Left ventricular diastolic dysfunction (LVDD) is highly prevalent in end-stage renal disease (ESRD) but remains difficult to assess accurately. The 2025 American Society of Echocardiography (ASE) update has introduced left atrial reservoir strain (LARS) as a novel parameter for estimating left ventricular filling pressure. This retrospective study included 109 maintenance hemodialysis (HD) patients who underwent comprehensive echocardiography immediately before and after dialysis, yielding a total of 218 paired examinations for analysis. Left ventricular (LV) diastolic function was evaluated according to both the 2016 ASE/EACVI and 2025 ASE algorithms. Concordance and reclassification between the two algorithms were assessed using Cohen's κ coefficient. Hemodynamic and echocardiographic parameters were compared to characterize volume-related changes. Hemodialysis significantly reduced LV volumes, cardiac output, ratio of early diastolic mitral inflow velocity to mitral annular velocity (E/e' ratio), and pulmonary artery systolic pressure. These findings indicate effective preload reduction after HD, whereas GLS and LARS also decreased in parallel with the reduction in volume load. Using the 2016 criteria, 32% of patients were classified as indeterminate in the pre-HD cohort. Application of the 2025 ASE algorithm eliminated all indeterminate cases: 29 cases previously labeled as "normal" were reclassified as Grade 1 LVDD, and 47 indeterminate cases were reassigned to normal (n = 13), Grade 1 (n = 20), or Grade 2 (n = 14) LVDD. Overall concordance between the two systems was good (κ = 0.682, p < 0.001). Together, these reclassifications effectively reduced the rate of indeterminate classifications. The updated 2025 criteria demonstrated improved classification specificity and reduced diagnostic uncertainty compared with the 2016 guidelines, facilitating earlier categorization of diastolic dysfunction and addressing the major limitation of a high rate of indeterminate classifications.

Diagnostic Accuracy of Machine Learning Algorithms in Electrocardiogram-Based Heart Failure Detection: A Systematic Review and Meta-Analysis.

Echocardiographic strain imaging and progression of atrial fibrillation in low-risk individuals.

Reconstitution of gut microbiota by medicinal plant isoflavones ameliorates heart failure with preserved ejection fraction.

ABSTRACTBackgroundDoppler‐based diastolic dysfunction assessment requires optimal apical views and specialized expertise, and up to 30% of evaluations yield indeterminate results. We investigated whether a parasternal long‐axis (PLAX)–only M‐mode scoring system derived from mitral valve anterior leaflet (MVAL) motion could provide clinically useful risk stratification for moderate‐to‐severe left ventricular diastolic dysfunction (LVDD).MethodsThis retrospective study analyzed echocardiographic data from 253 patients. Novel M‐mode parameters (EPSS, APSS, EPOL, APOL, and their ratios) were compared with conventional Doppler indices across LVDD severity grades (normal, grade 1, grade 2, grade 3). A logistic regression‐based scoring system combining five M‐mode parameters was developed and internally evaluated using five‐fold cross‐validation with bootstrap confidence intervals.ResultsThe EPOL/APOL ratio showed moderate correlations with the E/A ratio in both normal‐to‐mild (r = 0.353, p < 0.001) and moderate‐to‐severe (r = 0.397, p = 0.001) LVDD groups. The logistic regression–derived scoring system achieved an AUC of 0.754 (95% CI: 0.672–0.825), with 55.7% sensitivity and 85.9% specificity at the optimal cutoff of 63.5. Decision curve analysis demonstrated positive net benefit over default strategies across the clinically plausible threshold probability range of 0.15–0.35.ConclusionA PLAX‐only M‐mode scoring system provides acceptable discrimination and positive net clinical benefit for risk stratification of moderate‐to‐severe LVDD. External validation in independent populations is required before clinical implementation.

26-A-13708-ACC PACING-INDUCED LEFT VENTRICULAR DYSFUNCTION IN ASYMPTOMATIC PATIENTS WITH CHRONIC RV PACING: IS ROUTINE ECHOCARDIOGRAPHIC SCREENING JUSTIFIED?

