Ejection Fraction Research Articles (Page 1)

Abstract Aims Implantable cardioverter‐defibrillator (ICD) implantation is recommended in patients with heart failure with reduced ejection fraction (HFrEF) and left ventricular ejection fraction (LVEF) ≤ 35% after 3 months of optimized medical therapy (OMT). Whether recent advances in guideline‐directed medical therapy (GDMT), including angiotensin receptor‐neprilysin inhibitors (ARNI) and sodium‐glucose cotransporter 2 inhibitors (SGLT2i) alter the timing of ICD implantation remains uncertain. Methods In this single‐centre, prospective cohort study, 106 patients with newly diagnosed HFrEF (mean age 63 ± 13 years; 25% women; 53% non‐ischaemic aetiology) and baseline LVEF ≤35% were enrolled between 2019 and 2022. Echocardiographic assessments were performed at baseline, 3 months and 12 months to evaluate LVEF improvement. The primary endpoint was LVEF recovery >35% between 90 days and 1 year. Results Baseline mean LVEF was 27%. At 3 months, mean LVEF increased to 37% ( P < 0.001), and 58% of patients achieved LVEF >35%. These patients showed further improvement to a median LVEF of 45% at 12 months. Among those with LVEF ≤35% at 3 months ( n = 44), only eight patients (18%) recovered by 12 months, six of whom received cardiac resynchronization therapy. The rapid initiation and optimization of GDMT, particularly ARNI and SGLT2i, was associated with early LVEF improvement. Conclusions Early and intensive GDMT optimization resulted in significant LVEF improvement within the first 3 months post‐diagnosis for most patients. Those who failed to recover by this point exhibited limited improvement by 1 year. These findings suggest that the conventional 3 month window for ICD decision making remains appropriate, despite advancements in heart failure therapy.

Heart failure (HF) management increasingly requires multimodal assessment beyond cardiac function. Although echocardiography remains central, skeletal muscle and diaphragmatic dysfunction-key drivers of exercise intolerance-are underdiagnosed. This review synthesizes two critical aspects: (1) the pathophysiological heterogeneity of muscle involvement across HF subtypes [HF with reduced ejection fraction (HFrEF), HF with mildly reduced ejection fraction (HFmrEF), and HF with preserved ejection fraction (HFpEF)] and (2) the clinical utility of muscle ultrasound as a dynamic, bedside-compatible tool for risk stratification and personalized interventions. Emerging evidence reveals distinct mechanisms: HFrEF predominantly associates with diaphragmatic atrophy and mitochondrial dysfunction, whereas HFpEF is characterized by reduced diaphragmatic motion and skeletal muscle fat infiltration. Ultrasound-derived parameters, such as echo intensity for quadriceps fat quantification and diaphragm thickness ratio for inspiratory weakness, strongly correlate with functional outcomes (e.g., 6-min walk distance and peak VO2). Notably, a quadriceps echo intensity > 28 dB in HFrEF or a diaphragmatic excursion < 2.5 cm in HFpEF independently predicts adverse prognosis, guiding targeted interventions such as inspiratory muscle training or anti-inflammatory therapies. However, critical gaps persist, including the lack of standardized cutoff values for HF subtypes and insufficient data on ultrasound-guided therapeutic monitoring. Future research should prioritize subtype-specific protocols and validate cost-effective ultrasound algorithms against standard modalities. By bridging pathophysiology and clinical application, this review underscores muscle ultrasound's transformative potential in refining HF phenotyping, ultimately enhancing exercise capacity and reducing hospitalizations.

