We report the case of a 57-year-old man presenting with inferior ST elevation myocardial infarction. Initial electrocardiography demonstrated ST segment elevation in the inferior leads. After administration of aspirin and intravenous heparin, repeat electrocardiography showed partial improvement in ST segment elevation. Emergent coronary angiography revealed abrupt distal occlusion of branches of a dominant right coronary artery (RCA) with preserved proximal flow. Intravascular ultrasound (IVUS) demonstrated minimal coronary atherosclerosis without plaque rupture or dissection. Transthoracic and transesophageal echocardiography (TEE) demonstrated a patent foramen ovale with atrial septal aneurysm and right-to-left shunting. Hypercoagulable evaluation was unremarkable. Follow-up echocardiography identified a small left ventricular apical thrombus.

Rapid identification and localization of an acute coronary occlusion are vital to prevent myocardial damage, yet reliance on ST-segment ECG criteria misses many acute occlusion myocardial infarctions (OMI) and triggers unnecessary acute angiographies. Here, we present a trained and validated deep learning model using 540,372 emergency ECGs paired with definitive catheterization outcomes. The model has a C-statistic of ≥0.95 for OMI and ≥0.87 for non-OMI infarctions and can localize culprit lesions in the three main coronary branches, which can guide the angiographer. Performance is similar across age, sex, and ECG hardware subgroups. Obviating dependence on ST-elevations and troponins, this model for the identification and localization of OMI has the potential to shorten the time to reperfusion of an acute coronary occlusion and save resources. Because human oversight of OMI detection on the ECG is limited, randomized clinical trials with patient-relevant outcomes are warranted.

ST-segment elevation in lead aVR with diffuse ST depression is traditionally associated with left main or three-vessel coronary artery disease in acute coronary syndrome, although its diagnostic specificity remains controversial. We report a 60-year-old man presenting with chest pain and hemodynamic shock. The ECG showed diffuse ST depression with ST elevation in aVR, prompting urgent activation for coronary angiography. However, physical examination and echocardiography raised suspicion of type A aortic dissection, confirmed by computed tomography. This case highlights that, particularly in the setting of hemodynamic instability, this ECG pattern mandates careful differential diagnosis among the potential causes of coronary hypoperfusion.

Brugada syndrome (BrS) is a rare but potentially life-threatening condition that may lead to sudden cardiac death. Among the causes, dysfunctions of ion channels involved in the cardiac action potential (specifically in SCN5A and SCN10A genes) are particularly significant. Among diagnosed Brugada patients, fever-induced episodes occur in 20-30% of cases. Fever worsens sodium channel dysfunction, as elevated temperature further reduces their conductance. First clinical manifestation of BrS occurs usually during a febrile episode, especially in young people. We performed a multiparametric examination in addition to genetic analysis. We treated a 19-year-old man presenting with subfebrility. During the patient's subfebrile episodes, 12-lead ECG recordings revealed ST-segment elevations in leads V1-V3. Notably, the patient remained asymptomatic. Targeted genetic testing of SCN5A did not reveal any disease-causing variants as an underlying cause of the syndrome, but the temperature-inducing effect was demonstrated. The occurrence of the Brugada type 1 pattern has also been observed at subfebrile episodes, although significantly rarely. This case demonstrates that in susceptible patients, even a relatively mild elevation in body temperature can trigger ion channel dysfunctions. Timely diagnosis and follow-up are important in preserving quality of life and preventing fatal outcomes.

Congenital heart disease (CHD) and dermatologic conditions such as lymphedema and acquired melanocytic nevi (AMN) are common in Turner Syndrome (TS). We hypothesized that abnormalities of cranial neural crest cell derivatives drive the skin and heart manifestations of TS. We conducted joint cardiac and skin examinations of volunteers at a 2023 national TS conference. Electrocardiographic abnormalities were classified according to the Minnesota Codes. Aortic diameters and cardiac anatomy were assessed using a standardized echocardiographic protocol. The primary outcome was the association between ECG abnormalities and thoracic aortic aneurysms (TAA) or CHD. The secondary outcome was the association between AMN counts and CHD, TAA, or the corrected QT interval (QTc). Among 118 participants (median age 33 years; CHD 39%; TAA ~25%), 35% had major ECG abnormalities, most commonly T-wave inversions and ST depressions; QTc prolongation occurred in 7%. Major ECG abnormalities were associated with larger aortic diameter and were more frequent in CHD, with a trend toward increased TAA (OR 2.8). Notably, 17% without known CHD had ECG abnormalities, and > 25% of these had previously unrecognized TAA. Only 45,X karyotype independently predicted ECG abnormalities. AMN burden was markedly elevated and increased stepwise with combined CHD + TAA (adjusted OR per level 13.1) but was not associated with QTc. ECG abnormalities and AMN burden track with cardiovascular disease severity in TS and may identify individuals with unrecognized aortopathy. These preliminary findings support integrated multimodal screening for CHD in TS, pending validation in larger cohorts.

