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Titolo:
Electrical remodeling in atrial fibrillation - cellular and molecular mechanisms
Autore:
Bosch, RF; Grammer, JB; Kuhlkamp, V; Seipel, L;
Indirizzi:
Univ Tubingen, Med Klin, Abt 3, D-72076 Tubingen, Germany Univ Tubingen Tubingen Germany D-72076 Abt 3, D-72076 Tubingen, Germany
Titolo Testata:
ZEITSCHRIFT FUR KARDIOLOGIE
fascicolo: 9, volume: 89, anno: 2000,
pagine: 795 - 802
SICI:
0300-5860(200009)89:9<795:ERIAF->2.0.ZU;2-9
Fonte:
ISI
Lingua:
GER
Soggetto:
CHRONIC DOG-MODEL; SINUS RHYTHM; ELECTROPHYSIOLOGICAL CHARACTERISTICS; REFRACTORY PERIOD; GENE-EXPRESSION; ORAL VERAPAMIL; TACHYCARDIA; CARDIOVERSION; ARRHYTHMIAS; PERSISTENT;
Keywords:
atrial fibrillation; ion channels; action potentials; connexins; calcium homeostasis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Bosch, RF Univ Tubingen, Med Klin, Abt 3, Otfried Muller Str 10, D-72076 Tubingen, Germany Univ Tubingen Otfried Muller Str 10 Tubingen Germany D-72076 ny
Citazione:
R.F. Bosch et al., "Electrical remodeling in atrial fibrillation - cellular and molecular mechanisms", Z KARDIOL, 89(9), 2000, pp. 795-802

Abstract

Atrial fibrillation is associated with changes in atrial electrophysiologythat facilitate the initiation and persistence of the arrhythmia. The underlying cellular and molecular mechanisms are diverse; they have intensivelybeen investigated over the past few years. The results, that have substantially improved the understanding of the pathophysiology of atrial fibrillation are reviewed. On the cellular level, atrial fibrillation leads to a strong shortening and an impaired rate adaptation of the action potential as well as changes in action potential morphology. Atrial fibrillation is associated with an altered gene expression of the L-type calcium channel (I-Ca,I-L) and of potassium channels (I-to, I-Kl, I-KACh). The molecular mechanisms of intraatrial conduction slowing are less well understood; changes in the expression or distribution of gap junction proteins or a decrease of the fast sodium inward channel (I-Na) Seem to be involved. A trigger for many of the observations is an overload of the myocyte cytoplasm with Ca2+ and a consecutive decrease of the systolic calcium gradient, furthermore changes in calcium-handling proteins are detectable in atrial fibrillation. In the last part, the clinical relevance and potential new therapeutic approaches are discussed.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 01:28:37