Objective To identify the electrophysiological charateristics and cause of ridge gap related reentry after MI ablation in atrial ifbrillation patients. Methods Activation and entrainment mapping was performed in 82 redo cases for OAT recurrence in whom MI was ablated during the index produre. Once ridge gap related reentry was conifrmed, detailed mapping was performed in MI and ridge region. In addition, in 36 cases undergoing MI ablation and fulfilling criterion for bidirectional block, differential pacing was repeated at the ridge to identify a ridge gap. Results Out of 82 redo cases for OAT recurrence in whom MI was ablated during the index produre, 7 (8.5%) was found to be ridge gap related reentry. TCL was (247.9±19.2) ms, and the left atrial endocardial activation time was (145.4±17.7) ms, accounting for (58.5±3.2)%of TCL. However, wide double potential was recorded along the previous ablated MI line where PPI was (34.3±6.6) ms longer than TCL, while PPI was signiifcantly shorter at the ridge[PPI-TCL (11.4±3.9) ms, P<0.001]. Tachycardia was terminated at the ridge in 6 cases and at the corresponding site in coronary sinus in 1 case. No recurrence was found during follow-up for (11.1±4.5) months. In addition, in 36 patients undergoing MI ablation in whom criterion of bi-directional block was fuliflled, conduction gap located at the ridge was found in 5 (13.9%) cases. Conclusions MI ridge gap related reentry is a distinctive OAT, in which the ridge was used as the critical isthmus, whereas the previous ablated MI line is not part of the reentry. MI pseudo-block due to the ridge gap may lead to this type of recurrent tachycardia.

OBJECTIVES: Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α) controls mitochondrial biogenesis, but its role in cardiovascular diseases is unclear. The purpose of this study is to explore the effect of PGC1α on myocardial ischemia-reperfusion injury and the underlying mechanisms. METHODS: The transverse coronary artery of SD rat was ligated for 30 minutes followed by 2 hours of reperfusion. Triphenyltetrazolium chloride (TTC) staining was performed to measure the area of myocardial infarction. Immunohistochemistry and Western blotting were used to detect the PGC1α expression in myocardium. The rat cardiomyocyte H9C2 was subjected to hypoxia/reoxygenation (H/R) with the knockdown of PGC1α or hypoxia- inducible factor 1α (HIF-1α), or with treatment of metformin. Western blotting was used to detect the expression of PGC1α, HIF-1α, p21, BAX, and caspase-3. CCK-8 was performed to detect cell viability, and flow cytometry was used to detect apoptosis and mitochondrial superoxide (mitoSOX) release. RT-qPCR was used to detect the mRNA expression of PGC1α and HIF-1α. Besides, chromatin immunoprecipitation (ChIP)-qPCR and luciferase reporter gene assay were applied to detect the transcriptional regulation effect of HIF-1α on PGC1α. RESULTS: After I/R, the PGC1α expression was increased in infarcted myocardium. H/R induced H9C2 cell apoptosis ( CONCLUSIONS After I/R, HIF-1α up-regulates the expression of PGC1α, leading to an increase in ROS production and aggravation of injury. Metformin can inhibit the accumulation of HIF-1α during hypoxia and effectively protect myocardium from ischemia/reperfusion injury.
Animals ; Apoptosis ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics* ; Myocardial Reperfusion Injury/genetics* ; Myocytes, Cardiac/metabolism* ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism* ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury