Search

Abstract Introduction Chimeric antigen receptor T‐cell (CAR‐T) therapy is highly effective in B‐cell blood cancers, but there is limited data on its safety and efficacy in intra‐cardiac lymphoma, due to the potential risks of cardiotoxicity and pseudo‐progression. Discussion We discuss four high‐risk cases that were managed with a multi‐disciplinary approach, including baseline cardiac risk assessment and surveillance with multimodal cardiac imaging and serum cardiac biomarkers, elective supportive care in the intensive care unit, and early treatment of cytokine release syndrome. Conclusion CAR‐T therapy can be effective and safe in the treatment of B‐cell blood cancers with intra‐cardiac disease.

Background Cardiac screening of elite athletes is widely recommended by Australasian sporting federations, but data are not structured to be shared. Data are lacking from underrepresented groups to inform ECG interpretation guidelines. The ARENA (Australasian Registry of Screening ECGs in National Athletes) project is a retrospective and prospective, multicenter, longitudinal, observational registry of athlete cardiac screening results and outcomes. The aim is to create a repository to improve our understanding of the diagnoses and outcomes of screening. Methods Participating sports that conduct cardiac screening of athletes will contribute data. This includes an initial collection (retrospective data, waiver of consent) and future prospective data (opt‐out consent). Data include sex, age, sport/event, screening date, ECG findings, cardiac test results, follow‐up details, sport participation status, cardiac diagnoses, and major cardiovascular outcomes defined as sudden cardiac arrest/death, cardiac syncope or implanted cardioverter defibrillator shock, cardiac hospitalization, and arrhythmias requiring intervention. Comparisons will be made between diagnoses, outcomes, and ECG features and analyzed by sport and sex. The ARENA project was developed in collaboration with sporting bodies, team physicians, and players association representatives and endorsed by the Australasian College of Sport & Exercise Physicians and Sports Medicine Australia. Conclusions The ARENA project will provide a long‐term international data repository to improve our understanding of ECG interpretation, cardiac screening and diagnoses, and the prevalence of cardiovascular outcomes in screened athletes. A unique aim is to address evidence gaps in underrepresented athlete groups, specifically female athletes and Indigenous populations. Results will inform screening policies and guidelines.

Background: Despite historically being considered a channelopathy, subtle structural changes have been reported in Brugada syndrome (BrS) on histopathology and cardiac magnetic resonance (CMR) imaging. It is not known if these structural changes progress over time. Objective: The study sought to assess if structural changes in BrS evolve over time with serial CMR assessment and to investigate the utility of parametric mapping techniques to identify diffuse fibrosis in BrS. Methods: Patients with a diagnosis of BrS based on international guidelines and normal CMR at least 3 years prior to the study period were invited to undergo repeat CMR. CMR images were analyzed de novo and compared at baseline and follow-up. Results: Eighteen patients with BrS (72% men; mean age at follow-up 47.4 ± 8.9 years) underwent serial CMR with an average of 5.0 ± 1.7 years between scans. No patients had late gadolinium enhancement (LGE) on baseline CMR, but 4 (22%) developed LGE on follow-up, typically localized to the right ventricular (RV) side of the basal septum. RV end-systolic volume increased over time (P = .04) and was associated with a trend toward reduction in RV ejection fraction (P = .07). Four patients showed a reduction in RV ejection fraction >10%. There was no evidence of diffuse myocardial fibrosis observed on parametric mapping. Conclusions: Structural changes may evolve over time with development of focal fibrosis, evidenced by LGE on CMR in a significant proportion of patients with BrS. These findings have implications for our understanding of the pathological substrate in BrS and the longitudinal evaluation of patients with BrS.

