Background: Familial Mediterranean fever (FMF) is a chronic, recurrent auto-inflammatory disease characterised by self-terminating attacks of fever and sterile polyserositis. The main cause of death in auto-inflammatory diseases is cardiovascular events. Additionally, auto-inflammatory diseases have potential effects on the myocardial repolarisation parameters, including the T-wave peak-to-end (Tp-Te) interval, cTp-Te interval (corrected Tp-Te) and the cTp-Te/QT ratio. The aim of this study was to analyse the efficacy of myocardial repolarisation alterations in anticipation of cardiovascular risks in patients with FMF.
Methods: This study included 66 patients with FMF and 58 healthy control subjects. Tp-Te and cTp-Te intervals and the cTp-Te/QT ratio were measured from the 12-lead electrocardiogram.
Results: In electrocardiographic parameters, analysis of QT, QT dispersion, corrected QT (QTc) and QTc dispersion were similar between the groups. The Tp-Te and cTp-Te intervals and Tp-Te/QT and cTp-Te/QT ratios were significantly prolonged in FMF patients. Multivariate linear regression analyses indicated that erythrocyte sedimentation rate was an independent predictor of a prolonged cTp-Te interval.
Conclusions: Our study revealed that when compared with control subjects, Tp-Te and cTp-Te intervals and cTp-Te/QT ratio were increased in FMF patients.
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http://dx.doi.org/10.5830/CVJA-2016-074 | DOI Listing |
Elife
December 2024
Department of Computer Science, University of Oxford, Oxford, United Kingdom.
Sudden death after myocardial infarction (MI) is associated with electrophysiological heterogeneities and ionic current remodelling. Low ejection fraction (EF) is used in risk stratification, but its mechanistic links with pro-arrhythmic heterogeneities are unknown. We aim to provide mechanistic explanations of clinical phenotypes in acute and chronic MI, from ionic current remodelling to ECG and EF, using human electromechanical modelling and simulation to augment experimental and clinical investigations.
View Article and Find Full Text PDFAnn Cardiol Angeiol (Paris)
December 2024
Cardiology Department, Faculty of Medicine, Benha University, Benha, Egypt.
Background: Patients with anterior ST elevation myocardial infarction (STEMI) are vulnerable to life-threatening ventricular arrhythmia and arrhythmic death. This study aimed to investigate the predictive value of Tpeak-to-Tend (TpTe) and TpTe/QT ratio in patients with anterior STEMI on admission for the occurrence of in-hospital life-threatening ventricular arrhythmias and arrhythmic death.
Methods: This observational cross-sectional research was performed on patients with anterior STEMI who showed up within 12 hours of the beginning of symptoms and received the initial percutaneous coronary intervention (pPCI).
Dis Model Mech
August 2024
Victor Chang Cardiac Research Institute, Sydney, 2010, Australia.
Hypertrophic cardiomyopathy (HCM) is an inherited heart muscle disease that is characterised by left ventricular wall thickening, cardiomyocyte disarray and fibrosis, and is associated with arrhythmias, heart failure and sudden death. However, it is unclear to what extent the electrophysiological disturbances that lead to sudden death occur secondary to structural changes in the myocardium or as a result of HCM cardiomyocyte electrophysiology. In this study, we used an induced pluripotent stem cell model of the R403Q variant in myosin heavy chain 7 (MYH7) to study the electrophysiology of HCM cardiomyocytes in electrically coupled syncytia, revealing significant conduction slowing and increased spatial dispersion of repolarisation - both well-established substrates for arrhythmia.
View Article and Find Full Text PDFInt J Cardiol
November 2024
Oxford University Hospitals NHS Foundation Trust & University of Oxford, Oxford, UK. Electronic address:
Front Pharmacol
April 2024
Department of Computer Science, University of Oxford, Oxford, United Kingdom.
Hypertrophic cardiomyopathy (HCM) is a leading cause of lethal arrhythmias in the young. Although the arrhythmic substrate has been hypothesised to be amenable to late Na block with ranolazine, the specific mechanisms are not fully understood. Therefore, this study aimed to investigate the substrate mechanisms of safety and antiarrhythmic efficacy of ranolazine in HCM.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!