Efficacy of Complex Fractionated Atrial Electrogram-Guided Extensive Encircling Pulmonary Vein Isolation for Persistent Atrial Fibrillation.

Background: In persistent AF, the effect of adjunctive ablation in addition to PV isolation (PVI) is controversial. We considered a new modified PVI including complex fractionated atrial electrogram (CFAE) area. Methods and Results: In 57 patients with persistent AF undergoing first ablation, CFAE were mapped before ablation and CFAE-guided extensive encircling PVI (CFAE-guided EEPVI) was performed. The PVI line was designed to include the CFAE area near PV or to cross the minimum cycle length points of the CFAE area near PV (CFAE-guided EEPVI group). The outcome was compared with conventional PVI in 34 patients with persistent AF (conventional PVI group). During a mean follow-up of 365±230 days after the first procedure, AF in 13 and atrial tachycardia (AT) in 9 patients recurred in the CFAE-guided EEPVI group, while only AF in 17 patients recurred in the conventional PVI group. Eight of 9 AT in the CFAE-guided EEPVI group were successfully ablated at second procedure. After first and second procedures, the recurrence of atrial tachyarrhythmia in the CFAE-guided EEPVI group was significantly reduced compared with the conventional PVI group (8 patients, 14% vs. 11 patients, 32%, respectively; P<0.01, log-rank test). Conclusions: CFAE-guided EEPVI was more effective for persistent AF compared with conventional PVI after first and second procedures, because recurring AT as well as re-conduction of PV was successfully ablated.

Afadin Facilitates Vascular Endothelial Growth Factor-Induced Network Formation and Migration of Vascular Endothelial Cells by Inactivating Rho-Associated Kinase Through ArhGAP29.

OBJECTIVE: We previously reported that afadin, an actin filament-binding protein, regulated vascular endothelial growth factor-induced angiogenesis. However, the underlying molecular mechanisms are poorly understood. Here, we investigated the mechanisms of how Rho-associated kinase is activated in afadin-knockdown human umbilical vein endothelial cells (HUVECs) and how its activation is involved in defects of vascular endothelial growth factor-induced network formation and migration of the cells. APPROACH AND RESULTS: Knockdown of afadin or ArhGAP29, a GTPase-activating protein for RhoA, increased Rho-associated kinase activity and reduced the vascular endothelial growth factor-induced network formation and migration of cultured HUVECs, accompanied by the defective formation of membrane protrusions, such as lamellipodia and peripheral ruffles. Treatment of the afadin- or ArhGAP29-knockdown HUVECs with Rho-associated kinase inhibitors, Y-27632 or fasudil, partially restored the reduced network formation and migration as well as the defective formation of membrane protrusions. ArhGAP29 bound to afadin and was colocalized with afadin at the leading edge of migrating HUVECs. The defective formation of membrane protrusions in ArhGAP29-knockdown HUVECs was restored by expression of mutant ArhGAP29 that bound to afadin and contained a RhoGAP domain but not mutant ArhGAP29 that could bind to afadin and lacked the RhoGAP domain or mutant ArhGAP29 that could not bind to afadin and contained the RhoGAP domain. This suggested the requirement of both the interaction of afadin with ArhGAP29 and RhoGAP activity of ArhGAP29 for migration of HUVECs. CONCLUSIONS: Our results highlight a critical role of the afadin-ArhGAP29 axis for the regulation of Rho-associated kinase activity during vascular endothelial growth factor-induced network formation and migration of HUVECs.

Clinically suspected acute myopericarditis with cardiac tamponade associated with peripheral blood eosinophilia presenting in early pregnancy: a case report.

INTRODUCTION: The clinical presentation of eosinophilic myocarditis may vary from asymptomatic to the manifestation of severe symptoms, including cardiac tamponade and arrhythmias. In pregnant patients with this condition, drugs must be used cautiously up to approximately the 4th month of pregnancy because drug use should be limited during the period of fetal organogenesis. CASE PRESENTATION: A 30-year-old Asian woman at 14 weeks of pregnancy with progressive malaise was hospitalized. The electrocardiogram revealed ST elevation and low QRS voltage. Echocardiography revealed massive pericardial effusion and myocardial swelling. A laboratory examination revealed an increase in her white blood cell count, with a predominance of neutrophils. Pericardial drainage was performed for relief of the cardiac tamponade. The pericardial effusion revealed an abundance of eosinophils. Subsequently, the peripheral blood eosinophil count began to rise, and the patient was clinically diagnosed with eosinophilic myopericarditis. The patient's condition improved rapidly following the initiation of prednisolone treatment, and she finally delivered a full-term normal infant. CONCLUSIONS: A patient with clinically suspected myopericarditis in the early stage of pregnancy who improved rapidly with pericardial drainage and prednisolone therapy, and successfully delivered a normal full-term infant; the diagnosis was made in the early stage of the disease, based on the detection of an abundance of eosinophils in the pericardial effusion preceding the subsequent development of peripheral blood eosinophilia.