Abstract Background Computational fluid dynamics (CFD) is increasingly used for the assessment of blood flow conditions in patients with congenital heart disease (CHD). This requires patient-specific anatomy, typically obtained from segmented 3D cardiovascular magnetic resonance (CMR) images. However, segmentation is time-consuming and requires expert input. This study aims to develop and validate a machine learning (ML) method for segmentation of the aorta and pulmonary arteries for CFD studies. Methods 90 CHD patients were retrospectively selected for this study. 3D CMR images were manually segmented to obtain ground-truth (GT) background, aorta and pulmonary artery labels. These were used to train and optimize a U-Net model, using a 70-10-10 train-validation-test split. Segmentation performance was primarily evaluated using Dice score. CFD simulations were set up from GT and ML segmentations using a semi-automatic meshing and simulation pipeline. Mean pressure and velocity fields across 99 planes along the vessel centrelines were extracted, and a mean average percentage error (MAPE) was calculated for each vessel pair (ML vs GT). A second observer (SO) segmented the test dataset for assessment of inter-observer variability. Friedman tests were used to compare ML vs GT, SO vs GT and ML vs SO metrics, and pressure/velocity field errors. Results The network’s Dice score (ML vs GT) was 0.945 (interquartile range: 0.929–0.955) for the aorta and 0.885 (0.851–0.899) for the pulmonary arteries. Differences with the inter-observer Dice score (SO vs GT) and ML vs SO Dice scores were not statistically significant for either aorta or pulmonary arteries (p = 0.741, p = 0.061). The ML vs GT MAPEs for pressure and velocity in the aorta were 10.1% (8.5–15.7%) and 4.1% (3.1–6.9%), respectively, and for the pulmonary arteries 14.6% (11.5–23.2%) and 6.3% (4.3–7.9%), respectively. Inter-observer (SO vs GT) and ML vs SO pressure and velocity MAPEs were of a similar magnitude to ML vs GT (p > 0.2). Conclusions ML can successfully segment the great vessels for CFD, with errors similar to inter-observer variability. This fast, automatic method reduces the time and effort needed for CFD analysis, making it more attractive for routine clinical use.

Abstract The Pfizer COVID-19 vaccine is associated with increased myocarditis incidence. Constantly evolving evidence regarding incidence and case fatality of COVID-19 and myocarditis related to infection or vaccination, creates challenges for risk-benefit analysis of vaccination. Challenges are complicated further by emerging evidence of waning vaccine effectiveness, and variable effectiveness against variants. Here, we build on previous work on the COVID-19 Risk Calculator (CoRiCal) by integrating Australian and international data to inform a Bayesian network that calculates probabilities of outcomes for the delta variant under different scenarios of Pfizer COVID-19 vaccine coverage, age groups (≥12 years), sex, community transmission intensity and vaccine effectiveness. The model estimates that in a population where 5% were unvaccinated, 5% had one dose, 60% had two doses and 30% had three doses, there was a substantially greater probability of developing (239–5847 times) and dying (1430–384,684 times) from COVID-19-related than vaccine-associated myocarditis (depending on age and sex). For one million people with this vaccine coverage, where transmission intensity was equivalent to 10% chance of infection over 2 months, 68,813 symptomatic COVID-19 cases and 981 deaths would be prevented, with 42 and 16 expected cases of vaccine-associated myocarditis in males and females, respectively. These results justify vaccination in all age groups as vaccine-associated myocarditis is generally mild in the young, and there is unequivocal evidence for reduced mortality from COVID-19 in older individuals. The model may be updated to include emerging best evidence, data pertinent to different countries or vaccines and other outcomes such as long COVID.

The coronary microcirculation plays a cardinal role in regulating coronary blood flow to meet the changing metabolic demands of the myocardium. Coronary microvascular dysfunction (CMD) refers to structural and functional remodeling of the coronary microcirculation. CMD plays a role in the pathogenesis of obstructive and non-obstructive coronary syndromes as well as myocardial diseases, including heart failure with preserved ejection fraction (HFpEF). Despite recent diagnostic advancements, CMD is often under-appreciated in clinical practice, and may allow for the development of novel therapeutic targets. This review explores the diagnosis and pathogenic role of CMD across a range of cardiovascular diseases, its prognostic significance, and the current therapeutic landscape.

