Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Molecular aspects of arrhythmias associated with cardiomyopathies
Autore:
Tomaselli, GF; Rose, J;
Indirizzi:
Johns Hopkins Univ, Dept Med, Sect Mol & Cellular Cardiol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 ardiol, Baltimore, MD 21205 USA Univ Essen Gesamthsch Klinikum, Zentrum Innere Med, Abt Pathophys, D-4300 Essen, Germany Univ Essen Gesamthsch Klinikum Essen Germany D-4300 -4300 Essen, Germany
Titolo Testata:
CURRENT OPINION IN CARDIOLOGY
fascicolo: 3, volume: 15, anno: 2000,
pagine: 202 - 208
SICI:
0268-4705(200005)15:3<202:MAOAAW>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSIENT OUTWARD CURRENT; STAGE HEART-FAILURE; HUMAN VENTRICULAR MYOCYTES; TACHYCARDIA-INDUCED CARDIOMYOPATHY; CARDIAC SARCOPLASMIC-RETICULUM; CALCIUM-HANDLING PROTEINS; FAILING HUMAN HEART; DILATED CARDIOMYOPATHY; DOWN-REGULATION; CURRENT-DENSITY;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
74
Recensione:
Indirizzi per estratti:
Indirizzo: Tomaselli, GF Johns Hopkins Univ, Dept Med, Sect Mol & Cellular Cardiol, Ross 844,720 N Rutland Ave, Baltimore, MD 21205 USA Johns Hopkins Univ Ross 844,720 N Rutland Ave Baltimore MD USA 21205
Citazione:
G.F. Tomaselli e J. Rose, "Molecular aspects of arrhythmias associated with cardiomyopathies", CURR OPIN C, 15(3), 2000, pp. 202-208

Abstract

The increased risk of sudden cardiac death in patients with myocardial hypertrophy and heart failure is the result of remodeling that occurs in both the myocyte and interstitial compartments of the heart. Action potential prolongation is a hallmark of hypertrophied and failing myocardium and is a consequence of differential expression and function of membrane currents andtransporters. Functional downregulation of K currents in the ventricle is a recurring theme in hypertrophy and failure; the reduction in the density of the transient outward current (I-to) is the most consistent observation,whereas data on the density of the inward (I-K1) and the delayed rectifier(I-K) currents are more contradictory. The altered intracellular Ca handling of the myopathic hearts prolongs the decay of the L-type Ca current and favors extrusion of cytosolic Ca2+ via the Na+-Ca2+ exchanger. The interaction between such altered membrane currents and a changed neurohumoral milieu creates a substrate that is highly susceptible to potentially lethal ventricular arrhythmias. (C) 2000 Lippincott Williams & Wilkins, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 20:41:57