Abstract 12855: Left Atrial Reservoir Strain is an Early Marker of Atrial Fibrosis in Cardiovascular Surgery Patients

Introduction: Atrial fibrosis plays an important role in atrial remodeling and the development of atrial fibrillation (AF). Left atrium (LA) strain (LAS) measured by two-dimensional speckle tracking echocardiography (2DS) has been reported to be a useful method to predict the degree of atrial fibrosis. Hypothesis: To investigate whether LAS is an early marker of atrial fibrosis in cardiovascular surgery patients. Methods: Conventional echocardiography and 2DS method were performed in 131 patients (53 AF, 78 sinus rhythm (SR)) including cardiac valve disease (MR, AS, and CABG et al.). The mRNA and microRNA expression were analyzed by real-time reverse transcription polymerase chain reaction (RT-PCR) in 59 cases in which LA tissues were removed from the appendage. Results: Left atrial reservoir strain (LASr) negatively correlated with left atrial volume index (LAVI), and E/e’ and positively correlated with LVEF, and left atrial conduit strain (LAScd). LASr was significantly lower, and LAVI was higher in AF group. The fibrosis-related (COL1A, COL3A1, TGFβ1) and peroxisome proliferator-activated receptor-α (PPARα)-related (PPARα, PGC1α, CPT1B) genes expression as a metabolic remodeling showed a positive association with atrial ANP mRNA expression level, reflecting atrial pressure and mechanical stretching. The expression level of COL1A and TGFβ1 mRNA was higher in AF group, compared with SR group. LASr, but not LAVI, negatively correlated with the expression of COL1A1, TGFβ1, and miR21. Multivariate regression analysis showed that LASr was an independent predictor of COL1A1, TGFβ1, or miR21 expression. The PPARα-related gene expression did not correlate with LASr, and LVEF in SR group, while they had a significant negative correlation with LVEF in AF patients. AF patients (LVEF Conclusions: Low LASr exhibits increased atrial fibrosis, and LASr is extremely useful as an early marker for predicting atrial fibrosis and consequently AF in cardiovascular surgery patients. Furthermore, in progressed AF patients, overexpression of PPARα signaling may play a role in atrial degeneration eventually to leading to heart failure.