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Biomed Pharmacother. 2009 Dec;63(10):773-80. doi: 10.1016/j.biopha.2009.06.004. Epub 2009 Oct 13.

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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Cardiovascular Research Laboratory, Cardiac, Thoracic and Vascular Department, University of Pisa, Pisa, Italy.



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).


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.


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%.


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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