Anthracyclines, which are key to many chemotherapeutic protocols, have been associated with increased vascular stiffness, a major factor associated with cardiovascular morbidity and mortality. There is no evidence-based intervention to prevent anthracycline-associated vascular dysfunction. To investigate whether atorvastatin pretreatment is associated with attenuation of the anthracycline-induced increase in aortic stiffness. This study is a secondary analysis of a double-blind, randomized clinical trial (Statins to Prevent the Cardiotoxicity From Anthracyclines [STOP-CA]). Enrollment occurred between January 25, 2017, and September 10, 2021, with the last follow-up on October 10, 2022. Primary analyses were reported on August 8, 2023. STOP-CA was a multicenter trial across 9 academic centers in the US and Canada. Participants were patients with newly diagnosed lymphoma scheduled to undergo anthracycline-based chemotherapy with no clinical indication for a statin. Atorvastatin (40 mg, once daily) or placebo for 12 months. This subanalysis of the STOP-CA trial includes post hoc end points with cardiac magnetic resonance imaging-derived aortic arch pulse wave velocity (PWV) and aortic distensibility (AD). An intention-to-treat approach was applied. The proportions of participants with a 1 SD or more increase in PWV and a 1 SD or more decrease in ascending aortic distensibility (AAD) were calculated in each group over 12 months. An increase in PWV of 0.15 m per second or more, a previously defined annual rate in individuals of similar age, was also assessed as a secondary end point. Of the 300 participants (150 randomized to atorvastatin and 150 randomized to placebo), 152 (mean [SD] age, 51 [17] years; 72 female [47%]; 82 treated with atorvastatin) had paired PWV data, and 168 had paired AD data. The PWV values remained similar in the atorvastatin group (mean [SD], 6.5 [1.9] vs 6.5 [2.0] m per second) but increased in the placebo group (5.7 [1.8] vs 6.8 [2.0] m per second) over 12 months. A 1 SD or more increase (0.8 m per second) in PWV was observed among 4 of 82 patients (5%) with atorvastatin and 35 of 70 patients (50%) with placebo (odds ratio, 0.05; 95% CI, 0.02 to 0.16; P < .001) at 12 months. A 1 SD or more decrease (1.8 × 10-3 mm Hg-1) in AAD was observed among 6 of 88 patients (7%) with atorvastatin and in 14 of 80 patients (18%) with placebo. A 1 SD or more increase in PWV was associated with a mean left ventricular ejection fraction decline of 2.70% (95% CI, -4.65% to -0.81%; P = .006). Pretreatment with atorvastatin was associated with preservation of vascular function among patients with lymphoma undergoing anthracycline-based chemotherapy. ClinicalTrials.gov Identifier: NCT02943590.

Conceptual Models to Explain Heart Failure With a Preserved Ejection Fraction: a Tale of Futility, Frustration, and Perhaps, Fruition.

Adult survivors of childhood cancers are thought to be at high risk for late-onset cardiovascular complications of prior anti-cancer treatments. While cancer therapy-related cardiac dysfunction (CTRCD) has previously been observed in this population, data are limited regarding the utility of longitudinal echocardiographic monitoring. 124 adult survivors of childhood cancer who were previously treated with anthracyclines and/or radiation therapy as children were included in this longitudinal cohort study. Participants were enrolled in Northwestern Medicine's survivorship clinic: Survivors Taking Action and Responsibility (STAR) Program and followed for up to10 years between 2009 and 2022. Serial echocardiography was performed at baseline then at 1, 3, 5, and 7-10 years post-enrollment. Clinical data was collected by chart review. Major adverse cardiovascular events (MACE) and CTRCD were adjudicated according to ACC/AHA MACE criteria and the ESC Cardio-Oncology guidelines respectively. Over 10 years of follow-up in the STAR Program, 17.7% (22/124) of participants developed MACE, with the highest incidence observed in patients treated with radiation alone. 10.5% (13/124) of patients developed CTRCD by left ventricular ejection fraction (LVEF) criteria while 36.3% (45/124) developed CTRCD by global longitudinal strain (GLS) criteria. New incidence of MACE and CTRCD occurred as late as 7-10 years post-enrollment. Participants who developed CTRCD showed subsequent improvement in both LVEF and GLS by the end of 10 years of follow-up and treatment in the STAR Program. Survivors of childhood cancer are at high risk for both MACE and CTRCD even many years after initial diagnosis. Patients who received treatment for pediatric cancer, then subsequently enrolled in the STAR Program as adults and received appropriate cardiovascular monitoring and treatment showed improvement in both LVEF and GLS by the end of follow-up, underscoring the importance of a dedicated survivorship clinic for adult survivors of pediatric cancer.

