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Knowledge of toxicological findings among sports-related sudden cardiac death (SrSCD) is scarce.

Extracorporeal cardiopulmonary resuscitation (ECPR) in patients with prolonged or refractory out‐of‐hospital cardiac arrest (OHCA) is likely to be beneficial when used as part of a well developed emergency service system.ECPR is technically challenging to initiate and resource‐intensive, but it has been found to be cost‐effective in hospital‐based ECPR programs.ECPR expansion within Australia has thus far been reactive and does not provide broad coverage or equity of access for patients.Newer delivery strategies that improve access to ECPR for patients with OHCA are being trialled, including networked hospital‐based ECPR and pre‐hospital ECPR programs. The efficacy, scalability, sustainability and cost‐effectiveness of these programs need to be assessed.There is a need for national collaboration to determine the most cost‐effective delivery strategies for ECPR provision along with its place in the OHCA survival chain.

ObjectivesTo determine the impact of running a sub-4 min mile on longevity. It was hypothesised that there would be an increase in longevity for runners who successfully completed a sub-4 min mile compared with the general population.MethodsAs part of this retrospective cohort study, the Sub-4 Alphabetic Register was used to extract the first 200 athletes to run a sub-4 min mile. Each runner’s date of birth, date of their first successful mile attempt, current age (if alive) or age at death was compared with the United Nations Life Tables to determine the difference in each runner’s current age or age at death with their country of origin-specific life expectancy.ResultsOf the first 200 sub-4 min mile runners (100% male), 60 were dead (30%) and 140 were still alive. Sub-4 min mile runners lived an average of 4.7 years beyond their predicted life expectancy (95% CI 4.7 to 4.8). When accounting for the decade of completion (1950s, 1960s or 1970s), the longevity benefits were 9.2 years (n=22; 95% CI 8.3 to 10.1), 5.5 years (n=88; 95% CI 5.3 to 5.7) and 2.9 years (n=90; 95% CI 2.7 to 3.1), respectively.ConclusionSub-4 min mile runners have increased longevity compared with the general population, thereby challenging the notion that extreme endurance exercise may be detrimental to longevity.

ObjectiveTo explore the effect of left ventricular (LV) diastolic dysfunction (LVDD) in systemic sclerosis (SSc)-associated interstitial lung disease (ILD), and to investigate SSc-specific associations and clinical correlates of LVDD.MethodsThere were 102 Australian Scleroderma Cohort Study participants with definite SSc and radiographic ILD included. Diastolic function was classified as normal, indeterminate, or abnormal according to 2016 American Society of Echocardiography/European Association of Cardiovascular Imaging guidelines for assessment of LV diastolic function. Associations between clinical features and patient- and physician-reported dyspnea were evaluated using logistic regression. Survival analyses were performed using Kaplan-Meier survival estimates and Cox regression modeling.ResultsLVDD was identified in 26% of participants, whereas 19% had indeterminate and 55% had normal diastolic function. Those with ILD and LVDD had increased mortality (hazard ratio 2.4, 95% CI 1.0-5.7; P= 0.05). After adjusting for age and sex, those with ILD and LVDD were more likely to have severe dyspnea on the Borg Dyspnoea Scale (odds ratio [OR] 2.6, 95% CI 1.0-6.6; P= 0.05) and numerically more likely to record World Health Organization Function Class II or higher dyspnea (OR 4.2, 95% CI 0.9-20.0; P= 0.08). Older age (95% CI 1.0-6.4; P= 0.05), hypertension (OR 5.0, 95% CI 1.8-13.8; P< 0.01), and ischemic heart disease (OR 4.8, 95% CI 1.5-15.7; P< 0.01) were all associated with LVDD, as was proximal muscle atrophy (OR 5.0, 95% CI 1.9-13.6; P< 0.01) and multimorbidity (Charlson Comorbidity Index scores ≥ 4, OR 3.0, 95% CI 1.1-8.7; P= 0.04).ConclusionLVDD in SSc-ILD is more strongly associated with traditional LVDD risk factors than SSc-specific factors. LVDD is associated with worse dyspnea and survival in those with SSc-ILD.

People with schizophrenia account for approximately 1.0% of the population and seem to experience increased rates of sudden cardiac death (SCD).

Patients with heart failure with preserved ejection fraction (HFpEF) frequently develop atrial fibrillation (AF). There are no randomized trials examining the effects of AF ablation on HFpEF outcomes.

