total peripheral resistance (R). The LV is represented by a variable elastance (E) model, where by the LV pressure is a function of the LV elastance and the change in LV volume from its resting state, in this model E is represented by 2 values, Emax being representative of peak systolic LV contractility and Emin being representative of end diastolic LV stiffness. Using software such as OpenCell, (http://www.cellml.org/) model repository, which is a free to access store of computer based mathematical models, and run using OpenCell, an open source platform for working with CellML models, see LA) and left ventricle (ELV) are represented by variable capacitors to model the pumping action of the left side of the heart, the mitral (mi) and aortic (ao) valves are represented by diodes to model unidirectional flow, the total peripheral resistance by a resistor, systemic vascular compliance by a capacitor and blood vessels by wire allowing for flow of electrons, representing the flow of blood.For this study, a lumped parameter model with a variable elastance LV and 2 element (R and C) Windkessel afterload was chosen to model the LV in LVSD-HF To model the mean AHA/ACC PV loops, the Matlab  optimisation toolbox was used to find the combination of parameters that best fitted the data. This toolbox enabled running the lumped parameter model as an iterative process, whilst varying each variable  until the best-fit model for the patient derived mean LV PV loop for each stage was created. The resulting model PV loop data was exported to a spreadsheet and compared against the mean loops (see below).p values of <0.05 were considered significant.Statistical analysis was carried out using Microsoft Excel 2010 software . Parametric data is given as mean (± SD). Comparison of data between LVSD-HF stages using an unpaired 2 tailed Students t-test and The majority of the patients making up each category are males in their late fifties see . Some AHFor clarity, we have just shown the raw and mean loops from one stage, AHA/ACC D . It is eFor the modelled PV loops see  there isUsing Matlab , we compared the area error for the modelled loops to the mean, to give a measurement of accuracy see . This meThis is the first meta-analysis of all of the existing literature on PV loops in LVSD-HF, stratified by AHA/ACC stage. This study demonstrated that the pressure-volume data in the literature supports the existing theoretical ACC/AHA physiological paradigm for LVSD-HF, whereby as the left ventricle fails, it dilates. Thus, the contractile force is impaired and the volume it ejects with each beat is reduced. This study showed quantitatively the changes between each AHA/ACC stage. As the AHA/ACC stages are descriptive and qualitative, particularly stages C and D, it is remarkable how the stages could be delineated quantitatively in this study. Indeed, it demonstrates the strength of the EF, although typically used in echocardiography or cardiac magnetic resonance, as it is the only variable in the patient data, that is statistically and significantly different across all the stages, other than between O and A.For the first time, a LPM has been used to model all the existing PV loop data across the entire spectrum of heart disease, from healthy normal individuals to patients with end-stage LVSD-HF. The model, whilst simple, performed well, with a mean error of less than 10% and gives insight into how the heart, and the systemic vasculature fail.The lumped parameter model is true in physiological sense. Predictably, the pump function of the left ventricle deteriorates as LVSD-HF progresses, the left ventricular chamber dilates, the afterload and plasma volume increase, which will affect both R and C. The pressure-volume loops showed each stage as expected, thus: Stage O is indeed healthy, with normal left ventricular parameters that we would expect from a disease-free population. Patients in Stage A, the vast majority of whom have IHD, the systolic pressure rises reflecting increased afterload and the EF% and SV fall. However, all these parameters are still within normal limits. Following an ischaemic insult to the myocardium in Stage B, there is a rise in LVEDP reflecting increased stiffness, a fall in systolic pressure due to impaired contractile force and corresponding reduction in both the ejection fraction and the stroke volume. What is somewhat surprising is that whilst there is an increase in volume from stage C to D, both the systolic and diastolic pressures rise. This is not necessarily surprising as the process is not a simple mechanical process but it reflects the contribution of the compensatory mechanisms driven by the sympathetic drive and by the endocrine responses driven by the rennin-angiotensin-aldosterone system as well as the sympathetic system.The patients in stages A-B are asymptomatic from the LVSD-HF viewpoint, this is despite an increase of R and C, and decrease in LV Emax, by 60% (relative to Stage O). However, the remaining contractile force is sufficient to meet the demands of the body. The difference between the asymptomatic patients with structural heart disease (Stage B) and those with symptoms of (Stage C) is the reduction in LV Emax by a further 50%. The difference between symptomatic and refractory LVSD-HF is a further modest (13%) reduction in Emax . This is an important observation that illustrates the delicate tipping point between physiological compensation and decompensation. Indeed, as seen statistically, stage C and D were not significantly