Abstract 12560: Functional Characteristics of Monocytes Subsets in the Acute and Healing Phases of ST Elevation Myocardial Infarction and their Predictive Role for Major Adverse Cardiac Events
Background: Monocytes are implicated in the initiation of atherosclerosis, plaque instability and rupture during acute coronary syndromes (ACS). Little is known about the predictive role of the different monocyte subpopulations for major adverse cardiac events (MACE), following STEMI in humans. Mon1 is the "classical" monocytes with inflammatory action, whilst Mon3 is considered reparative with fibroblast deposition ability. The function of the newly described Mon2 subset is yet to be fully described. Hypothesis: MACE (recurrent ACS, heart failure or death), will be associated with (i) high count of Mon1, Mon2 and low Mon3 counts at 24 hours post STEMI; and (ii) impaired phagocytic activity and high IKKβ levels.
Method: 115 patients (aged 63±14; 66% male) were recruited within first 24 hours from admission with STEMI. Peripheral blood monocyte subsets were defined and enumerated by flow cytometry as CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2- (Mon3). Functional assessment of monocytes was measured by their phagocytic activity and activation of nuclear factor Kappa B (NFkB). MACE events were recorded at follow up for 293 (174-412) days.
Results . In total, 25 events (22%) occurred. On univariate analysis, the phagocytic activity of Mon2 was predictive of MACE [hazards ratio 0.988 (0.977- 0.999); p=0.03]. After adjusting for age, sex and troponin levels, Mon2 counts were predictive of MACE (p=0.012) [Table].
Conclusion: High counts of Mon2 and early excessive phagocytic activity are related to clinical outcome post-STEMI. The phagocytic activity of Mon2 (on univariate analysis) had a small protective impact whilst Mon2 count (on multivariate analysis) had a small detrimental effect on MACE. Monocytes might play a role in post-infarct remodelling and hence clinical outcome.
- © 2012 by American Heart Association, Inc.