Title:Atrial Fibrillation in Autoimmune Rheumatic Diseases: from Pathogenesis to Treatment
VOLUME: 13 ISSUE: 3
Author(s):Giuseppe Ciconte*, Manuel Conti, Martina Evangelista and Carlo Pappone
Affiliation:Arrhythmology Department, IRCCS Policlinico San Donato, San Donato Milanese, Milano, Arrhythmology Department, IRCCS Policlinico San Donato, San Donato Milanese, Milano, Cardiology Department, IRCCS Policlinico San Donato, University of Milano, San Donato Milanese, Milano, Arrhythmology Department, IRCCS Policlinico San Donato, San Donato Milanese, Milano
Keywords:Arrhythmia mechanism, atrial fibrillation, drivers, inflammation, mapping techniques, rheumatic diseases.
Abstract:Atrial Fibrillation (AF) is the most commonly described cardiac arrhythmia found in the
general population and can lead to adverse outcomes. Its onset and maintenance requires the presence
of an arrhythmogenic substrate that predisposes the patient for risk of these types of arrhythmias and
the occurrence of a trigger event. A major characteristic of AF-related structural remodelling is atrial
fibrosis, a process closely related to inflammation. Autoimmune rheumatic diseases constitute systemic
inflammatory disorders that can also present with cardiovascular manifestations, including a
high incidence of AF, thus supporting the idea of a link between AF and inflammation. A vicious
cycle exists in which inflammation leads to a higher prevalence of structural cardiovascular disease,
which in turn leads to more inflammation and AF; in fact, inflammation is known to affect signalling
pathways that lead to the development of AF. Therapy must first target systemic inflammation, since
decreasing the inflammatory burden has consistently shown to positively ameliorate the prognosis.
When this approach is not sufficient, rhythm or, when not feasible, rate control is indicated in addition
to anticoagulant therapy. As far as the rhythm control strategy is concerned, antiarrhythmic drugs
and/or catheter ablation should be considered. New mapping techniques allowing the characterization
of the arrhythmic substrate have opened new perspectives and may help in the treatment of AF in
these patients, since atrial tissue is the target of inflammation-induced arrhythmic alterations. In cases
where the natural history of the arrhythmia itself is more advanced, in order to minimize the impact of
AF on cardiac function as well as quality of life, a device-based therapy, including an “ablate and
pace” approach could be adopted.
