Cardiac Mechanical and Electrical Relevance Facilitating the Evolution of PAF to PRAF

Atrial Fibrillation (AF) is the commonest sustained arrhythmia. The absence of a reliable, cure for AF has fuelled research on its pathophysiology. This presentation will discuss electrical and mechanical abnormalities that initiate and perpetuate AF. AF has been known to require triggers, a suitable substrate and modifying factors. It is easy to understand that while the role of trigger is more important in paroxysmal AF, substrate abnormality is necessary for more permanent forms. The electrical triggers identified have been rapidly firing atrial focus, primarily from the pulmonary veins, atrial flutter and less commonly, supraventricular tachycardia. The substrate involves, first, an adequate mass capable of encompassing the number of wavelets required to maintain AF. Furthermore, in the presence of cardiac disease, heterogeneous electrophysiologic properties act to provide the milieu for sustained arrhythmia. Dilatation of the atria, fibrosis and loss of atrial muscle, can all lead to the necessary electrophysiologic substrate. Recent studies have pointed to more cellular and genetic abnormalities, including abnormalities of atrial angiotensin receptors in the, repolarisation alternans, enhanced and delayed atrial action potential repolarisation, cellular hyperexcitability, and conduction velocity hetrogenicity. Conventional compartmentalization of atrial fibrillation, into paroxysmal, persistent and permanent, has proven to be useful. However, pathophysiologically, they form a continuum, as demonstrated by presence of substrate abnormality in paroxysmal lone atrial fibrillation, and reverse remodeling of atria after treatment of mitral valve disease.