Increased 18F-fluorodeoxyglucose uptake in the cardiac atria: an evidence for increased atrial inflammation in patients with atrial fibrillation?

Type of funding sources: None. Atrial inflammation and fibrotic remodelling underlie the pathophysiology of atrial cardiomyopathy, which is associated with the development of atrial fibrillation (AF) and atrial flutter (AFL). 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) has been used to detect inflammatory processes. Recent studies have revealed an increased FDG-uptake in the atria of patients with AF, but also in patients with diagnosis of cardiac sarcoidosis with ventricular inflammation. This study aimed to assess the capability of PET/CT to detect and quantify the degree of atrial inflammation (FDG-uptake) in a population with dedicated cardiac FDG-PET/CT. We investigated 101 patients suspected of sarcoidosis (57±12 years, 72% male) who underwent 18F-FDG PET/CT scan with dedicated cardiac specific preparation (heparin infusion, 12 hours fasting, and high-fat low-carbohydrate diet). We excluded patients with active ventricular cardiac sarcoidosis or undergoing high-dose immunosuppressive therapy (prednisolone ≥20mg/day or prednisolone combined with other immunotherapy like methotrexate). We measured the maximum standardized uptake value (SUVmax) in atrial myocardium and mean standardized uptake value (SUVmean) in blood pool and calculated the target-to-background ratio (TBR) of SUVmax in atrial myocardium to SUVmean in blood pool. All medical records, ECG data on arrhythmia type and diagnosis of systemic sarcoidosis (with absence of ventricular involvement) were used for the analysis. Sarcoidosis was diagnosed based on the criteria established in 2006 by the Japanese Ministry of Health and Welfare. The collected data were sorted according to presence of arrhythmia and systemic sarcoidosis and TBR of each group were compared. AF or AFL was found in 30/101 patients. Systemic sarcoidosis was found in 37/101 patients. Patients with known AF/AFL had significantly increased TBR within the atrial tissue compared to those without AF/AFL: (median: 1.26, 1st-3rd quartile: 1.20-1.33) versus (median: 1.22, 1st-3rd quartile: 1.14-1.25; p = 0.004; figure A). Arrhythmia-associated atrial inflammation was consistently observed, independently of presence of concomitant systemic sarcoidosis (figure B). Patients with both atrial arrhythmias and systemic sarcoidosis had the highest atrial inflammation level, as identified by TBR (figure B). Development of atrial fibrillation or flutter is associated with an increased atrial FDG-uptake as metabolic marker of atrial inflammation. The level of atrial inflammation is further enhanced by additional presence of systemic sarcoidosis.