Introduction: The leadless pacemakers are implanted routinely under fluoroscopic image, yet the pacing sites and corresponding paced electrocardiography (ECG) remain unclear. This study was to determine the computed tomography (CT)-verified location of the leadless Micra™ pacemakers (Micra™) and ECG characteristics. Methods: 20 consecutive patients who met the pacemaker indications for bradycardia and underwent fluoroscopy assisted Micra TM implantation were enrolled. All subjects underwent a postoperative CT scan to determine the precise location of the Micra TM pacing tip. Paced 12-lead ECG characteristics were analysed and correlated with the Micra TM tip location. Results: In the nine partitions of fluoroscopic RAO images, 14 (70%) of 20 patients had the Micra TM tip in zone 5, 5 (25%) in zone 6 and 1 in zone 2. Reconstructed CT 3-D cardiac images found Micra TM tips mostly clustered near the anterior insertion between the RV septum and free wall with 12 cases at the insertion-septal side and 8 at the free-wall side. ECG morphological analysis found that the peak deviation index in ECG lead V1 was 0.402±0.061 for Micra TM tips at the insertion-septal side and 0.542±0.053 in the free-wall side (P <0.001 between two sides) and paced clumsy R wave was often observed for tips at the free-wall side though there was no difference in QRS duration between two sides. Conclusion. In routine Micra TM implantation, the pacing sites were often located in the anterior insertion region, either at the insertion-septal or free-wall side. The ventricular activation propagation likely depended on the pacing sites.

Brief Introduction: This article summarizes a case of successful radiofrequency ablation of atrial tachycardia in a patient with dextrocardia in combination with intracardiac echocardiography, and summarizes the relevant experience.

Polycystic ovary syndrome (PCOS), a metabolic and reproductive disease, is frequently associated with type 2 diabetes. We previously demonstrated that autoantibodies (AAb) directed toward the second extracellular loop (ECL2) of the gonadotropin-releasing hormone receptor (GnRHR) are present in a high percentage of PCOS patients. It is unclear whether GnRHR-AAb can induce peripheral tissue insulin resistance (IR) in animal models. In the present study, we examined the impact of GnRHR-AAb on glucose metabolism, inflammation, and insulin signaling in a recently established autoimmune rat model of PCOS. Sixteen rats were divided into two groups: a GnRHR ECL2 peptide-immunized group, and a control group. Sera GnRHR-AAb, luteinizing hormone (LH), and testosterone were measured by ELISA. All immunized rats produced elevated anti-GnRHR ECL2 antibody titers and higher concentration of testosterone and LH. Intraperitoneal glucose tolerance tests demonstrated higher blood glucose levels in immunized rats at 30 minutes and 60 minutes. A homeostatic model assessment of insulin resistance index was also higher. Furthermore, the mRNA expression levels of insulin signaling genes in peripheral tissue were decreased. The concentration of sera TNF-α, IL-1α, and IL-18 were increased, while IL-4 and IL-10 were inhibited in the immunized group. These data support the likelihood of GnRHR-ECL2 AAbs inducing IR in peripheral tissue. GnRHR-ECL2 AAb may alter the synthesis and pulsatile secretion of LH thus leading to hyperandrogenemia, inflammation, and IR. Our studies provide the realistic expectation of new knowledge regarding the etiology of IR in PCOS as well as a pathway for development of novel effective treatment.