Background.Increased exhaled breath acetone (EBA) concentrations might reflect impaired myocardial energetics and haemodynamic stress. We investigated the relation of EBA and cardiac structure, function, and exercise capacity in patients with or at risk of heart failure (HF).Methods.We enrolled outpatients with HF and reduced (<50%, HFrEF) or preserved (>50%, HFpEF) left ventricular ejection fraction (LVEF) and subjects with cardiovascular risk factors and/or structural heart disease without established HF. All participants underwent clinical and laboratory evaluation, resting transthoracic echocardiography, and a combined cardiopulmonary-echocardiographic stress test with EBA monitoring at rest (EBArest) and during exercise (EBAex).Results.Patients with HFpEF (n= 62) were older and more often female than those at risk of HF (n= 50) or with HFrEF (n= 41). EBArest(1.5, interquartile range (IQR) 1.0-3.1 vs 0.9, IQR 0.7-1.2 mcg l-1) and EBAex(2.4, IQR 1.5-4.4 vs 1.1, IQR 0.9-2.1 mcg l-1; allp< 0.0001) were significantly higher in patients with HF compared to others. Among HF patients, those in the highest EBAresttertile had lower LVEF, greater echocardiographic signs of congestion, higher NT-proBNP levels, and lower peak oxygen consumption, indicating impaired exercise capacity. In multivariate regression, NT-proBNP (p= 0.0004) and the slope of minute ventilation to carbon dioxide production (p= 0.0013) were independent predictors of EBArest(adjustedR2= 0.458).Conclusions.EBA concentrations are higher in patients with HF compared to those without, regardless of LVEF, and are associated with markers of disease severity. Further studies are needed to determine whether EBA measurement can aid in HF diagnosis and management.

Heart failure (HF) is slightly more common in primary aldosteronism (PA) than in essential hypertension, but early-onset HF remains rare. In such cases, underlying genetic cardiomyopathies should be considered. Autonomously secreted aldosterone and activation of the renin-angiotensin-aldosterone system can lead to extremely high aldosterone levels, worsening cardiac function and creating major therapeutic challenges. A 39-year-old male presented with progressive chest tightness and shortness of breath for 4 months. He had a 7-year history of hypertension and persistent hypokalemia. Electrocardiogram revealed a markedly reduced left ventricular ejection fraction of 18.3%. The patient was diagnosed with PA based on elevated plasma aldosterone concentration, an increased aldosterone-to-renin ratio, and a positive captopril challenge test. Computed tomography and adrenal vein sampling indicated unilateral PA. After initial HF management, the patient underwent laparoscopic adrenalectomy for PA treatment. According to the primary aldosteronism surgical outcome consensus criteria for postoperative evaluation of PA, complete biochemical remission (normalization of aldosterone-to-renin ratio and potassium) and partial clinical remission (stable blood pressure with reduced antihypertensive medication) were achieved 1 month postoperatively and have been maintained since. At the 8-month follow-up, his left ventricular ejection fraction had improved to 45.4% and BNP levels normalized. Whole-exon sequencing revealed a missense mutation of the dystrophin (DMD) gene. Certain DMD mutations are linked to X-linked dilated cardiomyopathy with absent or subclinical skeletal muscle involvement. Sanger sequencing confirmed the hemizygous mutation in the proband. The final diagnosis was poorly controlled PA with early-onset HF, potentially influenced by a coexisting DMD gene missense mutation that may modify both the onset and severity of PA-related HF. Early recognition and surgical treatment of PA with early-onset HF can substantially improve cardiac function, even in the presence of genetic susceptibility to cardiomyopathy. This case underscores the need to consider underlying cardiac genetic disorders in PA patients with atypical or early-onset HF and raises the hypothesis that the identified DMD variant may serve as a potential genetic modifier of HF severity in the context of PA.

