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