Acute coronary syndrome (ACS) remains a leading cause of emergency department presentations, yet triage based on the ST-elevation myocardial infarction (STEMI)/non-ST-elevation myocardial infarction (NSTEMI) paradigm misses approximately 25-34% of acute coronary occlusion myocardial infarction (OMI). Early artificial intelligence-electrocardiography (AI-ECG) models showed retrospective promise for detecting ischemic ECG patterns but lacked prospective validation. This review synthesizes emerging multicenter registry, prospective cohort, and pathway trial evidence for AI-ECG in ACS triage, including the Queen of Hearts registry, ROMIAE, and DIFOCCULT-3 studies. It is essential to distinguish two separate clinical tasks: (1) detecting OMI for emergent catheterization laboratory activation, and (2) ruling out acute myocardial infarction (MI), which requires serial high-sensitivity troponin and cannot be achieved by ECG alone. Contemporary findings suggest AI-ECG significantly improves OMI detection sensitivity (92% vs. 71% for standard care) and reduces false-positive catheterization laboratory activations by up to 91% among biomarker-negative patients. For acute MI rule-out, AI-ECG shows promise as an adjunct to troponin-based strategies, with a negative predictive value of approximately 99% when combined with high-sensitivity troponin and clinical risk scores. We propose a 'Second Opinion' framework in which AI augments physician judgment as a clinical decision support tool. Key implementation challenges include algorithmic bias, alert fatigue, documentation, and the risk of widening the digital divide. AI-ECG represents a shift toward a physiologically driven OMI vs. non-occlusive myocardial infarction (NOMI) diagnostic framework.

With the accelerated pace of modern life and the increasing pressure, the population affected by sleep disorders is expanding. Traditional polysomnography (PSG), though recognized as the gold standard for sleep monitoring, relies on wired connections and is restricted to hospital settings. This not only disrupts natural sleep patterns but also elevates the risk of data misinterpretation. Existing portable monitoring devices, however, have drawbacks such as limited monitoring parameters, inadequate medical-grade accuracy, or poor wearing comfort. In this study, a portable sleep monitoring system is developed, which adopts a modular wireless integrated architecture. A relay control box is used to receive data from electroencephalogram (EEG), electrocardiogram (ECG), and blood oxygen acquisition modules via Bluetooth. The system supports dual-path data transmission to the host computer through Wi-Fi/RS485, thus eliminating the constraints of wired connections. Performance tests confirm that the key performance indicators of the system meet national and industrial technical standards. Furthermore, the system is characterized by its compact size, easy wearing, and high comfort, making it applicable for popularization in home sleep monitoring scenarios.

The electrocardiogram is the pivotal triage instrument in suspected acute myocardial infarction, yet for three decades its interpretation has been reduced to a single feature: whether ST-segment elevation meets a fixed millimeter threshold. Approximately one-quarter to one-third of patients labeled non-ST-segment elevation myocardial infarction (NSTEMI) harbor total culprit artery occlusion at next-day angiography, sustain infarct sizes and mortality comparable to or worse than ST-segment elevation myocardial infarction (STEMI), and are younger and less comorbid - indicating that adverse outcomes reflect delayed reperfusion rather than baseline risk. The occlusion myocardial infarction versus non-occlusion myocardial infarction (OMI/NOMI) framework reorients electrocardiographic interpretation around acute coronary occlusion rather than a single morphological criterion. This review examines the principal arguments advanced in defense of the ST-elevation-only reading standard as electrocardiographic propositions: what the electrocardiogram is being asked to detect, what it predicts when read for occlusion, how its interpretation shapes the timing and selection of reperfusion, and whether an expanded reading standard can be operationalized without loss of diagnostic performance. The evidence shows that the call for dedicated randomized trials misunderstands a purely diagnostic paradigm, that early-invasive trials in NSTEMI were neither early nor selective, that fibrinolytic benefit in non-ST-elevation occlusion was obscured by heterogeneous pooling, and that expanded interpretation - increasingly scalable through artificial intelligence - improves sensitivity and specificity simultaneously. The electrocardiogram has not failed; the reading standard applied to it has.

BACKGROUND Prolonged exposure to high altitude can increase the risk of coronary artery disease, acute coronary syndrome, and other ischemic cardiovascular events. This report describes the case of a 34-year-old man with exercise-induced ST-segment elevation myocardial infarction (STEMI) 36 hours after descent from high altitude. CASE REPORT A previously healthy 34-year-old man presented with 9 hours of crushing substernal chest pain. Electrocardiogram (ECG) demonstrated anteroseptal ST-segment elevation in leads V1-V3 with reciprocal changes in inferior leads. Emergency coronary angiography (CAG) revealed total occlusion with a high thrombus burden of the proximal left anterior descending (LAD) artery with TIMI 0 flow, accompanied by diffuse non-culprit coronary plaques (30-40% stenosis). Primary percutaneous coronary intervention (PCI) with drug-eluting stent implantation restored TIMI 3 flow. The event occurred 36 hours after descent from 4200 m altitude, immediately following intensive exercise, suggesting a temporal association between early de-acclimatization and acute coronary events. CONCLUSIONS Multiple factors, including dyslipidemia, residual hemorheological changes after high-altitude exposure, and vigorous exercise, may be associated with the occurrence of acute myocardial infarction (AMI) during high-altitude de-acclimatization. This report highlights the importance of recognizing that patients with a history of living at high altitude can be at increased risk of acute coronary syndromes, particularly ST-segment elevation myocardial infarction, when undertaking exercise.