different from one another, but they were on almost every single variable compared to stages O-B. This information, whilst logical and perhaps inferred, was previously unknown. Also, there was no significant difference between any of the groups in Emin, representing LV end-diastolic stiffness, as one might expect, as this was a study investigating LVSD-HF, not HFPEF, although diastolic dysfunction can co-exist with systolic.Importantly, the creation of the lumped parameter model variables for the various LVSD-HF stages see , will saPreviously, it was felt that the LV afterload, comprising total peripheral resistance and systemic vascular compliance had an important role in modelling the LV performance accurately. However, this body of work, comprising the largest cohort of LVSD-HF models based on real patients to date, demonstrates there is no significant different in compliance or resistance between even healthy normals and end-stage. This is important as it demonstrates, that in LVSD-HF and in this this model at least, the most important factor is Emax or peak contractility of the LV. Of course, in reality, it is well known that increased afterload on the heart, due to diseases like hypertension, leads to increase LV wall shear stress, left ventricular hypertrophy and if untreated LVSD and eventually LVSD-HF. Afterload and compliance will also be influenced by other disease processes and medications, which were impossible to control for and very few of this patient cohort, particularly in stage A had hypertension. Our findings however, further strengthen the importance of using load-independent, repeatable and robust measures of LV performance such as elastance when modelling LVSD-HF.2 as undoubtedly in a cohort of over 200 patients, there will be large variations in patient size and anatomy. Hence, there is overlap amongst the disease stages and accounts for the non-significance difference in LV volume between the 5 stages. This further highlights the importance of objective differentiation of patient LVSD-HF stages, when creating models, rather than being based on the patient's subjective assessment  and objective echocardiographic measurements used in current clinical practice.There is wide distribution of the PV loops within each stage, as demonstrated in Stage D by It would be interesting to compare the PV loops of patients with HF of different aetiologies, such as ischaemic versus idiopathic DCM, and to model the effects of various therapies on the different parameters, such as cardiac resynchronisation therapy (CRT). Furthermore, comparing those PV loops of patients with different isolated risk factors for HF, such as obesity or essential hypertension or with differing structural heart diseases such as asymptomatic aortic stenosis or left ventricular hypertrophy to see how they progress from symptomless risk to symptomatic HF would also be of interest. Unfortunately, such data are not currently available. More PV loops are needed to inform stages O and B, as the mean loops and therefore the models, are based on a small number of cases. However, it is unlikely that ethical approval for invasive PV loop analysis would be granted for healthy subjects.Most of the information given about patients was not specific to the loop and so we were unable to control for age, body mass, sex, medications and other relevant co-morbidities , which could have an impact on the loop shape, size and position For the first time, the authors have created a visual and quantitative representation of the AHA/ACC stages of LVSD-HF, from normal to end-stage. The study demonstrates that robust, load-independent and reproducible parameters, such as elastance, can be used to categorise and model HF, complementing the existing classification. The modelled PV loops establish previously unknown physiological parameters for each AHA/ACC stage of LVSD-HF, such as LV elastance and highlight that it this parameter alone, in lumped parameter models, that determines the severity of HF. This is the largest collection of LV PV loop data, which has been used to create stage specific HF models, and as such, will enable cardiovascular modellers to create more accurate models of the heart as it fails and should be used as a reference for future work in this field.Checklist S1Search yield according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses.(DOC)Click here for additional data file.Diagram S1Flow diagram for search results according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses.(DOC)Click here for additional data file.


Acute exacerbation is a common cause of hospitalization in patients with chronic heart failure, and coronary heart disease is the most common cause. Shenfu injection, a Traditional Chinese Medicine injection, widely used in the adjuvant treatment of patients with acute exacerbation of chronic heart failure, shows some treatment effect in improving the symptoms and the quality of life, but it lacks the rigorous clinical evaluation of research reports. This paper describes the protocol for the clinical assessment of Shenfu injection loading in the treatment of patients with acute exacerbation of chronic heart failure.yang and qi deficiency syndrome). On the basis of the conventional therapy of western medicine, patients will be randomized to either the treatment group (100 ml 5% glucose injection + 50 ml Shenfu injection) or the control group (150 ml 5% glucose injection) for 7 ± 1 days and follow-up for 28 ± 3 days. The primary outcomes are New York