Supplemental Digital Content is Available in the Text.Bigaran, A, Howden, EJ, Foulkes, S, Janssens, K, Beaudry, R, Haykowsky, MJ, La Gerche, A, Fraser, SF, and Selig, SE. Prescribing exercise in early-stage breast cancer during chemotherapy: a simple periodized approach to align with the cyclic phases of chemotherapy. J Strength Cond Res36(10): 2934–2941, 2022—To evaluate whether a periodized aerobic and resistance training plan aligned to the anthracycline chemotherapy (AC) cycles would be well tolerated, feasible, and attenuate the decline in peak oxygen uptake (V̇o2peak) in breast cancer (BC) patients. Twenty-eight women with early-stage BC treated with AC self-selected to undertake exercise training (EX 47 ± 9 years, n= 14) or usual care (53 ± 9 years, n= 14) for 12 weeks as part of a nonrandomized controlled trial. The periodized EX was aligned to the cyclic phases of AC, including AC taper and nontaper weeks. Outcome measures included cardiopulmonary exercise testing. Attendance and adherence variables (relative dose intensity [RDI] and volume load) were calculated to quantify the dose of EX completed relative to the amount of EX prescribed. The mean session attendance was 76% (range 46–88%). The mean ± SDprescribed and completed dose of aerobic training was 332.3 ± 48.7 MET h·wk−1and 380.6 ± 53.2 MET h·wk−1(p= 0.02), equating to a mean RDI of 89 ± 17%. For resistance training, the prescribed and completed cumulative dose was 128,264 ± 54,578 and 77,487 ± 26,108 kg (p< 0.001), equating to an RDI of 60 ± 11%. Adherence to the AC taper week RDI (52 ± 14%) for resistance training was significantly lower than the non-AC taper week (72 ± 8%, p= 0.02). The most frequent cause for EX interruption was hospitalization (35%), whereas AC-related illness was the most common cause for missed (57%) or modified EX sessions (64%). This periodized approach was mostly well tolerated for patients with BC. We speculate that a periodized approach may be both more palatable and useful, although this requires further investigation in a randomized controlled trial.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) encompasses a group of conditions characterized by right ventricular fibrofatty infiltration, with a predominant arrhythmic presentation. First described in the late 1970s and early 1980s, it is now frequently recognized to have biventricular involvement. The prevalence is ∼1:2,000 to 1:5,000, depending on geographic location, and it has a slight male predominance. The diagnosis of ARVC is determined on the basis of fulfillment of task force criteria incorporating electrophysiological parameters, cardiac imaging findings, genetic factors, and histopathologic features. Risk stratification of patients with ARVC aims to identify those who are at increased risk of sudden cardiac death or sustained ventricular tachycardia. Factors including age, sex, electrophysiological features, and cardiac imaging investigations all contribute to risk stratification. The current management of ARVC includes exercise restriction, β-blocker therapy, consideration for implantable cardioverter-defibrillator insertion, and catheter ablation. This review summarizes our current understanding of ARVC and provides clinicians with a practical approach to diagnosis and management.

This study sought to define the feasibility and utility of postmortem cardiac implantable electronic device (CIED) interrogation.

This article provides an overview of the recommendations from the Sports Cardiology section of the European Association of Preventive Cardiology on sports participation in individuals with valvular heart disease (VHD). The aim of these recommendations is to encourage regular physical activity including sports participation, with reasonable precaution to ensure a high level of safety for all affected individuals. Valvular heart disease is usually an age-related degenerative process, predominantly affecting individuals in their fifth decade and onwards. However, there is an increasing group of younger individuals with valvular defects. The diagnosis of cardiac disorders during routine cardiac examination often raises questions about on-going participation in competitive sport with a high dynamic or static component and the level of permissible physical effort during recreational exercise. Although the natural history of several valvular diseases has been reported in the general population, little is known about the potential influence of chronic intensive physical activity on valve function, left ventricular remodelling pulmonary artery pressure, and risk of arrhythmia. Due to the sparsity of data on the effects of exercise on VHD, the present document is largely based on clinical experience and expert opinion.