This study aimed to examine the effects of sodium-glucose cotransporter 2 inhibitors (SGLT2i) on cardiac structure and cardiorenal function in older adults with hypertension and pre-heart failure. A total of 88 patients with hypertension and pre-heart failure who received care at the hospital between August 2022 and August 2024 were enrolled and randomly assigned to either a dapagliflozin group or a conventional treatment group. Changes in N-terminal pro-brain natriuretic peptide (NT-proBNP), troponin I (TnI), estimated glomerular filtration rate (eGFR), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP), procalcitonin (PCT), left ventricular end-diastolic volume (LVEDV), ejection fraction(EF), left atrial volume index (LAVI), and left ventricular mass index (LVMI) were assessed and compared between the two groups before and after three months of treatment. No significant differences were observed in NT-proBNP, TnI, eGFR, IL-6, and hsCRP levels between the two groups before treatment. Additionally, there were no differences in PCT, TnI, and LVEDV between the groups at three months post-treatment. However, IL-6, hsCRP, and eGFR levels were significantly lower in the dapagliflozin group compared to the conventional treatment group at three months post-treatment (P < 0.05). Additionally, the LAVI was significantly lower in the dapagliflozin group relative to the conventional treatment group, with the difference being statistically significant (P < 0.05). These findings indicate that SGLT2i therapy may contribute to early myocardial remodeling and improvement in cardiorenal function in older adults with hypertension and pre-heart failure. Furthermore, prolonged SGLT2i administration appears to exert anti-inflammatory effects.

Renin-angiotensin system (RAS) activation in heart failure (HF) increases circulating angiotensin II (AII). This increases blood pressure (BP) and promotes adverse ventricular remodeling that makes HF worse. Although human HF increases with age and differs between the sexes, preclinical studies have used young, mostly male animals. We investigated sex differences in AII-induced cardiac remodeling in aging C57BL/6 mice. Mice (≈16months) were infused with AII (3mg/kg/day; 6weeks; osmotic minipumps). BP (tail cuff), ventricular structure/function (echocardiography), M1 (Cd80/Mcp-1/Cd68), and M2 (Mrc1) macrophage markers and profibrotic markers (transforming growth factor beta (Tgfb1), collagen 1 (Col1a1), collagen 3 (Col3a1); qPCR/Western blot) were measured. AII treatment increased BP and heart weight/tibia length in both sexes. Interestingly, AII increased wall thickness in females but reduced it and caused left ventricular (LV) dilation in males only. AII increased E/A ratios in males and isovolumic relaxation time in both sexes, indicative of diastolic dysfunction. However, isovolumic contraction time (IVCT) increased (12.0 ± 0.7 vs. 24.3 ± 3.0ms; p = 0.0001) and ejection fraction (EF) declined in males (68.9 ± 1.9 vs. 46.1 ± 4.5; p = 0.0001), which indicates marked systolic dysfunction. By contrast, IVCT was unaffected, and EF declined but remained well above 50% in females (68.1 ± 1.3 vs. 55.9 ± 2.0; p = 0.01). mRNA for macrophage markers (Cd80, Mrc1), Tgfb1, Col1a1, and Col3a1, plus collagen 1 protein increased in treated male ventricles. By contrast, AII increased collagen 3 protein in females compared to treated males. Thus, AII promotes inflammatory/profibrotic signaling, which contributes to fibrosis and impairs systolic function in aging males. Older females appear resistant to these effects.

Takotsubo cardiomyopathy, also known as stress-induced cardiomyopathy, is a transient cardiac condition characterized by acute but reversible left ventricular dysfunction, typically triggered by emotional or physical stress. While Takotsubo cardiomyopathy usually occurs in the absence of significant coronary artery disease, its coexistence with severe coronary artery disease is uncommon and presents diagnostic and therapeutic challenges. We report the case of a 56-year-old Asian woman with a history of hypertension and diabetes who presented with acute chest pain following an intense emotional and physical altercation. On admission, she was hemodynamically stable, with electrocardiogram showing minor ST-segment elevation in the anterior leads and modest troponin rise. Bedside echocardiography revealed apical akinesia suggestive of Takotsubo cardiomyopathy. Coronary angiography demonstrated high-risk multivessel coronary artery disease, including significant left main disease. Cardiac function rapidly improved within 5 days, with normalization of left ventricular ejection fraction and global longitudinal strain, consistent with Takotsubo cardiomyopathy. Given her refusal of coronary artery bypass grafting, percutaneous coronary intervention to the left main and left anterior descending was successfully performed. She was discharged home on optimal medical therapy in stable condition. This case highlights the diagnostic complexity when Takotsubo cardiomyopathy coexists with severe coronary artery disease. It emphasizes the importance of considering Takotsubo cardiomyopathy in patients with acute chest pain even in the presence of significant coronary lesions, as Takotsubo cardiomyopathy may unmask otherwise silent but clinically important coronary artery disease.

