Related Experiment Video

Updated: Feb 18, 2026

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
08:30

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Published on: August 14, 2017

11.8K

Kinetics of plasma von Willebrand factor in acute myocardial infarction patients: a meta-analysis

Xia Wang1, Junyu Zhao2, Yong Zhang3

  • 1Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, 250014 Shandong, China.

Oncotarget
|November 23, 2017
PubMed

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.

Keywords:
acute myocardial infarctionkineticsmeta-analysisvon Willebrand factor

More Related Videos

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

19.5K
Microfluidics in Assessing Platelet Function06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

1.7K

Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
9.6K
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
9.2K
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
13.4K
Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
298
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
2.0K
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
468