Heart Association cardiac function classification and Traditional Chinese Medicine syndromes. The secondary outcomes are left ventricular ejection fraction, brain natriuretic peptide level, Lee’s heart failure score, 6-minute walking distance, and the incidence and readmission rate of cardiovascular events (including the emergency rate due to acute exacerbation of chronic heart failure).This protocol adopts the design of a prospective, randomized, multicenter, blind imitation, placebo-controlled trial to assess the efficacy and safety of Shenfu injection loading in the treatment of patients with acute exacerbation of chronic heart failure due to coronary heart disease. The research will be carried out in 12 hospitals in China and is expected to enroll 160 inpatients with acute exacerbation of chronic heart failure due to coronary heart disease (yang-qi deficiency syndrome) on the symptoms and signs of heart failure, exercise tolerance, and other aspects, and observe its influence on the short-term prognosis with follow-up. The results of the study will provide clinical research evidence for application of Shenfu injection in the treatment.This trial will assess the effect of loading Shenfu injection in the treatment of patients with acute exacerbation of chronic heart failure caused by coronary heart disease (ChiCTR-TRC-12002857).This trial was registered on 26 December 2012 at the Chinese Clinical Trials Register (Identifier: The online version of this article (doi:10.1186/s13063-015-0729-7) contains supplementary material, which is available to authorized users. Chronic Heart failure (CHF) is a chronic progressive disease, the terminal stage of various cardiovascular diseases and a cardiac dysfunction syndrome. The condition of CHF patients will remain stable after treatment, but will also dramatically worsen under the influence of various factors  and appears as acute decompensated CHF ) .The diagnosis and treatment guideline for heart failure of China in 2014  003) and other Institutional Review Boards of participating hospitals , and so forth, and has been demonstrated in clinical studies ,19.+-K+-ATP and Ca2+-ATP of the left ventricle [As a post-marketed herbal species used for nearly 30 years, the composition of SFI is clear and its quality is reliable. Some clinical reports showed that the conventional western medicine combined with SFI could further improve the symptoms of CHF patients, TCM syndrome, the quality of life and show a clinical curative effect, increase LVEF and decrease left ventricular end-diastolic diameter , reduce entricle , increasThe study design of this trial has three main points. (1) Selection of patients with AECHF due to CHD; this is a specific disease group and a study on the primary cause and the main type of hospitalization. (2) This is a superiority trial comparing a study drug with placebo. In view of the external characteristics of TCM injection, the study uses the method of blind imitation, with an intravenous drip of 5% GLI with a light-proof infusion cover. (3) The effective rate of heart functional class and TCM syndrome are primary outcomes; it will adopt the clinical effect evaluation methods of “the combination of disease and syndrome, systematic staging, multi-dimension index” , and wilThe trial was initiated in March 2013. Now, the study is in the stage of database testing and is ready to data input and statistics. The completion date of trial is estimated at December 2015.


Cardiac involvement in systemic light-chain amyloidosis (AL) is characterized by slightly decreased systolic left ventricular function (LV) function and typically a diastolic dysfunction including left atrial (LA) enlargement. Cardiac magnetic resonance (CMR) is often performed in AL to accurately assess chambers size and function. We aimed to compare features of LV systolic and diastolic function obtained by 2D transthoracic echocardiography (TTE), with morphological and functional myocardial LV (presence of late gadolinium enhancement: LGE) and LA (volume and emptying fraction) parameters as assessed by CMR in a consecutive series of patients with cardiac AL.Thirty-five consecutive patients in sinus rhythm  with confirmed systemic AL, underwent TTE and CMR within the same day. LVEF and LV 2D global longitudinal speckle tracking imaging obtained by TTE were stratified according to the presence or not by CMR, of myocardial late enhancement gadolinium (LV-LGE). Left atrial emptying fraction (LAEF) was calculated after assessing the maximal and minimal LA volume (by area/length formula) in CMR using 4 and 2 chambers views and the following formula: Max LAV-Min LAV/ Max LAV2D- LVEF and global longitudinal speckle tracking imaging were significantly decreased in patients with LV-LGE when compared to those without: 56.5±10.4% vs. 63.5±10.2%, p=0.04 and -10.8±2.8% vs. -16.6±5.02%, p=0.0005 respectively. Diastolic mitral deceleration time and E/A ratio and E/e' at lateral annulus were significantly altered in patients with low LA-EF < 24% median value) vs. those with higher LA-EF whereas, they were not significantly different according to max-LAV by CMR (Figure In systemic AL, reduced systolic LV 2D speckle tracking imaging is significantly associated with the presence of LV-LGE while impaired LV filling pressures are rather related to decreased in LA emptying fraction. Multimodality imaging in patients with AL may allow complementary and better assessment of LV hemodynamics. However, larger series are needed to confirm these results.None.


