De Winter's electrocardiogram (ECG) pattern, defined as upsloping ST-segment depression >1 mm at the J point with tall, symmetric T waves in the precordial leads, represents a rare acute ST-segment elevation myocardial infarction (STEMI) equivalent. Seen in only 2%-3% of proximal left anterior descending (LAD) occlusions, it is often missed by automated interpretation systems yet carries mortality similar to classic STEMI and mandates urgent reperfusion. We present the case of a 56-year-old male who collapsed during an Ironman triathlon after developing severe chest pain. Initial ECG showed hyperacute T waves in V2-V3, consistent with de Winter's pattern; high-sensitivity troponin was elevated. The patient underwent urgent catheterization, which revealed an acute mid-LAD occlusion and high-grade stenosis of the second diagonal branch. Primary percutaneous revascularization was performed with restoration of flow. Postprocedural echocardiography demonstrated moderately reduced left ventricular function, and the patient was discharged on guideline-directed medical therapy (GDMT) with an uncomplicated recovery. This case underscores the importance of recognizing de Winter's ECG pattern as a STEMI equivalent to facilitate rapid intervention and improve outcomes.

The authors present a case where the admission ECG showed extensive deep negative U-waves in the precordial leads, in addition to the precordial negative T-waves characteristic of Wellens syndrome. After stenting of the critical stenosis of the left anterior descending coronary artery, only the U-wave inversion disappeared, while the Wellens repolarization disorder persisted. The authors discuss the different dynamics of ischemic repolarization disorders in this case. Orv Hetil. 2026; 167(22): 885-888.

Histone deacetylase (HDAC) inhibitors are approved for cancer treatment and are being investigated for a wide range of other diseases. Despite their therapeutic promise, clinical studies have reported cardiac side effects, particularly electrocardiogram (EKG) abnormalities, with QT interval prolongation being one of the most consistently reported findings. The mechanisms underlying these cardiac effects remain unclear. In this study, we investigated the role of HDAC3 in cardiac electrophysiology. We found that postnatal depletion of cardiac HDAC3 in mice caused QT interval prolongation, recapitulating the EKG abnormalities reported with HDAC inhibitor use. Adult-onset inducible depletion of cardiac HDAC3 induced additional EKG abnormalities, including T-wave flattening, inversion, and biphasic T waves, which are also observed clinically. Loss of HDAC3 deacetylase activity, without affecting HDAC3 protein levels, was sufficient to induce QT prolongation. Disruption of HDAC3 function altered the expression of ion channel genes, including the downregulation of potassium channel genes such as Kcnh2, Kcne1, and Kcnip2. Moreover, a single dose of HDAC inhibitors, romidepsin or mocetinostat, caused reversible QT prolongation in mice. Consistent with these findings, HDAC inhibitor treatment altered the expression of potassium channel genes, with a predominant downregulation of multiple Kcn family members, including Kcnq1, Kcnh2, and Kcnip2. These findings establish HDAC3 enzymatic activity as a key regulator of cardiac repolarization and provide mechanistic insight into HDAC inhibitor-associated cardiotoxicity.

Ventricular repolarization abnormalities are among the most frequent electrocardiographic findings in pediatric athletes undergoing cardiovascular screening, yet their clinical significance remains a major source of diagnostic uncertainty. While most of them represent benign expressions of training-induced cardiac remodeling and developmental maturation, selected patterns may constitute the earliest phenotypic manifestation of cardiomyopathies or primary electrical disease. Distinguishing physiological adaptation from early pathology is therefore essential to prevent both sudden cardiac events and unnecessary restrictions on sports participation. This review integrates contemporary international electrocardiographic interpretation criteria with emerging pediatric evidence to provide a clinically oriented framework for evaluation and risk stratification of ventricular repolarization abnormalities in pediatric athletes. Early repolarization and anterior T-wave inversion are commonly benign when occurring within recognized age- and ethnicity-specific patterns and in the absence of symptoms, concerning family history, or structural abnormalities. Conversely, lateral or inferolateral T-wave inversion, atypical ST-segment morphology, complex ventricular arrhythmias, and abnormal imaging findings represent red flags requiring comprehensive investigation, including multimodality imaging when indicated. Due to the dynamic electrophysiological evolution during adolescence, longitudinal reassessment is crucial. A structured, risk-based approach integrating electrocardiographic features, demographic/familial context, clinical evaluation, imaging findings, and follow-up provides a pragmatic strategy to optimize risk detection while safeguarding appropriate athletic participation in young athletes.