Background: Despite developments in surgical techniques and medical care, people with a Fontan circulation still experience long-term complications; non-invasive therapies to optimize the circulation have not been established. Exercise intolerance affects the majority of the population and is associated with worse prognosis. Historically, people living with a Fontan circulation were advised to avoid physical activity, but a small number of heterogenous, predominantly uncontrolled studies have shown that exercise training is safe—and for unique reasons, may even be of heightened importance in the setting of Fontan physiology. The mechanisms underlying improvements in aerobic exercise capacity and the effects of exercise training on circulatory and end-organ function remain incompletely understood. Furthermore, the optimal methods of exercise prescription are poorly characterized. This highlights the need for large, well-designed, multi-center, randomized, controlled trials.Aims and Methods: The Fontan Fitness Intervention Trial (F-FIT)—a phase III clinical trial—aims to optimize exercise prescription and delivery in people with a Fontan circulation. In this multi-center, randomized, controlled study, eligible Fontan participants will be randomized to either a 4-month supervised aerobic and resistance exercise training program of moderate-to-vigorous intensity followed by an 8-month maintenance phase; or usual care (control group). Adolescent and adult (≥16 years) Fontan participants will be randomized to either traditional face-to-face exercise training, telehealth exercise training, or usual care in a three-arm trial with an allocation of 2:2:1 (traditional:telehealth:control). Children (

The coronavirus pandemic has given everyone in society an education on the harms of spread of respiratory illness. Young healthy athletes are far less likely to suffer severe adverse consequences of viral illnesses than the elderly and frail, but they are not completely immune. Chronic fatigue (overtraining) is an uncommon outcome and myocarditis a rare one, but they both warrant due consideration. It is, therefore, a sensible individual strategy to ‘stay home when sick’ if only for these risks. Traditionally though, athletes have tended to push through (train and play when ill) because of competing concerns, such as key events/matches and ‘not wanting to let teammates down’. Data from both low COVID-19 and high COVID-19 countries show that the number of cardiovascular deaths in a society correlates with the number of respiratory deaths at the same time, further linking respiratory viruses to cardiovascular deaths. We are now more aware of public health obligations to prevent the spread of respiratory illnesses, in particular to protect the more vulnerable members the community. This hopefully will correspond with a change in the culture of sport to one where it is considered ‘the right thing to do’, to ‘stay home when sick’.

Abstract Background The Task Force Criteria (TFC) for arrhythmogenic right ventricular cardiomyopathy (ARVC) was updated in 2010 to improve specificity. There was concern however that the revised cardiovascular magnetic resonance (CMR) criteria was too restrictive and not sensitive enough to detect early forms of the condition. We previously described patients with clinically suspected ARVC who satisfied criteria from non-imaging TFC categories and fulfilled parameters from the original but not the revised CMR criteria; as a result, these patients were not confirmed as definite ARVC but may represent an early phenotype. Methods Patients scanned between 2008 and 2015 who had either right ventricular (RV) dilatation or regional dyskinesia satisfying at least minor imaging parameters from the original criteria and without contra-indication underwent serial CMR scanning using a 1.5 T scanner. The aims were to assess the risk of progressive RV abnormalities, evaluate the accuracy of the revised CMR criteria and the need for guideline directed CMR surveillance in at-risk individuals. Results Overall, 48 patients were re-scanned; 24 had a first-degree relative diagnosed with ARVC using the revised TFC or a first-degree relative with premature sudden death from suspected ARVC and 24 patients had either left bundle branch morphology ventricular tachycardia or > 500 ventricular extra-systoles in 24-h. Mean follow up was 69+/− 25 months. The indexed RV end-diastolic, end-systolic volumes and ejection fraction were calculated for both scans. There was significant reduction in RV volumes and improvement in RV ejection fraction (EF) irrespective of changes to body surface area; − 11.7+/− 15.2 mls/m2, − 6.4+/− 10.5 mls/m2 and + 3.3 +/− 7.9% (p = 0.01, 0.01 and 0.04). Applying the RV parameters to the revised CMR criteria, two patients from the family history group (one with confirmed ARVC and one with a premature death) had progressive RV abnormalities satisfying major criteria. The remaining patients (n = 46) did not satisfy the criteria and either had normal RV parameters with regression of structural abnormalities (27,56.3%) or stable abnormalities (19,43.7%). Conclusion The revised CMR criteria represents a robust tool in the evaluation of patients with clinical suspicion of ARVC, especially for those with ventricular arrhythmias without a family history for ARVC. For patients with RV abnormalities that do not fulfill the revised criteria but have a family history of ARVC or an ARVC associated gene mutation, a surveillance CMR scan should be considered as part of the clinical follow up protocol.