There is an overlapping phenotype in patients with new-onset systolic heart failure due to myocarditis and dilative cardiomyopathy (DCM). Differentiation between both etiologies has important therapeutic and prognostic implications and is currently based on endomyocardial biopsy (EMB). In contrast, current cardiovascular magnetic resonance (CMR) techniques are of limited value in these patients with predominantly diffuse myocardial injury. This study evaluated the performance of quantitative T1- and T2-mapping CMR to differentiate between active myocarditis and DCM in patients with new-onset systolic heart failure.This study included 26 patients with new-onset systolic heart failure and reduced left ventricular (LV) ejection fraction (32 ± 12 %), who underwent EMB and CMR at 1.5 Tesla. The protocol included conventional sequences (T2w-STIR), Early- (T1w-TSE) and Late-Gadolinium-Enhancement (PSIR). Furthermore, T1 quantification was performed using the modified Look-Locker inversion-recovery (MOLLI) sequence before (native) and 15 minutes after administration of 0.075 mmol/kg Gadolinium-BOPTA. T2 quantification was performed using a free-breathing, navigator-gated multi-echo sequence. Native T1, post-contrast T1, extracellular volume (ECV) and T2 maps were calculated with a dedicated plug-in written for the OsiriX software.EMB revealed variants of active myocarditis in 13 (50 %) and DCM in the remaining 13 (50 %) patients. The ROC areas-under-the-curve (AUC) to discriminate between both etiologies was 0.54 (p = 0.77) for Early-Gadolinium-Enhancement, 0.63 (p = 0.23) for Late-Gadolinium-Enhancement, 0.68 (p = 0.11) for T2w-STIR, 0.66 (p = 0.17) for native global myocardial T1, 0.72 (p = 0.05) for post-contrast global myocardial T1, 0.61 (p = 0.36) for global myocardial ECV and 0.74 (p < 0.05) for global myocardial T2. Sensitivity and specificity were 50 % and 83 % to discriminate between myocarditis and DCM using global myocardial T2 .Assessing myocardial inflammation by T2-mapping CMR could be helpful to discriminate between active myocarditis and DCM in patients with new-onset systolic heart failure. T2-mapping CMR appears to be superior compared to conventional techniques but also to T1-mapping CMR in this context.No funding.


Accumulation of diffuse interstitial myocardial fibrosis in severe aortic stenosis relates to left ventricular (LV) functional impairment and determines the postoperative outcome in these patients. T1 mapping has been proposed for non-invasive quantification of diffuse interstitial fibrosis. We examined associations between T1 values and collagen volume fraction from endomyocardial biopsies from patients with severe aortic stenosis. We compared whether these relationships differ with respect to the post-processing approach.Ten patients  with isolated severe aortic stenosis and eligible for aortic valve replacement surgery underwent clinical cardiovascular magnetic resonance study at 3 clinical scanner. A mid- chamber myocardial biopsy was obtained from the left ventricular (LV) septum at the time of surgery and stained for collagen volume fraction (CVF) using Mason Trichrome technique and ImageJ analysis.T1 mapping was performed using MOLLI (3(3)3(3)5)) sequence prior to and 15 minutes after IV administration of 0.2 mmol/kg of gadobutrol. T1 measurements were performed using both a conservative septal ROI and the entire coverage of midventricular short-axis (SAX) slice. Areas of overt LGE were excluded from the analysis. T1 values were compared to fourteen age-matched healthy control subjects and correlated with CVF.Compared to controls, there were no significant differences in cardiac volumes and global systolic function. Patients had raised LV mass and wall thickness p<0.01), and mean native T1 values  comprehensive Biomedical Research Centre award to Guy's & St Thomas' NHS Foundation Trust in partnership with King's College London and King's College Hospital National Health Service Foundation Trust, and British Heart Foundation Research Centre of Excellence Award. King's Health Partners via MRC Confidence in Concept Grant.


Heart ventricular dysfunction has been characterized as reduced longitudinal function of the right ventricle (RV), and is associated with chronic alcohol abuse. This study investigated the use of two-dimensional speckle tracking echocardiography (2DSTE) to assess the longitudinal systolic and diastolic RV function of patients with alcoholic myocardial damage.We stratified 92 asymptomatic alcoholic men into three groups of increasing alcohol intake, Groups A–C. Thirty age-matched normal adult men served as the control group. Conventional echocardiography and tricuspid annulus peak systolic excursion (TAPSE) parameters were obtained. 2DSTE parameters were recorded from an apical 4-chamber view of the RV free wall. LV peak global longitudinal systolic strain was calculated from segmental averaging of the three apical long-axis views.r1=−0.84, r2=−0.72, respectively, P <0.05).In Group C, the RV end diastolic diameter (RVEDD) was dramatically higher than that of Groups A, B and the control, while TAPSE was significantly lower in Group C compared with the other experimental groups. In Group B, the longitudinal early diastolic strain rate (SRe) and late diastolic strain rate (SRa) of the RV free wall, and LV longitudinal strain were significantly lower than that of Group A or the control. In Group C, all the 2DSTE parameters were significantly lower than that of the other groups. A significant negative linear correlation was noted between global RV systolic parameters systolic strain peak (S), peak systolic strain rate (SRs) and TAPSE (Two-dimensional STE provided an effective and non-invasive method to assess the RV