The majority of cases of atrial fibrillation (AF) are the result of triggers originating in the area of the pulmonary veins. The reason for the predilection for that area remains unclear. We sought to examine the different mechanisms responsible for this observation through an extensive search of the medical literature, examining the development of the pulmonary veins, genetics of AF and left to -right cardiac chamber differentiation. Results confirm that the LAA is anatomically and embryologically different from other areas of the atrial walls and develops under distinct genetic and transcriptional pathways. Findings support an ablation strategy whose primary focus should be the creation of a 'box' lesion set, plus additional lines to prevent propagation to the left atrial appendage, the isthmus of the left atrium and the right atrium are likely to be more effective than simple pulmonary vein isolation.
Accessory chordae tendinae are exceedingly rare. We report an unusual case of severe mitral valve insufficiency caused by abnormal chordae tendinae tethering the middle scallop of the anterior mitral valve leaflet.
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