Abstract
Acute transmural ischaemia often shortens ventricular repolarization and increases repolarization dispersion, leading to life threatening ventricular arrhythmias in animal models and human subjects. Experimental studies and clinical observations have shown that acute subendocardial ischaemia rarely causes serious ventricular arrhythmia. We hypothesized that the different arrhythmia outcomes between transmural and subendocardial ischaemia are largely due to the homogenous prolongation in ventricular repolarization after acute subendocardial ischaemia. Further experimental studies on a subendocardial model are required to assess the changes in ventricular repolarization and its spatial dispersion, and to investigate the role of these changes in the pathogenesis of ventricular arrhythmias. These studies will facilitate our understanding on the mechanisms of life-threatening ventricular arrhythmias during acute myocardial ischaemia.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
