Hypertrophic cardiomyopathy is a common yet under-recognized genetic structural heart condition characterized by left ventricular hypertrophy. Patients may present with obstructive disease characterized by an elevated left ventricular outflow tract gradient or non-obstructive disease. Long established medical and surgical treatment options for patients with obstructive hypertrophic cardiomyopathy and refractory symptoms can be effective in eliminating outflow tract gradients and improving symptoms. Cardiac myosin inhibitors have emerged as a new class of evidence based medical therapy for patients with obstructive hypertrophic cardiomyopathy and an alternative to septal reduction therapies. However, effective treatments for patients with non-obstructive hypertrophic cardiomyopathy remain limited, with several clinical trials ongoing. Variants in cardiac sarcomeric genes are the primary genetic cause of hypertrophic cardiomyopathy and are being investigated as targets for gene based therapies. Stratification of the risk of sudden death is an important component of caring for patients with hypertrophic cardiomyopathy. Recommendations for implantable cardioverter-defibrillator implantation are based on well validated risk factors in combination with shared decision making. Atrial fibrillation is common in patients with hypertrophic cardiomyopathy, and anticoagulation is strongly recommended for stroke prevention. Rhythm control is essential for patients with symptomatic atrial fibrillation. Historically, vigorous exercise has been restricted; however, newer data suggest that the arrhythmic risk is less than previously thought and emphasize an individualized approach. Advanced heart failure is an uncommon but important cause of morbidity and mortality. Early identification is key to improving outcomes with advanced therapies including cardiac transplantation. The management of hypertrophic cardiomyopathy is rapidly evolving toward a more personalized approach, based on genotype and phenotype, to alter disease progression and improve patients' outcomes.

The feasibility and impact of high intensity exercise programmes in patients with hypertrophic cardiomyopathy (HCM) are unknown. This study was conducted to determine the feasibility of a high intensity exercise programme and explore safety and efficacy outcomes in patients with HCM.

Participants were randomized to a 12-week supervised exercise programme (n = 40) in addition to usual care, or usual care alone (n = 40). All participants underwent assessment at baseline and 12 weeks. The exercise group was re-evaluated 6 months post-programme. Feasibility was assessed by (i) recruitment, adherence, and retention rates; (ii) staffing ratios; (iii) logistics; and (iv) acceptability of the intervention. The primary exploratory safety outcome was a composite of arrhythmia-related events. Exploratory secondary outcomes included changes in (i) cardiorespiratory fitness; (ii) cardiovascular risk factors; and (iii) quality of life, anxiety, and depression scores.

Overall, 67 (84%) participants completed the study (n = 34 and n = 33 in the exercise and usual care groups, respectively). Reasons for non-adherence included travel, work, and family commitments. Resource provision complied with national cardiac rehabilitation standards. There was no difference between groups for the exploratory safety outcome (P = .99). At 12 weeks, the exercise group had a greater increase in peak oxygen consumption (VO2) [+4.1 mL/kg/min, 95% confidence interval (CI) 1.1, 7.1] and VO2 at anaerobic threshold (+2.3 mL/kg/min, 95% CI 0.4, 4.1), lower systolic blood pressure (-7.3 mmHg, 95% CI -11.7, -2.8) and body mass index (-0.8 kg/m2, 95% CI -1.1, -0.4), and greater improvement in hospital anxiety (-3, 95% CI -4.3, -1.7) and depression (-1.7, 95% CI -2.9, -0.5) scores, compared to the usual care group. Most exercise gains dissipated at 6 months.

A high intensity exercise programme is feasible in patients with HCM, with apparent cardiovascular and psychological benefits, and no increase in arrhythmias. A large-scale study is required to substantiate findings and assess long-term safety of high intensity exercise in HCM.

Exercise parameters can be altered in children with congenital heart disease or acquired heart disease compared with children with normal hearts. Exercise testing has proven a useful tool to predict patient outcomes and even the need for reintervention in several cardiovascular disease processes. There are established guidelines for serial exercise stress testing in adults with congenital heart disease, but corollary guidelines do not exist for the pediatric population.

A narrative literature review was completed. Evidence was ranked by a 4-point scale as outlined by the American College of Sports Medicine evidence categories. A survey was sent to experts in pediatric exercise physiology across the country regarding their current testing practices for 26 unique congenital heart disease or known or suspected acquired heart disease lesions. Survey questions were related to the frequency of testing, the age at which exercise testing is started, and if the frequency of testing is altered by a patient presenting with symptoms. Our literature search yielded 122 relevant studies pertaining to exercise stress testing in pediatric heart disease. We received 59 responses to our survey from 33 unique institutions in the United States and Canada.

Twenty-one summaries were provided regarding exercise stress testing in pediatric patients with heart disease. Multicentered or national stress testing registries may allow for adequate sample sizes of rare pediatric diseases to allow for development of improved guidelines regarding the type and timing of stress testing.

