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Titolo:
ARRHYTHMOGENESIS IN EXPERIMENTAL-MODELS OF HEART-FAILURE - THE ROLE OF INCREASED LOAD
Autore:
PYE MP; COBBE SM;
Indirizzi:
ROYAL INFIRM,DEPT MED CARDIOL,10 ALEXANDRA PARADE GLASGOW G31 2ER LANARK SCOTLAND ROYAL INFIRM,DEPT MED CARDIOL GLASGOW G31 2ER LANARK SCOTLAND
Titolo Testata:
Cardiovascular Research
fascicolo: 2, volume: 32, anno: 1996,
pagine: 248 - 257
SICI:
0008-6363(1996)32:2<248:AIEOH->2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONTRACTION-EXCITATION FEEDBACK; ACUTE VENTRICULAR DILATATION; ACTION-POTENTIAL DURATION; MYOCARDIAL-INFARCTION; CARDIAC-FAILURE; MECHANOELECTRICAL FEEDBACK; CANINE HEARTS; ANIMAL-MODEL; VOLUME LOAD; ARRHYTHMIAS;
Keywords:
HEART FAILURE; SUDDEN DEATH; MONOPHASIC ACTION POTENTIAL; VENTRICULAR FIBRILLATION; ARRHYTHMIAS; DOXORUBICIN; RABBIT, HEART;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
M.P. Pye e S.M. Cobbe, "ARRHYTHMOGENESIS IN EXPERIMENTAL-MODELS OF HEART-FAILURE - THE ROLE OF INCREASED LOAD", Cardiovascular Research, 32(2), 1996, pp. 248-257

Abstract

To assess the effects of cardiac failure due to doxorubicin cardiotoxicity err chronic myocardial infarction on arrhythmia induction, ventricular repolarization and refractoriness in isolated perfused rabbit hearts under different loading conditions. Methods: Cardiac failure wasinduced by doxorubicin injection (1-1.25 mg . kg(-1) twice weekly for8 weeks, n = 16) or coronary ligation (n = 12), with 12 controls, Cardiac failure was defined by an echocardiographic ejection fraction less than or equal to 0.40. Arrhythmia susceptibility was assessed by programmed ventricular stimulation and fibrillation threshold measurementduring Langendorff and during working heart perfusion under baseline conditions and at maximum tolerated preload and afterload, Monophasic action potential duration, dispersion of refractoriness, conduction time and effective refractory period were measured al each level of load, Results: During unloaded (Langendorff) perfusion, there was a low incidence of arrhythmia induction in all hearts, Increasing load did notalter arrhythmogenesis significantly in normal hearts, but led to increases in arrhythmia inducibility and falls in fibrillation threshold which were significantly greater in failing than in non-failing hearts, Monophasic action potential duration was significantly (P < 0.05) shorter in failing than in non-failing hearts in the doxorubicin-treated[mean (s.e.m,) 140(2) vs, 147(2) ms] and post-infarction groups [146(2) vs, 154 (3) ms] during working heart perfusion, The shortening in action potential duration and effective refractory period during increased preload tended to be greater in failing than in non-failing hearts, There were no changes in conduction times in response to changes in loading, Conclusions: The inducibility of ventricular arrhythmias is greater in failing than in non-failing hearts and is further enhanced by increases in preload, Shortening of repolarization and refractoriness due to increased preload may contribute to the increased risk of ventricular tachyarrhythmias and sudden death in cardiac failure.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 14:54:24