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VWF in Cardiac Disorders

In the Rutgers CLSD 5124 Advanced Hemostasis graduate course, a participant responded to  the question, “Show how VWF and platelets appear to be involved in cardiac insufficiency and atrial fibrillation.” The question referred to our Coag Conversation with Dr. Emmanuel Favaloro, The Many Faces of VWF. The response:

VWF is a glycoprotein heavily engaged in arterial clot development. It is released into circulation through the secretion from endothelial cell Weibel-Palade bodies and platelet α-granules. Many factors go into determining plasma VWF levels such as ABO blood group, VWF mutations, aging, inflammation, production of nitric oxide, diabetes, and production of free radicals.1 VWF levels have long been suggested as indicators of endothelial cell dysfunction. As VWF has been proven to have critical functions in platelet aggregation and adhesion, high levels of VWF may lead to thrombus formation and atherosclerosis.2

High VWF concentrations are thought of as risk factors for cardiovascular incidents. Though only feebly correlated with the risk of coronary heart disease [CHD] in the general public, there is a more significant association in high-risk populations such as those with diabetes, previous cardiovascular events, or the elderly. 1 Associations between VWF and ischemic heart disease are well-established, suggesting that endothelial dysfunction plays a function in the pathogenesis of coronary artery disease [CAD]. In patients with previously diagnosed myocardial infarction, it is common to find increased VWF concentrations. There is also a significant correlation between the clinical severity of angina and increasing VWF concentrations. It is to be noted that there is no circadian difference found in VWF concentration levels, unlike fibrinolytic counterparts.2

Atrial fibrillation leads to an increased risk of stroke. Increased VWF levels correlate with the severity of left atrial blood stasis, left atrial appendage thrombosis, and increased stroke risk in non-valvular atrial fibrillation (NVAF) patients.  The intensity of VWF elevation is directly correlated in conjunction with the degree of left atrial blood stasis, left atrial appendage thrombus formation, left atrial appendage emptying velocity, and dysrhythmia.3

The exact process through which VWF increases cardiovascular risks in patients with post-myocardial infarction or angina has yet to be fully elucidated. It could potentially be through increased endothelial injury in CAD that may lead to both amplified VWF concentrations and higher levels of thrombin generation. Or perhaps, the heightened concentrations of VWF boost the possibility of thrombogenesis in those patients with pre-existing vascular wall disease since VWF plays a part in the adhesion and aggregation of platelets, therefore leading to additional reinfarctions.2

  1. Vischer UM. Von Willebrand factor, endothelial dysfunction, and cardiovascular disease. J Thromb Haemost 2006; 4: 1186–1193,
  2. Lip G. Von Willebrand factor: A marker of endothelial dysfunction in vascular disorders? Cardiovascular Research 1997;34:255–65,
  3. Wysokinski WE et al. Effect of atrial fibrillation duration on plasma von Willebrand factor level. Eur J Haematol 2017; 99: 569–76,
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