The patient with cardiac sarcoidosis experienced progressive LV dilatation and persistent ventricular tachycardia despite immunosuppressive therapy and antiarrhythmic treatment.
This case highlights the complementary role of CMR and PET in monitoring cardiac sarcoidosis, differentiating inflammatory from scar-mediated arrhythmias, and informing the timing of advanced interventions.
Absolute Event Rate: 0% vs 0%
Abstract Background Cardiac sarcoidosis (CS) is a potentially life-threatening granulomatous inflammatory cardiomyopathy associated with conduction abnormalities, ventricular arrhythmias (VA), and heart failure (HF). Multimodality imaging plays a key role in diagnosis, risk stratification, and guiding therapy. Case summary A 53-year-old male presented with an out-of-hospital ventricular fibrillation arrest (OHVFA) in May 2022. Initial transthoracic echocardiography (TTE) demonstrated moderate left ventricular (LV) systolic impairment with hypokinesis of the basal inferoseptum, anteroseptal, and basal to mid-inferior walls. Invasive coronary angiography raised the possibility of spontaneous coronary artery dissection (SCAD) of the distal left anterior descending (LAD) artery. He subsequently underwent implantation of a cardiac resynchronisation therapy defibrillator (CRT-D) for secondary prevention. A cardiac magnetic resonance (CMR) scan was performed in February 2024, but image quality was suboptimal due to device artefact. It showed generalised hypokinesia with thinning and akinesia of the basal to mid-septum; late gadolinium enhancement (LGE) was present but difficult to characterise. Over the following eighteen months, serial CMR and ¹8F-fluorodeoxyglucose positron emission tomography (¹8F-FDG PET) demonstrated progressive LV dilatation with worsening LV systolic function, extensive non-ischaemic fibrosis, and intermittent low-grade inflammation. In June 2024, he was discussed at the Sarcoidosis Multidisciplinary Team (MDT) meeting, which included a consultant cardiologist with expertise in cardiac sarcoidosis (CS), consultant respiratory physicians, and imaging specialists, where a definite diagnosis (i. e. . 90% likelihood) of CS was established. Immunosuppression with intravenous methylprednisolone followed by oral prednisolone and methotrexate achieved partial disease control; however, recurrent ventricular tachycardia (VT) persisted despite antiarrhythmic therapy. A PET scan in May 2025 showed a stable scar burden (16% LV myocardium) with subtle new FDG uptake in the mid-inferolateral and inferoseptal walls. The MDT reached a definite diagnosis of CS (90% likelihood) based on concordant multimodality imaging findings demonstrating extensive myocardial scarring in the absence of active cardiac inflammation, consistent with established disease. Given ongoing VT and biventricular dysfunction, he was referred for VT ablation and heart transplant assessment. Discussion This case highlights the complementary role of CMR and PET in monitoring CS, differentiating inflammatory from scar-mediated arrhythmias, and informing timing of advanced interventions. It illustrates the need for ongoing risk reassessment and integration of emerging arrhythmia management strategies in advanced CS.
Sharma et al. (Fri,) reported a other. The patient with cardiac sarcoidosis experienced progressive LV dilatation and persistent ventricular tachycardia despite immunosuppressive therapy and antiarrhythmic treatment.