How does β-adrenergic signalling affect the transitions from ventricular tachycardia to ventricular fibrillation?

Autor: Donald M. Bers, Yuanfang Xie, Daisuke Sato, Eleonora Grandi
Rok vydání: 2014
Předmět:
medicine.medical_specialty
Heart Ventricles
Clinical Sciences
Action Potentials
Cardiovascular
Ventricular tachycardia
Action potential duration restitution
Adrenergic stimulation
Focused Issue: Original Research
Heart Conduction System
Models
Tachycardia
Physiology (medical)
Internal medicine
Receptors
Adrenergic
beta
Receptors
Animals
Medicine
Computer Simulation
Ventricular myocytes
Fibrillation
business.industry
Models
Cardiovascular
Ventricular
Spiral wave
Cardiac arrhythmia
Fetal Restitution
medicine.disease
β-Adrenergic stimulation
Heart Disease
Signalling
Cardiovascular System & Hematology
Adrenergic
Ventricular Fibrillation
Ventricular fibrillation
Tachycardia
Ventricular
Disease Progression
cardiovascular system
Cardiology
beta
Rabbits
Electrical conduction system of the heart
medicine.symptom
Cardiology and Cardiovascular Medicine
business
Signal Transduction
Zdroj: Xie, Y; Grandi, E; Bers, DM; & Sato, D. (2014). How does β-adrenergic signalling affect the transitions from ventricular tachycardia to ventricular fibrillation?. Europace, 16(3), 452-457. doi: 10.1093/europace/eut412. UC Davis: Retrieved from: http://www.escholarship.org/uc/item/3kg2n349
Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology, vol 16, iss 3
ISSN: 1532-2092
1099-5129
DOI: 10.1093/europace/eut412
Popis: Aims: Ventricular tachycardia (VT) and fibrillation (VF) are the most lethal cardiac arrhythmias. The degeneration of VT into VF is associated with the breakup of a spiral wave of the action potential in cardiac tissue. β-Adrenergic (βAR) signalling potentiates the L-type Ca current (ICaL) faster than the slow delayed rectifier potassium current (IKs), which transiently prolongs the action potential duration (APD) and promotes early after depolarizations. In this study, we aimed at investigating how βAR signalling affects the transition from VT to VF. Methods and results: We used a physiologically detailed computer model of the rabbit ventricular myocyte in a two-dimensional tissue to determine how spiral waves respond to βAR activation following administration of isoproterenol. A simplified mathematical model was also used to investigate the underlying dynamics. We found that the spatiotemporal behaviour of spiral waves strongly depends on the kinetics of βAR activation. When βAR activation is rapid, a stable spiral wave turns into small fragments and its electrocardiogram reveals the transition from VT to VF. This is due to the transiently steepened APD restitution induced by the faster activation of ICaLvs. IKsupon sudden βAR activation. The spiral wave may also disappear if its transient wavelength is too large to be supported by the tissue size upon sudden strong βAR activation that prolongs APD transiently. When βAR activation is gradual, a stable spiral wave remains such, because of more limited increase in both APD and slope of APD restitution due to more contemporaneous ICaLand IKsactivation. Conclusion: Changes in APD restitution during βAR activation revealed a novel transient spiral wave dynamics; this spatiotemporal characteristic strongly depends on the protocol of isoproterenol application. © The Author 2014.
Databáze: OpenAIRE
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