Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Cardiomyocyte apoptosis and progression of heart failure to transplantation
Autore:
Saraste, A; Pulkki, K; Kallajoki, M; Heikkila, P; Laine, P; Mattila, S; Nieminen, MS; Parvinen, M; Voipio-Pulkki, LM;
Indirizzi:
Turku Univ, Dept Anat, Turku, Finland Turku Univ Turku FinlandTurku Univ, Dept Anat, Turku, Finland Turku Univ, Dept Med, Turku, Finland Turku Univ Turku FinlandTurku Univ, Dept Med, Turku, Finland Turku Univ, Dept Clin Chem, Turku, Finland Turku Univ Turku FinlandTurku Univ, Dept Clin Chem, Turku, Finland Turku Univ, Dept Pathol, Turku, Finland Turku Univ Turku FinlandTurku Univ, Dept Pathol, Turku, Finland Univ Helsinki, Dept Pathol, Helsinki, Finland Univ Helsinki Helsinki Finland Helsinki, Dept Pathol, Helsinki, Finland Univ Helsinki, Dept Surg, Helsinki, Finland Univ Helsinki Helsinki Finland v Helsinki, Dept Surg, Helsinki, Finland Univ Helsinki, Dept Med, Helsinki, Finland Univ Helsinki Helsinki Finland iv Helsinki, Dept Med, Helsinki, Finland Wihuri Res Inst, SF-00140 Helsinki, Finland Wihuri Res Inst Helsinki Finland SF-00140 st, SF-00140 Helsinki, Finland
Titolo Testata:
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
fascicolo: 5, volume: 29, anno: 1999,
pagine: 380 - 386
SICI:
0014-2972(199905)29:5<380:CAAPOH>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOCYTE CELL-DEATH; VENTRICULAR MYOCYTES; RAT; MYOCARDIUM; DOGS;
Keywords:
apoptosis; dilated cardiomyopathy; heart failure; ischaemia; remodelling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
21
Recensione:
Indirizzi per estratti:
Indirizzo: Voipio-Pulkki, LM Turku Univ, Cent Hosp, Dept Med, POB 52, FIN-20521 Turku, Finland Turku Univ POB 52 Turku Finland FIN-20521 urku, Finland
Citazione:
A. Saraste et al., "Cardiomyocyte apoptosis and progression of heart failure to transplantation", EUR J CL IN, 29(5), 1999, pp. 380-386

Abstract

Background Cardiomyocyte apoptosis has been found in congestive heart failure, but its clinical significance has been difficult to study. We comparedthe occurrence of cardiomyocyte apoptosis in explanted hearts with the progression of severe heart failure until the need for transplantation. Design Using the TUNEL assay, apoptotic cardiomyocytes were quantified in explanted failing hearts from patients with either idiopathic dilated cardiomyopathy (n = 21) or ischaemic heart disease (n = 14). The percentage was compared with the clinical severity and progression of endstage heart failure. Samples obtained at autopsy and during open heart surgery served as controls. Results The number of apoptotic cardiomyocytes was significantly increasedin failing hearts regardless of aetiology (medians 0.075% in ischaemic heart disease and 0.119% in dilated cardiomyopathy) compared with control myocardium. In patients with dilated cardiomyopathy, apoptotic cardiomyocytes were more numerous in subjects with a rapidly deteriorating clinical course (0.192%, n = 10) than in patients with intermediate (0.093%, n = 6, P = 0.03) or slow (0.026%, n = 5, P = 0.003) progression. No such association was observed in patients with ischaemic heart disease, in whom we found significantly increased cardiomyocyte apoptosis adjacent to scars of previous infarctions (0.576%) in contrast to the diffuse distribution seen in dilated cardiomyopathy. Expression of Bcl-2, an antiapoptotic protein, was increased in all failing hearts by immunohistochemistry. Conclusion Cardiomyocyte apoptosis is a consistent feature of end-stage heart failure in man and appears to be quantitatively related to the clinicalseverity of deterioration in dilated cardiomyopathy. Increased expression of Bcl-2 in cardiomyocytes indicates activation of an antiapoptotic response. These observations suggest that cardiomyocyte apoptosis is a clinically relevant and potentially modifiable pathophysiological phenomenon in severeheart failure.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 21:52:48