| Inflammatory markers and cardiac function in acute coronary syndrome: difference in ST-segment elevation myocardial infarction (STEMI) and in non-STEMI models. | |
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MedLine Citation:
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PMID: 19906505 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: No studies have been addressed to the differences in inflammation kinetics between ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). PATIENTS AND METHODS: Forty consecutive patients with acute coronary syndrome (ACS) (n=23 STEMI, age=61.7+/-10.3 years; n=17 NSTEMI, age=65.6+/-11.3 years) were enrolled within 12h after symptoms. All patients received therapy according to the current Guidelines. Blood samples were collected at admission (t0), on days 7 (t1) and 30 (t2) to evaluate CD40 ligand (CD40L), transforming growth factor (TGF)-beta, interleukin (IL)-6, tumor necrosis factor (TNF)-alpha and its receptors TNFRI and TNFRII, high sensitivity C-reactive protein (hs-CRP), serum amyloid A (SAA) and white blood cells (WBC). Echocardiographic parameters were also evaluated. RESULTS: STEMI patients, at admission, had significantly higher median values of hs-CRP (p<0.001), WBC (p<0.01), ferritin (p<0.0005) and IL-6 (p<0.05) than NSTEMI. On the contrary, NSTEMI patients had lower median levels of every inflammatory marker except for CD40L (p<0.05) that was significantly higher. Moreover, three out of four deceased patients presented levels of CD40L higher than the median. At admission, STEMI showed a reduced ejection fraction (EF, p<0.01) and increased wall motion score index (WMSI, p<0.001) and end-diastolic volume (EDV, p<0.05) vs NSTEMI. An inverse correlation between admission values of inflammatory markers (SAA and WBC) and cardiac function was observed (p<0.05). Moreover, the necrosis marker troponin I was positively correlated with both WMSI (p<0.05) and hs-CRP (p<0.05). Regarding the inflammation kinetics, a difference was observed in the two groups only for WBC (p<0.05) and SAA (p<0.05). SAA showed higher values in STEMI at t0 and t1. In both groups, TGF-beta had an increase at t1 and t2 with respect to admission, while IL-6 had a decreasing trend. The total incidence of major adverse clinical events (MACE) was 22.5% at t2, with a mortality rate of 10%. CONCLUSION: These observations suggest a differential inflammatory pattern in STEMI and NSTEMI patients. The absence of significant correlations between inflammatory indexes and myocardial infarction in NSTEMI supports the hypothesis that a different pattern of inflammation occurs in these patients. CD40L may have an important role as a marker for risk stratification in patients with ACS. |
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Authors:
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Rossella Di Stefano; Vitantonio Di Bello; Maria Chiara Barsotti; Chrysanthos Grigoratos; Chiara Armani; Matteo Dell'Omodarme; Angelo Carpi; Alberto Balbarini |
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Publication Detail:
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Type: Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't Date: 2009-10-13 |
Journal Detail:
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Title: Biomedicine & pharmacotherapy = Biom??decine & pharmacoth??rapie Volume: 63 ISSN: 1950-6007 ISO Abbreviation: Biomed. Pharmacother. Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2009-11-30 Completed Date: 2010-02-03 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8213295 Medline TA: Biomed Pharmacother Country: France |
Other Details:
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Languages: eng Pagination: 773-80 Citation Subset: IM |
Affiliation:
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Cardiovascular Research Laboratory, Cardiac, Thoracic and Vascular Department, University of Pisa, Pisa, Italy. r.distefano@ao-pisa.toscana.it |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Coronary Syndrome
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drug therapy,
physiopathology* Aged Biological Markers / blood CD40 Ligand / blood* Echocardiography Female Follow-Up Studies Humans Inflammation / etiology, physiopathology* Inflammation Mediators / blood Male Middle Aged Myocardial Infarction / drug therapy, physiopathology* Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Inflammation Mediators; 147205-72-9/CD40 Ligand |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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