Fluorouracil (5-FU) is frequently used in chemotherapy for several cancers, but adverse effects such as electrocardiography (ECG) ST-T changes and vascular spasms have been reported. Here, we present a case in which 5-FU triggered coronary vasospastic angina and takotsubo syndrome. A 65-year-old woman was admitted to our hospital for treatment of esophageal adenocarcinoma and initiated on 5-FU, leucovorin, and oxaliplatin. Three days after administration, she experienced chest pain that resolved spontaneously. On the fifth day, she was referred to our department. ECG showed ST-segment elevation in leads II, III, and aVF, with T-wave inversion in leads I, aVL, and V1-6. Echocardiography revealed wall motion abnormalities predominantly at the apex. Cardiac computed tomography showed no significant coronary artery stenosis. An acetylcholine provocation test was performed, revealing multi-vessel spasm, leading to a diagnosis of coronary vasospastic angina. Coronary vasodilators were initiated, and the chemotherapy regimen was changed to discontinue 5-FU. The patient experienced no recurrence of chest pain, and improvements were observed in both echocardiographic and ECG findings. Reports of takotsubo syndrome caused by 5-FU are rare, and its mechanism remains unclear. In this case, the presence of coronary vasospastic angina suggests that it may have contributed to the development of takotsubo syndrome.

Refractory ventricular fibrillation (VF) during out-of-hospital cardiac arrest is associated with high mortality, particularly when resuscitation is prolonged. Early cardiopulmonary resuscitation (CPR), rapid defibrillation, and comprehensive post-return of spontaneous circulation (ROSC) care are critical determinants of survival. A 46-year-old previously healthy man collapsed during exercise. Immediate bystander CPR was initiated. Emergency medical services identified VF as the initial rhythm and delivered multiple defibrillation shocks along with antiarrhythmic therapy. On hospital arrival, the patient remained in persistent VF, and advanced cardiac life support was continued. ROSC was achieved after prolonged resuscitation but was followed by a brief re-arrest. Sustained ROSC occurred after a total CPR duration of approximately 85 minutes, during which 20 defibrillation shocks were administered. Advanced airway management and pharmacologic therapy, including epinephrine, amiodarone, lidocaine, and magnesium, were provided. Following ROSC, the patient developed severe hemodynamic instability requiring mechanical ventilation, intravenous fluids, and high-dose vasopressors. Electrocardiography demonstrated diffuse ST-segment depression with subtle ST-segment elevation in leads aVR, aVL, and V1, suggestive of an acute ischemic etiology. Neurological examination revealed preserved brainstem reflexes. Active temperature control was initiated, and the patient was transferred for urgent coronary angiography and management in the coronary care unit. Coronary angiography confirmed complete proximal left anterior descending artery occlusion, and primary percutaneous coronary intervention with drug-eluting stent implantation was performed. The subsequent hospital course was complicated by cardiogenic shock, complete atrioventricular block requiring temporary transvenous pacing, and recurrent ventricular tachycardia/ventricular fibrillation triggered by frequent premature ventricular complexes with an R-on-T pattern. Repeat coronary angiography confirmed a patent left anterior descending artery (LAD) stent with TIMI (Thrombolysis in Myocardial Infarction) III flow. The patient survived and achieved good neurological recovery, with a Glasgow Coma Scale score of 15/15 after extubation. This case illustrates survival after prolonged resuscitation for refractory VF, emphasizing the importance of early bystander CPR, persistent advanced life support, urgent coronary revascularization, careful rhythm management, and comprehensive post-cardiac arrest care. In selected patients, extended resuscitative efforts may result in meaningful survival despite prolonged cardiac arrest.

Hypocalcaemic cardiomyopathy is a rare but potentially reversible cause of heart failure (HF), yet it remains under-recognized in clinical practice. Evidence supporting a direct causal relationship is limited, particularly with regard to relapse and long-term follow-up.