longitudinal function of patients with alcoholic myocardial damage. This methodology may be useful for diagnosing, directing treatment, and judging prognosis of alcoholic cardiac damage. Alcohol is a risk factor of heart disease, and long-term alcohol abuse may have detrimental effects on ventricular function , 2, possLongitudinal LV dysfunction is one of the earliest biomarkers of ventricular damage , 5. Two-Although the prognostic value of right ventricular (RV) systolic and diastolic function has been documented for cardiac symptoms and exercise capacity , prior sThe limitations of other echocardiographic techniques are overcome with 2DSTE, as the focus is on endocardial structures interference from the RV wall is avoided. Prior studies have suggested that RV dysfunction can be determined quantitatively by the change in longitudinal movement of the RV, relative to that of the normal RV , 14. SinIn this setting, we hypothesized that 2DSTE could be used for early evaluation of changes in RV longitudinal function in patients with alcoholic myocardial damage. While there have been several studies of deformation that have touched upon this topic, none have used 2D-STE to study the RV.Ninety-two male asymptomatic alcoholics, 42–65 years old, were examined between June 2009 and March 2013 and served as the experimental group. These patients were categorized into three groups according to the amount and duration of alcohol consumption: Group A, ≥90 mg ethanol or ≥2–3 bottles of beer, 3–5 days/week for 5–8 years; Group B, ≥90 mg ethanol or ≥2–3 bottles of beer, 3–5 days/week for 9–20 years; and Group C, ≥150 mg ethanol or ≥4 bottles of beer, 6–7 days/week for >10 years, which met the standard for diagnosis of alcoholic cardiomyopathy (ACM) .Thirty age-matched (40–65 years) healthy male volunteers served as the control group (Group D). Control subjects did not exhibit any cardiovascular abnormalities.The exclusion criteria included a history of congenital heart disease, hypertension, diabetes, ischemic or vascular heart diseases, rhythm problems and atrial fibrillation, pulmonary hypertension, systemic and metabolic diseases that could adversely affect cardiac structure and function such as valvular heart disease, or using cardiac medications.All procedures were carried out in accordance with institutional guidelines. The local medical ethics committee  approved the study, and all patients provided written informed consent before entering the study.Recordings were obtained with a GE Vingmed Vivid 7  scanner equipped with a 1.7–3.4 MHz transducer (M3S probe). Standard echocardiography and 2DSTE measurements of the RV and LV were analyzed off-line using dedicated software .The examination focused on the measurement of LV and RV dimensions. The end diastolic diameters, ejection fractions, and tricuspid annulus peak systolic excursion (TAPSE) were captured as follows. RV and LV end diastolic diameters  were measured in the parasternal long-axis view. From the apical four-chamber view, the LV ejection fraction (LVEF) was obtained using a commercially available software program that applied the biplane Simpson’s method in the four-chamber view. The RV ejection fraction (RVEF) was calculated from the RV fractional area change.TAPSE acquisition was performed by M-mode echocardiography in the four-chamber view: an M-mode cursor was steered through the lateral portion of the tricuspid annulus, which delineates the RV atrioventricular plane. The magnitude of the tricuspid valve ring along the M-mode line was determined by measuring the maximal distance between the leading edge of the highest and lowest echoes during each cardiac cycle.Two-dimensional dynamic images were recorded for subsequent analyses. High frame rate acquisition was used (≥100 frames/s). At least three cardiac cycles were stored for offline analysis. All 2DSTE data were measured by averaging data over three heartbeats.A crucial part of the analysis was based on the correct adjudication of event timing. For example, end-diastole was defined at the peak R of the electrocardiographic QRS complex, and end-systole was defined as the first negative crossover of the velocity curve. Offline analysis was performed using a special software program (EchoPAC 6.1.0 GE Vingmed).Out of the cardiac cycles recorded, the RV endocardial surface was manually defined using the clearest  of apical 4-chamber views. To train the software to track automatically the relevant myocardial motion, a region of interest was manually defined on the RV wall. Myocardial deformation was defined as longitudinal strain and strain rate was examined at basal, middle, and apical segments of the RV wall, including peak systolic displacement (P), systolic strain peak (S), peak systolic strain rate (SRs), peak early diastolic strain rate (SRe) and late diastolic strain rate peak (SRa).In addition, LV peak global longitudinal systolic strain was calculated from segmental averaging of the three apical long-axis views . The LV region of interest was defined by tracking the endocardial and epicardial borders, and adjusted to accommodate wall thickness.P-value <0.05 was considered statistically significant. Intra-observer analysis of RV longitudinal strain in the 4-chamber view was conducted 2 months after completion of the initial measurements (by author MSS). For inter-observer variability, a second observer (LGS) analyzed 20 % of the initial images. Intra-observer variability and inter-observer variability were assessed using the intra-class correlation coefficient (ICC) [All analyses were performed using SPSS version 17.0 for Windows . Variables are presented as mean ± standard deviation. One-way analysis of variance was used to assess changes among the four