Timely reperfusion is central to the management of ST-segment elevation myocardial infarction (STEMI), but dynamic coronary processes such as vasospasm may complicate primary percutaneous coronary intervention (PCI). We present a 50-year-old male with hyperlipidemia, active tobacco use, daily nicotine vaping, and a family history of heart disease who presented approximately three hours after the onset of persistent chest pain, following three days of intermittent left arm pain radiating to the left shoulder. Initial troponin was negative. His initial electrocardiogram was unremarkable, but repeat electrocardiography 30 minutes later demonstrated inferior ST-segment elevation, prompting emergent transfer for primary PCI. Coronary angiography demonstrated a smooth proximal right coronary artery narrowing and a separate distal stenotic lesion. The proximal narrowing resolved completely after intracoronary nitroglycerin, and intravascular ultrasound showed no plaque or thrombus at that site. ST-segment elevations did not improve after intracoronary nitroglycerin alone. Despite nitroglycerin administration, the distal lesion persisted and was treated with balloon angioplasty followed by stent implantation, with a door-to-balloon time of 117 minutes. He was discharged on vasodilator therapy (initially nitrates, later transitioned to a calcium channel blocker due to intolerance). This case highlights how coronary vasospasm may accompany fixed obstructive disease during STEMI and create additional diagnostic complexity during primary PCI, with implications for lesion assessment, avoidance of unnecessary intervention, and post-PCI vasodilator therapy.

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.

Atrioventricular block and cardiogenic shock are critical complications of inferior wall myocardial infarction with high mortality, especially in resource-limited settings lacking percutaneous coronary intervention. We report a 53-year-old male smoker presenting to a rural hospital with acute chest pain, dyspnea, and profound hemodynamic instability with electrocardiogram showing inferior wall ST-segment elevation myocardial infarction with Mobitz type I atrioventricular block. This case highlights reversal of atrioventricular block with return of hemodynamic stablility using Streptokinase and ionotropes in a rural setting. Therefore, timely fibrinolysis and inotropes in managing inferior wall myocardial infarction with atrioventricular block and cardiogenic shock in percutaneous coronary intervention -inaccessible regions and strengthening rural ST segment elevation myocardial infarction care networks is crucial.

Heart failure is clinical syndrome with many different underlying cardiac diseases. The definition of heart failure includes the presence of typical symptoms and the proof of a structural cardiac abnormality, which is responsible for a reduced cardiac output and/or elevated cardiac filling pressures at rest or on exertion. The identification and exact description of the main mechanism of heart failure is key for the introduction of an appropriate treatment, which when appropriately selected improves symptoms and prognosis. In patients with suspected heart failure, a basic assessment including history, physical examination, ECG, measurement of natriuretic peptides, and a comprehensive transthoracic echocardiogram should always be performed. Based on the finding of this initial assessment additional imaging modalities are selected on a case-to-case basis. In this review, we discuss the role of advanced echocardiography techniques, cardiac magnetic resonance imaging, computed tomography, cardiac catheterization and nuclear medicine examinations in this context.

Russell's viper envenomation is known to cause complications such as coagulopathy, acute kidney injury and haemolysis. Cardiac involvement, though rare, has been reported in the form of arrhythmias, myocardial infarction and ECG changes such as ST-segment elevation or T-wave inversions. We report a case of a middle-aged farmer who presented to our centre with Russell's viper envenomation, characterised by local envenomation, coagulopathy, haemolysis and ocular manifestations. His ECG showed a Brugada pattern, with no evidence of any structural cardiac abnormalities or elevated cardiac enzymes. A repeat ECG performed 72 hours after anti-snake venom therapy showed resolution of the ECG findings. A diagnosis of Brugada phenocopy secondary to Russell's viper envenomation was made. The most likely mechanism causing a Brugada phenocopy in Russell's viper envenomation may be due to phospholipase A2 present in the venom, causing alteration in the cardiac voltage-gated sodium channels.