26-CCC-12585-ACC WALKING INTO SUDDEN DEATH: BECKER’S MUSCULAR DYSTROPHY AND THE HIDDEN BURDEN OF SEVERE LEFT VENTRICULAR DYSFUNCTION

Coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) are the two dominant revascularisation strategies for obstructive coronary artery disease, yet their relative roles continue to shift because they address coronary pathophysiology differently with ever-evolving techniques. PCI has advanced through iterative improvements, including balloon angioplasty, bare-metal stents, and drug-eluting stents, with contemporary outcomes increasingly driven by procedural optimisation using intracoronary imaging and physiology-guided lesion selection rather than device category alone. CABG has progressed through perioperative management, improvements in operative safety, and, critically, conduit durability. Recognition of progressive saphenous vein graft failure has underpinned a conduit-optimisation era in which the left internal mammary artery to left anterior descending artery remains the gold standard. Further, broader arterial grafting (including radial artery use, multiple arterial grafting, and selected total-arterial strategies) has been increasingly applied, albeit with deliverability and competing-risk constraints highlighted in randomised evidence. This perspective review reframes the CABG versus PCI comparison not as a binary contest, but as a context-dependent assessment in which the relative value of each strategy depends on the specific technologies, techniques, and conduits available at the time of comparison. We summarise comparative effectiveness where evidence is most consistent and where it remains sensitive to anatomy, comorbidity, and endpoint definitions. In diabetes with multivessel disease, trial data favour CABG for long-term survival and clinical outcomes despite higher stroke risk. In left main disease, outcomes depend on lesion pattern and overall complexity, with trial-era stent technology and composite endpoint definitions influencing conclusions. In ischaemic left ventricular dysfunction, a long-term survival benefit is established for CABG added to medical therapy, while multi-vessel PCI has not demonstrated comparable prognostic modification in contemporary data. We then examine hybrid coronary revascularisation as territory-specific allocation, highlighting its physiological rationale, program dependence, and limited, adequately powered randomised evidence. Finally, we outline how artificial intelligence (AI) and robotics may accelerate a precision revascularisation paradigm by standardising lesion assessment, supporting procedural planning, improving procedural reproducibility, and enabling more patient-specific selection among PCI, contemporary CABG with optimised conduits, and hybrid pathways.

Takotsubo syndrome (TTS) is an acute and reversible form of heart failure characterised by transient left ventricular (LV) dysfunction in the absence of obstructive coronary artery disease and often triggered by emotional or physical stress. Although the clinical presentation may mimic acute coronary syndrome, the underlying mechanisms remain incompletely understood. Recent evidence highlights coronary microvascular dysfunction (CMD) as a key factor contributing to myocardial ischaemia and transient LV dysfunction in TTS.CMD in TTS appears multifactorial, involving autonomic dysregulation, endothelial dysfunction, inflammation and myocardial oedema, all contributing to transient impairment of myocardial perfusion. Invasive studies consistently demonstrate elevated microvascular resistance and reduced coronary flow reserve during the acute phase, with gradual recovery and improvement in LV function. CMD in TTS has also been associated with adverse prognosis, including higher mortality and persistent LV dysfunction.This narrative review summarises current evidence supporting the pivotal role of CMD in the pathophysiology and prognosis of TTS. We discuss the invasive and non-invasive techniques used to assess CMD, explore the neuro-immune-cardiac interplay underlying TTS and discuss ongoing clinical trials that may refine future diagnostic and therapeutic strategies targeting CMD in TTS.

Primary cardiac tumors are exceedingly rare in the pediatric population, with cardiac fibromas (CFs) representing the second most common benign neoplasm. Although histologically benign, these intramural tumors frequently precipitate life-threatening, intracavitary obstruction, and sudden cardiac death. We present the case of a 9-year-old male who presented with exercise-induced syncope and was found to have a large, arrhythmogenic interventricular septal fibroma. The patient underwent successful complete surgical excision with patch reconstruction, resulting in immediate resolution of his arrhythmia burden. However, 5 years postoperatively, he developed a late, infiltrative recurrence at the patch margin, precluding complete re-resection. Despite partial debulking and implantable cardioverter-defibrillator placement, the patient experienced progressive left ventricular dysfunction and refractory heart failure, ultimately succumbing to the disease at age 19 while awaiting heart transplantation. This case underscores the unpredictable long-term biological behavior of cardiac fibroma. It highlights the critical diagnostic role of multimodal imaging, the surgical challenges of septal reconstruction, and the rare but devastating potential for late recurrence. Furthermore, it emphasizes the necessity of lifelong surveillance and the complex interplay between repeated surgical interventions, chronic arrhythmia, and progressive myocardial failure in pediatric patients with recurrent cardiac fibromas.

