Pathophysiology of atrial fibrillation: current aspects

The existence of independent wandering wavelets as the basis for fibrillation was postulated by Moe and coworkers in their multiple wavelet theory and was later confirmed in both animal and human atria. The process of initiation of fibrillation however is less clear but probably depends on a) an increase in inhomogeneity in conduction and b) a decrease in the length of the excitation wave. Recently a method has been introduced to quantify inhomogeneity in conduction in isolated rabbit atria. Already during slow basic rhythm, inhomogeneties based on structural inhomogeneities could be identified. Premature activation increased conduction inhomogeneities in the neighborhood of the premature stimuli while rapid pacing induced the highest degree of inhomogeneity throughout the myocardium. The role of the second prerequisite for atrial fibrillation, the length of the excitation wave, has also recently been studied in chronic instrumented conscious dogs. Conduction velocities, refractory periods and wavelengths were measured during the administration of a variety of drugs and correlated with the induction of atrial arrhythmias. The predictive power of the wavelength was much higher than for refractory period or conduction velocity alone. Upon gradual reduction of the wavelength, first rapid repetitive responses, then atrial flutter, and finally atrial fibrillation was observed. In summary, at least two factors are of importance for the initiation of atrial fibrillation: inhomogeneity in conduction and a short excitation wave. Other factors, such as abnormalities in atrial structure and function will certainly modify the contribution of these factors to an extent that remains to be investigated.