This case report describes a 55-year-old asymptomatic woman with persistent T-wave inversion who was initially suspected of having arrhythmogenic cardiomyopathy (ACM) based on cardiac magnetic resonance findings of epicardial lipomatosis and a dyskinetic right ventricular segment. Advanced CMR with T1 mapping later reclassified the dyskinetic segment as a benign anatomical variant-a "butterfly apex"-and confirmed isolated epicardial fat without myocardial infiltration. Over long-term follow-up, no arrhythmias or structural progression occurred. The case highlights the critical role of multimodal imaging in differentiating ACM from benign anatomical mimics, thereby preventing misdiagnosis and unnecessary intervention.

Fluoropyrimidines, such as 5-fluorouracil (5-FU), when used in combination with bevacizumab are associated with diverse cardiotoxic effects, including vasospasm, myocarditis, and myopericarditis. These toxicities may closely mimic acute coronary syndrome, creating diagnostic uncertainty and risk of inappropriate management. Cardiac magnetic resonance (CMR) is central in distinguishing inflammatory myocardial injury from ischaemic pathology.

Apical hypertrophic cardiomyopathy (ApHCM), or Yamaguchi syndrome, is a morphological variant of hypertrophic cardiomyopathy that frequently mimics acute coronary syndrome (ACS) due to ischemic-type chest pain and characteristic electrocardiographic changes. A 46-year-old woman presented with angina and deep T-wave inversion in precordial leads. Coronary angiography showed normal epicardial arteries. Transthoracic echocardiography revealed localized left ventricular apical hypertrophy with preserved systolic function and the typical "ace-of-spades" cavity configuration, confirming ApHCM. She was managed conservatively with beta-blockers and guideline-directed therapy, with symptomatic improvement. Early recognition prevents unnecessary invasive procedures and facilitates appropriate long-term management.

Isolated T-wave inversion (TWI) in lead aVL is commonly regarded as a benign normal variant in asymptomatic individuals during routine electrocardiogram (ECG) interpretation. In patients presenting with chest pain, however, this subtle abnormality may represent early high lateral myocardial ischemia, often involving diagonal branch disease, and may be overlooked when the remainder of the ECG appears normal. The diagnostic challenge in such cases is not a lack of knowledge regarding lead aVL, but the ease with which isolated abnormalities can be discounted when patients appear clinically stable, and ECGs are reviewed outside the full clinical context.

The transition-metal dichalcogenide MoTe2 has been proposed as an ideal platform to intertwine superconductivity with band topology, yet a key experiment-tracking how its properties evolve across a pressure-tuned structural and topological phase transition-has remained elusive. Here, we map the superconducting landscape across these high-pressure regimes from the noncentrosymmetric type-II Weyl semimetal Td phase to the centrosymmetric 1T' phase using surface-sensitive soft point-contact Andreev spectroscopy combined with quantitative theoretical analysis. In the Td phase, our spectra consistently reveal two distinct superconducting gaps that remain resolvable under an external magnetic field, implying robust and pressure-independent multi-gap superconductivity consistent with muon-spin-rotation evidence for two s-wave gaps at ambient pressure. In the 1T' phase, reached by pressure along a topological pathway that connects the Weyl to the higher-order topological phase, we observe an s + p-wave surface response whose p-wave component follows the s-wave gap in temperature and is rapidly suppressed by a magnetic field-fingerprints of proximity-induced p-wave pairing between a bulk s-wave superconducting band and second-order topological surface states. This phenomenology aligns with theoretical analysis showing that the Td phase hosts type-II Weyl points, whereas the 1T' phase realizes a higher-order topological insulator arising from double-band inversion. Finally, we further propose that the resulting higher-order hinge boundary channels provide a natural route toward potential zero-energy Majorana corner modes under the observed s + p-wave proximity pairing, suggesting MoTe2 as an intrinsic, pressure-tunable platform for multi-gap and s + p-wave topological superconductivity.