Background. Yellow phosphorus is a highly toxic rodenticide known to cause fulminant hepatic failure and cardiotoxicity. Adolescent ingestions are often impulsive and associated with emotional distress. Case presentation. We report a 16-year-old girl who ingested approximately 5 g of yellow phosphorus and developed progressive hepatitis, coagulopathy, and severe reversible left ventricular dysfunction. Early administration of N-acetylcysteine and six cycles of plasma exchange led to full hepatic and cardiac recovery. Cardiac dysfunction developed during the acute hepatic failure phase and resolved within 10 days. The patient was followed up for 14 days until discharge. Conclusion. Early aggressive management, including therapeutic plasma exchange, may improve survival in severe yellow phosphorus poisoning. Cardiac dysfunction may be reversible. Psychiatric care is essential in adolescent toxic ingestions.

Abstract Introduction Spontaneous Coronary Artery Dissection (SCAD) is a significant cause of non-atherosclerotic acute myocardial infarction (AMI), predominantly affecting young to middle-aged women. It is also a leading cause of post-partum MI. Typically; SCAD occurs in patients with fewer cardiovascular risk factors than atherosclerotic AMI. Approximately 3-5% of SCAD patients present with cardiac arrest (CA). According to current ESC guidelines, patients with an LVEF below 40% at discharge following an acute myocardial infarction should undergo repeat Left Ventricular Ejection Fraction (LVEF) assessment 6–12 weeks later, and ICD implantation is recommended if significant and persistent left ventricular dysfunction is present. A previous cohort study in a SCAD population suggested an increased future risk of ventricular arrhythmia in SCAD patients whose first presentation was with ventricular fibrillation or ventricular tachycardia. Clinicians often adopt a precautionary approach, resulting in variability in real-world practice. Purpose This study investigated whether SCAD patients with cardiac arrest received ICDs despite preserved LVEF, potentially in discordance with ESC post-AMI guidelines. Results Of 2,742 SCAD patients, 100 (3.65%) presented with CA. The median age of all patients presenting with CA was 47.0 years and predominantly female (95%). Co-morbidities included hypertension (24.2%), diabetes (4.04%), a smoking history (38.4%), and a mean body mass index of 27.3 kg/m2. On initial ECG, 19.7% had ST-elevation myocardial infarction. The most common SAW class was Type 2, with 2a being most common at 44.8%, and 2b being second most common at 28.1% of cases. Type 4 SCAD was seen in 13.5% of cases. Most commonly affected vessel was the Left Anterior Descending artery (62.3%), with 10.9% having a multi-vessel SCAD. Twenty patients (20.0%) received an ICD, with no significant difference in demographics between patients with, and without ICDs. Presenting ECG showing STEMI was numerically more frequent in the ICD group (31.3% vs 17.1%, p=0.21). There was no statistical difference in SAW class, and vessel distribution (p=0.10). Overall, 50% had preserved LVEF, 45% had mildly impaired LVEF, and 3% had severely impaired LVEF. Within the ICD group, 10 patients had preserved LVEF, 7 had mildly impaired LVEF, and 3 had severely impaired LVEF. Hence, only three patients met guideline-based criteria for ICD implantation based on LVEF. Discussion: We found that 85% of ICD implantations in this SCAD cohort were outside current guidelines. This likely reflects clinician uncertainty regarding the true risk of sudden cardiac death in this group, and emphasises the need for improved risk stratification. Further study is required to evaluate long-term outcomes and recurrence risk in this subgroup. In order to better inform the balance between potential protection from sudden death, and the procedural and psychological risks of ICD implantation.

High risk and low incidence diseases: Peripartum cardiomyopathy.

Beta Blockers After Acute Myocardial Infarction Without Left Ventricular Systolic Dysfunction: A Meta-Analysis of Randomized Controlled Trials.

Peripartum cardiomyopathy (PPCM) is a potentially life-threatening condition. The histological characteristics of PPCM as risk factors for poor outcomes have not been thoroughly investigated. This study evaluated the pathological findings of PPCM, with a particular focus on inflammatory factors such as tenascin-C (TNC) and interleukin-6, which may predict left ventricular dysfunction and the prognosis of PPCM. We conducted a retrospective single-center observational study involving endomyocardial biopsies (from 27 patients) as clinically diagnosed PPCM. We assessed the association between the histology and cardiac events, namely cardiac death, left ventricular assist device implantation, and/or heart transplantation. During the median follow-up period of 2,100 days, 7 (25.9%) composite events were documented. Kaplan-Meier survival curves demonstrated that patients with advanced cardiac fibrosis had significantly poorer long-term outcomes than those with mild cardiac fibrosis (log-rank P=0.0003). Furthermore, TNC-positive patients with advanced fibrosis had significantly worse event-free survival than TNC-negative patients with advanced fibrosis and patients with mild fibrosis (Bonferroni-adjusted P=0.016 and P<0.0001, respectively). Interleukin-6 expression was higher in cardiac tissue from PPCM patients who were TNC positive (P=0.03). Cardiac histopathology in PPCM patients can predict long-term prognosis; both advanced fibrosis and immunohistochemical TNC expression are associated with poor prognosis.