Altermagnets are a recently discovered class of magnetic materials that combine a collinear, zero-magnetization spin structure, characteristic of antiferromagnets, with spin-split electronic bands, a hallmark of ferromagnets. This unique behavior arises from the breaking of combined time-reversal and spatial symmetries (such as inversion or lattice translation), which are preserved in conventional antiferromagnets. To date, research has mainly focused on altermagnetic phases in periodic crystals, where the order is linked to rotational symmetries compatible with translational periodicity. In this Letter, we demonstrate that quasicrystals, which possess rotational symmetries incompatible with periodicity, can host exotic altermagnetic orders. Using symmetry analysis and self-consistent mean-field theory, we predict stable g-wave and i-wave altermagnetism in octagonal and dodecagonal quasicrystals, respectively. These phases are characterized by global C_{8}T and C_{12}T symmetries and exhibit anisotropic spin-splittings in their spectral functions and spin conductance, with characteristic eight and twelvefold nodal structures that establish a theoretical framework for identifying these phases in future experiments. Our findings establish quasicrystals as a versatile platform for realizing unconventional altermagnetic orders beyond the constraints of periodicity.

Most patients with acute central nervous system (CNS) lesions, including acute ischemic stroke, intracranial bleeding, traumatic brain or spinal cord injury, exhibit electrocardiographic (ECG) abnormalities. These are generally transient and considered secondary to the neurological condition. The most common neurogenic ECG alterations include ST-segment elevation or depression, T wave inversion, prominent U wave, prolonged QTc interval, sinus bradycardia and atrioventricular block. The primary mechanism involves autonomic nervous system alterations due to damage to the central autonomic network, causing regional changes in myocardial action potential duration, altered ventricular repolarization gradients, altered automaticity, or altered atrioventricular node conduction. These may promote arrhythmias including atrial fibrillation and ventricular arrhythmias. Sympathetic hyperactivation may additionally induce non-ischemic acute myocardial injury characterized by contraction band necrosis. The functional neuroanatomy of the central autonomic network determines the diverse cardiac manifestations observed with distinct CNS injuries. Insular cortex lesions typically result in sympathetic hyperactivation, whereas brain stem or spinal cord lesions above T6 can cause autonomic failure with reduced sympathetic tone and altered autonomic reflexes. While most patients exhibit asymptomatic ECG abnormalities, initial clinical evaluation should identify underlying cardiac conditions such as Takotsubo cardiomyopathy, myocardial infarction, or pre-existing chronic coronary syndromes. Serial ECG, cardiac biomarkers and echocardiography are key. Additional targeted work-up may be useful in selected patients. The implications of distinct ECG findings for neurological and cardiovascular prognosis should also be considered.

Pheochromocytoma is a rare catecholamine-secreting tumour with diverse cardiovascular manifestations. Presentation with chest pain and troponin elevation may closely mimic acute coronary syndrome (ACS), potentially leading to diagnostic delay.

Leptospirosis is a potentially fatal disease that can lead to dysfunction across multiple organ systems. Although cardiovascular complications are relatively rare, they are frequently underestimated and may result in severe outcomes if not addressed promptly. A 46-year-old farmer presented with complaints of palpitations and chest pain. He reported a history of fever, chills, rigors, diaphoresis, myalgia, nausea, low back pain, and headaches that began 7 days prior. An electrocardiogram showed diffuse T-wave inversions and sinus tachycardia; a troponin test was positive, indicating myocardial injury. Echocardiography revealed generalized wall motion abnormalities and left ventricular systolic dysfunction. After 5 days of antibiotic treatment and a 3-day course of corticosteroids, the patient fully recovered and was discharged without any complications. His angiography was normal, and leptospiral IgM was highly positive. Severe leptospirosis should be considered a potential cause of myocarditis, especially in patients with occupational risk factors and those living in endemic regions. Given the non-specific clinical features and diagnostic findings of leptospirosis, it is essential to maintain a high level of suspicion. Timely clinical recognition and laboratory confirmation are crucial, as delays can lead to higher mortality.