Remodeling of the Purkinje Network in Congestive Heart Failure in the Rabbit.
Action Potentials
/ physiology
Animals
Cardiac Pacing, Artificial
/ adverse effects
Electrocardiography
/ methods
Heart Failure
/ physiopathology
Heart Rate
/ physiology
Heart Ventricles
/ physiopathology
Male
Models, Animal
Rabbits
Ventricular Remodeling
/ physiology
X-Ray Microtomography
/ adverse effects
Purkinje fibers
electron microscopy
heart failure
ion channels
rabbits
tomography
Journal
Circulation. Heart failure
ISSN: 1941-3297
Titre abrégé: Circ Heart Fail
Pays: United States
ID NLM: 101479941
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
pubmed:
1
7
2021
medline:
15
12
2021
entrez:
30
6
2021
Statut:
ppublish
Résumé
Purkinje fibers (PFs) control timing of ventricular conduction and play a key role in arrhythmogenesis in heart failure (HF) patients. We investigated the effects of HF on PFs. Echocardiography, electrocardiography, micro-computed tomography, quantitative polymerase chain reaction, immunohistochemistry, volume electron microscopy, and sharp microelectrode electrophysiology were used. Congestive HF was induced in rabbits by left ventricular volume- and pressure-overload producing left ventricular hypertrophy, diminished fractional shortening and ejection fraction, and increased left ventricular dimensions. HF baseline QRS and corrected QT interval were prolonged by 17% and 21% (mean±SEMs: 303±6 ms HF, 249±11 ms control; n=8/7; Severe volume- followed by pressure-overload causes rapidly progressing HF with extensive remodeling of PFs. The PF network is central to both arrhythmogenesis and contractile dysfunction and the pathological remodeling may increase the risk of fatal arrhythmias in HF patients.
Sections du résumé
BACKGROUND
Purkinje fibers (PFs) control timing of ventricular conduction and play a key role in arrhythmogenesis in heart failure (HF) patients. We investigated the effects of HF on PFs.
METHODS
Echocardiography, electrocardiography, micro-computed tomography, quantitative polymerase chain reaction, immunohistochemistry, volume electron microscopy, and sharp microelectrode electrophysiology were used.
RESULTS
Congestive HF was induced in rabbits by left ventricular volume- and pressure-overload producing left ventricular hypertrophy, diminished fractional shortening and ejection fraction, and increased left ventricular dimensions. HF baseline QRS and corrected QT interval were prolonged by 17% and 21% (mean±SEMs: 303±6 ms HF, 249±11 ms control; n=8/7;
CONCLUSIONS
Severe volume- followed by pressure-overload causes rapidly progressing HF with extensive remodeling of PFs. The PF network is central to both arrhythmogenesis and contractile dysfunction and the pathological remodeling may increase the risk of fatal arrhythmias in HF patients.
Identifiants
pubmed: 34190577
doi: 10.1161/CIRCHEARTFAILURE.120.007505
pmc: PMC8288482
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e007505Subventions
Organisme : British Heart Foundation
ID : RG/11/18/29257
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/15/16/31330
Pays : United Kingdom
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