Bursting dynamics in the normal and failing hearts.
Sci Rep
; 7(1): 5927, 2017 07 19.
Article
en En
| MEDLINE
| ID: mdl-28725037
ABSTRACT
A failing heart differs from healthy hearts by an array of symptomatic characteristics, including impaired Ca2+ transients, upregulation of Na+/Ca2+ exchanger function, reduction of Ca2+ uptake to sarcoplasmic reticulum, reduced K+ currents, and increased propensity to arrhythmias. While significant efforts have been made in both experimental studies and model development to display the causes of heart failure, the full process of deterioration from a healthy to a failing heart yet remains deficiently understood. In this paper, we analyze a highly detailed mathematical model of mouse ventricular myocytes to disclose the key mechanisms underlying the continual transition towards a state of heart failure. We argue that such a transition can be described in mathematical terms as a sequence of bifurcations that the healthy cells undergo while transforming into failing cells. They include normal action potentials and [Ca2+]i transients, action potential and [Ca2+]i alternans, and bursting behaviors. These behaviors where supported by experimental studies of heart failure. The analysis of this model allowed us to identify that the slow component of the fast Na+ current is a key determining factor for the onset of bursting activity in mouse ventricular myocytes.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Potenciales de Acción
/
Insuficiencia Cardíaca
Tipo de estudio:
Health_economic_evaluation
/
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Sci Rep
Año:
2017
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
ENGLAND
/
ESCOCIA
/
GB
/
GREAT BRITAIN
/
INGLATERRA
/
REINO UNIDO
/
SCOTLAND
/
UK
/
UNITED KINGDOM