Automated Framework for the Inclusion of a His–Purkinje System in Cardiac Digital Twins of Ventricular Electrophysiology

Personalized models of cardiac electrophysiology (EP) that match clinical observation with high fidelity, referred to as cardiac digital twins (CDTs), show promise as a tool for tailoring cardiac precision therapies. Building CDTs of cardiac EP relies on the ability of models to replicate the ventricular activation sequence under a broad range of conditions. Of pivotal importance is the His–Purkinje system (HPS) within the ventricles. Workflows for the generation and incorporation of HPS models are needed for use in cardiac digital twinning pipelines that aim to minimize the misfit between model predictions and clinical data such as the 12 lead electrocardiogram (ECG). We thus develop an automated two stage approach for HPS personalization. A fascicular-based model is first introduced that modulates the endocardial Purkinje network. Only emergent features of sites of earliest activation within the ventricular myocardium and a fast-conducting sub-endocardial layer are accounted for. It is then replaced by a topologically realistic Purkinje-based representation of the HPS. Feasibility of the approach is demonstrated. Equivalence between both HPS model representations is investigated by comparing activation patterns and 12 lead ECGs under both sinus rhythm and right-ventricular apical pacing. Predominant ECG morphology is preserved by both HPS models under sinus conditions, but elucidates differences during pacing.

Key factors behind autofluorescence changes caused by ablation of cardiac tissue

Radiofrequency ablation is a commonly used clinical procedure that destroys arrhythmogenic sources in patients suffering from atrial fibrillation and other types of cardiac arrhythmias. To improve the success of this procedure, new approaches for real-time visualization of ablation sites are being developed. One of these promising methods is hyperspectral imaging, an approach that detects lesions based on changes in the endogenous tissue autofluorescence profile. To facilitate the clinical implementation of this approach, we examined the key variables that can influence ablation-induced spectral changes, including the drop in myocardial NADH levels, the release of lipofuscin-like pigments, and the increase in diffuse reflectance of the cardiac muscle beneath the endocardial layer. Insights from these experiments suggested simpler algorithms that can be used to acquire and post-process the spectral information required to reveal the lesion sites. Our study is relevant to a growing number of multilayered clinical targets to which spectral approaches are being applied.

Atrial Ectopy Increases Asynchronous Activation of the Endo- and Epicardium at the Right Atrium

The predisposition of atrial extrasystoles (AES) to trigger cardiac tachyarrhythmia may arise from intramural conduction disorders causing endo-epicardial asynchrony (EEA). This study aimed to determine whether spontaneous AES disturb endo-epicardial conduction. Simultaneous endo-epicardial mapping of the right atrium was performed in patients during cardiac surgery with two 128-electrode arrays. Sixty spontaneous AES were observed in 23 patients and were analyzed for incidence of conduction delay, conduction block and amount of EEA compared to the previous sinus rhythm beat. Both conduction delay and block occurred more often in AES compared to sinus rhythm. The difference in lines of conduction block between the epicardium and endocardium increased in AES causing a greater imbalance of conduction disorders between the layers. The incidence of EEA with differences ≥10 ms increased significantly in AES. AES caused delays between the epicardium and endocardium up to 130 ms and EEA to increase for up to half (47%) of the mapping area. Conduction disturbances between the epicardial and endocardial layer giving rise to EEA increase during AES. Asynchronous activation of the atrial layers increases during AES which may be a mechanism for triggering cardiac tachyarrhythmia under the right conditions but EEA cannot be recognized by current mapping tools.

Assessment of Strain Changes in the Triple Layers of Left Ventricle in Normotensive Versus Hypertensive Patients

