A decade of complex fractionated electrograms catheter-based ablation for atrial fibrillation: Literature analysis, meta-analysis and systematic review

AbstractBackgroundIt has been a decade since the complex fractionated atrial electrograms (CFAEs) were first established following the publication of Nademanee's standards. However, the status and focus of CFAE research are unclear, as is the efficacy of additional CFAE ablation in atrial fibrillation (AF). This literature review and meta-analysis were designed to determine the status of CFAE research and the efficacy and complications of CFAE ablation alone, pulmonary vein isolation (PVI) alone and PVI plus CFAE ablation in AF.MethodsWith the assistance from reference librarians and investigators trained in systematic review, we conducted a literature search of MEDLINE (via PubMed), Embase, the Cochrane Library, ScienceDirect, Wiley Blackwell and Web of Knowledge, using “complex fractionated atrial electrograms” for MeSH and keyword search.ResultsThe literature on CFAEs increased from 2007, mainly focusing on mapping studies, with mechanism studies increasing significantly from 2012. Fifteen trials with 1525 patients were qualified for our meta-analysis. Success rates were as follows. Overall (P < 0.001): CFAE ablation alone, 23.5–26.2%; PVI, 64.7%; PVI plus CFAE ablation, 67.0%. Single ablation: PVI, 60.4%; PVI plus CFAEs, 68.8% (OR 1.53, 95% CI 1.07–2.20, P = 0.02). Re-ablation: PVI, 69.0%; PVI plus CFAEs, 77.2% (OR 1.54, 95% CI 1.06–2.24, P = 0.02). Paroxysmal AF: PVI, 76.7%; PVI plus CFAEs, 79.1% (OR 1.20, 95% CI 0.79–1.81, P = 0.39). Persistent or permanent AF: PVI, 47.9%; PVI plus CFAEs, 58.7% (OR = 1.59, 95% CI 1.13–2.24, P = 0.008). Complication rates: PVI, 2.6%; PVI plus CFAEs, 3.4% (OR 1.22, 95% CI 0.58–2.57, P = 0.61).ConclusionsIn the literature, CFAE mapping studies preceded mechanism studies. CFAE ablation alone is insufficient for the treatment of AF. Additional CFAE ablation after adequate PVI or PVI plus linear ablation improves the outcome of single ablation and re-ablation without increasing complications, especially in persistent or permanent AF. There are insufficient data to support a similar improvement in paroxysmal AF or inducible AF after PVI for paroxysmal AF

Effects of Low-Level Autonomic Stimulation on Prevention of Atrial Fibrillation Induced by Acute Electrical Remodeling

Background. Rapid atrial pacing (RAP) can induce electrical and autonomic remodeling and facilitate atrial fibrillation (AF). Recent reports showed that low-level vagosympathetic nerve stimulation (LLVNS) can suppress AF, as an antiarrhythmic effect. We hypothesized that LLVNS can reverse substrate heterogeneity induced by RAP. Methods and Results. Mongrel dogs were divided into (LLVNS+RAP) and RAP groups. Electrode catheters were sutured to multiple atrial sites, and LLVNS was applied to cervical vagosympathetic trunks with voltage 50% below the threshold slowing sinus rate by ⩽30 msec. RAP induced a significant decrease in effective refractory period (ERP) and increase in the window of vulnerability at all sites, characterized by descending and elevated gradient differences towards the ganglionic plexi (GP) sites, respectively. The ERP dispersion was obviously enlarged by RAP and more significant when the ERP of GP-related sites was considered. Recovery time from AF was also prolonged significantly as a result of RAP. LLVNS could reverse all these changes induced by RAP and recover the heterogeneous substrate to baseline. Conclusions. LLVNS can reverse the electrical and autonomic remodeling and abolish the GP-central gradient differences induced by RAP, and thus it can recover the homogeneous substrate, which may be the underlying mechanism of its antiarrhythmic effect

Mechanism of and Therapeutic Strategy for Atrial Fibrillation Associated with Diabetes Mellitus