Background: Growing evidence suggests that men exposed to androgen deprivation therapy (ADT) have an increased risk of cardiovascular disease. While exercise has shown to attenuate some adverse effects of ADT, the effects on cardiometabolic health have not been systematically evaluated. Objective: To evaluate the effect of exercise on cardiometabolic health in men with prostate cancer (PCa) receiving ADT. Methods: A systematic literature search of MEDLINE, EMBASE, CINHAL, SCOPUS, WEB OF SCIENCE and SPORTSDICUS from database inception to April 2020 was performed. A quantitative synthesis using Cohens deffect size and a meta-analysis using random-effects models were conducted. Results: Overall, fourteen randomised controlled trials (RCTs) and four non-randomised studies were included. Eleven RCTs (n= 939 patients) were included in the meta-analysis. Exercise training improved the 400-m-walk test (MD −10.11 s, 95% CI [−14.34, −5.88]; p&lt; 0·00001), diastolic blood pressure (−2.22 mmHg, [−3.82, −0.61]; p= 0.007), fasting blood glucose (−0.38 mmol/L, [−0.65, −0.11]; p= 0.006), C-reactive protein (−1.16 mg/L, [−2.11, −0.20]; p= 0.02), whole-body lean mass (0.70 kg, [0.39, 1.01]; p&lt; 0.0001), appendicular lean mass (0.59 kg, [0.43, 0.76]; p&lt; 0.00001), whole-body fat mass (−0.67 kg, [−1.08, −0.27]; p= 0.001), whole-body fat percentage (−0.79%, [−1.16, −0.42]; p&lt; 0.0001), and trunk fat mass (−0.49 kg, [−0.87, −0.12]; p= 0.01), compared to usual care. No significant effects on systolic blood pressure or blood lipid metabolism were detected. Conclusions: In a small subset of evaluated studies, exercise may favourably improve some but not all markers of cardiometabolic health. Future exercise intervention trials with cardiometabolic outcomes as primary endpoints are needed to confirm these initial findings.

Exercise capacity is frequently reduced in people with diabetes mellitus (DM) and may be due to subclinical cardiac dysfunction. Speckle-tracking echocardiography is now widely available; however, the clinical utility and significance of left ventricular (LV) strain and twist parameters remain uncertain. We hypothesized that LV strain and twist would be reduced in DM subjects during exercise.

This article has been withdrawn because it is a duplicate. The correct published version of the article can be found at http://dx.doi.org/10.1016/j.jacep.2015.03.007. The Publisher apologizes for any inconvenience this may cause.

Cardiovascular disease is a competing cause of death in patients with cancer with early-stage disease. This elevated cardiovascular disease risk is thought to derive from both the direct effects of cancer therapies and the accumulation of risk factors such as hypertension, weight gain, cigarette smoking, and loss of cardiorespiratory fitness. Effective and viable strategies are needed to mitigate cardiovascular disease risk in this population; a multimodal model such as cardiac rehabilitation may be a potential solution. This statement from the American Heart Association provides an overview of the existing knowledge and rationale for the use of cardiac rehabilitation to provide structured exercise and ancillary services to cancer patients and survivors. This document introduces the concept of cardio-oncology rehabilitation, which includes identification of patients with cancer at high risk for cardiac dysfunction and a description of the cardiac rehabilitation infrastructure needed to address the unique exposures and complications related to cancer care. In this statement, we also discuss the need for future research to fully implement a multimodal model of cardiac rehabilitation for patients with cancer and to determine whether reimbursement of these services is clinically warranted.

Background Anthracycline chemotherapy may be associated with decreased cardiac function and functional capacity measured as the peak oxygen uptake during exercise (V·O2peak). We sought to determine (a) whether a structured exercise training program would attenuate reductions in V·O2peak and (b) whether exercise cardiac imaging is a more sensitive marker of cardiac injury than the current standard of care resting left ventricular ejection fraction (LVEF).Methods Twenty-eight patients with early stage breast cancer undergoing anthracycline chemotherapy were able to choose between exercise training (mean ± SD age 47 ± 9 years, n= 14) or usual care (mean ± SD age 53 ± 9 years, n= 14). Measurements performed before and after anthracycline chemotherapy included cardiopulmonary exercise testing to determine V·O2peak and functional disability (V·O2peak < 18 ml/min/kg), resting echocardiography (LVEF and global longitudinal strain), cardiac biomarkers (troponin and B-type natriuretic peptide) and exercise cardiac magnetic resonance imaging to determine stroke volume and peak cardiac output. The exercise training group completed 2 × 60 minute supervised exercise sessions per week.Results Decreases in V·O2peak during chemotherapy were attenuated with exercise training (15 vs. 4% reduction, P= 0.010) and fewer participants in the exercise training group met the functional disability criteria after anthracycline chemotherapy compared with those in the usual care group (7 vs. 50%, P= 0.01). Compared with the baseline, the peak exercise heart rate was higher and the stroke volume was lower after chemotherapy (P= 0.003 and P= 0.06, respectively). There was a reduction in resting LVEF (from 63 ± 5 to 60 ± 5%, P= 0.002) and an increase in troponin (from 2.9 ± 1.3 to 28.5 ± 22.4 ng/mL, P< 0.0001), but no difference was observed between the usual care and exercise training group. The baseline peak cardiac output was the strongest predictor of functional capacity after anthracycline chemotherapy in a model containing age and resting cardiac function (LVEF and global longitudinal strain).Conclusions The peak exercise cardiac output can identify patients at risk of chemotherapy-induced functional disability, whereas current clinical standards are unhelpful. Functional disability can be prevented with exercise training.