Inflammatory cardiomyopathy is a condition that is characterised by the presence of inflammatory cells in the myocardium, which can lead to a significant deterioration in cardiac function. The etiology of this condition involves multiple factors, both infectious and non-infectious causes. While it is primarily associated with viral infections, other potential causes include bacterial, protozoal, or fungal infections, as well as a wide variety of toxic substances and drugs, and systemic immune-mediated pathological conditions. In spite of comprehensive investigation, the presence of inflammatory cardiomyopathy accompanied by left ventricular dysfunction, heart failure or arrhythmia is indicative of an unfavourable outcome. The reasons for the occurrence of either favourable outcomes, characterised by the absence of residual myocardial injury, or unfavourable outcomes, marked by the development of dilated cardiomyopathy, in patients afflicted by the condition remain to be elucidated. The relative contributions of pathogenic agents, genomic profiles of the host, and environmental factors in disease progression and resolution remain subjects of ongoing discourse. This includes the determination of which viruses function as active inducers and which merely play a bystander role. It remains unknown which changes in the host immune profile are critical in determining the outcome of myocarditis caused by various viruses, including coxsackievirus B3 (CVB3), adenoviruses, parvoviruses B19 and SARS-CoV-2. The objective of this review is unambiguous: to provide a concise summary and comprehensive assessment of the extant evidence on the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy. Its focus is exclusively on virus-induced and virus-associated myocarditis. In addition, the extant lacunae of knowledge in this field are identified and the extant experimental models are evaluated, with the aim of proposing future directions for the research domain. This includes differential gene expression that regulates iron and lipid and metabolic remodelling. Furthermore, the current state of knowledge regarding the cardiovascular implications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is also discussed, along with the open questions that remain to be addressed.

Larry A. Allen, MD, MHS, FAHA, FACC; Mats Börjesson, MD, PhD, FACC; Alan C. Braverman, MD, FACC; Julie A. Brothers, MD; Silvia Castelletti, MD, MSc, FESC; Eugene H. Chung, MD, MPH, FHRS, FAHA, FACC; Timothy W. Churchill, MD, FACC; Guido Claessen, MD, PhD; Flavio D'Ascenzi, MD, PhD; Douglas Darden, MD; Peter N. Dean, MD, FACC; Neal W. Dickert, MD, PhD, FACC; Jonathan A. Drezner, MD; Katherine E. Economy, MD, MPH; Thijs M.H. Eijsvogels, PhD; Michael S. Emery, MD, MS, FACC; Susan P. Etheridge, MD, FHRS, FAHA, FACC; Sabiha Gati, BSc (Hons), MBBS, PhD, MRCP, FESC; Belinda Gray, BSc (Med), MBBS, PhD; Martin Halle, MD; Kimberly G. Harmon, MD; Jeffrey J. Hsu, MD, PhD, FAHA, FACC; Richard J. Kovacs, MD, FAHA, MACC; Sheela Krishnan, MD, FACC; Mark S. Link, MD, FHRS, FAHA, FACC; Martin Maron, MD; Silvana Molossi, MD, PhD, FACC; Antonio Pelliccia, MD; Jack C. Salerno, MD, FACC, FHRS; Ankit B. Shah, MD, MPH, FACC; Sanjay Sharma, BSc (Hons), MBChB, MRCP (UK), MD; Tamanna K. Singh, MD, FACC; Katie M. Stewart, NP, MS; Paul D. Thompson, MD, FAHA, FACC; Meagan M. Wasfy, MD, MPH, FACC; Matthias Wilhelm, MD.

This American Heart Association/American College of Cardiology scientific statement on clinical considerations for competitive sports participation for athletes with cardiovascular abnormalities or diseases is organized into 11 distinct sections focused on sports-specific topics or disease processes that are relevant when considering the potential risks of adverse cardiovascular events, including sudden cardiac arrest, during competitive sports participation. Task forces comprising international experts in sports cardiology and the respective topics covered were assigned to each section and prepared specific clinical considerations tables for practitioners to reference. Comprehensive literature review and an emphasis on shared decision-making were integral in the writing of all clinical considerations presented.

In the clinical setting of acute myocarditis, existing guidelines recommend refraining from moderate-intensity to high-intensity sports for 3-6 months, yet the extent to which these recommendations are implemented by clinicians and followed by patients remains unclear.

From January 2020 to December 2023, consecutive patients with myocarditis according to European Society of Cardiology criteria were prospectively enrolled. Myocarditis was categorised into acute, subacute and non-acute myocarditis. Patients completed a sports questionnaire and sports behaviour was categorised into no sports (NSP), recreational (REC) or competitive sports (COMP).

A total of 165 patients with myocarditis (mean age 50±17 years, 35% women) completed the questionnaire. Overall 73 (44%) patients received sports counselling. A total of 44 (72%) patients engaged in sports (REC+COMP) with acute or subacute myocarditis, received sports counselling with 38 (87%) adhering. Overall COMP patients (all male) received more counselling (11/11; 100%) compared with REC (53/105; 50%) and NSP (9/49; 18%). Of 39 women in the REC group, 14 (36%) received recommendations, whereas of 66 men 39 (59%) received recommendations (p<0.001). Of all patients engaged in sports, 55% received recommendations. Self-reported adherence to recommendations was significantly lower in COMP (73%) compared with REC (92%, p<0.001).

Although only half of the myocarditis patients received counselling regarding sports activity, adherence to these recommendations was generally high but varied by activity level. Women received fewer recommendations overall compared with men. While competitive athletes were counselled more frequently than recreational athletes, they were less likely to adhere to the recommendations.

Myocarditis is a potentially fatal complication of coronavirus disease 2019 (COVID-19), which is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. COVID-19 myocarditis appears to have distinct inflammatory characteristics that distinguish it from other viral etiologies. COVID-19 myocarditis can present with symptoms ranging from dyspnea and chest pain to acute heart failure and death. It is critical to detect any cases of myocarditis, especially fulminant myocarditis, which can be characterized by signs of heart failure and arrhythmias. Serial troponins, echocardiography, and electrocardiograms should be performed as part of the initial workup for suspected myocarditis. The second step in detecting myocarditis is cardiac magnetic resonance imaging and endomyocardial biopsy. Treatment for COVID-19 myocarditis is still debatable; however, combining intravenous immunoglobulins and corticosteroids may be effective, especially in cases of fulminant myocarditis. Overall, more research is needed to determine the incidence of COVID-19 myocarditis, and the use of intravenous immunoglobulins and corticosteroids in combination requires large randomized controlled trials to determine efficacy. The purpose of this review is to summarize current evidence on the subject.

