A proinflammatory monocyte response is associated with myocardial injury and impaired functional outcome in patients with ST-segment elevation myocardial.

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A proinflammatory monocyte response is associated with myocardial injury and impaired functional outcome in patients with ST-segment elevation myocardial infarction  Anja M. van der Laan, MD, Alexander Hirsch, MD, PhD, Lourens F.H.J. Robbers, MD, Robin Nijveldt, MD, PhD, Ingrid Lommerse, Ronak Delewi, MD, Pieter A. van der Vleuten, MD, PhD, Bart J. Biemond, MD, PhD, Jaap Jan Zwaginga, MD, PhD, Wim J. van der Giessen, MD, PhD, Felix Zijlstra, MD, PhD, Albert C. van Rossum, MD, PhD, Carlijn Voermans, PhD, C. Ellen van der Schoot, PhD, Jan J. Piek, MD, PhD  American Heart Journal  Volume 163, Issue 1, Pages 57-65.e2 (January 2012) DOI: 10.1016/j.ahj.2011.09.002 Copyright © 2012 Mosby, Inc. Terms and Conditions

Figure 1 The association between circulating levels of classical and nonclassical monocytes and baseline myocardial injury and LV function. Baseline LV ejection fraction, infarct size, and percentage of patients with STEMI with microvascular obstruction, stratified according to tertiles of circulating classical (A) and nonclassical monocytes (B). Data are presented as mean ± SD. For the association between monocyte subsets and LV ejection fraction and infarct size, P values were determined by the Spearman correlation test. P values for trend were determined by 1-way analysis of variance. MVO indicates microvascular obstruction. American Heart Journal 2012 163, 57-65.e2DOI: (10.1016/j.ahj.2011.09.002) Copyright © 2012 Mosby, Inc. Terms and Conditions

Figure 2 The association between circulating levels of classical and nonclassical monocytes and recovery of regional myocardial function. The change in wall thickening in dysfunctional segments from baseline to 4 months is depicted for tertiles of classical monocytes (A) and nonclassical monocytes (B). Data are presented as mean ± SD. P values for the change between baseline and follow-up within each tertile were calculated with paired Student t test. For the change in wall thickening from baseline to 4-month follow-up, P values were determined by the Spearman correlation test. Base denotes baseline; FU, follow-up. American Heart Journal 2012 163, 57-65.e2DOI: (10.1016/j.ahj.2011.09.002) Copyright © 2012 Mosby, Inc. Terms and Conditions

Figure 3 The regional myocardial function at 4-month follow-up according to tertiles of circulating classical or nonclassical monocytes, stratified by the transmural extent of infarction at baseline. (A) Wall thickening at follow-up, stratified by the transmural extent of infarction at baseline. Outcomes were further stratified by tertiles of classical monocytes (B) and nonclassical monocytes (C). Data are presented as mean ± SD. P values derived from the multilevel linear analysis using monocytes as a continuous variable are shown. American Heart Journal 2012 163, 57-65.e2DOI: (10.1016/j.ahj.2011.09.002) Copyright © 2012 Mosby, Inc. Terms and Conditions

Appendix Figure S1 Fluorescence-activated cell scanner analysis of monocytes. A, Peripheral blood mononuclear cells were gated in a forward scatter/sideward scatter dotplot. The expression of CD14 and CD62L was measured on the gated PBMCs to determine the classical (CD14++CD62L+) and nonclassical (CD14+CD62L−) monocyte subset. B, In addition, the expression of Mac-1 (CD11b), VLA-4 (CD49d), ICAM-1 (CD54), and coexpression of glycoprotein 1b (CD42b) were measured after gating of the monocytes (CD14+ cells). FSC indicates forward scatter; SSC, sideward scatter. American Heart Journal 2012 163, 57-65.e2DOI: (10.1016/j.ahj.2011.09.002) Copyright © 2012 Mosby, Inc. Terms and Conditions