The most important determinant of long-term survival in patients with idiopathic pulmonary fibrosis is the right ventricular (RV) adaptation to the increased pulmonary vascular resistance. Our aim was to explore RV contractile reserve during stress echocardiography in early-stage IPF.

This study sought to compare electrocardiogram (ECG) variants in athletic and arrhythmogenic right ventricular cardiomyopathy (ARVC) cohorts matched for the confounders of age, sex, and ethnicity.

This study sought to determine the impact of regular alcohol consumption on left atrial (LA) mechanical and reservoir function.

The Right Heart International Network is a multicenter international study aiming to prospectively collect exercise Doppler echocardiography tests of the right heart pulmonary circulation unit (RHPCU) in large cohorts of healthy subjects, elite athletes, and individuals at risk of or with overt pulmonary hypertension. It is going to provide standardization of exercise stress echocardiography of RHPCU and explore the full physiopathologic response.

Cardiomyopathies (CM) are a heterogeneous group of muscle heart diseases, divided into 3 main categories (dilated, hypertrophic, and restrictive). In addition to these subgroups, athlete’s heart and hypertensive cardiopathy are both the result of heart adaptation to increased loading conditions, making it possible to include them in the CM group. Right heart involvement is clear in some CM as arrhythmogenic CM, carcinoid syndrome, and endomyocardial fibrosis, whereas in others, like hypertrophic or dilated CM, it is known that the right heart has a prognostic impact but less clear is its pathogenic role.

Exercise and competitive sports should be associated with a wide range of health benefits with the potential to inspire a positive community health legacy. However, the reputation of sports is being threatened by an ever-expanding armamentarium of agents with real or perceived benefits in performance enhancement. In addition to the injustice of unfair advantage for dishonest athletes, significant potential health risks are associated with performance-enhancing drugs. Performance-enhancing drugs may have an effect on the cardiovascular system by means of directly altering the myocardium, vasculature, and metabolism. However, less frequently considered is the potential for indirect effects caused through enabling athletes to push beyond normal physiological limits with the potential consequence of exercise-induced arrhythmias. This review will summarize the known health effects of PEDs but will also focus on the potentially greater health threat posed by the covert search for performance-enhancing agents that have yet to be recognized by the World Anti-Doping Agency. History has taught us that athletes are subjected to unmonitored trials with experimental drugs that have little or no established efficacy or safety data. One approach to decrease drug abuse in sports would be to accept that there is a delay from when athletes start experimenting with novel agents to the time when authorities become aware of these drugs. This provides a window of opportunity for athletes to exploit with relative immunity. It could be argued that all off-label use of any agent should be deemed illegal.

Heart transplantation (HTP) is a life-saving therapy for selected individuals with end-stage refractory heart failure. Despite improvements in quality of life and survival, HTP recipients’ peak aerobic power (peak VO2) remains up to 50% lower than age-matched healthy control subjects owing to abnormal cardiovascular and skeletal muscle function. Currently, little is known regarding the effect of exercise training (ET) to improve peak VO2after HTP. This brief review aims to summarise existing evidence regarding the role of ET on peak VO2and its determinants, highlights the upper limits of endurance performance in highly trained HTP athletes, and identifies areas for future HTP exercise rehabilitation research.