The management of acute myocarditis (AM) is addressed in multiple clinical guidelines. We systematically reviewed current guidelines developed by national and international medical organizations on the management of AM to aid clinical practice. Publications in MEDLINE, EMBASE and Cochrane were identified between 1 January 2013 and 12 April 2024. Additionally, the websites of relevant organizations and the Guidelines International Network, Guideline Central, and NHS knowledge and library hub were reviewed. Two reviewers independently screened titles and abstracts, two reviewers assessed the rigour of guideline development, and one reviewer extracted the recommendations. Two of the three guidelines identified showed good rigour of development. Those rigorously developed agreed on the definition of AM, sampling serum troponin as part of the workflow for AM, testing for B-type natriuretic peptides in heart failure, key diagnostic imaging in the form of cardiovascular magnetic resonance, coronary angiography to exclude significant coronary disease, indications for endomyocardial biopsy (EMB), and indications for immunosuppression and advanced treatment options. Discrepancies exist in sampling creatine kinase-myocardial bound as a marker of myocardial injury, indications for EMB, and indications for immunosuppression and treatment of uncomplicated AM. Evidence is lacking for the use of 18F-Fluorodeoxyglucose Positron Emission Tomography for myocardial imaging, exercise restriction, follow-up measures, and genetic testing, and there are few high-quality randomized trials to support treatment recommendations. Recommendations for management of AM in the guidelines have largely been developed from expert opinion rather than trial data.

This systematic review aimed to review existing evidence to evaluate the effects of physical cardiac rehabilitation on cardio-pulmonary outcomes in the patients with hypertrophic cardiomyopathy (HCM).

We conducted a systematic search of the databases PubMed, Web of Science, Embase, Scopus, and Google Scholar. The initial search led to 1222 citations after removing duplicate results. We included only English-written studies published since 2013 (2013-2023). Ultimately, we retrieved five studies, involving 235 participants. We used the Cochrane Risk of Bias Tool for randomized trials (RoB2) and risk of bias in non-randomized studies of intervention (ROBINS-I) for evaluating the risk of bias in randomized and non-randomized studies, respectively.

Results showed that four training programs improved participants' functional capacity by up to 46%. Improvements in weight, BMI, echocardiography, and remodeling parameters (left atrium volume index, premature ventricular contraction burden, pulmonary artery systolic pressure), exercise test results (minute ventilation/carbon dioxide production, peak workload, heart rate reserve, exercise duration, peak heart rate, peak systolic pressure, and blood pressure response to exercise normalization), and a decrease in N- Terminal Pro-Brain Natriuretic Peptide (NT-pro BNP) were reported in these studies. No major adverse events, including sustained tachyarrhythmia, implantable cardioverter-defibrillator discharge, and sudden cardiac death were reported.

Supervised exercise training is safe and helpful for patients diagnosed with HCM. It can improve exercise capacity and is considered an adjunctive therapeutic option.

Hypertrophic cardiomyopathy (HCM) is traditionally associated with exercise restriction due to potential risks, yet recent evidence and guidelines suggest a more permissive stance for low-risk individuals. The aim of this comprehensive review was to examine existing research on the impact of exercise on cardiovascular outcomes, safety, and quality of life in this population and to consider implications for clinical practice. Recent studies suggest that regular exercise and physical activity in low-risk individuals with HCM are associated with positive outcomes in functional capacity, haemodynamic response, and quality of life, with consistent safety. Various studies highlight the safety of moderate-intensity exercise, showing improvements in exercise capacity without adverse cardiac remodelling or significant arrhythmias. Psychological benefits, including reductions in anxiety and depression, have been also reported following structured exercise programmes. These findings support the potential benefits of integrating individualised exercise regimens in the management of low-risk individuals with HCM, with the aim of improving their overall well-being and cardiovascular health. Adoption of the FITT (frequency, intensity, time, and type of exercise) principle, consideration of individual risk profiles, and shared decision-making are recommended. Future research is warranted to clarify the definition of 'low risk' for exercise participation and investigate the influence of physical activity on disease progression in HCM. Innovation in therapeutic strategies and lifestyle interventions, alongside improved patient and provider education, will help advance the care and safety of individuals with HCM engaging in exercise.

Myocarditis is a condition marked by inflammation of the heart muscle, which can lead to serious outcomes such as sudden cardiac death (SCD) and life-threatening arrhythmias. While myocarditis can affect any population, athletes, especially those engaged in high-intensity training, are at increased risk due to factors such as reduced immunity and increased exposure to pathogens. This review examines the clinical presentation, current guidelines, diagnostic challenges, and the significance of cardiac magnetic resonance imaging (CMR) in detecting myocardial inflammation and scarring. Current guidelines recommend a period of exercise restriction followed by thorough reassessment before athletes can return-to-play (RTP). However, there are several knowledge gaps, including the implications of persistent late gadolinium enhancement (LGE) on CMR and the optimal duration of exercise restriction. Additionally, the psychological impact of myocarditis on athletes highlights the importance of incorporating mental health support in the recovery process. A shared decision-making approach should be encouraged in RTP, considering the athlete's overall health, personal preferences, and the potential risks of resuming competitive sports. We have proposed an algorithm for RTP in athletes following myocarditis, incorporating CMR. Future research is warranted to refine RTP protocols and improve risk stratification, particularly through longitudinal studies that examine recovery and outcomes in athletes.

