Abstract
Previous studies have shown a variation in plasma level of von Willebrand factor (vWF) in acute myocardial infarction (AMI) patients but with contentious results. In this study, we performed a meta-analysis to evaluate the kinetics of plasma vWF after AMI. A total of 11 qualified studies were obtained through systematical search in PubMed, Web of science, Cochrane Library database and CNKI, followed by search of reference lists, involving 519 AMI patients and 466 non-AMI controls. The standard mean difference (SMD) and 95% confidence intervals (95% CI) were calculated using random-effects model. Results indicated that the plasma vWF was significantly increased in the first several hours after onset of AMI (SMD = 1.94, 95% CI = 1.39–2.48, P < 0.001) and stayed at high level until 24 h (SMD = 1.17, 95% CI = 0.45–1.89, P = 0.001). Elevated level of vWF appeared to persist for one week and reduced to normal until the fourteenth day after AMI (SMD = 0.44, 95% CI = −0.14–1.02, P = 0.14). Subgroup analysis revealed that the high level of vWF lasted just for 1 day in patients with a symptom duration ≤ 6 h before admission. For patients with a symptom duration > 6 h, elevated vWF was found in all 7 days except day 1. Our findings determined the kinetics of plasma vWF after AMI, and might provide a new insight in monitoring AMI progression.
Highlights
Acute myocardial infarction (AMI) is one of leading causes of mortality
Patients in study of Zhou et al [24] were classified into two groups according to Thrombolysis in Myocardial Infarction (TIMI) grade after reperfusion therapy, and these two groups were independently incorporated in our meta-analysis
Over the 11 studies, 519 acute myocardial infarction (AMI) patients and 466 healthy or non-acute coronary syndromes (ACS) controls were included in this metaanalysis
Summary
Acute myocardial infarction (AMI) is one of leading causes of mortality. In 2008, over 3,000,000 individuals developed ST-elevated myocardial infarction (SETMI) and 4,000,000 developed non-ST-elevated myocardial infarction (non-STEMI) worldwide [1]. AMI is caused by rupture of atherosclerotic plaques, exposure of sub-endothelial procoagulant factors, and subsequent thrombus formation, which leads to the complete or incomplete occlusion of coronary arteries [2]. As the most serious type of acute coronary syndromes (ACS), AMI may lead to cardiac death and/or heart failure [3]. The current diagnosis for AMI is mainly dependent on electrocardiograph (ECG) and circulating myocardial enzymes such as ultrasensitive troponin I or T and creatine kinase MB [4]. No clinical marker is available for the accurate assessment of AMI process [5]
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