Dr. Ning Wei, Purdue University
Abstract:
Myocardial ischemia is an imbalance between myocardial blood supply and demand, which affects 785,000 people annually in the United States alone. If the blockage is severe, the region of tissue downstream of the obstruction site is deprived of blood supply required for survival, creating a region of nonperfused tissue known as myocardial infarction (MI). As a result, a border zone (BZ) between perfused and nonperfused regions is created due to differences in blood and oxygen supplies. It has been well documented that heterogeneities and electrophysiological gradients developed at MI BZ are pro-arrhythmic. Recent experimental findings reveal a complex ``finger"-like geometry in MI BZ, however, its effect on arrhythmogenicity is not clear. Ephaptic coupling, which relies on the intercalated disk between cell ends, has been suggested to play an active role in mediating intercellular electrical communication when gap junctions are impaired. In this talk, we explore the interplay between detailed geometry of MI BZ and ephaptic coupling on arrhythmogenicity. Our study is the first instance to show that ephaptic coupling plays an anti-arrhythmic role during myocardial ischemia, which lays a solid ground for understanding and developing anti-arrhythmic strategies and therapies for patients with MI. Ventricular arrhythmias are fatal complications observed in patients with MI, which exhibit a diurnal rhythm with a peak in the morning. The biophysical mechanisms underlying these daily rhythms in adverse cardiovascular events are not fully understood. We use biophysical modeling and dynamical systems analysis to study how circadian variation in ionic conductances affects early afterdepolarization (EAD) and its progression to ventricular arrhythmias. This is the first study to connect circadian clock and ventricular arrhythmia.
Zoom
Meeting ID: 912 3803 3561
Passcode: 735393