Structural Basis of Atrial Arrhythmogenesis in Metabolic Syndrome

Abstract

Individual components of metabolic syndrome (MetS) have been correlated with atrial fibrillation (AF), but as a whole, the exact mechanism underlying the increased susceptibility of AF still remains unclear. This study identifies key structural substrates in a robust obesogenic dietary model of MetS in the rabbits. The rabbit atria from both MetS and controls (N=3 each) were processed and incubated in wheat germ agglutinin (WGA) to label cell membranes and collagen. Confocal microscopy was used to image the tissue. The collagen and cell membranes were segmented using a robust machine learning architecture, V-net. Quantification of fibrosis was done by calculating the ratio of total pixels of collagen to those of atrial tissue in each of the segmented images. Cell hypertrophy measurements were calculated by measuring means of individual cell diameters. We discovered atrial dilation, increased collagen, cell hypertrophy and reduction in axial-tubules in MetS atria. These are established arrhythmogenic phenotypes which might lead to increased AF susceptibility.