Volume 104, Issue 9 , Pages 1179-1183, 1 November 2009
The Chemokine Network in Relation to Infarct Size and Left Ventricular Remodeling Following Acute Myocardial Infarction
Increased circulating chemokines have been reported during acute myocardial infarction and might give prognostic information about future ischemic events. However, data on the chemokine network in relation to infarct size and measures of left ventricular remodeling after successful percutaneous coronary intervention (PCI) are lacking. A total of 42 patients with first-time ST-segment elevation acute myocardial infarction with a single occluded vessel were recruited, and cardiac magnetic resonance was used for serial assessment (2, 7, and 60 days) of infarct size and left ventricular remodeling. The chemokines were analyzed before and after PCI. After PCI, high levels of CCL4, CXCL16, CXCL10, and, in particular, CXCL8 within the first week after PCI correlated positively with the degree of myocardial damage, as reflected by correlations with the maximum troponin T levels and infarct size after 2 months, as assessed by cardiac magnetic resonance, and with impaired myocardial function after 2 months as assessed by cardiac magnetic resonance and neurohormonal methods. In contrast, the plasma levels of CCL3 and CXCL7 during the first week correlated negatively with myocardial dysfunction after 2 months. In conclusion, our findings suggest a role for chemokines in both adaptive and maladaptive responses after myocardial infarction and might support a role for CCL4, CXCL16, CXCL10, and, in particular, CXCL8 in postmyocardial infarction reperfusion and remodeling.
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This work was supported by Helse Vest Grant 911017, Bergen, Norway; the Norwegian Association of Heart and Lung Patients, Oslo, Norway; Helse og Rehabilitering Grant 2003/2/0211, Oslo, Norway; the University of Oslo, Oslo, Norway; the Norwegian Council on Cardiovascular Disease, Oslo, Norway; and the Family Blix Foundation, Oslo, Norway.
PII: S0002-9149(09)01254-5
doi:10.1016/j.amjcard.2009.06.028
© 2009 Elsevier Inc. All rights reserved.
Volume 104, Issue 9 , Pages 1179-1183, 1 November 2009