Diabetes mellitus (DM) is one of the most important risk factors for atrial fibrillation (AF) and is a predictor of stroke and thromboembolism. DM may increase the incidence of AF, and when it is combined with other risk factors, the incidence of stroke and thromboembolism may also be higher; furthermore, hospitalization due to heart failure appears to increase. Maintenance of well-controlled blood glucose and low levels of HbA1c in accordance with guidelines may decrease the incidence of AF. The mechanisms of AF associated with DM are autonomic remodeling, electrical remodeling, structural remodeling, and insulin resistance. Inhibition of the renin-angiotensin system is suggested to be an upstream therapy for this type of AF. Studies have indicated that catheter ablation may be effective for AF associated with DM, restoring sinus rhythm and improving prognosis. Catheter ablation combined with hypoglycemic agents may further increase the rate of maintenance of sinus rhythm and reduce the need for reablation

<i>Bacteroides fragilis</i> Supplementation Deteriorated Metabolic Dysfunction, Inflammation, and Aorta Atherosclerosis by Inducing Gut Microbiota Dysbiosis in Animal Model

Background: The gut microbial ecosystem is an important factor that regulates host health and the onset of chronic diseases, such as inflammatory bowel diseases, obesity, hyperlipidemia, and diabetes mellitus, which are important risk factors for atherosclerosis. However, the links among diet, microbiota composition, and atherosclerotic progression are unclear. Methods and results: Four-week-old mice (-/- mice, C57Bl/6) were randomly divided into two groups, namely, supplementation with culture medium (control, CTR) and Bacteroides fragilis (BFS), and were fed a high-fat diet. The gut microbiota abundance in feces was evaluated using the 16S rDNA cloning library construction, sequencing, and bioinformatics analysis. The atherosclerotic lesion was estimated using Oil Red O staining. Levels of CD36, a scavenger receptor implicated in atherosclerosis, and F4/80, a macrophage marker in small intestine, were quantified by quantitative real-time PCR. Compared with the CTR group, the BFS group showed increased food intake, fasting blood glucose level, body weight, low-density lipoprotein level, and aortic atherosclerotic lesions. BFS dramatically reduced Lactobacillaceae (LAC) abundance and increased Desulfovibrionaceae (DSV) abundance. The mRNA expression levels of CD36 and F4/80 in small intestine and aorta tissue in the BFS group were significantly higher than those in the CTR group. Conclusions: gut microbiota dysbiosis was induced by BFS. It was characterized by reduced LAC and increased DSV abundance and led to the deterioration of glucose/lipid metabolic dysfunction and inflammatory response, which likely promoted aorta plaque formation and the progression of atherosclerosis

Overlap phenotypes of the left ventricular noncompaction and hypertrophic cardiomyopathy with complex arrhythmias and heart failure induced by the novel truncated DSC2 mutation

10.1186/s13023-021-02112-9Orphanet Journal of Rare Diseases16149

Case report of familial sudden cardiac death caused by a DSG2 p.F531C mutation as genetic background when carrying with heterozygous KCNE5 p.D92E/E93X mutation

Abstract Background Sudden cardiac death (SCD) induced by malignant ventricular tachycardia (MVT) among young adults with right ventricular cardiomyopathy/dysplasia (ARVC/D) is a devastating event. Parts of ARVC/D patients have a mutation in genes encoding components of cardiac desmosomes, such as desmoglein-2 (DSG2), plakophilin-2 and desmoplakin. Case presentation Here we report a potentially pathogenic mutation in the DSG2 gene, which was identified in a family with ARVC/D using Whole Exome Sequencing (WES) and Sanger Sequencing. In all, Patient III:1 with ARVC/D carried the compound heterozygous mutations of DSG2 p.F531C and KCNE5 p.D92E/E93X, which were both inherited from her mother (II:2), who died of SCD. Carriers of DSG2p.F531C showed various phenotypes, such as ARVC/D, SCD, MVT and dilated cardiomyopathy. For III:1, there were significant low-voltage regions in the inferior-apical, inferior-lateral wall of the right ventricular epicardium and outflow tracts of the right ventricle. Under the guidance of a three-dimensional mapping system, MVT was successfully ablated with an epicardial–endocardial approach targeting for late, double or fragmental potentials after implantable cardioverter-defibrillator (ICD) electrical storms. No VT recurrence was observed during the one year of follow-up. Conclusions When coexisting with heterozygous KCNE5 p.D92E/E93X, heterozygous DSG2 p.F531C as a genetic background was found to predispose to ARVC/D, SCD and MVT, which were successfully ablated using an epicardial–endocardial approach

Genomic Analyses Yield Markers for Identifying Agronomically Important Genes in Potato

International audienc