Background: Coronary artery in-stent restenosis is the negative response caused by the decrease in the artery diameters. Prolidase is an enzyme, whichplays a role in the formation of new matrix, collagen metabolism and cell development. There is no study evaluating the serum levels of prolidase enzyme in patients developing in-stent restenosis. Therefore, the objective of our study was to reveal the relationship between serum prolidase levels and in-stent restenosis. Methods: A total of 70 patients who were at medium-to-high risk based on non-invasive tests or clinical evaluation, and who underwent a coronary angiography in the cardiology and emergency polyclinics of our hospital from 2013 through 2014 were included in the study. In-stent restenosis was identified in 40 patients. In the other 30 patients, there was no angiographically determined critical lesion. Serum prolidase levels were measured in all patients. Results: The mean serum level of prolidase was found to be statistically significantly higher in the in-stent restenosis group compared to restenosis free group (p=0.02). The mean serum level of prolidase level was significantly higher in smokers compared to the non-smoker patients (p=0.04). It was observed that serum prolidase levels statistically significantly increased proportionally to the in-stent restenosis percentage (p=0.04). Conclusions: The results of this study indicate that, prolidase enzyme levels may enable timely and and correct assessment of in-stent restenosis, and may contribute to the decision for changing the treatment or timing to increase intensity of the treatment in patients undergoing percutaneous coronary intervention (PCI) with coronary stenting.

Purpose:Atrial fibrillation(AF) causes structural, electrical, and cellular remodeling in the atrium. Evaluation of intra- and interatrial conduction time, which is measured by tissue doppler echocardiography, indicates structural and electrical remodeling in the atrium. The aim of this study was to evaluate the effect of pulmonary vein isolation applied with RF ablation therapy on intra- and interatrial conduction time and to investigate the structural and electrically remodeling after treatment. Methods:Fifty-two patients with symptomatic PAF despite at least one antiarrhythmic drug and without structural heart disease were included in the study. Two patients were excluded because of complications developed during and after the operation. Fifty patients (28 female; mean age: 51.68 ± 11.731; mean left atrial diameter: 36.79 ± 4.318) who underwent CARTO® 3D pulmonary vein isolation applied with the RF ablation system were followed-up. Intra- and the inter-atrial electromechanical delay was measured in all patients by tissue doppler echocardiography before and three months after RF ablation. Results:All intra- and interatrial conduction times were significantly decreased 3 months after RF ablation procedure(PA lateral p = 0.022; PA septum p = 0.002; PA tricuspid p = 0.019, interatrial conduction delay p= 0,012, intra-atrial conduction delay p = 0.029). Conclusion:The results of our study suggest that providing stable sinus rhythm by the elimination of the AF triggering mechanisms with RF ablation of pulmonary vein isolation may slow down,stop or even improve structural remodeling at substrate level secondary to AF even in patients who did not yet develop atrial fibrosis and permanent structural changes.