Abstract
Objectives: We present a case series of patients with granulomatous myocarditis presenting as atrial arrhythmias accompanied by lymphadenopathy.
Background: Atrial myocarditis (AM) may be the cause of atrial arrhythmias in patients without risk factors for atrial fibrillation. (AF).
Methods: Patients with atrial arrhythmias without traditional risk factors for AF underwent 18F Fluorodeoxyglucose positron emission tomography (18F FDG PET). We performed biopsy of either the myocardium or draining lymph nodes in patients with atrial uptake of 18F FDG PET. We found evidence of AM in 15 patients.
Results: The mean age of the patients was 43.33±12.59 years with a male predominance (73.3%). The left ventricular ejection fraction (LVEF) at presentation was 48.07±12.29% and the left atrial volume was 37.6±10.64 ml. All patients had AF at presentation, atrial flutter was noted in 4 patients (26.7%) and 2 patients (13.3%) had atrioventricular nodal reentrant tachycardia (AVNRT). 18F FDG PET uptake was noted in the atria in all patients and in the ventricles in 3 patients (20%). Cardiac sarcoidosis was the diagnosis in 12 patients (80%) while 3 patients (20%) had evidence of tuberculosis. The mean CHA2DS2 Vasc score of the patients was 1.06±0.93. Four patients (26.7%) presented with ischemic stroke. All patients were treated with disease specific therapy (immunosuppression or anti-tuberculosis therapy) in addition to standard anti-arrhythmic medications. Over a mean follow up of 30.53± 13 months we observed a significant improvement in clinical status commensurate with a decline in atrial uptake. There was a non-significant improvement in LVEF to 56±12.07% with disease specific therapy. (p=0.0853)
Conclusions: Atrial arrhythmias with granulomatous lymphadenopathy may be a presenting feature of Atrial myocarditis. The risk of stroke seems to be high in these individuals. This syndrome should be suspected in young individuals presenting with atrial arrhythmias and stroke without conventional risk factors.
The pathophysiology of Atrial fibrillation (AF) involves complex changes such as electrical remodelling and structural remodelling, with fibrosis being a central pathological feature. 1 Replacement fibrosis where connective tissue ousts the atrial myocardium is the net result of myriad insults to the myocardium. Atrial inflammation has been recognized to be an important feature of certain AF aetiologies, namely Post-operative AF, obesity, infection, and autoimmune diseases.2,3 The role of myocarditis involving predominantly the atrial musculature has been recognised but its role in the pathogenesis of AF has not been firmly established.4,5The potential causes of inflammatory atrial myocarditis (AM) include infections, sarcoidosis, giant cell myocarditis, rheumatic heart disease, connective tissue disorders and drugs. The manifestations of atrial myocarditis could range from atrial arrhythmias, stroke, valve dysfunction to sinus nodal dysfunction. 6,7
Detection of inflammation and its management has been established in the management of ventricular arrhythmias due to granulomatous myocarditis.8 The important diagnostic modalities in this aspect being nuclear imaging and biopsies, either of the myocardium or draining lymph nodes. In this study we describe the presentation, clinical features, diagnostic strategies, and management of patients presenting with atrial arrhythmias with atrial inflammation on imaging and histopathological studies, in the absence of conventional risk factors