The phenomenon of left ventricular remodeling caused by hypertension is a well-known affair that can be evaluated through echocardiography techniques. In recent decade, modern echocardiographic methods such as speckle tracking echocardiography have been used to evaluate left ventricular mechanical changes in hypertensive conditions. The evaluation of the strain index as an important part of the evaluation of the ventricular wall in various ventricular layers has been highly regarded in hypertensive patients. In this regard, the left global ventricular longitudinal strain (GLS) especially in the three ventricular wall layers can strongly predict mortality and morbidity of cardiovascular disease. Given that hypertensive disease is one of the most important risk factors for the development of heart failure and systolic and diastolic cardiovascular dysfunction, even in cases with preserved left ventricular ejection fraction, the exact determination of ventricular strain changes in various layers in hypertensive states would be beneficial for preventing hypertensive cardiomyopathy. In a cross-sectional study, we assessed strain changes in the triple layers of the ventricular wall in hypertensive and normotensive individuals with presence or absence of left ventricular diastolic dysfunction. In this study, both global longitudinal strain (GLS) and global circumferential strain (GCS) indices in endocardial, myocardial and epicardial layers were evaluated. We also considered the effect of diastolic ventricular dysfunction as an important confounder with the effect of hypertension on the ventricular strain. An important finding of this study was the significant effect of hypertension on reducing GLS and GCS in mid myocardial and epicardial layers in the presence of left ventricular diastolic dysfunction. At first, in case of hypertension, the presence of diastolic dysfunction in reducing the strain of the left ventricular wall seems to be necessary as a trigger factor; thus in hypertensive cases with preserved diastolic function, the strain change in left ventricular wall may not be evident. Secondly, reduction in the ventricular wall strain in the endocardial layer was not revealed but it seems that the exacerbation of uncontrolled hypertension may also lead to endocardial involvement as shown by prior studies. In total, proper control of blood pressure in patients with a history of hypertension, especially in the field of left ventricular diastolic dysfunction will improve the function of the left ventricular wall and thus improve the prognosis of these patients.Disturbance in left ventricle wall layers in the field of hypertension has been studied and confirmed in several studies, although the effective role of diastolic dysfunction has been studied less. For instance, in a study by Tadic et al., GLS was significantly lower in hypertensive than in normotensive patients (1). In Navarini et al study, although no difference was found in left ventricular volume or ejection fraction, both GLS and GCS reduced significantly in hypertensive status (2). In a study by Craciunescu et al, LV mass was higher and both the GLS and GCS parameters were significantly lower in the uncontrolled hypertension group than in patients with controlled hypertension (3). In a study by Nagata et al., the values of GLS and GCS in the endocardial layer were higher than the other layers, and this could justify the preservation of the strain in the field of hypertension in the endocardial layer (4). Finally, in a study by Sharif et al, patients with diastolic dysfunction experienced a relative decrease in GLS in all three layers of myocardial infarction, compared with those without diastolic dysfunction, which was consistent with our findings (5). What can be emphasized as the final result is that prolonged and uncontrolled hypertension with an effect on cell growth as well as cardiomyocyte fibrosis through the secretion of inflammatory and growth factors leading left ventricular hypertrophy can reduce strain in various ventricular wall layers particularly in myocardial and epicardial layers. Of course, the role of the presence of diastolic ventricular dysfunction is highly indicative in these changes.

570 Myocardial deformation imaging after STEMI: can we better predict one-year mortality and heart failure development?

Prognosis after STEMI is still challenging. One-year mortality ranges between 10-12% and the incidence of heart failure (HF) is between 4% and 28%. Early and accurate identification of high-risk patients necessitates therapy intensification. Aim this study is a part of PREDICT-VT study (NCT03263949). The aim was to test whether deformation imaging based on spackle tracking echocardiography predict MACE (total mortality, HF hospitalization and NYHA class ≥3 development) better than conventional echocardiography and clinical parameters. Methods in 264 consecutive pts enrolled in PREDICT-VT study early echocardiography (5 ± 2 days after pPCI) was done including LA and multilayer LV deformation analysis with longitudinal (L), radial (R) and circumferential (C) strain (S; %) and strain rate (SR, 1/sec). LV index of post systolic shortening for longitudinal (PSS LS) and circumferential (PSS CS) strain were calculated as average of PSS over 18 LV segments. Results 198 patients completed 1-year follow-up and 22 patients (11.1%) experienced MACE. Significant echo, clinical and laboratory predictors with the ROC analysis are listed in the table according to AUC . Conclusion peak systolic longitudinal and to a lesser degree peak systolic circumferential deformation predict mortality and HF development after pPCI better than conventional echo and even clinical parameters. From diastolic parameters only radial SR during atrial contraction was better MACE predictor compared to conventional echocardiography. AUC p Cut-off Senz Spec Peak systolic LS epicardial layer 0.757 <0.001 -11 75 63 Radial SR during atrial contraction 0.754 <0.001 -0.63 65 80 Peak systolic LS mid-wall layer 0.750 <0.001 -12.58 80 60 PSS LS endocardial layer 0.744 <0.001 0.1409 70 61 Peak systolic CS endocardial layer 0.744 <0.001 -18.08 70 67 Wall Motion Score Index 0.740 0.001 1.53 70 70 Peak systolic CS mid-wall layer 0.730 0.001 -13.66 80 60 Peak radial LV strain 0.722 0.001 14.08 80 60 Creatine kinase peak level 0.698 0.003 2155 64 73 LV EF 0.692 0.004 47.5 67 60 TAPSE 0.685 0.015 1.95 75 60 LA strain 0.676 0.012 18.33 63 64 Killip class 0.644 0.028

