Universität zu Köln

Burashnikov, Alexander, Di Diego, Jose M., Sicouri, Serge, Doss, Michael Xavier, Sachinidis, Agapios, Barajas-Martinez, Hector, Hu, Dan ORCID: 0000-0002-0994-8434, Minoura, Yoshino, Moise, N. Sydney, Kornreich, Bruce G., Chi, Liguo, Belardinelli, Luiz and Antzelevitch, Charles ORCID: 0000-0001-7349-1582 (2014). A temporal window of vulnerability for development of atrial fibrillation with advancing heart failure. Eur. J. Heart Fail., 16 (3). S. 271 - 281. HOBOKEN: WILEY-BLACKWELL. ISSN 1879-0844

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Abstract

Aims Heart failure (HF) is associated with development of AF and life-threatening ventricular tachycardia and fibrillation (VT/VF). Vulnerability to development of AF and VT/VF at different stages of HF and the underlying pathophysiological mechanisms are poorly defined. The present study was designed to determine the time-course of development of electrical and structural remodelling of the atria and ventricles, and their contribution to induction of AF and VT/VF in a canine model of HF. Methods and results Dogs were ventricular tachypaced (VTP) for 2-3 weeks or 5-6 weeks ('early' and 'late' HF, respectively). Electrophysiological studies were performed in isolated atrial and ventricular preparations and correlated with cardiac dimensions and haemodynamic parameters recorded in vivo. Vulnerability to programmed electrical stimulation-induced AF was greater in early vs. late stages of HF (78% vs. 38%). In contrast, VT/VF was inducible in late but not in early stages of HF (38% vs. 0%). The temporal distinction in atrial and ventricular arrhythmia susceptibility was associated with a much more rapid development of electrical and structural remodelling in atria. Vulnerability to AF developed following moderate electro-structural remodelling and waned with further progression to severe remodelling, which averted rapid atrial activation. Conclusions A temporal window of vulnerability for AF appears relatively early during development of VTP-induced HF in dogs, whereas VT/VF vulnerability is observed at more advanced stages of HF. These findings, if confirmed in humans, may have clinical implications with regard to prognosis and approach to therapy of patients with HF.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Burashnikov, Alexander UNSPECIFIED UNSPECIFIED UNSPECIFIED Di Diego, Jose M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Sicouri, Serge UNSPECIFIED UNSPECIFIED UNSPECIFIED Doss, Michael Xavier UNSPECIFIED UNSPECIFIED UNSPECIFIED Sachinidis, Agapios UNSPECIFIED UNSPECIFIED UNSPECIFIED Barajas-Martinez, Hector UNSPECIFIED UNSPECIFIED UNSPECIFIED Hu, Dan UNSPECIFIED orcid.org/0000-0002-0994-8434 UNSPECIFIED Minoura, Yoshino UNSPECIFIED UNSPECIFIED UNSPECIFIED Moise, N. Sydney UNSPECIFIED UNSPECIFIED UNSPECIFIED Kornreich, Bruce G. UNSPECIFIED UNSPECIFIED UNSPECIFIED Chi, Liguo UNSPECIFIED UNSPECIFIED UNSPECIFIED Belardinelli, Luiz UNSPECIFIED UNSPECIFIED UNSPECIFIED Antzelevitch, Charles UNSPECIFIED orcid.org/0000-0001-7349-1582 UNSPECIFIED
URN:	urn:nbn:de:hbz:38-445261
DOI:	10.1002/ejhf.28
Journal or Publication Title:	Eur. J. Heart Fail.
Volume:	16
Number:	3
Page Range:	S. 271 - 281
Date:	2014
Publisher:	WILEY-BLACKWELL
Place of Publication:	HOBOKEN
ISSN:	1879-0844
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language PRESERVED EJECTION FRACTION; FAILING HUMAN HEARTS; GROWTH-FACTOR; RISK; DOGS; TACHYCARDIA; DYSFUNCTION; PREVALENCE; FIBROSIS; MODEL Multiple languages Cardiac & Cardiovascular Systems Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/44526