Kuan-Liang Liu1, Shu-Min Lin2, Chih-Hsiang Chang3, Yung-Chang Chen3, Pao-Hsien Chu4. 1. Division of Cardiology, Department of Internal medicine, Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Taipei, Taiwan. 2. Department of Thoracic Medicine, Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Taipei, Taiwan. 3. Department of Nephrology, Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Taipei, Taiwan. 4. Division of Cardiology, Department of Internal medicine, Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Taipei, Taiwan; Healthcare Center, Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Taipei, Taiwan; Heart Failure Center, Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Taipei, Taiwan. Electronic address: pchu@adm.cgmh.org.tw.
Abstract
OBJECTIVES: Patients with acute myocardial infarction (AMI) are frequently complicated with major cardiovascular events (MACEs). Endothelial dysfunction has been found to be involved in pathogenesis of AMI, but its role in development of MACEs after AMI is not clearly investigated. This study aimed to determine whether the plasma markers of endothelial dysfunction could serve as independent predictors for MACEs in patients with AMI. METHODS: This prospective study was conducted from March 2010 to July 2012 and enrolled consecutive 132 patients with acute ST elevation myocardial infarction (STEMI) receiving primary percutaneous coronary intervention (PCI). Plasma levels of thrombomodulin (TM), von Willebrand factor (vWF), angiopoietin (Ang)-1, Ang-2, Tie-2, and vascular endothelial growth factor (VEGF) were measured on day 1 of AMI. The development of MACEs at 1-year follow-up was recorded. RESULT: Patients with STEMI who developed MACEs had increased heart rate on admission (86±24 vs. 74±20bpm, p=0.006), lower left ventricular ejection fraction (LVEF) (49.0±12.4 vs. 57.2±12.4%, p=0.002), and higher incidence of multivessel disease (66.7% vs. 42.2%, p=0.018) comparing with those without MACEs. Plasma level of Ang-1 was lower in patients with MACEs than in those without (21,165±16,281 vs. 31,411±21,593pg/mL, p=0.018). In multivariate analysis, Ang-1 level<median value (OR 2.977, 95% CI 1.16-7.63, p=0.023), LVEF (OR 0.958, 95% CI 0.92-0.99, p=0.022) and multivessel disease (OR 3.013, 95% CI 1.19-7.60, p=0.019) independently predicted 1-year MACEs. CONCLUSION: Decreased plasma Ang-1 levels on admission, LVEF and multivessel disease independently predicted the development of 1-year MACEs in patients with STEMI. These results suggest that endothelial dysfunction may play an important role in mediating MACEs in patients with STEMI.
OBJECTIVES:Patients with acute myocardial infarction (AMI) are frequently complicated with major cardiovascular events (MACEs). Endothelial dysfunction has been found to be involved in pathogenesis of AMI, but its role in development of MACEs after AMI is not clearly investigated. This study aimed to determine whether the plasma markers of endothelial dysfunction could serve as independent predictors for MACEs in patients with AMI. METHODS: This prospective study was conducted from March 2010 to July 2012 and enrolled consecutive 132 patients with acute ST elevation myocardial infarction (STEMI) receiving primary percutaneous coronary intervention (PCI). Plasma levels of thrombomodulin (TM), von Willebrand factor (vWF), angiopoietin (Ang)-1, Ang-2, Tie-2, and vascular endothelial growth factor (VEGF) were measured on day 1 of AMI. The development of MACEs at 1-year follow-up was recorded. RESULT: Patients with STEMI who developed MACEs had increased heart rate on admission (86±24 vs. 74±20bpm, p=0.006), lower left ventricular ejection fraction (LVEF) (49.0±12.4 vs. 57.2±12.4%, p=0.002), and higher incidence of multivessel disease (66.7% vs. 42.2%, p=0.018) comparing with those without MACEs. Plasma level of Ang-1 was lower in patients with MACEs than in those without (21,165±16,281 vs. 31,411±21,593pg/mL, p=0.018). In multivariate analysis, Ang-1 level<median value (OR 2.977, 95% CI 1.16-7.63, p=0.023), LVEF (OR 0.958, 95% CI 0.92-0.99, p=0.022) and multivessel disease (OR 3.013, 95% CI 1.19-7.60, p=0.019) independently predicted 1-year MACEs. CONCLUSION: Decreased plasma Ang-1 levels on admission, LVEF and multivessel disease independently predicted the development of 1-year MACEs in patients with STEMI. These results suggest that endothelial dysfunction may play an important role in mediating MACEs in patients with STEMI.
Authors: Brandon S Peplinski; Brian A Houston; David A Bluemke; Steven M Kawut; Todd M Kolb; Richard A Kronmal; Joao A C Lima; David D Ralph; Samuel G Rayner; Zachary L Steinberg; Ryan J Tedford; Peter J Leary Journal: J Card Fail Date: 2021-04-17 Impact factor: 6.592
Authors: Elcha Charles; Benjamin L Dumont; Steven Bonneau; Paul-Eduard Neagoe; Louis Villeneuve; Agnès Räkel; Michel White; Martin G Sirois Journal: BMC Immunol Date: 2021-08-03 Impact factor: 3.615