Atherosclerosis, which is a primary cause of cardiovascular disease (CVD) deaths around the world, is a chronic inflammatory disease that is characterised by the accumulation of lipid plaques in the arterial wall, triggering inflammation that is regulated by cytokines/chemokines that mediate innate and adaptive immunity. This review focuses on IL-32, -34 and -37 in the stable vs. unstable plaques from atherosclerotic patients. Dysregulation of the novel cytokines IL-32, -34 and -37 has been discovered in atherosclerotic plaques. IL-32 and -34 are pro-atherogenic and associated with an unstable plaque phenotype; whereas IL-37 is anti-atherogenic and maintains plaque stability. It is speculated that these cytokines may contribute to the explanation for the increased occurrence of atherosclerotic plaque rupture seen in patients with COVID-19 infection. Understanding the roles of these cytokines in atherogenesis may provide future therapeutic perspectives, both in the management of unstable plaque and acute coronary syndrome, and may contribute to our understanding of the COVID-19 cytokine storm.

The increasing prevalence of congenital heart disease (CHD) can be attributed to major improvements in diagnosis and treatment. Although echocardiography is the most commonly used imaging modality for diagnosis and follow up of subjects with CHD, the evolution of both cardiovascular magnetic resonance (MR) imaging and computed tomography (CT) does offer new ways to visualize the heart and the great vessels. The development of cardiovascular MR techniques such as spinecho and gradient-echo imaging, velocity-encoded phase contrast MR and gadolinium-enhanced MR angiography allow comprehensive assessment of cardiac anatomy and function. This provides information about the long-term sequelae of the underlying complex anatomy, hemodynamic assessment of residual post-operative lesions and complications of surgery. As much of the functional data in CHD patients is usually acquired with invasive X-ray angiography, non-invasive alternatives such as cardiovascular MR and CT are desirable. This review evaluates the role of both these modalities in the management of subjects with CHD, particularly detailing recent developments in imaging techniques as they relate to the various CHD diagnoses we commonly encounter in our practice.

Left ventricular non-compaction (LVNC) is a complex clinical condition with no diagnostic gold standard. At present, there is trepidation about the accuracy of the diagnosis, the correlation to clinical outcomes and the long-term medical management. This article reviews the current imaging criteria, the limitations of echocardiography and cardiac magnetic resonance and the consequences of LV hypertrabeculation in athletes.

Increasing evidence suggests the presence of structural changes affecting the right ventricular outflow tract (RVOT) in patients with Brugada Syndrome (BrS). The aim of this study was to characterise the RV morphology in BrS and explore associations between morphologic, clinical, electrical, and genetic parameters using non-invasive multimodality testing.Consecutive BrS patients (recruited 2013-2015) underwent clinical assessment, dedicated RV imaging using cardiac magnetic resonance (CMR) imaging (unless contra-indicated), electrical assessment (electrocardiogram, Holter monitoring, signal-averaged ECG[SAECG]) and genotyping. Morphologic data were compared to matched control and unmatched ARVC (arrhythmogenic right ventricular cardiomyopathy) cohorts, and potential associations between morphologic parameters and other variables were explored.BrS patients (n = 42, male 86%, age 46±12 years) exhibited normal global RV volume and function, comparable to control, in contrast to significantly larger, impaired RVs in ARVC cohort (RVESV p = 0.0001; RVEDV p

Sinus venosus atrial septal defects (SV-ASDs) are inter-atrial communications caused by a deficiency of the common wall between the superior or inferior vena cava and the right-sided pulmonary veins. The diagnosis can be challenging, especially in adults with delayed presentation. We present images that illustrate an example of the role of cardiac magnetic resonance imaging (CMRI) in the diagnosis and follow-up of a patient with SV-ASD.