Document Detail


Inflammatory markers and cardiac function in acute coronary syndrome: difference in ST-segment elevation myocardial infarction (STEMI) and in non-STEMI models.
MedLine Citation:
PMID:  19906505     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-10-13
Journal Detail:
Title:  Biomedicine & pharmacotherapy = Biom??decine & pharmacoth??rapie     Volume:  63     ISSN:  1950-6007     ISO Abbreviation:  Biomed. Pharmacother.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-30     Completed Date:  2010-02-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8213295     Medline TA:  Biomed Pharmacother     Country:  France    
Other Details:
Languages:  eng     Pagination:  773-80     Citation Subset:  IM    
Affiliation:
Cardiovascular Research Laboratory, Cardiac, Thoracic and Vascular Department, University of Pisa, Pisa, Italy. r.distefano@ao-pisa.toscana.it
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MeSH Terms
Descriptor/Qualifier:
Acute Coronary Syndrome / 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:
0/Biological Markers; 0/Inflammation Mediators; 147205-72-9/CD40 Ligand

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