One in five patients with CS had PAF, which occurred at low burden and long after stroke. Future studies should determine the role of implantable cardiac monitors after stroke and determine the potential therapeutic benefit of OAC treatment of patients with PAF.

Background - Recurrent paroxysmal atrial fibrillation (PAF) after catheter ablation is presumably caused by failure to achieve durable pulmonary vein isolation (PVI). The primary methods of PVI are radiofrequency (RF) and cryoballoon (CRYO) catheter ablation, but these methods have not been directly compared with respect to PVI durability and the effect thereof on AF burden (% of time in AF). Methods - Accordingly, we performed a randomized trial including 98 patients (68% male, 61 [55-67] years) with PAF assigned 1:1 to PVI by contact-force sensing, irrigated RF catheter or second-generation CRYO catheter. Implantable cardiac monitors were inserted ≥1 month before PVI for assessment of AF burden and recurrence, and all patients, irrespective of AF recurrence, underwent a second procedure 4-6 months after PVI to determine PVI durability. Results - In the second procedure, 152/199 (76%) pulmonary veins (PVs) were found durably isolated after RF and 161/200 (81%) after CRYO (NS), corresponding to durable isolation of all veins in 47% of patients in both groups (NS). Median AF burden before PVI was 5.4% (interquartile range: 0.5-13.0%) vs. 4.0% (0.6-18.1%), RF vs. CRYO, and reduced to 0.0% (0.0-0.1%) and 0.0% (0.0-0.5%), respectively - a reduction of 99.9% (92.9-100.0%) and 99.3% (85.9-100.0%) (all NS). AF burden after PVI significantly correlated to the number of durably isolated PVs (p < 0.01), but 9/45 (20%) patients with durable isolation of all veins had recurrence of AF within 4-6 months after PVI (excluding a 3-month blanking period). Conclusions - PVI by RF and CRYO catheter ablation produce similar moderate to high PVI durability. Both treatments lead to marked reductions in AF burden, which is related to the number of durably isolated PVs. However, for one fifth of PAF patients, complete and durable PVI was not sufficient to prevent even short-term AF recurrence.

Abstract-AngotensmII faclhtates epmephrme release durmg msuhn-induced hypoglycenua, and this effect appears to be independent of type 1 angotensm II (AT,) receptors m man In the present study, we hypothesized that the action of anglotensm II on adrenomedullary epmephrme release IS mediated by an AT2 receptor-dependent mechamsm In conscious chronically mstrumented rats, we measured plasma concentrations of catecholammes durmg acute msuhninduced hypoglycenua m groups of rats pretreated with the AT, receptor antagonist losartan (10 mg/kg IV), the AT, receptor antagonist PD123319 (30 mg/kg IV), combined losartan + PD123319, the convertmg enzyme mhlbltor enalapnl (1 mg/kg IV), or vehicle In vehicle-treated rats, the area under the curve for changes m plasma epmephrme concentration [AUC ( However, in contrast with other sympathoexcltatory stlmuh such as hemorrhage, exercise, or environmental stress, severe hypoglycemia produces a relatlvely selective stimulation of the adrenal medulla Thus, m humans, severe hypoglycenua causes a 50-fold increase in the plasma concentration of epmephrme while the plasma concentration of norepmephnne only Increases about 3-fold ' The increased level of epmephnne 1s considered one of the most important counterregulatory hormones released dunng severe hypoglycerma, and therefore, any substance that impairs the release of epmephrme may potentially provoke episodes of hypoglycemia m patients with insulin-dependent diabetes mellitus ' Anglotensm II interacts with the sympathetic nervous system at several levels It stimulates central sympathetic outflow and neurotransmlsslon m sympathetic ganglia, and it facilitates norepmephrme release from sympathetic nerve endings 3 Furthermore, several lines of evidence suggest that anglotensm II may also stimulate adrenomedullary epmephrme release High concentrations of anglotensm II sttmulate epmephrme release m the isolated perfused rat adrenal gland 4s In anesthetized cats, it was reported that nonselective anglotensm II receptor blockade with Sar-Ile-Ang II abolished adrenomedullary catecholamme release durmg msulm-induced hypoglycemia" as well as durmg hemorrhage ' Slmllar findings were reported m anesthetized rats, where the increase m plasma epmephrme concentration observed during hypoglycemia was reduced by CEI ' To examine the role of the remn-angotensm system for adrenomedullary epmephnne release dunng msulm-induced hypoglycenua m humans, we studled the effect of CEI with enalapnl and the effect of AT, receptor blockade with losartan m healthy subJects "" Whereas captopnl attenuated epmephnne release dunng hypoglycemia, losartan did not affect the plasma epmephnne concentration either dunng rest or dunng hypoglycemia These findings are consistent with the hypothesis that the AT, receptor may be involved m the action of anglotensm II on adrenomedullary epmephnne release m humans This nooon 1s supported by recent studies which have demonstrated that the AT2 receptor 1s the predominant angotensm II receptor m both human and rat adrenal medulla " I...