Exercise capacity is a spectrum that reflects an individual’s functional capacity and the dynamic nature of cardiac remodelling along with respiratory and skeletal muscle systems. The relationship of increasing physical activity, increased cardiac mass and volumes, and improved cardiorespiratory fitness (CRF) is well established in the endurance athlete. However, less emphasis has been placed on the other end of the spectrum, which includes individuals with a more sedentary lifestyle and small hearts who are at increased risk of functional disability and poor clinical outcomes. Reduced CRF is an independent predictor of all-cause mortality and cardiovascular events determined by multiple inter-related exogenous and endogenous factors. In this review, we explore the relationship of physical activity, cardiac remodelling, and CRF across the exercise spectrum, emphasising the critical role of cardiac size in determining exercise capacity. In contrast to the large compliant left ventricle of the endurance athlete, an individual with a lifetime of physical inactivity is likely to have a small, stiff heart with reduced cardiac reserve. We propose that this might contribute to the development of heart failure with preserved ejection fraction in certain individuals, and is key to understanding the link between low CRF and increased risk of heart failure.

Background: Skeletal muscle can be directly affected by systemic sclerosis (SSc); however, a significant burden of SSc-associated myopathy is undetected because clinical parameters such as weakness and creatine kinase (CK) are unreliable biomarkers of muscle involvement. This study presents qualitative and quantitative magnetic resonance imaging (MRI) findings that quantify the prevalence of myopathy and evaluate any association between skeletal and cardiac muscle involvement in SSc. Methods: Thirty-two patients with SSc who fulfilled the 2013 American College of Rheumatology/European League Against Rheumatism classification criteria underwent skeletal muscle MRI in addition to cardiac MRI. Skeletal muscles were independently assessed by two musculoskeletal radiologists for evidence of oedema, fatty infiltration and atrophy. Skeletal muscle T2 mapping times and percentage fat fraction were calculated. Linear regression analysis was used to evaluate the clinical and myocardial associations with skeletal muscle oedema and fatty infiltration. Cardiac MRI was performed using post gadolinium contrast imaging and parametric mapping techniques to assess focal and diffuse myocardial fibrosis. Results: Thirteen participants (40.6%) had MRI evidence of skeletal muscle oedema. Five (15.6%) participants had fatty infiltration. There was no association between skeletal muscle oedema and muscle strength, creatine kinase, inflammatory markers or fibroinflammatory myocardial disease. Patients with skeletal muscle oedema had higher T2-mapping times; there was a significant association between subjective assessments of muscle oedema and T2-mapping time (coef 2.46, p= 0.02) and percentage fat fraction (coef 3.41, p= 0.02). Diffuse myocardial fibrosis was a near-universal finding, and one third of patients had focal myocardial fibrosis. There was no association between skeletal myopathy detected by MRI and burden of myocardial disease. Conclusions: MRI is a sensitive measure of muscle oedema and systematic assessment of SSc patients using MRI shows that myopathy is highly prevalent, even in patients without symptoms or other signs of muscle involvement. Similarly, cardiac fibrosis is highly prevalent but occurs independently of skeletal muscle changes. These results indicate that novel quantitative MRI techniques may be useful for assessing sub-clinical skeletal muscle disease in SSc.

Exercise training can have a profound effect on cardiac structure. Recent evidence suggests that the greatest determinants of exercise-induced cardiac remodeling are the intensity, duration, and frequency of training. This also has overlap with athlete fitness. There are many additional factors that are important in determining cardiac remodeling, but while further refinements evolve, the authors argue that the best means of predicting the degree of expected physiologic remodeling is to either quantify training (intensity times total training time) or its by-product (exercise capacity). A uniform approach to estimating the degree of exercise-induced cardiac remodeling will enable more consistent research.

The emerging controversy related to the potential cardiotoxic effects of high doses of intense exercise need to be considered among the much stronger evidence that supports the pleomorphic benefits of exercise as a whole. However, there is fairly compelling evidence to support the association between long-term sport practice and an increased prevalence of atrial fibrillation and the fact that this relates to a chronic altered atrial substrate. This article was designed to challenge the reader with speculative science that suggests that exercise might promote permanent structural changes in the myocardium which can, in some individuals, predispose to arrhythmias. In terms of long-term health outcomes, it would seem that these small risks are outweighed by the many other benefits of exercise, including a likely decrease in atherosclerotic vascular events, although some recent results have brought into question whether the protective benefits of exercise on vascular events also extends to high-intensity exercise training. Above all else, in this article we sought to highlight current controversies to stimulate research on the many unanswered questions. In particular, there is a lack of adequately powered prospective studies from which we can measure health outcomes and their relationship to exercise-induced cardiac remodelling.

