Fibrosis, myocardial crossings, disconnections, abrupt turns, and epicardial reflections: do they play an actual role in human permanent atrial fibrillation? A controlled necropsy study

Abstract Atrial myocardium fibrosis and other alterations of fiber continuity and potential circuit reentrancy (disconnections, abrupt turns, crossings, and epicardial reflections) are thought to play an important role in permanent atrial fibrillation. However, few studies have been performed in human beings. Some of them are only descriptive, and controls were usually normal hearts; thus, differences between cases and controls could be related to the underlying disease rather than the arrhythmia. We quantified by histomorphometry the above characteristics in nine samples (three from the left atrium, three from around fat pads, one from the right atrium, one from the cavum–tricuspid isthmus, and one from the ventricular septum) from 13 necropsy hearts of patients with permanent atrial fibrillation and compared the findings with those from 13 control cases with the same diseases but without any atrial arrhythmia. Statistical analysis was performed using generalized estimating equations and a normal linear mixed model for repeated measures, with significance defined as P ≤.05. No differences were found in fibrosis (estimated as collagen/(collagen+myocardium) ratio—0.26 vs. 0.23, P =.35), the presence of disconnections (70.1 vs. 61.5, P =.09), abrupt turns (43.6 vs. 45.3, P =.84), or epicardial reflections (9.4 vs. 14.5, P =.12). The only difference identified was that cases with permanent atrial fibrillation exhibited fewer crossings than those without (79.5 vs. 91.5, P =.02). In conclusion, alterations in myocardial fiber continuity, including fibrosis, seem to reflect a generalized myocardial disorganization of the atria in cardiac disease but are not specifically related to permanent atrial fibrillation.