Myocarditis is a rare cardiomyocyte inflammatory process, typically caused by viruses, with potentially devastating cardiac sequalae in both competitive athletes and in the general population. Investigation into myocarditis prevalence in the Coronavirus disease 2019 (COVID-19) era suggests that infection with Severe acute respiratory syndrome coronavirus (SARS-CoV-2) is an independent risk factor for myocarditis, which is confirmed mainly through cardiovascular magnetic resonance imaging. Recent studies indicated that athletes have a decreased risk of myocarditis after recent COVID-19 infection compared to the general population. However, given the unique nature of competitive athletics with their frequent participation in high-intensity exercise, athletes possess distinct factors of susceptibility for the development of myocarditis and its subsequent severe cardiac complications (e.g., sudden cardiac death, fulminant heart failure, etc.). Under this context, this review focuses on comparing myocarditis in athletes versus non-athletes, owing special attention to the distinct clinical presentations and outcomes of myocarditis caused by different viral pathogens such as cytomegalovirus, Epstein-Barr virus, human herpesvirus-6, human immunodeficiency virus, and Parvovirus B19, both before and after the COVID-19 pandemic, as compared with SARS-CoV-2. By illustrating distinct clinical presentations and outcomes of myocarditis in athletes versus non-athletes, we also highlight the critical importance of early detection, vigilant monitoring, and effective management of viral and non-viral myocarditis in athletes and the necessity for further optimization of the return-to-play guidelines for athletes in the COVID-19 era, in order to minimize the risks for the rare but devastating cardiac fatality.

To investigate the burden of disease of myocarditis in Germany and identify similarities and differences in myocarditis with or without COVID-19.

All patients hospitalized with myocarditis in Germany were included in this nationwide retrospective analysis. Data were retrieved from the Federal Statistical Office of Germany (DESTATIS) for the years from 2007 to 2022. The primary endpoint was hospital mortality.

A total of 88,159 patients hospitalized with myocarditis were analyzed. Annual cases increased from 5100 in 2007 to 6593 in 2022 (p < 0.001 for trend) with higher incidence during winter months. Incidence per 100,000 inhabitants was 6.2 in 2007 rising to 7.8 in 2022 (p < 0.001 for trend). Hospital mortality remained constant at an average of 2.44% (p = 0.164 for trend). From 2020 to 2022, 1547/16,229 (9.53%) patients were hospitalized with both, myocarditis and COVID-19 (incidence 0.62/100,000 inhabitants and 180/100,000 hospitalizations with COVID-19). These patients differed significantly in most patient characteristics and had a higher rate of hospital mortality compared to myocarditis without COVID-19 (12.54% vs. 2.26%, respectively, p < 0.001).

Myocarditis hospitalizations were slowly rising over the past 16 years with hospital mortality remaining unchanged. Incidence of hospitalizations with combined myocarditis and COVID-19 was low, but hospital mortality was high.

Hypertrophic cardiomyopathy (HCM), a common genetic heart condition, is characterized by thickening of the left ventricle, which can result in a range of health issues, such as arrhythmias, heart failure, and sudden death. Despite traditional cautions against exercise in HCM patients due to potential exacerbation of symptoms and risk of sudden death, recent evidence suggests a paradigm shift toward the benefits of structured exercise rehabilitation. The pathogenesis of HCM, the physical and psychological effects of the illness on patients, and changing views on exercise as a therapeutic intervention are all covered in this review. Recent research shows that modest physical activity can considerably enhance functional ability, psychological health, and overall quality of life in individuals with heart failure without increasing the risk of unfavorable cardiac events, challenging earlier recommendations. Moreover, exercise rehabilitation has been shown to induce favorable myocardial remodeling and enhance cardiovascular fitness, suggesting a revaluation of exercise prescriptions tailored to individual patient profiles. Despite the promising role of exercise in managing HCM, this review also acknowledges the complexities of implementing rehabilitation programs, including the need for comprehensive patient assessment, personalized exercise regimens, and monitoring for potential complications. Future research should focus on optimizing exercise recommendations, understanding long-term outcomes, and integrating exercise rehabilitation into standard care protocols for HCM to foster a more holistic approach to patient management. Underscoring the necessity of a multidisciplinary strategy that balances the benefits of physical activity with the unique risks associated with HCM with the aim of improving patient outcomes through evidence-based, patient-centered care.

While pediatric myocarditis incidence has increased since the coronavirus disease 2019 (COVID-19) pandemic, there remain questions regarding diagnosis, risk stratification, and optimal therapy. This review highlights recent publications and continued unanswered questions related to myocarditis in children.

Emergence from the COVID-19 era has allowed more accurate description of the incidence and prognosis of myocarditis adjacent to COVID-19 infection and vaccine administration as well that of multi-system inflammatory disease in children (MIS-C). As cardiac magnetic resonance technology has shown increased availability and evidence in pediatric myocarditis, it is important to understand conclusions from adult imaging studies and define the use of this imaging biomarker in children. Precision medicine has begun to allow real-time molecular evaluations to help diagnose and risk-stratify cardiovascular diseases, with emerging evidence of these modalities in myocarditis.

Recent information regarding COVID-19 associated myocarditis, cardiac magnetic resonance, and molecular biomarkers may help clinicians caring for children with myocarditis and identify needs for future investigations.

The "2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy" provides recommendations to guide clinicians in the management of patients with hypertrophic cardiomyopathy.

