126 Dynamics of the three human monocyte subsets over 30 days in ST-elevation myocardial infarction. (16th May 2012)

• Record Type: Journal Article
• Authors: Tapp, L D; Wrigley, B J; Pamukcu, B; Shantsila, E; Lip, G Y H
• Is Part Of: Heart. Volume 98(2012)Supplement 1
• Page Start: A71
• Page End: A71
• Publication Date: 2012-05-16
• Subjects: Monocytes -- acute coronary syndromes -- myocardial infarction; Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/heartjnl-2012-301877b.126
• Languages: English
• ISSNs: 1355-6037

Abstract

Abstract : Introduction: Monocytes are intimately involved in the pathophysiology of myocardial infarction (MI), with different subsets thought to have distinct roles in cardiac repair. We have described that human monocytes can be divided phenotypically into 3 subsets by their surface expression of CD14, CD16 and CCR2: CD14+CD16−CCR2+ (Mon1, "classical" monocytes), CD14+CD16+CCR2+ (Mon2) and CD14lowCD16+CCR2− (Mon3). Having observed a threefold increase in Mon2 at admission with STEMI, we aimed to establish the dynamics in total monocyte count, subset count and relative proportions of the subsets in the 30 days following ST elevation myocardial infarction (STEMI) treated by primary percutanous coronary intervention (PPCI). Methods: Monocyte subsets were measured by flow cytometry in 50 patients (57.5±11.7 years, 86% male) with STEMI at 4 time points: within 24 h after PPCI, day 3, day 7 and day 30 after MI onset. All patients underwent PPCI. Exclusion criteria comprised factors known to affect monocyte count. Results: The peak number of total monocytes, Mon1 and Mon2 occurred on day 1, with comparable values on day 3. The total monocyte count and Mon1 reduced significantly by day 30, to levels seen is stable coronary artery disease. Mon2 count reduced significantly earlier, by day 7. No changes were seen in Mon3 count. Mon2 predominates over Mon3 on day 1, with the reverse pattern seen at day 30, where the Mon2 proportion had reduced significantly and the Mon3 proportion had increased significantly. Conclusions: We observed prominent differences in the dynamics of monocyte subsets, particularly the minor subsets (Mon2 and Mon3) which have been suggested to play distinct roles in myocardial reparative processes. The dramatic increase in number of Mon2 after STEMI followed by significant reduction by day suggests a specific role in the acute phase of MI. These novel findings may contribute to further understanding the pathophysiology of the recovery processes following acute MI.