Abstract Introduction Heart Failure is a highly prevalent condition that can lead to a reduced Ejection Fraction (HFrEF) due to deterioration in cardiac output. It remains a condition with some of the highest morbidity and mortality rates. Novel therapies (ACE inhibitors or ARNIs, beta-blockers, MRAs, and SGLT2 inhibitors) – also named the four pillars of heart failure management have proven to slow progression and reduce hospital readmissions. However, despite their proven effectiveness, under-prescribing of these agents remains a significant concern. Aim This study aimed to review prescribing patterns for patients with HFrEF within the Primary Care Networks (PCNs) of the Dudley area, to identify gaps in the utilisation of the four pillars of HF therapy, and to develop recommendations to improve prescribing practices. Methodology A retrospective review was conducted across six PCNs in the Dudley area. Patients were identified using SNOMED codes within the EMIS electronic patient record system. The dataset included anonymised data for 3,940 patients coded with a diagnosis of HF and a reduced ejection fraction, and who were receiving at least one of the four pillar medications (ACE inhibitors, Beta Blockers, MRAs, and SGLT2 inhibitors). Descriptive data analysis was performed using Microsoft Excel. Since the study used anonymised retrospective data collected for service evaluation purposes, it did not require formal ethical approval. Results Among the 3,940 identified patients, 85% had been prescribed a Beta Blocker. However, prescribing rates for the remaining three pillar drugs were significantly lower, with only 62% of patients receiving three out of four recommended therapies. Dosing data revealed that a large proportion of patients were prescribed less than 50% of the target optimal dose, suggesting suboptimal titration practices. Discussion The findings reveal a significant gap in the optimisation and comprehensive prescribing of the four pillars of HF therapy in primary care across the Dudley PCNs. Although Beta Blocker usage is high, the underuse and underdosing of the other three pillar drugs suggest a need for improved clinical decision-making and medication titration. Limitations of this study include its retrospective nature and the reliance on coded data, which may not fully capture all clinical decision factors. The results highlight the importance of multidisciplinary collaboration and targeted educational interventions to support guideline-concordant prescribing and ultimately improve clinical outcomes for HF patients in the Dudley health economy.

Hypertrophic cardiomyopathy (HCM) is the most common myocardial genetic disease characterized by left ventricular hypertrophy (LVH) and diastolic dysfunction with preserved or elevated ejection fraction. Thirty-five years after the identification of the first genetic variant in myosin heavy chain 7, other variants have been discovered in numerous components of the sarcomere, pointing to a primary defect in cardiomyocyte contractility. Still, a large portion of HCM patients does not have a pathogenic variant and others present with LVH of another genetic origin. Research has uncovered a primary driver of hypercontractility at the sarcomere level and diverse molecular and cellular mechanisms contributing to HCM, including alterations of calcium handling and proteolysis, microtubule modifications, energy deficiency, and the impact of noncardiomyocyte cell types. These discoveries have fueled preclinical and translational research, leading to the development of myosin inhibitors, which are now on the market, and gene-based therapeutic products. This review summarizes current knowledge on the genetics, mechanisms, and targeted treatments of HCM.

