Atrial Fibrillation: Are Associated Risk Factors Surrogates for an Inflammatory State?

Abstract

Today’s understanding of the inflammatory process has evolved far beyond what was initially described by Celsus in the 1st Century A.D [1]. Terms like oxidative stress, reactive oxygen species (ROS), cytokines, and fibrosis have been thrown around in everyday scientific discussions for some time now. Well-known pathways of the “inflammatory state” have underpinned many common cardiovascular diseases such as the atherosclerotic process. However, there are less recognized entities where inflammation seems to play a key role in their mechanisms of origin. The concept of inflammation in atrial fibrillation (AF) is not a novel one, but this characteristic of its pathophysiology seems to have been overshadowed by the inherent dangers of its complications. More emphasis has been placed instead on its associated risk factors, which alone, or in combination, contribute to the development of AF. The risk factor burden and the arrhythmia it produces are generally considered uniform in a presentation in most studies. Some researchers, however, allude to ethnic or racial differences in AF [2,3]. This small retrospective study of an Afro-Mestizo Caribbean cohort of patients with AF will corroborate findings of associated risk factors with those commonly encountered globally in predominantly White populations. It will also point out, through numerous bibliographical references, how an “inflammatory state” may be identified in each AF-associated risk factor. If it holds true that the whole is nothing more than a sum of its parts, we should then accept the oversimplified view that AF, like atherosclerosis, is indeed inflammatory in nature. To this end, a fresh focus could be placed on new upstream therapeutic opportunities designed to complement our current downstream interventions, in an effort to prevent the occurrence and recurrence of AF.