Searching the Resource Information Network
Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.
Mutations in the gene encoding the main cardiac sodium channel (SCN5A) are the commonest genetic cause of Brugada syndrome (BrS). However, the effect of SCN5A mutations on the outcomes of ventricular fibrillation (VF) and syncope remains uncertain. To clarify this relationship, a meta-analysis was performed. A comprehensive search was conducted to identify all eligible studies from PubMed, MEDLINE, EBSCO, ProQuest, Science Direct, Clinical Key, and Cochrane database for cohort studies of BrS populations that had been systematically tested for SCN5A mutations. We did meta-analysis to see the relationship between SCN5A mutations and the occurrence of VF and/or syncope using RevMan 5.3. Five clinical studies met our criteria and included a total of 665 BrS patients. These studies included 45 patients with VF and 178 patients with syncope. We found that in BrS patients with SCN5A mutations the rate of VF event was 30.7% while in patients without mutations was 28.5% (Risk Ratio [RR] = 1.11, [95% CI: 0.61, 2.00], P = 0.73, I 2 = 0%). The occurrence of syncope events was 35.9% in patients with SCN5A mutations and 34.5% in patients without mutations (RR = 1.12, [95% CI: 0.87, 1.45], P = 0.37, I 2 = 39%). Furthermore, the occurrence of combined VF and syncope events were similar between the 2 groups (RR = 1.12, [95% CI: 0.89, 1.42], P = 0.34, I 2 = 11%). BrS patients with SCN5A mutations exhibit a similar risk of future occurence of VF and/or syncope as compared to those without SCN5A mutations.
Pubmed ID: 30327691
Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.
A premier bibliographic database that contains over 18 million references to journal articles in life sciences with a concentration on biomedicine. A distinctive feature is that the records are indexed with NLM Medical Subject Headings (MeSH). PubMed provides free access to MEDLINE and links to full text articles when possible. The great majority of journals are selected for MEDLINE based on the recommendation of the Literature Selection Technical Review Committee (LSTRC), an NIH-chartered advisory committee of external experts analogous to the committees that review NIH grant applications. Some additional journals and newsletters are selected based on NLM-initiated reviews, e.g., history of medicine, health services research, AIDS, toxicology and environmental health, molecular biology, and complementary medicine, that are special priorities for NLM or other NIH components. These reviews generally also involve consultation with an array of NIH and outside experts or, in some cases, external organizations with which NLM has special collaborative arrangements. MEDLINE is the primary component of PubMed, part of the Entrez series of databases provided by the NLM National Center for Biotechnology Information (NCBI). MEDLINE may also be searched via the NLM Gateway. Time coverage: generally 1946 to the present, with some older material. Source: Currently, citations from approximately 5,516 worldwide journals in 39 languages; 60 languages for older journals. Citations for MEDLINE are created by the NLM, international partners, and collaborating organizations.
View all literature mentionsTHIS RESOURCE IS NO LONGER IN SERVICE. Documented on January 5, 2023.A software package that does meta-analysis and provides results in tabular format and graphically.
View all literature mentionsPublic bibliographic database that provides access to citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites. PubMed citations and abstracts include fields of biomedicine and health, covering portions of life sciences, behavioral sciences, chemical sciences, and bioengineering. Provides access to additional relevant web sites and links to other NCBI molecular biology resources. Publishers of journals can submit their citations to NCBI and then provide access to full-text of articles at journal web sites using LinkOut.
View all literature mentions