Exercise intolerance and volume overload are key symptoms that characterize the complex syndrome called heart failure with preserved ejection fraction (HFpEF). The increased pulmonary capillary wedge pressure (PCWP) also contributes significantly to these symptoms. A promising intervention, greater splanchnic nerve (GSN) ablation, is an approach that alleviates this volume overload by modulating sympathetic tone. This mini-narrative review discusses data from six (6) clinical trials investigating the effects of GSN ablation in HFpEF. These studies focus on procedural safety, hemodynamic outcomes (PCWP), clinical measures (NYHA class, KCCQ score), and adverse events. The trials varied in terms of sample size, patient characteristics, and follow-up durations, with a total of 259 patients. In addition, the outcomes were assessed at 1, 3, 6, and 12months. The studies report positive outcomes with reductions in PCWP, especially during exercise. The NYHA classes and KCCQ scores were also improved in patients. Exercise capacity was measured by the 6-min walk test, and studies reported notable gains. NT-proBNP levels were also decreased, indicating an improvement in heart failure status. Some trials reported mild procedural complications such as pain and site injection; however, no significant adverse events were reported. GSN ablation presents a therapeutic approach for patients with HFpEF. While short-term benefits are evident, further large-scale randomized trials are necessary to confirm the long-term efficacy and safety of this procedure. In addition, its application in patients with diverse characteristics and comorbidities needs to be investigated and validated before it is incorporated into clinical practice.

Cardiac Biomarkers, Intensive Lifestyle Intervention, and Heart Failure Subtypes in Diabetes: Look AHEAD Cardiac Biomarker Ancillary Study.

Low dose of landiolol does not prevent postoperative atrial fibrillation after cardiac surgery in non-Asian patients: a multicentre randomised study.

The development of atrial fibrillation (AF) has important prognostic implications in patients undergoing percutaneous coronary intervention (PCI), due to the concurrent need for both antiplatelet and anticoagulant therapies. This study aimed to evaluate the long-term incidence and predictors of AF in patients with acute coronary syndrome (ACS) undergoing PCI. We prospectively enrolled 337 consecutive ACS patients in sinus rhythm who underwent PCI and did not develop AF during hospitalization. Patients were followed every six months for up to 72 months. Follow-up data were available for 300 patients (89%); 37 patients were lost to follow-up. At the end of follow-up, 34 patients (11.3%) had developed AF. Kaplan-Meier analysis demonstrated that mitral annular calcification (MAC) was significantly associated with an increased incidence of AF from the early stages (χ2 = 24.620, log-rank p < 0.001). Multivariate Cox regression identified body mass index (BMI) (HR: 1.070; 95% CI: 1.010-1.130; p = 0.022), left ventricular ejection fraction (LVEF) (HR: 0.942; 95% CI: 0.918-0.916; p < 0.001), mitral annular late diastolic velocity (Am) (HR: 0.785; 95% CI: 0.707-0.872; p < 0.001), and mitral annular calcification (MAC) (HR: 4.066; 95% CI: 1.976-8.368; p < 0.001) as independent predictors. These findings provide important insights into the long-term risk of AF after PCI in ACS patients and may support early identification and management of high-risk individuals.

Non-ST-segment elevation acute coronary syndrome (NSTE-ACS) is a major contributor to cardiovascular mortality, yet reliable tools for individualized mortality prediction remain limited. Machine learning offers the potential to enhance prognostic accuracy in this high-risk population. A total of 1,495 patients with NSTE-ACS who underwent percutaneous coronary intervention (PCI) were retrospectively analyzed. Eight clinical and laboratory variables were selected through univariate and multivariate logistic regression. Five machine learning models-logistic regression, random forest, XGBoost, LightGBM, and naïve Bayes-were constructed. Model performance was evaluated using area under the curve (AUC) and calibration curves. Age, diabetes mellitus, and ejection fraction were identified as independent predictors of all-cause mortality. Among all models, LightGBM achieved the highest AUC (0.847), followed by XGBoost (0.822), both of which demonstrated superior discrimination and calibration compared to traditional logistic regression and other algorithms. Calibration analysis showed excellent agreement between predicted and observed mortality in both training and test cohorts. Gradient boosting models, particularly LightGBM and XGBoost, significantly improve mortality prediction in NSTE-ACS patients after PCI. These models may facilitate more accurate risk stratification and guide personalized post-procedural management strategies in clinical practice.