A comprehensive literature search was conducted from September 14, 2022, to November 22, 2022, encompassing studies, reviews, and other evidence on human subjects that were published in English from PubMed, EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline. Additional relevant studies, published through May 23, 2023, during the guideline writing process, were also considered by the writing committee and added to the evidence tables, where appropriate.

Hypertrophic cardiomyopathy remains a common genetic heart disease reported in populations globally. Recommendations from the "2020 AHA/ACC Guideline for the Diagnosis and Treatment of Patients With Hypertrophic Cardiomyopathy" have been updated with new evidence to guide clinicians.

Until recently, implantable cardioverter defibrillators (ICDs) were considered a contraindication to competitive athletics. Recent prospective observational registry data in athletes with ICDs who participated in sports against the societal recommendations at the time have demonstrated the safety of sports participation. While athletes did receive both appropriate and inappropriate shocks, these were not more frequent during sports participation than other activity, and there were no sports-related deaths or need for external resuscitation in the 440 athlete cohort (median followup 44 months). Optimization of medical therapies, device settings and having an emergency action plan allow many athletes to safely continue athletic activity.

Myocarditis is one of the presentations of multisystemic inflammatory syndrome in children (MIS-C) following coronavirus disease 2019 (COVID-19). Although the reported short-term prognosis is good, data regarding medium-term functional capacity and limitations are scarce. This study aimed to evaluate exercise capacity as well as possible cardiac and respiratory limitations in children recovered from MIS-C related myocarditis.

Fourteen patients who recovered from MIS-C related myocarditis underwent spirometry and cardiopulmonary exercise testing (CPET), and their results were compared with an age-, sex-, weight- and activity level-matched healthy control group (n = 14).

All participants completed the CPET with peak oxygen uptake (peak [Formula: see text]), and the results were within the normal range (MIS-C 89.3% ± 8.9% and Control 87.9% ± 13.7% predicted [Formula: see text]). Five post-MIS-C patients (35%) had exercise-related cardio-respiratory abnormalities, including oxygen desaturation and oxygen-pulse flattening, compared to none in the control group. The MIS-C group also had lower peak exercise saturation (95.6 ± 3.5 vs. 97.6 ± 1.1) and lower breathing reserve (17.4% ± 7.5% vs. 27.4% ± 14.0% of MVV).

Patients who recovered from MIS-C related myocarditis may present exercise limitations. Functional assessment (e.g., CPET) should be included in routine examinations before allowing a return to physical activity in post-MIS-C myocarditis. Larger, longer term studies assessing functional capacity and focusing on physiological mechanisms are needed.

While most children with multisystem inflammatory syndrome in children have rapid recovery of cardiac dysfunction, little is known about the long-term outcomes regarding exercise capacity. We aimed to compare the exercise capacity among patients with multisystem inflammatory syndrome in children versus viral/idiopathic myocarditis at 3-6 months after initial diagnosis.

We performed a retrospective cohort study among patients with multisystem inflammatory syndrome in children in June 2020 to May 2021 and patients with viral/idiopathic myocarditis in August 2014 to January 2020. Data from cardiopulmonary exercise test as well as echocardiographic and laboratory data were obtained. Inclusion criteria included diagnosis of multisystem inflammatory syndrome in children or viral/idiopathic myocarditis, exercise test performed within 3-6 months of hospital discharge, and maximal effort on cardiopulmonary exercise test as determined by respiratory exchange ratio >1.10.

Thirty-one patients with multisystem inflammatory syndrome in children and 25 with viral/idiopathic myocarditis were included. The mean percent predicted peak VO2 was 90.84% for multisystem inflammatory syndrome in children patients and 91.08% for those with viral/idiopathic myocarditis (p-value 0.955). There were no statistically significant differences between the groups with regard to percent predicted maximal heart rate, metabolic equivalents, percent predicted peak VO2, percent predicted anerobic threshold, or percent predicted O2 pulse. There was a statistically significant correlation between lowest ejection fraction during hospitalisation and peak VO2 among viral/idiopathic myocarditis patients (r: 0.62, p-value 0.01) but not multisystem inflammatory syndrome in children patients (r: 0.1, p-value 0.6).

Patients with multisystem inflammatory syndrome in children and viral myocarditis appear to, on average, have normal exercise capacity around 3-6 months following hospital discharge. For patients with viral/idiopathic myocarditis, those with worse ejection fraction during hospitalisation had lower peak VO2 on cardiopulmonary exercise test.

Background Moderate intensity exercise training (MIT) is safe and effective for patients with hypertrophic cardiomyopathy, yet the efficacy of high intensity training (HIT) remains unknown. This study aimed to compare the efficacy of HIT compared with MIT in patients with hypertrophic cardiomyopathy. Methods and Results Patients with hypertrophic cardiomyopathy were randomized to either 5 months of MIT, or 1 month of MIT followed by 4 months of progressive HIT. Peak oxygen uptake (V˙O2; Douglas bags), cardiac output (acetylene rebreathing), and arteriovenous oxygen difference (Fick equation) were measured before and after training. Left ventricular outflow gradient and volumes were measured by echocardiography. Fifteen patients completed training (MIT, n=8, age 52±7 years; HIT, n=7, age 42±8 years). Both HIT and MIT improved peak V˙O2 by 1.3 mL/kg per min (P=0.009). HIT (+1.5 mL/kg per min) had a slightly greater effect than MIT (+1.1 mL/kg per min) but with no statistical difference (group×exercise P=0.628). A greater augmentation of arteriovenous oxygen difference occurred with exercise (Δ1.6 mL/100 mL P=0.005). HIT increased left ventricular end-diastolic volume (+17 mL, group×exercise P=0.015) compared with MIT. No serious arrhythmias or adverse cardiac events occurred. Conclusions This randomized trial of exercise training in patients with hypertrophic cardiomyopathy demonstrated that both HIT and MIT improved fitness without clear superiority of either. Although the study was underpowered for safety outcomes, no serious adverse events occurred. Exercise training resulted in salutary peripheral and cardiac adaptations. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT03335332.