BACKGROUND Subarachnoid hemorrhage (SAH) is a neurological emergency accounting for 5% of all strokes, with mortality exceeding 50% in patients over 80 years of age. Aneurysmal SAH is particularly lethal in the elderly due to atypical presentations, including ECG abnormalities mimicking acute coronary syndromes, leading to delayed diagnosis and high complication rates. This case report highlights the diagnostic pitfalls of SAH-induced STEMI mimicry. CASE REPORT A in their 90s White woman with a remote history of diabetes presented to the Emergency Department (ED) with sudden-onset occipital headache, nausea, and hypertensive crisis (214/68 mmHg). Initial electrocardiography (ECG) showed ST-segment elevations (STEMI) in leads I/aVL with reciprocal depressions in III/aVF, prompting STEMI activation despite normal troponin levels. Emergency computed tomography angiography (CTA) revealed a ruptured 3×1 mm anterior communicating artery (ACOM) aneurysm with Fisher Grade 3 SAH. Echocardiography at admission showed normal ejection and no wall motion abnormalities. ECG performed 1 day after admission showed complete resolution of the ST-T segment changes and the patient did not require any coronary intervention. Despite successful endovascular coiling, her hospital course was complicated by Cronobacter sakazakii bacteremia, embolic infarcts, and refractory cachexia. Palliative care was initiated on hospital day 14 due to irreversible functional decline, culminating in hospice transition. CONCLUSIONS SAH-mediated autonomic dysregulation can produce STEMI-like ECG changes even in the absence of coronary ischemia. Geriatric SAH management requires balancing intervention risks against frailty and comorbidities. Early recognition of SAH-induced ECG changes from autonomic-mediated repolarization abnormalities is essential to avoid misdiagnosis and guide appropriate intervention, particularly in older patients in whom comorbidities and frailty complicate recovery trajectories.

ST-segment elevation on electrocardiography is classically associated with acute myocardial infarction and often prompts urgent invasive evaluation. However, non-ischemic causes may complicate diagnostic decision-making, particularly in elderly patients with acute non-cardiac illnesses. We report a 95-year-old woman admitted with COVID-19-associated pneumonia and aspiration pneumonia, whose admission electrocardiogram demonstrated ST-segment elevation with T-wave inversion in the lateral precordial leads, mimicking ST-elevation myocardial infarction. She had no chest pain, no elevation of cardiac biomarkers, and preserved left ventricular systolic function without regional wall motion abnormalities on echocardiography. Review of prior records revealed that similar electrocardiographic abnormalities had been consistently present for more than a decade. Serial imaging demonstrated no overt structural heart disease. However, the electrocardiographic pattern-localized and persistent ST-segment elevation with repolarization abnormalities-is most consistent with chronic localized myocardial remodeling, possibly related to unrecognized myocardial fibrosis. This case highlights the importance of integrating clinical presentation, biomarkers, and longitudinal electrocardiographic findings. Persistent ST-segment elevation does not always indicate acute coronary occlusion, but may reflect an underlying structural myocardial substrate not detectable by routine imaging.

Cardiac metastases are rare in clinical practice. Herein, we describe the case of a 61-year-old male patient who underwent radical left lung cancer surgery > 2 years before the current admission. The postoperative diagnosis was left lung squamous cell carcinoma (stage pT2N1M0/IIB). Post-surgery, he received adjuvant chemotherapy and did not undergo chest radiotherapy. At the current admission, the patient presented with a dull pain in the left side of his chest. Electrocardiography (ECG) revealed ST-segment elevation; repeat troponin and cardiac enzyme levels were negative. Coronary CT showed 55%-77% stenosis in the proximal-mid left anterior descending artery, but no severe occlusive disease in the other major branches. Cardiac ultrasound revealed a 104 × 49 mm hypoechoic mass at the lateral apex without regional wall motion abnormalities or pericardial effusion. Contrast-enhanced chest CT revealed a metastatic tumor in the left anterior mediastinum with invasion of the pericardium and local left ventricular wall. ST-segment elevation on ECG does not always indicate acute myocardial infarction. In patients with advanced cancer, if unexplained persistent ST elevation without pathological Q waves is observed, the possibility of cardiac metastasis should be considered.