groups. Multiple comparisons between the groups were performed using the Student–Newman–Keuls method. Correlation coefficients, 95 % confidence intervals (CIs) and percentage errors were reported. A nt (ICC) .P >0.05; Table P <0.05).All study subjects were in sinus rhythm at rest, and none had a history of cardiac surgery. The four groups showed an average distribution in age, body weight, height, body mass index and body surface area, which were similar among the groups .The RVEDD of Group C was significantly higher than that of the other groups, and the TAPSE was significantly lower (P >0.05). The SRe and SRa of each RV free wall segment were significantly lower in Group B than in either Group A or the control group (P <0.05). However, the parameters P, S, and SRs of Groups A, B, and the control group were similar (P >0.05). Notably, all the diastolic parameters and the systolic parameters P, S, and SRs were significantly lower in Group C than in the other groups . Changes in myocardial strain within each segment  between the four groups are presented in Figs. The LV longitudinal strain was less in Group B and C compared with both Group A and the control Table . The aver1=−0.84, r2=−0.72, respectively, P <0.05; Fig. TAPSE was significantly lower in Group C compared with that of the other experimental groups Figs.  and 6. AUsing 2D-STE to evaluate alcoholic cardiac damage, inter- and intra-observer results had good reproducibility and small variability Table .Table 5IVentricular dysfunction is consistent with the sympathetic depressant effect of high alcohol consumption. Findings of reduced longitudinal function in the RV have been shown to reflect global ventricular dysfunction , 19; furAnatomically, the structure of the RV is more complex than that of the LV, appearing triangular when viewed from the side and crescentic when viewed in cross-section. RV myocardial fibers are three times thinner than LV fibers, making the RV myocardial wall relatively thin. The RV wall is mainly composed of two layers: the superficial layer fibers that are aligned circumferentially and parallel to the AV groove, and the deep layer fibers arranged longitudinally, from base to apex, which predominate RV contractile motion. Importantly, RV and LV share a common interventricular septum and the epicardial fibers are mutually encircled, thus ventricular interdependence cannot be overlooked.Due to the complex shape of the RV, conventional transthoracic echocardiography assessment of the RV is nearly always based on qualitative estimation . Thus, fTo assess ventricular function in a variety of different cardiovascular diseases, 2D-STE has been confirmed to be a feasible and sensitive method –29. EstiBecause circulatory support functions of the RV are performed by longitudinal muscle, some researchers have suggested that peak longitudinal strain could be a biomarker for assessment of RV function . FurtherCompared with the control group, the RVEDD of patients in Group C was significantly higher, based on conventional ultrasound parameters. However, 2D-STE analysis of Re and SRa in Group B were significantly lower than in Group A and the control, indicating altered diastolic RV function. This finding suggests that 2DSTE reflects RV function in chronic asymptomatic alcoholics more reliably as compared to conventional ultrasonic methods.Alcoholic damage in ventricular pathology is generally considered to consist of both diastolic and systolic dysfunction. RV diastolic dysfunction is possibly related to myocardial relaxation and myocardial stiffness. Pathological changes are reflected mainly in myocardial conditions and myocardial fibrosis. Ethanol does affect tissue remodeling and causes ACM , 36, whiAlcohol injury may cause severe cardiac dysfunction in chronic asymptomatic alcoholics , 40. TheVentricular interdependence has an important role in the pathophysiology of RV dysfunction . InterdeBecause most heavy drinkers remain asymptomatic in the early stages of disease progression, early detection of morphological changes may allow early intervention in the pathogenesis of cardiovascular dysfunction . The resMurata et al.  used 2DSNotably, 2DSTE is strongly associated with RV contractile function confirmed by magnetic resonance imaging (MRI) –55. As wFor the assessment of RV function, 2DSTE offers improvements over conventional ultrasonic evaluation. The results of this study suggest that 2DSTE can be applied in the evaluation of RV function in chronic asymptomatic alcoholics. However, further studies are warranted to fully elucidate the clinical benefit of this imaging modality.The present study has several limitations. Firstly, it was conducted using a small number of male subjects, leading to uncertainty in extrapolation of these results across diverse sub-populations. Another limitation is that 2DSTE requires acceptable 2D image quality. Poor 2D image quality could confound interpretation of the results and negatively influence predictive validity of this imaging modality. In addition, several studies concluded that real-time 3-dimensional echocardiography had higher discriminating power than 2DSTE . To testAlcohol may increase the risk of RV diastolic and systolic dysfunction and ethanol-induced alterations in early cardiac function have the potential to develop into ACM. Although conventional echocardiography fails to detect RV function at an early disease stage, 2DSTE is a novel and sensitive technique to assess RV function. Our study demonstrates that 2DSTE is a promising imaging modality to detect early changes in cardiac function in chronic asymptomatic alcoholics. Future confirmatory studies are warranted to further evaluate RV function using 2DSTE in this patient population.