This scientific statement from the American Heart Association focuses on treatment strategies and modalities for cardiomyopathy (heart muscle disease) in children and serves as a companion scientific statement for the recent statement on the classification and diagnosis of cardiomyopathy in children. We propose that the foundation of treatment of pediatric cardiomyopathies is based on these principles applied as personalized therapy for children with cardiomyopathy: (1) identification of the specific cardiac pathophysiology; (2) determination of the root cause of the cardiomyopathy so that, if applicable, cause-specific treatment can occur (precision medicine); and (3) application of therapies based on the associated clinical milieu of the patient. These clinical milieus include patients at risk for developing cardiomyopathy (cardiomyopathy phenotype negative), asymptomatic patients with cardiomyopathy (phenotype positive), patients with symptomatic cardiomyopathy, and patients with end-stage cardiomyopathy. This scientific statement focuses primarily on the most frequent phenotypes, dilated and hypertrophic, that occur in children. Other less frequent cardiomyopathies, including left ventricular noncompaction, restrictive cardiomyopathy, and arrhythmogenic cardiomyopathy, are discussed in less detail. Suggestions are based on previous clinical and investigational experience, extrapolating therapies for cardiomyopathies in adults to children and noting the problems and challenges that have arisen in this experience. These likely underscore the increasingly apparent differences in pathogenesis and even pathophysiology in childhood cardiomyopathies compared with adult disease. These differences will likely affect the utility of some adult therapy strategies. Therefore, special emphasis has been placed on cause-specific therapies in children for prevention and attenuation of their cardiomyopathy in addition to symptomatic treatments. Current investigational strategies and treatments not in wide clinical practice, including future direction for investigational management strategies, trial designs, and collaborative networks, are also discussed because they have the potential to further refine and improve the health and outcomes of children with cardiomyopathy in the future.

Diabetes mellitus (DM) is one of the most frequent comorbidities in patients suffering from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with a higher rate of severe course of coronavirus disease (COVID-19). However, data about post-COVID-19 syndrome (PCS) in patients with DM are limited.

This multicenter, propensity score-matched study compared long-term follow-up data about cardiovascular, neuropsychiatric, respiratory, gastrointestinal, and other symptoms in 8,719 patients with DM to those without DM. The 1:1 propensity score matching (PSM) according to age and sex resulted in 1,548 matched pairs.

Diabetics and nondiabetics had a mean age of 72.6 ± 12.7 years old. At follow-up, cardiovascular symptoms such as dyspnea and increased resting heart rate occurred less in patients with DM (13.2% vs. 16.4%; p = 0.01) than those without DM (2.8% vs. 5.6%; p = 0.05), respectively. The incidence of newly diagnosed arterial hypertension was slightly lower in DM patients as compared to non-DM patients (0.5% vs. 1.6%; p = 0.18). Abnormal spirometry was observed more in patients with DM than those without DM (18.8% vs. 13; p = 0.24). Paranoia was diagnosed more frequently in patients with DM than in non-DM patients at follow-up time (4% vs. 1.2%; p = 0.009). The incidence of newly diagnosed renal insufficiency was higher in patients suffering from DM as compared to patients without DM (4.8% vs. 2.6%; p = 0.09). The rate of readmission was comparable in patients with and without DM (19.7% vs. 18.3%; p = 0.61). The reinfection rate with COVID-19 was comparable in both groups (2.9% in diabetics vs. 2.3% in nondiabetics; p = 0.55). Long-term mortality was higher in DM patients than in non-DM patients (33.9% vs. 29.1%; p = 0.005).

The mortality rate was higher in patients with DM type II as compared to those without DM. Readmission and reinfection rates with COVID-19 were comparable in both groups. The incidence of cardiovascular symptoms was higher in patients without DM.

Infection with SARS-CoV-2, the virus that causes COVID, is associated with numerous potential secondary complications. Global efforts have been dedicated to understanding the myriad potential cardiovascular sequelae which may occur during acute infection, convalescence, or recovery. Because patients often present with nonspecific symptoms and laboratory findings, cardiac imaging has emerged as an important tool for the discrimination of pulmonary and cardiovascular complications of this disease. The clinician investigating a potential COVID-related complication must account not only for the relative utility of various cardiac imaging modalities but also for the risk of infectious exposure to staff and other patients. Extraordinary clinical and scholarly efforts have brought the international medical community closer to a consensus on the appropriate indications for diagnostic cardiac imaging during this protracted pandemic. In this review, we summarize the existing literature and reference major societal guidelines to provide an overview of the indications and utility of echocardiography, nuclear imaging, cardiac computed tomography, and cardiac magnetic resonance imaging for the diagnosis of cardiovascular complications of COVID.

Multisystem inflammatory syndrome in children (MIS-C) is a severe life-threatening manifestation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection that often presents with acute cardiac dysfunction and cardiogenic shock. While recovery from acute illness is excellent, the long-term myocardial impact is unknown.

To compare cardiac MRI findings in children 6-9 months after their hospitalization with MIS-C against MRI findings in healthy controls to assess for residual myocardial disease.