Takotsubo syndrome (TTS) is an acute cardiomyopathy characterized by transient left ventricular systolic dysfunction, often mimicking acute coronary syndrome. Current pathophysiological concepts emphasize sympathetic overactivity and catecholamine excess as major determinants of myocardial stunning, and experimental models further suggest that high epinephrine concentrations may induce a beta-2 adrenoceptor Gs-to-Gi signaling switch, contributing to severe but reversible myocardial dysfunction. Neurological triggers, particularly epileptic seizures, are increasingly recognized and may be associated with distinctive clinical profiles, arrhythmic complications, recurrence, and variable ventricular morphology. We report the case of a 57-year-old woman with epilepsy and chronic obstructive pulmonary disease who presented with acute chest pain immediately after a generalized tonic-clonic seizure. She had experienced a previous TTS episode 11 months earlier, documented as a mid-ventricular variant with a left ventricular ejection fraction (LVEF) of 50%. During the recurrent episode, electrocardiography showed sinus rhythm without ST-segment elevation, with known anteroseptal T-wave inversion. Serial laboratory testing demonstrated a relatively modest peak high-sensitivity troponin T level of 140 pg/mL despite severe left ventricular dysfunction, together with markedly elevated N-terminal pro-B-type natriuretic peptide. Transthoracic echocardiography showed an LVEF of 20%-25%, with apical hypokinesia extending to the adjacent mid-ventricular segments and relative basal hypercontractility. Coronary angiography showed no acute culprit lesion and was unchanged from the prior examination. Left ventriculography confirmed apical ballooning with mid-ventricular extension. By day 3, LVEF had improved to 52%, while cardiac magnetic resonance imaging showed normalized wall motion with mild residual myocardial edema. This case highlights recurrent seizure-triggered TTS with documented phenotypic switching and rapid functional recovery, emphasizing the value of multimodality imaging and coordinated neuro-cardiac management.

We present the case of an 8-year-old male with frequent premature ventricular contractions and mild left ventricular dysfunction, who was found to carry heterozygous variants in both FLNC and CTNNA3. Medical therapy resulted in improved systolic function and reduced arrhythmia burden. This rare combination suggests a potential genotype-phenotype correlation in paediatric arrhythmogenic cardiomyopathy.

Patient: Female, 48-year-oldFinal Diagnosis: Reverse takotsubo cardiomyopathySymptoms: Dry cough • acute-onset chest pain • fatigue • feverClinical Procedure: Clinical observation and conservative managementSpecialty: Cardiology • Laboratory Diagnostics • PulmonologyObjective: Unusual clinical courseBackgroundReverse takotsubo cardiomyopathy (rTTC) is a rare variant of stress-induced cardiomyopathy typically associated with neurological triggers. Recent evidence suggests that hyperinflammatory states, such as cytokine storm as seen in some COVID-19 cases, may precipitate rTTC. We present a unique case of rTTC occurring during SARS-CoV-2 infection with the omicron variant, highlighting diagnostic and therapeutic implications.Case ReportA 48-year-old Hispanic woman with morbid obesity, hypertension, and rheumatoid arthritis, fully vaccinated against COVID-19, presented with chest pain, fever, and respiratory symptoms. SARS-CoV-2 infection was confirmed by RT-PCR. Initial laboratory test results showed hyperferritinemia (peak: 14 707 ng/mL). On Day 4, cardiac biomarkers were elevated (troponin T: 28 ng/L; NT-proBNP: 1582 pg/mL). Transthoracic echocardiography revealed basal hypokinesia with preserved apical contractility and moderately reduced left ventricular ejection fraction (LVEF) (45%), consistent with reverse takotsubo cardiomyopathy. She received colchicine and spironolactone as anti-inflammatory therapy. Gradual clinical and echocardiographic improvement followed. At her 6-month follow-up, her LVEF had normalized to 63%, and she remained asymptomatic. No cardiac sequelae were detected at 12 months.ConclusionsThis case illustrates how COVID-19–associated cytokine storm can precipitate rTTC in the absence of obstructive coronary disease, even in vaccinated individuals. The temporal alignment between inflammatory marker peaks and left ventricular dysfunction supports a transient, inflammation-mediated myocardial stunning. Clinicians should consider rTTC in COVID-19 patients presenting with atypical chest pain and modest biomarker elevation. Early echocardiography and targeted anti-inflammatory therapy may facilitate diagnosis and promote full recovery.