The establishment of radiofrequency catheter ablation techniques as the mainstay in the treatment of tachycardia has renewed new interest in cardiac anatomy. The interventional arrhythmologist has drawn attention not only to the gross anatomic details of the heart but also to architectural and histological characteristics of various cardiac regions that are relevant to the development or recurrence of tachyarrhythmias and procedural related complications of catheter ablation. In this review, therefore, we discuss some anatomic landmarks commonly used in catheter ablations including the terminal crest, sinus node region, Koch's triangle, cavotricuspid isthmus, Eustachian ridge and valve, pulmonary venous orifices, venoatrial junctions, and ventricular outflow tracts. We also discuss the anatomical features of important structures in the vicinity of the atria and pulmonary veins, such as the esophagus and phrenic nerves. This paper provides basic anatomic information to improve understanding of the mapping and ablative procedures for cardiac interventional electrophysiologists. The adoption of catheter ablation techniques for treatment of tachyarrhythmias has increased interest in learning cardiac anatomy. Interventional arrhythmologists are paying more attention to study the gross morphologic and architectural features of the heart. As a result of this interest a new wave of investigation has emerged to study cardiac anatomic topics that were not completely studied in the past. Recent investigations have unraveled anatomic features, architectural aspects, and histologic details of certain components of the heart, of interest to understanding of the substrates of tachycardias and their ablation.The right atrium (RA) is of utmost importance to electrophysiologist. It is the anatomic of major parts of the conduction system of the heart and the gateway to perform complex electrophysiological procedures that involve passing through the RA and interatrial septum. Each atrium is composed of a venous component, an appendage, body, and a vestibule. The venous component is located posterolaterally and receives the systemic venous flow, from the superior caval vein (SCV), inferior caval vein (ICV), and coronary sinus. The right atrial vestibule is a smooth muscular wall around the tricuspid orifice and supports the leaflets of the tricuspid valve. The characteristic of the vestibule is that it is surrounded by the pectinate muscles of the right atrium. The atrial chambers are separated from one another by the interatrial septum.Viewed from outside, the RA is dominated by its large, triangular appendage, which points anterosuperiorly and extends laterally . UsuallyThe sinus node (SN) is the source of the cardiac impulse. In the human heart, the SN is described as an almost crescent-shaped or cigar-shaped structure usually lodged immediately subepicardially within the sulcus terminalis, lying just inferior to the crest of the atrial appendage. Our studies have shown the head and body of the node to occupy a location within the anterolateral course of the terminal groove in the vast majority of hearts . OverallThis sinus node artery  is the iAnother area of significance to electrophysiologists is the triangle of Koch that delineates the location of the atrioventricular node (AVN) . This trThe body of the AVN is found near the apex of the triangle and the His bundle penetrates the CFB at the apex. The penetrating His bundle can readily be distinguished from the compact node at the point where the conduction axis itself becomes completely surrounded by tissues of the CFB  and condThe inferior pyramidal space is the extracardiac fibroadipose tissue wedging between the atrial and ventricular musculatures . ImportaThe cavotricuspid isthmus (CTI) in the lower part of the right atrium between the ICV and the tricuspid valve is considered crucial in producing a conduction delay and, hence, favoring the perpetuation of a reentrant circuit. Atrial flutter (AFL) can be categorized as being dependent on the CTI  and non-isthmus-dependent . The commonest type of AFL is isthmus-dependent AFL, which is a stable macroreentrant circuit that has its basis in the anatomical structure of the right atrium. The wave-fronts progress around the tricuspid annulus in a counterclockwise direction, resulting in the typical sawtooth-like P-wave morphology. The target for ablation is at the level of the isthmus of right atrium wall between the orifices of the inferior vena cava and the tricuspid valve . The fluAnatomical studies with CT scan using image data obtained during different cardiac phases have shown that the CTI is longest at all three parallel levels during midventricular systole . In thisFor the electrophysiologist entering the right atrium via the inferior route, the first structure encountered is the Eustachian valve (EV) guarding the orifice of the ICV. Normally, it is a thin, insignificant, crescentic flap. Occasionally, the flap is large and may impede access to the most posterior part of the isthmus. The free border of the EV continues as the tendon of Todaro that runs in the musculature of the Eustachian ridge . It has The sub-Eustachian recess is an extension of a pouch-like isthmus under the orifice of the coronary sinus . AttitudThe anatomy of the interatrial septum (IS) is particularly important for interventional cardiologists. The fact that the left atrium (LA) is posterior and superior to the RA determines the orientation of the atrial septum. Generally, the septal plane is at an angle to the median sagittal plane when viewed from the front of the chest, and a right anterior oblique projection will view the septal plane more or less “en face.”On heart specimens, the septal aspect of the RA gives an erroneous impression of there being an extensive atrial septum. The true septum, as defined by the area that can be excised without exiting the heart, is