Angiotensin II receptor blockers suppress the release of stromal cell-derived factor-1α from infarcted myocardium in patients with acute myocardial infarction

Background: Although angiotensin II receptor blockers (ARBs) have been shown to have anti-inflammatory effects on infarcted myocardium in experimental models, little is known in humans. Stromal cell-derived factor-1 alpha (SDF-1 alpha), a pro-inflammatory chemokine, is released from infarcted tissue in patients with acute myocardial infarction (AMI). This study examined whether ARBs suppress SDF-1 alpha production in the infarcted lesion in patients with AMI. Methods: SDF-1 alpha levels were measured by enzyme-linked immunosorbent assays in plasma obtained from the aortic root (AO) and the anterior interventricular vein (AIV) in 50 patients with an anterior AMI. Measurement of SDF-1 alpha levels and left ventriculography were repeated at discharge and 6 months after AMI. Patients were divided into 2 groups according to treatment with ARBs, which were administered at the discretion of the attending physician after admission. Results: The AIV-AO gradient of SDF-1 alpha, reflecting SDF-1 alpha release from the infarcted myocardial region, decreased between the time of discharge and 6 months after AMI in patients taking an ARB. In contrast, the SDF-1 alpha transcardiac gradient did not change in patients not taking an ARB. Among the clinical parameters tested, only the use of ARBs was significantly associated with percent changes in the SDF-1 alpha transcardiac gradient from the time of discharge to 6 months after AMI in a linear regression analysis (r = -0.31, p = 0.03). The SDF-1 alpha transcardiac gradient 6 months after AMI was inversely correlated with the percent change in left ventricular (LV) ejection fraction (r = -0.52, p < 0.01) and positively correlated with the percent change in LV end-diastolic volume index (r = 0.57, p < 0.01) and LV end-systolic volume index (r = 0.54, p < 0.01) during 6 months after AMI. Conclusions: ARB treatment suppressed SDF-1 alpha release from the infarcted myocardial region, which was associated with improvement in LV dysfunction and adverse remodeling in AMI survivors. (C) 2017 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.