Predictive role of specific monocyte subsets for major adverse cardiac events after ST-elevation myocardial infarction

Background: Monocytes are implicated in the initiation of the atheroscleroticplaque through to plaque instability and rupture during presentation with an acutecoronary syndrome (ACS). Little is known about the predictive role for the threephenotypically and functionally different monocyte subpopulations in predictingmajor adverse cardiac events (MACE), defined as recurrent ACS, heart failure ordeath, following ST elevation myocardial infarction (STEMI) in humans. Monocytepopulations 1 and 2 are thought to be the “classical” monocytes with inflammatoryaction, whilst monocyte subpopulation 3 is considered to be the reparativesubpopulation with assumed fibroblast deposition ability.
Method: Ninety six patients (aged 6±14; 65% male) were recruited within first24 hours from admission with STEMI treated with percutaneous revascularization.Peripheral blood monocyte subsets were enumerated and characterisedusing flow cytometry. Monocyte subsets were defined as CD14++CD16-CCR2+(Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2- (Mon3) cells.MACE events were recorded at follow up for median of 187 days (112-222 days).
Results: MACE events occurred in 14 patients (14.6%). Using logistic regressionanalysis, increased total monocyte count (p<0.032), and Mon 2 count (P<0.047) were significantly predictive of future MACE. Only Mon2 counts were an independentpredictor of MACE after adjusting for age and sex (Table 1).Table 1. Predictive value of monocytes in MACEMonocytes Odds ratio (95% confidence intervals) P-valuePhenotypic Characterisation and enumerationTotal Monocytes (cells/μl) 1.002 (1-1.004) 0.032Mon1 1.001 (0.998-1.003) 0.111Mon2 1.008 (1.003-1.013) 0.047Mon3 1.01 (0.999-1.022) 0.388Conclusion: Increased total monocyte and Mon 2 counts in the first 24 hourspost infarction are predictive of MACE in STEMI patients. Mon 3, despite an assumedrole in reparation and fibroblast deposition, was not predictive of MACE inpost-STEMI patients. This suggests a specific role for Mon2 monocyte subset inpost-infarct recovery in STEMI, and a potential role of this subset as a future therapeutictarget. Remodelling data from cardiac magnetic resonance is awaited.