Deep septal deployment of a thin, lumenless pacing lead: a translational cadaver simulation study

Aims The recently introduced technique of direct transseptal pacing of the left bundle branch is poorly characterized with many questions with regard to the optimal implantation strategy and safety concerns largely left unanswered. We developed a cadaver model for deep septal lead deployment in order to investigate the depth of penetration in relation to lead behaviour, lead tip position, and the number of rotations. Methods and results Five fresh human hearts and five lumenless, 4.1-Fr pacing leads were used for deep septal deployment simulations. The leads were positioned with the use of a dedicated delivery sheath and screwed into the interventricular septum at several sites progressively more distal from the atrioventricular ring with a predetermined number of lead rotations. During each lead deployment, the depth of tip penetration was measured and the lead behaviour was noted. Four distinct lead behaviours were observed: (i) helix only penetration, no matter how many rotations were performed, due to the ‘endocardial entanglement effect’ (43.1% cases) or (ii) ‘endocardial barrier effect’ (19.6% cases), (iii) shallow/moderate penetration, with ensuing ‘drill effect’ when more rotations were added (9.8% cases), and (iv) deep progressive penetration with each additional rotation, occurring when the ‘screwdriver effect’ was present (27.4% cases, including three septal perforations). These different lead behaviours seemed to be determined by the lead position—mainly the strength of the initial endocardial layer—and the number of fully transmitted rotations. Conclusion New insights into deep septal lead deployment technique were gained with regard to safe and successful implantation.

Impact of apical foreshortening on deformation measurements: a report from the EACVI-ASE Strain Standardization Task Force

Aims Foreshortening of apical views is a common problem in echocardiography. It results in an abnormally thick false apex and a shortened left ventricular (LV) long axis. We sought to evaluate the impact of foreshortened (FS) on LV ejection fraction (LVEF) and layer-specific 2D speckle tracking based segmental (S) and global (G) longitudinal strain (LS) measurements. Methods and results We examined 72 participants using a GE Vivid E9 system. FS apical views were collected from an imaging window one rib-space higher than the optimal images. Ejection fraction as well as layer-specific GLS and SLS measurements were analysed by GE EchoPAC v201 and TomTec Image Arena 4.6 and compared between optimal and FS images. On average, LV long axis was 10% shorter in FS images than in optimal images. FS induced a relative change in LVEF of 3.3% and 6.9% for GE and TomTec, respectively (both, P < 0.001). Endocardial GLS was 9.0% higher with GE and 23.2% with TomTec (P < 0.001). Midwall GLS measurements were less affected (7.8% for GE and 14.1% for TomTec, respectively, both P < 0.001). Segmental strain analysis revealed that the mid-ventricular and apical segments were more affected by foreshortening, and endocardial measurements were more affected than midwall. Conclusion Optimal image geometry is crucial for accurate LV function assessment. Foreshorhening of apical views has a substantial impact on longitudinal strain measurements, predominantly in the apex and in the endocardial layer. Our data suggest that measuring midwall strain might therefore be the more robust approach for clinical routine use.

Intramyocardial dissecting haematoma mimicking left ventricular clot, a rare complication of myocardial infarction: a case report

Background Intramyocardial dissecting haematoma is a rare complication of myocardial infarction (MI) associated with high mortality rates. Studies and research of this occurrence are limited largely to isolated case reports or case series. Case summary We report a case of late presenting MI, where on initial echocardiogram had what was thought to be an intraventricular clot. However, upon further evaluation, the patient actually had an intramyocardial haematoma, with the supporting echocardiographic features to distinguish it from typical left ventricular (LV) clot. While this prevented the patient from receiving otherwise unnecessary anticoagulation, this diagnosis also put him at a much higher risk of mortality. Despite exhaustive medical and supportive management, death as consequence of pump failure occurred after 2 weeks. Discussion This report highlights the features seen on echocardiography which support the diagnosis of an intramyocardial haematoma rather than an LV clot, notably the various acoustic densities, a well visualized myocardial dissecting tear leading into a neocavity filled with blood, and an independent endocardial layer seen above the haematoma. Based on this report, we wish to highlight the importance of differentiating intramyocardial haematomas from intraventricular clots in patients with recent MI.