limited to the area marked by the valve of the oval fossa (the embryonic septum primum) and the anterior buttress of the atrial septum that is the true “secondary septum” . The supTwo main anatomic variants of the interatrial septum are lipomatous hypertrophy of the septum  and largBecause the left atrium (LA) is the main target of catheter ablation in patients with atrial fibrillation (AF), we review the gross morphological features of this chamber, the anatomy of pulmonary veins (as major target sites), and their relations with collateral extracardiac structures  which is key to successful and, more importantly, safe ablation.As with the RA, the LA possesses a venous component, a vestibule, a body, and an appendage. The pulmonary venous component, with the venous orifices at each corner, is found posteriorly. The vestibular component surrounds the mitral orifice . The majThe walls of the left atrial body are composed of several overlapping layers of differently aligned myocardial strands, and there are marked regional variations in muscular thickness . In the The epicardial fibers of the superior wall are composed of longitudinal or oblique fibers from the septopulmonary bundle  Figure  that ariIn addition to Bachmann's bundle, there are other interatrial muscular connections of varying thicknesses and widths that cross the interatrial groove  and connThe venous component of the LA receives the PVs, whereas the vestibular components surround the opening to the mitral valve. There are no endocardial landmarks to separate the vestibule from the pulmonary venous components Figures  and 7. TUnlike the RA, the LA lacks a terminal crest. The most prominent ridge in the LA is the left lateral ridge between the orifices of the left PVs and the ostium of the LAA  Figure . This stIn formalin fixed adult cadaveric hearts normal pulmonary vein (PV) anatomy consists of two right-sided and two left-sided PVs with separate ostia  Figures and 10, The musculature of the left atrial wall extends to varying lengths over the outer surface of the venous wall, with the longest sleeves along the upper veins . The sle(a) Esophagus. Due to the close proximity of the esophagus to the posterior wall of the LA . In. In70]. The septomarginal trabeculation itself is a Y-shaped muscular band that is adherent to the septal surface. Between its limbs lies the infolding of the heart wall forming the ventricular roof, an area also known as the supraventricular crest that separates the inflow and outflow components of the RV and supports the pulmonary valve . The sepThe inlets also differ notably in the normal ventricles, as do the outlets  Figure . The MV The right ventricular outflow tract (RVOT) passes superiorly and cephalad over the left ventricular outflow tract (LVOT), which is directed rightward, resulting in a crossover relationship between the two tracts, in fact most of the RVOT is to the left of the LVOT Figures  and 15, The LVOT is much more reduced in size because of the fibrous continuity between two of the leaflets of the aortic valve and the aortic leaflet of the MV . TherefoPremature ventricular contractions, ventricular tachycardias (VTs), and initiating beats for ventricular fibrillation have all been localized at the level of the right and left ventricular outflow tracts (RVOT and LVOT) , 81. AbsUnderstanding the image detail of the heart obtained with echocardiography and CT has an imperative role in outlining and anatomically delineating the cardiac landmarks related to the conduction system. Learning classic anatomy of the heart provided by cadaveric specimens is the prerequisite to understand what imaging delivers. Since anatomic variation of the cardiac conduction system landmarks and associated structures is common, it is also crucial to learn more about these normal variants, especially prior to interventional procedures.


Cardiac involvement in systemic sclerosis (SSc) is mainly characterised by diffuse myocardial fibrosis and impairment of the microcirculation; even if clinically silent, it is increasingly recognized to be responsible for higher morbidity and mortality rate. Cardiovascular magnetic resonance (CMR) is the most accurate non-invasive method able to detect myocardial inflammation and fibrosis, even though traditional CMR techniques such as T2-weighted and late gadolinium enhancement (LGE) are inaccurate to assess diffuse myocardial disease.Our aim was to investigate diffuse cardiac damage and perfusion abnormalities in asymptomatic SSc patients without known cardiac disease, using newer non-invasive imaging technique, such as T1 mapping and extracellular volume fraction (ECV), in pre-clinical stage.30 SSc patients  and 10 healthy controls  underwent CMR at 1.5 T unit . CMR protocol included: cineMR sequences, STIR T2w, MOLLI T1 mapping pre-contrast. LGE imaging and MOLLI sequence for ECV quantification were acquired 10-15 min after administration of a bolus 0.1 mmol/Kg of Gadobenate dimeglumine (Gd-BOPTA)LGE imaging was found to be positive in 7 SSc patients (23%) but none of controls. T2 weighted imaging found focal areas of inflammation in 3 SSc patients (10%), being negative in all controls. Native myocardial T1 values were significantly higher in SSc patients compared to controls (1043±37 vs. 980±33 p<0.01) and a significant difference in ECV expansion was found as well . Notably, T1 values and ECV did not correlate with the presence of LGE but they were associated to higher disease activity and severity.SSc patients with no cardiac symptoms and preserved left ventricular size and function have nonetheless cardiac involvement, which can be detected with conventional T2 weighted and LGE imaging. Newer techniques are much more sensible in identifying diffuse cardiac pathology, since the elevated T1 values and expanded ECV fractions found in patients are probably due to the underlying low-grade inflammation and diffuse fibrosis.