We prospectively performed cardiac MRI on 13 children 6-9 months following their hospitalization with MIS-C: eight of these children had a history of left ventricle ejection fraction (LVEF) < 50%, persistent symptoms, or electrocardiogram (ECG) abnormalities and underwent clinical MRI; five of these children without cardiac abnormalities during their hospitalization underwent research MRIs. We compared their native T1 and T2 mapping values with those of 20 normal controls.

Cardiac MRI was performed at 13.6 years of age (interquartile range [IQR] 11.9-16.4 years) and 8.2 months (IQR 6.8-9.6 months) following hospitalization. Twelve children displayed normal ejection fraction: left ventricle (LV) 57.2%, IQR 56.1-58.4; right ventricle (RV) 53.1%, IQR 52.0-55.7. One had low-normal LVEF (52%). They had normal extracellular volume (ECV) and normal T2 and native T1 times compared to controls. There was no qualitative evidence of edema. One child had late gadolinium enhancement (LGE) with normal ejection fraction, no edema, and normal T1 and T2 times. When stratifying children who had MIS-C according to history of LVEF <55% on echocardiography, there was no difference in MRI values.

Although many children with MIS-C present acutely with cardiac dysfunction, residual myocardial damage 6-9 months afterward appears minimal. Long-term implications warrant further study.

Cardiovascular involvement is a major cause of inpatient and intensive care unit morbidity related to Multisystem inflammatory syndrome in children (MIS-C). The objective of this study was to identify long-term cardiovascular manifestations of MIS-C. We included 80 consecutive patients admitted to the intensive care unit with MIS-C who were evaluated for a year in our follow-up clinic using an institution protocol. The outcome measures were cardiac biomarkers (troponin and BNP), electrocardiogram changes, echocardiographic findings cardiovascular magnetic resonance (CMR) and graded-exercise stress test (GXT) findings. The cohort included patients aged between 6 months and 17 years (median 9 years; 48.8% females). At the peak of the disease 81.3% had abnormal BNP and 58.8% had troponin leak which reduced to 33.8% and 18.8% respectively at discharge with complete normalization by 6 weeks post-discharge. At admission 33.8% had systolic dysfunction, which improved to 11.3% at discharge with complete resolution by 2 weeks. Coronary artery abnormalities were seen in 17.5% during the illness with complete resolution by 2 weeks post discharge except one (1.9%) with persistent giant aneurysm at 1 year-follow up. CMR was performed at 6 months in 23 patient and demonstrated 4 patients with persistent late gadolinium enhancement (17.4%). Normal exercise capacity with no ectopy was seen in the 31 qualifying patients that underwent a GXT. There is significant heterogeneity in the cardiovascular manifestations of MIS-C. Although majority of the cardiovascular manifestations resolve within 6 weeks, diastolic dysfunction, CAA and myocardial scar may persist in a small subset of patients warranting a structured long-term follow-up strategy.

Background. Exercise stress test (EST) has been scarcely investigated in patients with arrhythmic myocarditis. Objectives. To report the results of EST late after myocarditis with arrhythmic vs. nonarrhythmic presentation. Methods. We enrolled consecutive adult patients with EST performed at least six months after acute myocarditis was diagnosed using gold-standard techniques. Patients with ventricular arrhythmia (VA) at presentation were compared with the nonarrhythmic group. Adverse events occurring during follow-up after EST included cardiac death, disease-related rehospitalization, malignant VA, and proven active myocarditis. Results. The study cohort was composed of 128 patients (age 41 ± 9 y, 70% males) undergoing EST after myocarditis. Of them, 64 (50%) had arrhythmic presentation. EST was performed after 15 ± 4 months from initial diagnosis, and was conducted on betablockers in 75 cases (59%). During EST, VA were more common in the arrhythmic group (43 vs. 4, p < 0.001), whereas signs and symptoms of ischemia were more prevalent in the nonarrhythmic one (6 vs. 1, p = 0.115). By 58-month mean follow-up, 52 patients (41%) experienced adverse events, with a greater prevalence among arrhythmic patients (39 vs. 13, p < 0.001). As documented both in the arrhythmic and nonarrhythmic subgroups, patients had greater prevalence of adverse events following a positive EST (40/54 vs. 12/74 with negative EST, p < 0.001). Electrocardiographic features of VA during EST correlated with the subsequent inflammatory restaging of myocarditis. Nonarrhythmic patients with uneventful EST both on- and off-treatment were free from subsequent adverse events. Conclusions. Late after the arrhythmic presentation of myocarditis, EST was frequently associated with recurrent VA. In both arrhythmic and nonarrhythmic myocarditis, EST abnormalities correlated with subsequent adverse outcomes.

The objective of this study was to determine the utility of "standard" cardiac screening with EKG, echocardiography, and serum troponin T (hs-Tn T) testing after COVID infection in competitive college athletes.

Prospective cohort study.

Tertiary cardiology clinic, university training room.

Sixty-five Division 1 athletes recovered from COVID-19 and 465 controls.

All COVID-recovered athletes underwent cardiac screening on return to campus in fall 2020. Controls were screened if indicated by preparticipation examination. Students cleared for sports participation were followed for the development of cardiac complications.

Incidence of cardiac complications after COVID infection.

Infected athletes experienced mild (26/65), moderate (8/65), or no (31/65) COVID symptoms. No athletes had severe symptoms. Men were more likely to have been asymptomatic (20/31), and women were more likely to have had moderate (7/8) symptoms (P = 0.015). All athletes, except 2 with anosmia, were asymptomatic at the time of cardiac testing. One athlete had persistently elevated hs-Tn T but no evidence of myocarditis on cardiac MRI. All other cardiac testing was negative. No athletes were diagnosed with myocarditis (95% CI: 0%-5.5%). All athletes were cleared for athletic participation. None suffered complications over the next 9 months.

