Heart failure (HF) is a culmination of pathological processes presenting with debilitating symptoms that highlight a complex interplay between immunological, hormonal, and metabolic systems resulting in impaired cardiac function. HF has a major impact on the quality of life and longevity of the affected patients. 1 Inflammation has been shown to play a pivotal role in the pathogenesis of HF within animal studies, but there has been limited translation of these findings into human research. 2, 3

Monocytes and monocyte-derived macrophages play a role in the development of HF. In human immunology, monocytes undertake phagocytosis to provide protection from foreign pathogens such as bacteria and viruses. Nevertheless, there are distinct subsets of monocytes with potential for beneficial or detrimental effects on HF pathogenesis, although intimate details of the involved processes are not yet fully determined. 4, 5 Of importance is the fact that the role of monocytes in cardiovascular diseases is complex and includes inflammation, which subsequently contributes to processes of regeneration, repair, and modulation of the prothrombotic state. 6, 7 All these functions are highly relevant to patients with HF, who show progressive impairment of cardiac function and frequently develop atrial fibrillation (AF), an arrhythmia with a high risk of thrombotic complications. Therefore, of equal interest is the role of the immune system in AF, a very common arrhythmia in HF, which has been strongly linked to inflammation. 8 Atrial and ventricular fibrosis have been documented in patients with AF, with