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Inflammatory markers and cardiac function in acute coronary syndrome: difference in ST-segment elevation myocardial
Rossella Di Stefano1, Vitantonio Di Bello, Maria Chiara Barsotti
1Cardiovascular Research Laboratory, Cardiac, Thoracic and Vascular Department, University of Pisa, Pisa, Italy. r.distefano@ao-pisa.toscana.it
Insights
This study reveals distinct inflammation patterns in ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) patients, with CD40 ligand (CD40L) showing potential as a risk stratification marker in acute coronary syndrome (ACS).
Area of Science:
- Cardiovascular Medicine and Research
- Inflammation and Immunology in Cardiovascular Disease
Background:
- Acute coronary syndrome (ACS) encompasses ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI).
- Differences in inflammatory kinetics between STEMI and NSTEMI have not been previously investigated.
Purpose of the Study:
- To investigate and compare the inflammation kinetics between STEMI and NSTEMI patients.
- To explore the role of specific inflammatory markers and their correlation with cardiac function and clinical outcomes in ACS.
Main Methods:
- Forty consecutive ACS patients (23 STEMI, 17 NSTEMI) were enrolled within 12 hours of symptom onset.
- Blood samples were collected at admission (t0), day 7 (t1), and day 30 (t2) to measure inflammatory markers (CD40L, TGF-beta, IL-6, TNF-alpha, hs-CRP, SAA, WBC).
- Echocardiographic parameters were assessed, and correlations between inflammatory markers, cardiac function, and clinical events were analyzed.
Main Results:
- STEMI patients exhibited higher admission levels of hs-CRP, WBC, ferritin, and IL-6 compared to NSTEMI patients.
- NSTEMI patients showed higher CD40L levels, which was also associated with mortality.
- STEMI presented with reduced ejection fraction and impaired cardiac function at admission, inversely correlated with SAA and WBC.
Conclusions:
- A differential inflammatory pattern exists between STEMI and NSTEMI patients.
- CD40L may serve as a valuable marker for risk stratification in ACS patients.
- Further research is warranted to elucidate the distinct inflammatory mechanisms in NSTEMI.
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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