1998
DOI: 10.1016/s0735-1097(98)80799-7
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Angiotensin II receptor antagonist improves the immune activations of patients with chronic heart failure

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Cited by 4 publications
(3 citation statements)
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“…43 The upregulations of inflammatory cytokines such as IL-6 and TNF-α have both been reported to depress cardiac function. 44,45 PGE 2 is one of the most abundant prostaglandins and involved in all processes leading to inflammation. 46 Anti- MCP-1 therapy exerted a beneficial action on the infarcted ventricle, reducing mortality, attenuating chamber dilation, and improving systolic function.…”
Section: ■ Results and Discussionmentioning
confidence: 99%
“…43 The upregulations of inflammatory cytokines such as IL-6 and TNF-α have both been reported to depress cardiac function. 44,45 PGE 2 is one of the most abundant prostaglandins and involved in all processes leading to inflammation. 46 Anti- MCP-1 therapy exerted a beneficial action on the infarcted ventricle, reducing mortality, attenuating chamber dilation, and improving systolic function.…”
Section: ■ Results and Discussionmentioning
confidence: 99%
“…The mechanism by which IL-6 exerts its deleterious effects is not known, but there is initial evidence that it is involved in the development of ventricular hypertrophy by an interaction with a receptor known as glycoprotein 130 (gp130), expressed on the cardiac myocyte (39). IL-6 levels are high in patients with left ventricular dysfunction even in the absence of the clinical syndrome of CHF (40) and are con-Clinical Reviews in Allergy and Immunology Volume 23, 2002 sidered a prognostic marker associated with poor prognosis in CHF (41,42). Although in the left ventricular dysfunction trial (SOLVD), no relation was found between IL-6 plasma levels and survival (14), the VEST trial on 1200 patients found that IL-6, like TNF and TNF receptors, were an independent predictors of mortality in patients with CHF (27).…”
Section: Interleukin-6mentioning
confidence: 99%
“…Φαίνεται μάλιστα ότι το σύνδρομο της ΚΑ εν πολλοίς οφείλεται στη σχετική ανισορροπία που επικρατεί στην αύξηση των φλεγμονωδών και αντιφλεγμονωδών μεσολαβητών 124. Τα επίπεδα των προφλεγμονωδών κυτοκινών του πλάσματος, που περιλαμβάνουν τον παράγοντα νέκρωσης των όγκων-α (TNF-a)125,126 , την ιντερλευκίνη 6 (IL-6)127,128 , και τους υποδοχείς τους 125 είναι αυξημένα ανάλογα με τη βαρύτητα της νόσου και προβλέπουν την έκβαση. Οι κυτοκίνες ασκούν άμεσες αρνητικές επιδράσεις στα μυοκύτταρα της καρδιάς και στην εξωκυττάρια ουσία και έχουν ενοχοποιηθεί ότι συμμετέχουν στην αναδιαμόρφωση των κοιλιών και στην εξέλιξη της νόσου 129.…”
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