Evidence-based and/or consensus guidance regarding exercise and return-to-play for the adolescent and young adult (AYA) athlete with cardio-oncology concerns is lacking. Many of the recommendations utilized for the diagnosis, surveillance, and management of cancer therapeutic-related cardiotoxicity in children have been extrapolated from adult literature and myocarditis guidelines, the latter of which are primarily concerned with potential for arrhythmias secondary to inflammation and myocardial scarring. In addition, the athlete's heart itself brings about several diagnostic challenges including physiologic changes due to endurance or isometric training. Exercise-induced cardiac remodeling, with enlarged cavity size, lower resting ejection fraction and increased left ventricular wall thickness, depending on the type of exercise, can mimic disease states including both underlying pathologies and the response to cancer therapeutics. A high school cancer survivor had borderline ejection fraction and abnormal strain indices. He was able to return to competitive sports without complication after clinical evaluation and through a shared decision-making process. The difficulty in differentiating physiologic from potentially pathologic echocardiographic changes can result in unnecessary disqualification, depriving athletes from social, psychological, and possibly financial benefits. Stress echocardiography indices, such as contractile reserve and mitral E/e' ratio, may inform assessment of systolic and diastolic function, respectively, and may be helpful in risk stratifying and understanding potential performance limitations in AYA athletes with cardio-oncology concerns for exercise and return-to-play. Most recent consensus statements regarding sports participation in the athlete with heart disease focus on a shared decision-making process amongst all stakeholders involved to formulate an informed, safe, and cohesive prescription to enable the athlete to safely re-engage in sports after recovering from a cardiac illness or surgery. Multidisciplinary recommendations emphasize the importance of exercise before, during, and after chemotherapy in an individualized approach to reduce risk factors in oncology patients and improve cardiovascular outcomes. Further research is needed to delineate protocols for the adolescent and young adult cardio-oncology athlete regarding exercise prescriptions and their return-to-play following oncology treatment.

Background: Takotsubo syndrome (TTS) is an acute cardiac condition characterized by transient left ventricular dysfunction. Although generally considered reversible, early arrhythmias are a dreaded complication and their prognostic significance remains incompletely understood. Methods: In this study, 104 consecutive patients diagnosed with TTS (January 2007 to September 2024) were examined for the prognostic relevance of in-hospital arrhythmias during monitoring at the time of diagnosis. The median follow-up was 2.1 years. The primary combined endpoint included cardiac death, TTS recurrence, occurrence of arrhythmias, and rehospitalization for cardiac causes. Results: In-hospital arrhythmias occurred in 35.6% of the patients. Ventricular arrhythmias were significantly associated with an increased risk of adverse cardiac events (odds ratio 3.94, 95% confidence interval 1.22–12.69; p = 0.021). Reduced left ventricular ejection fraction and QTc prolongation, while frequently observed, were not independently associated with adverse outcomes when analyzed separately from arrhythmic events. Supraventricular arrhythmias exhibited a non-significant trend (p = 0.145). Conclusions: In a large registry of consecutive TTS patients, in-hospital ventricular arrhythmias at diagnosis were significantly associated with adverse outcomes, underscoring the importance of early rhythm monitoring.

Heart failure with preserved ejection fraction (HFpEF) currently accounts for half of the heart failure (HF) cases world-wide, affecting nearly 32 million people. HFpEF has a skewed prevalence toward females and those older than 65 years old. The pathophysiology of HFpEF is suggestive of a conglomerate of inflammatory, hypertensive, as well as metabolic dysfunction, giving rise to the syndrome. Disruptions in ceramide metabolism do occur in heart failure as well as within the HFpEF-associated risk factors, both modifiable inflammation, obesity, hypertension, diabetes, and non-modifiable-aging, and female sex. The focus of this review is to draw attention to the links between changes in female biophysiology, such as pregnancy, menopause and aging, in which ceramide is dysregulated and consequently gives rise to the same pathologies that are labeled as risk factors for HFpEF. Our objective is to highlight ceramides as potential biomarkers for prevention and initial diagnostic tools for HFpEF, especially for women later in life.