Takotsubo syndrome (also known as stress-induced cardiomyopathy or takotsubo cardiomyopathy) is an acute, reversible left ventricular dysfunction typically triggered by emotional or physical stress. TS is a rare but dangerous disease. In-hospital mortality in patients with TS is identical to mortality of patients with ST-segment elevation myocardial infarction. There is no obstructive coronary plaque or thrombosis in patients with TS, but there is injury of both cardiomyocytes and endothelial cells. The main manifestations of TS are apical akinesia and apical ballooning. The main cause of death in patients with TSis cardiogenic shock. The excessive release of endogenous catecholamines is a trigger of TS. There is evidence that TS is a consequence of β1-adrenergic receptor (β1-AR) overstimulation by catecholamines. The protein kinase Ainhibitor H-89 partially reversed stress-induced cardiac injury in rats with TS model (TSM). Theβ2-ARantagonist ICI-118,551 exacerbated cardiac injury in TSM. The β2-AR agonist formoterol partially reversed cardiac injury in TSM. The β3-AR antagonist L-748337 had no effect on TSM. These findings indicate that the activation of β1-AR plays a key role in the pathogenesis of cardiac injury inTSM. In contrast, β2-AR stimulation protects the heart against stress-induced damage. However, thereisevidence that β2-AR overstimulation can cause a negative inotropic effect. It remains unclear why β1-AR antagonists protect the heart against cardiac injury in TSM, but β1-AR antagonists do not demonstrate a significant clinical effect in patients with TS. Administration of isoproterenol and immobilization stress can be used for TSM, because both impacts induce apical akinesia, but only immobilization causes apical ballooning. There is indirect evidence on the involvement of progesterone in cardiac injury in TSM.

Heart failure with preserved ejection fraction (HFpEF) represents a common subtype of heart failure, accounting for approximately 50% of all heart failure cases. It is characterised by a left ventricular ejection fraction of ≥50%, alongside persistent symptoms and signs of heart failure. The pathophysiology of HFpEF is complex and multifactorial, involving mechanisms such as hypertension, coronary artery disease, left ventricular dysfunction, right ventricular impairment, systemic inflammation and metabolic abnormalities. Although pharmacological therapies play a central role in the management of HFpEF, non-pharmacological interventions have also demonstrated potential in improving patients' symptoms and quality of life. However, there remains no consensus regarding which non-pharmacological approach is most effective. This study will aim to systematically compare the efficacy of different non-pharmacological therapies in patients with HFpEF by conducting a systematic review and network meta-analysis. We will systematically search the following electronic databases from their inception to 14 February 2026: PubMed, MEDLINE, Embase, the Cochrane Library, Web of Science, Chinese databases China National Knowledge Infrastructure (CNKI) and SinoMed. The search will be restricted to studies published in English or Chinese. The primary outcomes will comprise all-cause and cardiovascular mortality, together with heart failure-related rehospitalisation. Pairwise meta-analyses will be performed using RevMan V.5.3 (The Cochrane Collaboration, Copenhagen, Denmark), while network meta-analyses will be conducted using ADDIS V.1.16.6 (Drugis, Groningen, The Netherlands) and Stata V.16.1 (StataCorp) within a Bayesian framework employing Markov chain Monte Carlo methods to compare the relative efficacy of different non-pharmacological therapies. To ensure transitivity assumptions are met, we will conduct separate network meta-analyses for lifestyle and behavioural interventions (exercise training, dietary interventions and multidisciplinary management), device-based and surgical interventions (interatrial shunts, implantable haemodynamic monitors, cardiac contractility modulation and splanchnic nerve ablation), and a full network including all modalities. To ensure accuracy and reliability, study screening, data extraction, risk of bias assessment and certainty of evidence evaluation will be carried out independently by two reviewers. We will assess the risk of bias in individual studies with the Cochrane Risk of Bias tool and evaluate the certainty of evidence using both the Grading of Recommendations, Assessment, Development and Evaluations framework and the Confidence in Network Meta-Analysis tool. Ethical approval is not required for this study, as it is a systematic review of previously published literature. The findings will be submitted for publication in a peer-reviewed journal and/or presented at relevant academic conferences. CRD420251165545.