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Titolo:
Altering ventricular activation remodels gap junction distribution in canine heart
Autore:
Patel, PM; Plotnikov, A; Kanagaratnam, P; Shvilkin, A; Sheehan, CT; Xiong, W; Danilo, P; Rosen, MR; Peters, NS;
Indirizzi:
Univ London Imperial Coll Sci Technol & Med, Sch Med, St Marys Hosp, Dept Cardiol, London W2 1NY, England Univ London Imperial Coll Sci Technol & Med London England W2 1NY ngland Columbia Univ Coll Phys & Surg, New York, NY 10032 USA Columbia Univ Coll Phys & Surg New York NY USA 10032 w York, NY 10032 USA
Titolo Testata:
JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY
fascicolo: 5, volume: 12, anno: 2001,
pagine: 570 - 577
SICI:
1045-3873(200105)12:5<570:AVARGJ>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
RENIN-ANGIOTENSIN SYSTEM; CARDIAC MEMORY; ATRIAL-FIBRILLATION; T-WAVE; MYOCARDIUM; CONNEXIN43; MYOCYTES; EXPRESSION; CONDUCTION; HYPERTROPHY;
Keywords:
ventricular pacing; gap junctional remodeling; connexin43; T wave;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Peters, NS Univ London Imperial Coll Sci Technol & Med, Sch Med, St Marys Hosp, Dept Cardiol, Praed St, London W2 1NY, England Univ London Imperial Coll Sci Technol & Med Praed St London England W2 1NY
Citazione:
P.M. Patel et al., "Altering ventricular activation remodels gap junction distribution in canine heart", J CARD ELEC, 12(5), 2001, pp. 570-577

Abstract

Gap Junctional Remodeling in Paced Ventricle. Introduction: Prolonged arrhythmic or paced ventricular activation causes persistent changes in myocardial conduction and repolarization that may result from altered electrotoniccurrent flow, for which gap junctional coupling is the principal determinant. Remodeling of gap junctions and their constituent connexins modifies conduction and has been causally implicated in reentrant arrhythmogenesis. Wehypothesized conversely that altering the pattern of ventricular activation causes gap junctional remodeling. Methods and Results: Seven dogs were paced from the left ventricular (LV) epicardium (VVO, similar to 120 beats/min) for 21 days before excision of transmural LV samples that were divided into endomyocardial, mid-myocardial,and epimyocardial layers. Another five paced dogs had recording electrodesattached to multiple LV sites. All 12 dogs developed characteristic pacing-induced persistent T wave changes of cardiac memory. After 21 days of pacing, the ventricularly paced QRS duration prolonged by a mean of 4 msec overbaseline (P < 0.05), a change that was associated with significant slowingof intraventricular conduction to local sites. These changes in QRS duration and repolarization were associated with a reduction in epimyocardial connexin43 expression on quantitative Western blotting of LV myocardium from close to, but not distant from, the pacing site (61.7 +/- 18.4 vs 100.9 +/- 34.0; P < 0.02) and a marked disruption in imnunolabeled connexin43 distribution in epimyocardium only. Conclusion: Spatially distinct transmural and regional gap junctional remodeling is a consequence of abnormal ventricular activation and is associated with consistent changes in activation that may alter patterns of repolarization and facilitate reentrant arrhythmogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 10:21:24