Abstract 352: Pulmonary Vein Thrombosis can make Pulmonary Vein Acidic States, which may be Associated with Atrial Fibrillation.

Abstract

Atrial fibrillation can cause ischemic stroke. To prevent atrial fibrillation (AF) is crucial to prevent ischemic stroke. The pulmonary vein has a myocardial layer that can generate spontaneous or triggered action potentials. The myocardial layer is extended from the left atrial myocardium. Pulmonary vein myocardium sleeve is known to be associated with generating and maintaining AF. Pulmonary vein myocardium can be classified into two types. One is short and thin myocardium sleeve, which has no potential to cause atrial fibrillation (AF). And the other is long and thick myocardium sleeve, which has potential to cause AF. The mechanisms of such myocardium sleeve changes are not understood well. Pulmonary vein thrombosis (PVT) is believed to be rare, which was reported as a rare complication of chest surgeries such as lobectomy or lung cancers. But since 2012, I reported seven cases of PVT in elderly patients without such conditions, which suggests that PVT is not uncommon. That is a novel notion. PVT prevents arterial blood flow, which inhibits oxygen and nourishment supply and carbon dioxide excretion. Hypoxia activates hypoxia inducible factors (HIFs), and HIFs can modulate epigenetic changes, reprogramming and ES cells. Undernourishments may activate nuclear respiratory factor-1 (NRF-1) and the aryl hydrocarbon receptor (AhR). PVT can make pulmonary vein acidic states by inhibiting excretion of carbon dioxide and may modulate pulmonary vein myocardium. Under acidic states, pulmonary vein cells such as pulmonary vein myocardium cells may obtain some kinds of multipotency. After obtaining multipotency, the cells may turn into new cells to adapt changed surroundings. The changes of myocardium sleeve may be caused by acidic state conditions and HIFs, AhR and NRF-1, which seemed to modulate pulmonary vein myocardium functions. To clear these, more studies are needed.