Inflammatory biomarkers and left ventricular thrombus formation after ST-elevation myocardial infarction
C Gansted, F J Olsen, M Pareek, S Lindberg, S Pedersen, N E Magnusson, M Bjerre, R Moegelvang, T Biering-SoerensenAbstract
Background
ST-segment elevation myocardial infarction (STEMI) may be complicated by left ventricular thrombus (LVT) formation, which increases the risk of systemic thromboembolism five-fold. Given the role of inflammation in LVT formation, inflammatory biomarkers could be useful markers of LVT risk.
Purpose
To investigate whether inflammatory biomarkers are associated with LVT formation in patients treated with primary percutaneous coronary intervention (pPCI) after STEMI.
Methods
Patients were sampled from a single-center prospective cohort study of STEMI patients treated with pPCI from 2006-2008. Inflammatory biomarkers were analyzed in samples obtained immediately before pPCI and included, C-reactive protein (CRP), white blood cell (WBC) count, mannose-binding lectin (MBL), osteoprotegerin (OPG), ostepontin (OPN), alpha-defensin, and neutrophil gelatine-associated lipocalin (NGAL). The endpoint was LVT detected on echocardiography during the index event or any follow-up echocardiogram. Univariable and multivariable logistic regression was applied to investigate the association between log-transformed inflammatory biomarkers and LVT. A p-value<0.05 was considered statistically significant.
Results
The study included 372 patients with STEMI treated with pPCI of whom 177 (48%) had an anterior infarction. The mean age was 62 ± 11 years, and 280 (75%) were men. Of these, 31 (8%) developed LVT. No significant difference was found in troponin I (TnI), CRP, or WBC count between patients who developed LVT formation compared with patients who did not (TnI: 148 vs 100 ng/L, p=0.17; CRP: 4 vs 3 mg/L, p=0.11; WBC count: 13.6 vs 12.4 x 109/L, p=0.058). By extension, no differences in MBL, OPG, or OPN were observed. However, patients with LVT formation had significantly higher alpha-defensin (280 vs 223 μg/L, p=0.009) and NGAL (154 vs 118 μg/L, p=0.005) levels at baseline. Similarly, only alpha-defensin and NGAL were significantly associated with LVT in univariable logistic regression (alpha-defensin: OR 1.10 (1.03-1.17), p=0.005, per 10% increase; NGAL: 1.09 (1.02-1.17), p=0.013, per 10% increase, Figure 1a-b, respectively). After multivariable adjustment, the results were unchanged (alpha-defensin: OR 1.12 (1.04-1.20), p=0.002, per 10% increase; NGAL: 1.10 (1.01-1.20), p=0.025, per 10% increase). Both alpha-defensin and NGAL increased AUC compared with established predictors of LVT formation (LVEF, LAD culprit lesion, LV aneurysm), albeit not significantly (AUC baseline 0.787; AUC baseline and alpha-defensin=0.813, p=0.17; AUC baseline and NGAL=0.833, p=0.056).
Conclusion
In patients with STEMI treated with pPCI, alpha-defensin and NGAL were associated with LVT formation, indicating that these inflammatory biomarkers may be useful for identifying patients at risk of LVT formation.Figure 1aFigure 1b