Myocardial infarction with non-obstructive coronary arteries (MINOCA) represents a diagnostic challenge with multiple underlying mechanisms, including coronary embolism. We report the case of a 50-year-old woman with a history of rheumatic fever who was admitted for acute chest pain. Electrocardiography showed atrial fibrillation with inferolateral ischemic changes, and elevated troponin levels confirmed myocardial infarction. Transthoracic echocardiography revealed moderate mitral stenosis, severe aortic stenosis, and left atrial enlargement. Coronary angiography demonstrated thrombotic occlusion of the second obtuse marginal branch without significant atherosclerotic disease. Transesophageal echocardiography identified a left atrial appendage thrombus, supporting a cardioembolic mechanism. This case emphasizes the importance of considering coronary embolism in MINOCA, particularly in patients with valvular atrial fibrillation, and highlights the role of a structured diagnostic approach in guiding diagnosis and management.

Raynaud's phenomenon is characterized by episodic vasospasm of the extremities, often triggered by cold or stress. It is a hallmark of systemic sclerosis (SSc) and is frequently associated with pulmonary arterial hypertension (PAH). PAH may cause right atrial dilatation, predisposing to atrial fibrillation (AF). While Raynaud's and PAH are well-documented, their coexistence with AF is rarely reported. A 71-year-old male presented with rapid AF and pulmonary oedema. On admission, vital signs were stable, but he developed symmetrical discoloration of the fingers, palms, and feet after cold exposure in the ICU, accompanied by numbness and pain. Laboratory tests revealed prolonged PT, high ESR (65/121 mm/hr), and positive ANA (44.8 IU/mL). ECG showed rapid AF with left ventricular hypertrophy. Chest X-ray demonstrated pulmonary artery dilatation and cardiomegaly. Echocardiography revealed moderate tricuspid regurgitation and severe PAH. This case illustrates a rare combination of Raynaud's phenomenon, PAH, and AF, likely secondary to autoimmune vascular dysfunction. PAH-induced atrial dilatation may trigger AF, while endothelial dysfunction may worsen Raynaud's symptoms. A positive ANA suggests underlying SSc or SLE. Early recognition and multidisciplinary management targeting pulmonary pressure, arrhythmia control, and vasospasm are crucial to prevent complications. Long-term outcome was not assessed due to loss to follow-up.

Long-term cardiac rhythm monitoring has become a central component of the diagnostic evaluation of patients with ischemic stroke in whom atrial fibrillation (AF) is suspected but not initially detected. Implantable loop recorders (ILRs) substantially increase AF detection compared with conventional short-term monitoring, particularly when surveillance is extended over months to years. However, increased detection has not consistently translated into fewer strokes, underscoring important limitations in current paradigms. Growing evidence supports atrial cardiopathy as the underlying substrate predisposing to thromboembolism, with AF representing a variable electrical manifestation rather than the primary disease itself. Electrocardiographic and echocardiographic markers of atrial cardiopathy, including abnormal P-wave indices, left atrial enlargement, and impaired atrial function, help identify patients most likely to benefit from prolonged monitoring. This review examines the role of ILRs in post-stroke patients through the lens of atrial cardiopathy, emphasizing biologic plausibility, patient selection, and disciplined interpretation of monitoring results to optimize clinical relevance and avoid uncritical escalation of therapy.

A 61-year-old woman presented to our hospital with palpitations and dyspnea persisting for several months. Electrocardiography revealed atrial tachycardia, and X-ray revealed bilateral hilar enlargement. Computed tomography (CT) was performed for suspected sarcoidosis of the respiratory system, which revealed hilar lymph node enlargement in the bilateral lungs. 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography-CT revealed abnormal 18F-FDG uptake in the hilar lymph nodes, liver, and left atrium (LA), but not in the left ventricle. Contrast-enhanced cardiac magnetic resonance imaging revealed late gadolinium enhancement (LGE) in the LA. Mediastinal lymph node, transbronchial lung, and right ventricular biopsies were performed, but no specific pathological findings were observed. Echocardiography-guided liver biopsy was also performed, which revealed non-caseating epithelioid granulomas. We definitively diagnosed systemic sarcoidosis, including cardiac lesions. Following the initiation of immunosuppressive therapy, abnormal 18F-FDG uptake in the liver, lymph nodes, and LA resolved, and atrial tachycardia improved, likely owing to the suppression of atrial inflammation. However, LGE in the LA persisted after immunosuppressive therapy, suggesting that structural damage had persisted. In this case, multimodality imaging helped us understand the disease state and post-treatment course.

To examine the clinical characteristics of sintilimab-induced myocarditis and to provide evidence for its diagnosis and management. Retrospective analysis was conducted on clinical case reports of sintilimab-induced myocarditis documented before July 31, 2025. A total of 34 patients were included, with a median age of 64 years (range: 33-85), including 23 (67.6%) male cases. The onset of myocarditis ranged from 1 to 120 days post-treatment, with a median onset of 21 days. The primary clinical presentations included dyspnea (41.2%), chest tightness (35.3%), palpitations (17.6%), and shortness of breath (14.7%), with some cases remaining asymptomatic (8.8%). Comorbid immune-related adverse events included myasthenia gravis (44.1%), myositis (17.6%), and hepatitis (17.6%). Laboratory findings often revealed elevated cardiac troponin I, N-terminal probrain natriuretic peptide, creatine kinase MB, and lactate dehydrogenase. The electrocardiogram mainly showed atrioventricular block (41.2%), ST-T segment changes (44.1%), and atrial or ventricular arrhythmias (50.0%). Echocardiography examination can show normal (34.5%), left ventricular diastolic dysfunction (31.0%), left atrial enlargement (13.8%), and pericardial effusion (13.8%). Cardiac magnetic resonance imaging may show normal (42.9%), myocardial edema (28.6%), and delayed myocardial enhancement (28.6%). Coronary angiography showed normal (73.3%) and coronary artery stenosis of the lumen (26.7%). All patients discontinued sintilimab and received steroid and intravenous immunoglobulin treatment. Outcomes indicated that 79.4% recovered from myocarditis, while 20.6% succumbed. Sintilimab-induced myocarditis has nonspecific manifestations and a high mortality rate. Myasthenia gravis and myositis can occur simultaneously with myocarditis. During simtimab treatment, it is necessary to closely monitor cardiac parameters and symptoms.