After COVID-19 infection, no college athletes with mild, moderate, or no symptoms had signs of myocarditis, and all returned to play without cardiac complication. These findings support consensus opinion recommendations that college-age athletes who recovered from COVID-19 and who experienced mild or no symptoms may return to play without cardiac testing.

There are four main myocarditis presentations identified in the context of severe acute respiratory coronavirus 2 (SARS-CoV-2): myocarditis associated with acute coronavirus disease 2019 (COVID-19) infection, post-acute COVID-19 syndrome, multisystem inflammatory syndrome, and vaccination-associated myocarditis. This article reviews the clinical features and current management strategies for each of these presentations. The overall prevalence of myocarditis is considered to be rare, although accurate estimation is affected by heterogeneity in diagnostic criteria and reporting, as well as infrequent use of gold-standard diagnostic endomyocardial biopsy. Severity of disease can range from mild symptoms to fulminant myocarditis. Therapeutic interventions are typically supportive and extrapolated from treatment for non-COVID-19 viral myocarditis. Several pathogenic mechanisms for the development of myocarditis have been proposed, and ongoing research is critical for elucidating disease pathogenesis and potentially identifying therapeutic targets. The long-term cardiovascular sequelae of SARS-CoV-2 infections and associated myocarditis require further elucidation and understanding.

Myocarditis has been discovered to be a significant complication of coronavirus disease 2019 (COVID-19), a condition caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. COVID-19 myocarditis seems to have distinct inflammatory characteristics, which make it unique to other viral etiologies. The incidence of COVID-19 myocarditis is still not clear as a wide range of figures have been quoted in the literature; however, it seems that the risk of developing myocarditis increases with more severe infection. Furthermore, the administration of the mRNA COVID-19 vaccine has been associated with the development of myocarditis, particularly after the second dose. COVID-19 myocarditis has a wide variety of presentations, ranging from dyspnea and chest pain to acute heart failure and possibly death. It is important to catch any cases of myocarditis, particularly those presenting with fulminant myocarditis which can be characterized by signs of heart failure and arrythmias. Initial work up for suspected myocarditis should include serial troponins and electrocardiograms. If myocardial damage is detected in these tests, further screening should be carried out. Cardiac magnetic resonance imagining and endomyocardial biopsy are the most useful tests for myocarditis. Treatment for COVID-19 myocarditis is still controversial; however, the use of intravenous immunoglobulins and corticosteroids in combination may be effective, particularly in cases of fulminant myocarditis. Overall, the incidence of COVID-19 myocarditis requires further research, while the use of intravenous immunoglobulins and corticosteroids in conjunction requires large randomized controlled trials to determine their efficacy.

COVID-19 is associated with myocardial injury caused by ischemia, inflammation, or myocarditis. Cardiovascular magnetic resonance (CMR) is the noninvasive reference standard for cardiac function, structure, and tissue composition. CMR is a potentially valuable diagnostic tool in patients with COVID-19 presenting with myocardial injury and evidence of cardiac dysfunction. Although COVID-19-related myocarditis is likely infrequent, COVID-19-related cardiovascular histopathology findings have been reported in up to 48% of patients, raising the concern for long-term myocardial injury. Studies to date report CMR abnormalities in 26% to 60% of hospitalized patients who have recovered from COVID-19, including functional impairment, myocardial tissue abnormalities, late gadolinium enhancement, or pericardial abnormalities. In athletes post-COVID-19, CMR has detected myocarditis-like abnormalities. In children, multisystem inflammatory syndrome may occur 2 to 6 weeks after infection; associated myocarditis and coronary artery aneurysms are evaluable by CMR. At this time, our understanding of COVID-19-related cardiovascular involvement is incomplete, and multiple studies are planned to evaluate patients with COVID-19 using CMR. In this review, we summarize existing studies of CMR for patients with COVID-19 and present ongoing research. We also provide recommendations for clinical use of CMR for patients with acute symptoms or who are recovering from COVID-19.

Coronavirus disease 2019 (COVID-19) is the third deadly coronavirus infection of the 21st century that has proven to be significantly more lethal than its predecessors, with the number of infected patients and deaths still increasing daily. From December 2019 to July 2021, this virus has infected nearly 200 million people and led to more than 4 million deaths. Our understanding of COVID-19 is constantly progressing, giving better insight into the heterogeneous nature of its acute and long-term effects. Recent literature on the long-term health consequences of COVID-19 discusses the need for a comprehensive understanding of the multisystemic pathophysiology, clinical predictors, and epidemiology to develop and inform an evidence-based, multidisciplinary management approach. A PubMed search was completed using variations on the term post-acute COVID-19. Only peer-reviewed studies in English published by July 17, 2021 were considered for inclusion. All studies discussed in this text are from adult populations unless specified (as with multisystem inflammatory syndrome in children). The preliminary evidence on the pulmonary, cardiovascular, neurological, hematological, multisystem inflammatory, renal, endocrine, gastrointestinal, and integumentary sequelae show that COVID-19 continues after acute infection. Interdisciplinary monitoring with holistic management that considers nutrition, physical therapy, psychological management, meditation, and mindfulness in addition to medication will allow for the early detection of post-acute COVID-19 sequelae symptoms and prevent long-term systemic damage. This review serves as a guideline for effective management based on current evidence, but clinicians should modify recommendations to reflect each patient's unique needs and the most up-to-date evidence. The presence of long-term effects presents another reason for vaccination against COVID-19.