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Association between inflammation and left ventricular thrombus formation following ST-elevation myocardial infarction
Ivan Lechner1, Martin Reindl1, Christina Tiller1
1University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria.
Background:
Current evidence suggests a link between the inflammatory state and left ventricular (LV) thrombus formation following ST-elevation myocardial infarction (STEMI). However, a comprehensive study investigating the association between inflammatory biomarkers and LV thrombus diagnosed by cardiac magnetic resonance (CMR) is lacking.
Methods:
We studied 309 patients with acute STEMI treated with primary percutaneous coronary intervention (pPCI) from the prospective MARINA-STEMI cohort study. Concentrations of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), white blood cell count (WBCc), fibrinogen and D-dimer were measured two days after STEMI. Infarct characteristics and presence of LV thrombi were assessed with the use of contrast-enhanced CMR at a median of 4 (interquartile range [IQR] 3-5) days after pPCI.
Results:
In total, 309 STEMI patients (18% female) with a median age of 57 (IQR 52-65) years were included. A LV thrombus was observed in 8% (n = 24) of the overall cohort and in 15% of patients with an anterior STEMI. Hs-CRP (OR 2.16, 95% CI 1.54-3.02, p < 0.001), IL-6 (OR 2.38, 95% CI 1.48-3.81, p < 0.001) and fibrinogen levels (OR 2.05, 95% CI 1.40-3.00, p < 0.001) were significantly associated with presence of LV thrombus. Among all assessed inflammatory biomarkers, only hs-CRP was independently associated with LV thrombus after adjustment for markers of inflammation and CMR parameters (OR 1.77, 95% CI 1.21-2.59, p = 0.004).
Conclusion:
In patients with STEMI treated with pPCI, inflammatory markers (hs-CRP, IL-6 and fibrinogen) are associated with the presence of LV thrombus. However, only hs-CRP was independently associated with the occurrence of LV thrombi, highlighting the key role of CRP as clinical risk marker for LV thrombus formation in STEMI patients treated with pPCI.
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