Introduction In an era of appreciation of inflammatory role in MI, we describe a potential mechanism through which the innate immune system affects both outcome and ventricular remodelling in STEMI patients.
Method STEMI patients were recruited within 24 hours of presentation. Monocyte subsets and their phagocytic functional activity were measured by flow cytometry using nuclear differentiation of surface markers: CD14; CD16 and CCR2. Patients underwent echocardiograms during the index events and 6 months post STEMI, to assess LV remodelling and global longitudinal strain (GLS) and global circumferential strain (GCS). Patients were followed up at six months and annually for MACE.
Results In total 211 patients with STEMI were recruited ( 69% males; Age 61±11). MACE occurred in 76 patients during a median follow up of 37 months. A multivariate COX regression model indicated total counts of monocytes, Mon 1, and Mon 2 as well as their phagocytic activity were predictive of MACE. High Mon1 and Mon 2 counts in the 3rd and 4th quartiles, were strongly predictive of MACE, an effect that was maintained for more than 2 years. Incorporating Mon1 and Mon2 counts in TIMISTEMI score improved the ability to predict poor clinical outcome in STEMI patients: C-statistics indicated the area under the curve (AUC) improved from 0.67 (for TIMI STEMI score), to an AUC 0.77 when including total monocyte counts (TIMI Mon score). Total monocyte count, Mon 1 and Mon 2 were predictive of negative ventricular remodelling (>15% in LVESVi). GLS and GCS were also significantly correlated with total monocyte, Mon 1 and Mon 2 levels.
Conclusion Mon1 and Mon2 through their phagocytic activity alter both patient outcome and ventricular remodelling post STEMI. These results could be a stepping stone into targeted anti-inflammatory therapy in management of myocardial infarction.
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