Matches in SemOpenAlex for { <https://semopenalex.org/work/W4377014746> ?p ?o ?g. }
Showing items 1 to 63 of
63
with 100 items per page.
- W4377014746 endingPage "S658" @default.
- W4377014746 startingPage "S658" @default.
- W4377014746 abstract "Sepsis-induced cardiomyopathy (SIC) is one major cause of death in sepsis. Evidence of various cardiac arrhythmias in septic patients has been reported previously. Acquired QT prolongation (aQTP) is associated with an increased risk of polymorphic VT and Torsade de Pointes. However, data on the clinical analysis of aQTP, or acquired long QT syndrome (aLQTS) in sepsis and their potential mechanism is limited. We aimed to investigate the prevalence and characteristics of aQTP/aLQTS in sepsis and explore the underlying mechanism. Patients diagnosed with sepsis from 2018 to 2022 were enrolled. Occurrence of aQTP as well as cardiac arrhythmias were described. Correlation analysis was performed to investigate associated factors, followed analysis on prognosis. Mouse model for SIC was thereafter established, in which bulk-RNA sequencing of the heart was performed. The gene expression of myocardial tissue was then determined by RT-quantitative polymerase chain reaction. Biostatistical analysis based on Gene Expression Omnibus database were performed. Among 110 patients diagnosed with sepsis, aQTP was found in 13 (11.8%) subjects with a mean QTc of 502 msec, in which 2 typical aLQTS cases with progressive QTP was observed to develop electrical storm during sepsis following pacemaker implantation and esophagectomy, respectively. In correlation analysis, the prevalence of aQTP was found statistically associated with heart failure (p=0.009) and all-cause shock (p=0.02). As for primary endpoints, aLQTS was shown relevant with the length of ICU stay (p=0.037) and as an independent risk factor for all-cause death (p=0.026) in sepsis. Sequencing of myocardium on SIC mice revealed multiple genes associated with electrical ion channels were significantly altered in SIC, e.g., KCNQ1 (p<0.001, R2=0.84), KCNJ5(p<0.001, R2=0.97), SCN5A (p<0.001, R2=0.86), CALMl4 (p-0038, R2=0.36) etc., which affect cardiac repolarization by regulating potassium, sodium and calcium channels, and was in accordance with the results of qPCR for the hub genes. Externally validation based on GEO database demonstrated similar results. aQTP is not infrequently observed in sepsis-induced myocardial injury, which is associated with poor prognosis in septic patients. It requires more clinical awareness of regular monitoring for related aLQTS and other complications. Sepsis-induced myocardial inflammation may have an impact on the expression of multiple genes related to myocardial repolarization." @default.
- W4377014746 created "2023-05-19" @default.
- W4377014746 creator A5008260213 @default.
- W4377014746 creator A5019703798 @default.
- W4377014746 creator A5022816342 @default.
- W4377014746 creator A5052883326 @default.
- W4377014746 creator A5061526092 @default.
- W4377014746 creator A5083496482 @default.
- W4377014746 date "2023-05-01" @default.
- W4377014746 modified "2023-09-28" @default.
- W4377014746 title "PO-05-161 ACQUIRED LONG QT SYNDROME IN SEPSIS-INDUCED MYOCARDIAL INJURY: INVESTIGATION ON CLINICAL CHARACTERISTICS AND MECHANISM VIA ION CHANNEL REPROGRAMMING" @default.
- W4377014746 doi "https://doi.org/10.1016/j.hrthm.2023.03.1375" @default.
- W4377014746 hasPublicationYear "2023" @default.
- W4377014746 type Work @default.
- W4377014746 citedByCount "0" @default.
- W4377014746 crossrefType "journal-article" @default.
- W4377014746 hasAuthorship W4377014746A5008260213 @default.
- W4377014746 hasAuthorship W4377014746A5019703798 @default.
- W4377014746 hasAuthorship W4377014746A5022816342 @default.
- W4377014746 hasAuthorship W4377014746A5052883326 @default.
- W4377014746 hasAuthorship W4377014746A5061526092 @default.
- W4377014746 hasAuthorship W4377014746A5083496482 @default.
- W4377014746 hasBestOaLocation W43770147461 @default.
- W4377014746 hasConcept C118441451 @default.
- W4377014746 hasConcept C126322002 @default.
- W4377014746 hasConcept C164705383 @default.
- W4377014746 hasConcept C2777628635 @default.
- W4377014746 hasConcept C2778198053 @default.
- W4377014746 hasConcept C2778384902 @default.
- W4377014746 hasConcept C2778797674 @default.
- W4377014746 hasConcept C2779703243 @default.
- W4377014746 hasConcept C2781300812 @default.
- W4377014746 hasConcept C71924100 @default.
- W4377014746 hasConceptScore W4377014746C118441451 @default.
- W4377014746 hasConceptScore W4377014746C126322002 @default.
- W4377014746 hasConceptScore W4377014746C164705383 @default.
- W4377014746 hasConceptScore W4377014746C2777628635 @default.
- W4377014746 hasConceptScore W4377014746C2778198053 @default.
- W4377014746 hasConceptScore W4377014746C2778384902 @default.
- W4377014746 hasConceptScore W4377014746C2778797674 @default.
- W4377014746 hasConceptScore W4377014746C2779703243 @default.
- W4377014746 hasConceptScore W4377014746C2781300812 @default.
- W4377014746 hasConceptScore W4377014746C71924100 @default.
- W4377014746 hasIssue "5" @default.
- W4377014746 hasLocation W43770147461 @default.
- W4377014746 hasOpenAccess W4377014746 @default.
- W4377014746 hasPrimaryLocation W43770147461 @default.
- W4377014746 hasRelatedWork W2065102252 @default.
- W4377014746 hasRelatedWork W2189484333 @default.
- W4377014746 hasRelatedWork W2234542263 @default.
- W4377014746 hasRelatedWork W2262340557 @default.
- W4377014746 hasRelatedWork W2319071034 @default.
- W4377014746 hasRelatedWork W2413296737 @default.
- W4377014746 hasRelatedWork W2474037268 @default.
- W4377014746 hasRelatedWork W2742862736 @default.
- W4377014746 hasRelatedWork W3207127851 @default.
- W4377014746 hasRelatedWork W4311219518 @default.
- W4377014746 hasVolume "20" @default.
- W4377014746 isParatext "false" @default.
- W4377014746 isRetracted "false" @default.
- W4377014746 workType "article" @default.