Introduction:Post-acute COVID-19 sequalae (PASC) is a poorly understood constellation of symptoms that persist or emerge following the post-viral convalescent period. We sought to comprehensively evaluate cardiac and autonomic function and deconditioning as possible contributors to PASC associated fatigue.Methods:Thirty individuals with PASC (20F:10M; 41±11yrs; 137-730 days post-infection) prospectively underwent measures of autonomic function (heart rate [HR] and muscle sympathetic nerve activity [MSNA] response to passive head-up tilt 60° [HUT]); cardiac function (echocardiogram); arrhythmia burden (24-hour Holter monitor); exercise capacity (cardiopulmonary exercise test); hemoglobin and inflammatory biomarkers (CRP, troponin, IL-6, TNFα, IL-10). Participants were stratified by ongoing fatigue and symptoms of breathlessness (SOB+ or SOB-). Individuals with pre-existing conditions associated with fatigue were excluded.Results:Sixteen individuals (53%) reported breathlessness. Other common symptoms were palpitations (n=9; 30%) and light-headedness (n=5; 17%). Exercise capacity normalised for age and gender was lower in breathless subjects (SOB+) than in non-breathless subjects (SOB-); 70±11% vs 85±15%, p=0.004. The SOB+ group tended to have a blunted MSNA response to HUT when compared to SOB- (p=0.06), with similar prevalence of postural orthostatic tachycardia (SOB+ n=5 vs SOB- n=5). Echocardiography revealed that global longitudinal strain trended higher in the SOB+ group compared with SOB- (p=0.075), with similar prevalence of participants who fulfilled diastolic dysfunction criteria (SOB+ 5 vs SOB- 4). There were no significant sustained arrhythmias on 24-hour Holter monitoring. Hemoglobin, troponin and cytokines were all similar (p>0.05), but CRP was higher in the breathless group (p=0.016).Conclusions:This is the first comprehensive phenotyping of PASC with ongoing fatigue and breathlessness. We found that these symptoms were associated with reduced exercise capacity but without any associated cardiac impairment, arrhythmias, or autonomic dysfunction. These findings suggest that deconditioning may contribute to the pathophysiology of PASC.

Introduction:Global longitudinal strain (GLS) can predict cancer therapeutics-related cardiac dysfunction (CTRCD) and guide initiation of cardioprotection (CPT) at the time of chemotherapy. No prospective randomized controlled trial (RCT) has identified the impact on LV function in survivors.Hypothesis:GLS-guided CPT provides less cardiac dysfunction in survivors of potentially cardiotoxic chemotherapy, compared with usual care.Methods:In this international (28 sites) multicenter prospective RCT, patients (pts) were included if they were administrated anthracyclines and had another risk factor for HF. They were randomly allocated into undergoing GLS-guided CPT for >12% relative reduction in GLS or EF-guided CPT for >10% absolute reduction of EF. Primary endpoint was the change in EF (ΔEF) from baseline to 3 years by 3D echocardiography.Results:Among 331 pts enrolled, 255 (77%, 60±16 years, 95% women) completed 3-year follow-up (123 in EF-guided group and 132 in GLS-guided). Most had breast cancer (236, 93%), 67 (26%) with hypertension and 32 (13%) with diabetes mellitus. A regimen of anthracycline and trastuzumab was the most common chemotherapy regimen (84%). The baseline LVEF was 61±4% with GLS of 20.7±2.3% in the entire population. CPT was administrated in 18 pts (15%) in EF-guided and 41 (31%) in GLS-guided (p=0.02). Most patients showed recovery in EF and GLS after chemotherapy (Figure). ΔEF was -2.0±4.8 in EF-guided and -1.4±5.4 in GLS-guided (p=0.25), but LVEF at 3 years in EF-guided was lower than that of GLS-guided (58.0±5.6% vs 59±4.9%, p=0.043). Ten pts in EF-guided developed CTRCD, and 6 in GLS-guided (p=0.24).Conclusions:Most of the enrolled pts were taking potentially cardiotoxic chemotherapy for breast cancer. Almost all improved LV function over 3 years, and although GLS-guided CPT was associated with higher EF at 3 years, there was no difference in ΔEF compared with EF-guided surveillance.

An introduction is presented in which editor discusses various articles within the issue on topics including causes of sudden cardiac death in young athletes, limitations of assessing environmental risk for heat related illness and automated external defibrillators.

Abdominal obesity is an independent risk factor for cardiovascular disease. The effect of abdominal obesity on myocardial function in young obese women remains unknown. Therefore, we aimed to investigate cardiac morphology and function, myocardial deformation, and mechanical indices, in young women with and without abdominal obesity.