High-power short-duration (HPSD) setting during radiofrequency ablation has become an attempt to improve atrial fibrillation (AF) treatment outcomes. This study ought to compare the efficacy, safety, and effectiveness between HPSD and conventional settings. PubMed, Embase, and Cochrane Library were searched. Studies that compared HPSD and conventional radiofrequency ablation settings in AF patients were included while studies performed additional ablations on nonpulmonary vein targets without clear recording were excluded. Data were pooled with random-effect model. Efficacy endpoints include first-pass pulmonary vein isolation (PVI), acute pulmonary vein (PV) reconnection, free from AF, and free from atrial tachycardia (AT) during follow-up. Safety endpoints include esophagus injury rate and major complication rate. Effectiveness endpoints include complete PVI rate, total procedure time, PVI time, and PVI radiofrequency ablation (PVI RF) time. We included 22 studies with 3867 atrial fibrillation patients in total (2393 patients received HPSD radiofrequency ablation). Perioperatively, the HPSD group showed a higher first-pass PVI rate (risk ratio, RR = 1.10 , P = 0.0001 ) and less acute PV reconnection rate ( RR = 0.56 , P = 0.0004 ) than the conventional group. During follow-up, free from AF ( RR = 1.11 , P = 0.16 ) or AT ( RR = 1.06 , P = 0.24 ) rate did not differ between HPSD and conventional groups 6-month postsurgery. However, the HPSD group showed both higher free from AF ( RR = 1.17 , P = 0.0003 ) and AT ( RR = 1.11 , P < 0.0001 ) rate than the conventional group 12-month postsurgery. The esophagus injury ( RR = 0.99 , P = 0.98 ) and major complications ( RR = 0.76 , P = 0.70 ) rates did not differ between the two groups. The HPSD group took shorter total procedure time ( MD = − 33.71 95% CI: -43.10 to -24.33, P < 0.00001 ), PVI time ( MD = − 21.60 95% CI: -25.00 to -18.21, P < 0.00001 ), and PVI RF time ( MD = − 13.72 , 95% CI: -14.45 to -13.00, P < 0.00001 ) than conventional groups while complete procedure rate did not differ between two groups ( RR = 1.00 , P = 0.93 ). HPSD setting during AF radiofrequency ablation has better effectiveness, efficacy, and similar safety compared with the conventional setting.
Background. Exosomes derived from cardiac microvascular endothelial cells (CMECs) under hypoxia can mediate cardiac repair functions and alleviate pyroptosis and oxidative stress during ischemia-reperfusion (I/R) injury. This study is aimed at investigating the effect and mechanism of miR-27b-3p underlying hypoxic CMECs-derived exosomes against I/R injury. Methods. CMECs were isolated from the left ventricle of Sprague-Dawley rats, followed by culturing under hypoxic conditions or pretreatment with the miR-27b-3p inhibitor. CMECs-derived exosomes were added into H9C2 cells before hypoxia/reoxygenation (H/R) or injected into the rat heart before I/R injury. An in vivo I/R injury model was established by ligating and releasing the left anterior descending coronary artery. Expression of pyroptosis-related factors was detected using Western blot, and heart infarcted size was determined by the 2,3,5-triphenyl-2H-tetrazpinolium chloride staining method. Dual-Luciferase Reporter assays were performed to analyze the interactions of nmiR-27b-3p-forkhead box O1 (Foxo1) and Gasdermin D- (GSDMD-) Foxo1. Chromatin-immunoprecipitation (ChIP) assays were performed to validate the interactions between forkhead box O1 (Foxo1) and Gasdermin D (GSDMD) and Foxo1-mediated histone acetylation of GSDMD. Results. CMECs were successfully identified from left ventricle of Sprague-Dawley rats. The expressions of Foxo1 and pyroptosis-related proteins (GSDMD, NLPR3, cleaved caspase 1, IL-1β, and IL-18) were upregulated in the rat heart after I/R injury. Treatment of CMEC-derived exosomes, especially that under hypoxic conditions, significantly reduced pyroptosis in the rat heart. miR-27b-3p was significantly upregulated in CMEC-derived exosomes under hypoxic conditions, and miR-27b-3p inhibition in exosomes alleviated its cytoprotection and inhibited oxidative stress in H9C2 cells. Treatment with Foxo1 overexpression plasmids aggravated in vitro H/R and in vivo I/R injury by upregulating pyroptosis-related proteins. Further experiments validated that miR-27b-3p negatively targeted Foxo1, which bound to the promoter region of GSDMD. Conclusions. These results demonstrated a great therapeutic efficacy of miR-27b-3p overexpression in hypoxic CMEC-derived exosomes in preventing the development of myocardial damage post I/R injury through inhibiting Foxo1/GSDMD signaling-induced oxidative stress and pyroptosis.
Background: It is known that dietary consumption of ω-3 fatty acids is correlated with a reduced incidence of cardiovascular events. Here, we investigated the effect of dietary ω-3 fatty acids on atrial fibrillation (AF) vulnerability in a canine model of AF and explored the related mechanisms. Methods: 24 male beagle dogs (weight, 8-10 kg) were randomly divided into four groups: (a) sham-operated group (normal chow), (b) AF group ( AF with normal chow), (c) AF+FO (AF and chow supplemented with fish oil (FO, 0.6 g ω-3 PUFA/kg/day)), (d) FO (chow supplemented with FO). Daily oral administration FO was initiated 1 week before surgery and continued throughout the study period. Results: Dietary FO significantly reversed atrial electric remodeling post rapid atria pacing (RAP). FO treatment also attenuated the elevated levels of biomakers for ER stress (all P<0.05 vs. AF). RAP-induced upregulation of inflammation factors IL-1β, IL-6, TNF-α in LA were significantly attenuated by FO treatment (all p<0.05 vs. AF). In addition, Masson staining revealed increased interstitial fibrosis in LA was significantly reduced in AF+FO group as compared to AF group (P<0.01). FO treatment also alleviated RAP-induced myocardial apoptosis (p<0.05). Conclusions: Dietary ω-3 fatty acids reduced RAP-induced AF vulnerability, possibly via attenuating myocardial ER stress and inflammation in this canine model of AF.
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