Recent advances have raised the hope of effective pharmacological or non-pharmacological treatments of atrial fibrillation (AF), and of better understanding of the pathophysiological mechanisms involved in the initiation and persistence of the arrhythmia. Inflammatory changes in the atrial structure have been observed after cardiac surgery1 but also in patients with non-postoperative AF. Atrial histological abnormalities have been shown to be present in lone AF and in 66% of patients the biopsies were compatible with myocarditis.2
Recently C reactive protein (CRP) concentration, a sensitive marker of systemic inflammation, was found to be twice as high in patients with AF as in a control group with no history of atrial arrhythmia.3 A potential non-cardiovascular disease that predisposes to AF may be chronic gastritis caused by chronic Helicobacter pylori infection. Thus, we hypothesised that H pylori may be involved in the chronic atrial inflammation resulting in AF.
This study aimed: (1) to confirm the data previously reported that showed higher concentrations of CRP in patients with AF; and (2) to assess the possible association between H pylori infection and AF in patients without demonstrable structural cardiac disease, by comparing them with a group of normal healthy volunteers.