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Titolo:
When calcium turns arrhythmogenic: Intracellular calcium handling during the development of hypertrophy and heart failure
Autore:
Zaugg, CE; Buser, PT;
Indirizzi:
Univ Basel Hosp, Dept Res, Cardiovasc Res Grp, CH-4031 Basel, Switzerland Univ Basel Hosp Basel Switzerland CH-4031 rp, CH-4031 Basel, Switzerland Univ Basel Hosp, Dept Internal Med, Div Cardiol, CH-4031 Basel, Switzerland Univ Basel Hosp Basel Switzerland CH-4031 ol, CH-4031 Basel, Switzerland
Titolo Testata:
CROATIAN MEDICAL JOURNAL
fascicolo: 1, volume: 42, anno: 2001,
pagine: 24 - 32
SICI:
0353-9504(200102)42:1<24:WCTAIC>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPONTANEOUSLY HYPERTENSIVE RATS; CARDIAC SARCOPLASMIC-RETICULUM; PRESSURE-OVERLOAD HYPERTROPHY; FAILING HUMAN MYOCARDIUM; HUMAN DILATED CARDIOMYOPATHY; PHOSPHOLAMBAN MESSENGER-RNA; VENTRICULAR-FIBRILLATION; GENE-EXPRESSION; EXCHANGE ACTIVITY; PROTEIN-LEVELS;
Keywords:
arrhythmia; calcium; heart; hypertrophy, left ventricular; hypertrophy, right ventricular; myocardium; death, sudden, cardiac; ventricular fibrillation;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
80
Recensione:
Indirizzi per estratti:
Indirizzo: Zaugg, CE Univ Basel Hosp, Dept Res, Cardiovasc Res Grp, ZLF 319,Hebelstr 20, CH-4031 Basel, Switzerland Univ Basel Hosp ZLF 319,Hebelstr 20 Basel Switzerland CH-4031 d
Citazione:
C.E. Zaugg e P.T. Buser, "When calcium turns arrhythmogenic: Intracellular calcium handling during the development of hypertrophy and heart failure", CROAT MED J, 42(1), 2001, pp. 24-32

Abstract

Alterations of intracellular Ca2+ handling in hypertrophied myocardium have been proposed as a mechanism of ventricular tachyarrhythmias, which are amajor cause of sudden death in patients with heart failure. In this review, alterations in intracellular Ca2+ handling and Ca2+ handling proteins in the development of myocardial hypertrophy and the transition to heart failure are discussed. The leading question is at what stage of hypertrophy or heart failure Ca2+ handling can turn arrhythmogenic. During the development of myocardial hypertrophy and the transition to failure, Ca2+ handling is progressively altered. Recordings of free myocyte Ca2+ concentrations duringa cardiac cycle (Ca2+ transients) are prolonged early in the development of hypertrophy. However, resting (or diastolic) Ca2+ does not increase before end-stage heart failure has developed. These alterations are due to progressively defective Ca2+ uptake into the sarcoplasmic reticulum that scums to be caused by quantitative changes of gene expression of the Ca2+ ATPase of the sarcoplasmic reticulum. Increased expression and activity of the Na+/Ca2+ exchanger might compensate for this defective Ca2+ uptake, probably atthe expense of increased arrhythmogenicity. When the Ca2+ handling proteins no longer efficiently counterbalance increasing intracellular Ca2+ - during stress conditions, resulting Ca2+ overload can lead to spontaneous intracellular Ca2+ oscillations, after depolarizations. Thus, after the transition to heart failure, Ca2+ overloaded sarcoplasmic reticulum, increasing resting intracellular Ca2+, and increased Na+/Ca2+ activity may all provoke afterdepolarizations, triggered activity, and finally, life-threatening ventricular arrhythmias. This increased susceptibility to ventricular arrhythmias in heart failure should not be treated with calcium antagonists.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 11:46:45