Abstract
Objectives Coagulation mechanisms and fibrinolytic assembly are important components role players of acute myocardial infarction (AMI) progression. Our study objective was to see the serial variations in the levels of Von Willebrand factor (VWF) and A Disintegrin and Metalloprotease with ThromboSpondin motif (ADAMTS13) over the course of AMI and to determine their relationship with the cardiovascular risk markers and the patient's clinical characteristics. Methods This project was done at the departments of Emergency Medicine, Physiology and Cardiac sciences of King Saud University Medical City. We studied ADAMTS13, VWF, fibrinogen, and CRP levels in 80 patients with AMI when patients were admitted; post AMI by 3-4 days and at follow-up of 3 months. We compared them with a control group consisting of 36 subjects. Results AMI had significantly lower levels of ADAMTS13 at AMI and after 3-4 days; at follow-up the difference in levels was nonsignificant, when compared with controls. Similarly, VWF levels were significantly higher in AMI and remained high even at follow-up compared to control subjects. VWF/ADAMTS13 ratio was also significantly higher at AMI and 3-4 days while at follow-up difference was nonsignificant compared to control subjects. Regression analysis between hsCRP and ADAMTS13 showed an inverse relationship (r = 0.376, p < 0.01), while correlation with VWF was significantly positive (r = 0.376, p < 0.01), while correlation with VWF was significantly positive (Conclusions Increased levels of VWF and reduced levels of ADAMTS13 activity may contribute to the pathogenesis of acute myocardial infarction and might prove to be important mediators of AMI progression.
Highlights
Coagulation assembly and its fibrinolytic components are the leading cause of mortality worldwide and has estimated management burden of higher than $250 billion that is expected to be tripled by the year 2030 [1]
Another study demonstrated that higher Von Willebrand factor (VWF)/ADAMTS13 ratio may be a significant predictor for adverse cardiovascular episodes a er acute myocardial infarction (AMI) [12]. erefore, we aimed to examine serial changes in plasma ADAMTS13 antigen and VWF levels a er AMI progression and to determine their relationship with the cardiovascular risk markers and the patient’s clinical characteristics
We compared them with a control group consisting of 36 subjects who were matched for gender, age, and body mass index (BMI). ey were free of any clinical manifestations of coronary, peripheral or cerebral artery disease by detailed relevant history, clinical examination, and had normal electrocardiographic findings
Summary
Coagulation assembly and its fibrinolytic components are the leading cause of mortality worldwide and has estimated management burden of higher than $250 billion that is expected to be tripled by the year 2030 [1]. In addition management of thrombotic and haemorrhagic attacks may add to increase incidence and cost of management of coagulation disorders [2]. E VWF is synthesised in endothelial cells and is stored. It mediates platelet aggregation and adhesion [3]. It carries factor VIII in circulation and mediates initial platelets that stick to the sub endothelium following vascular endothelial damage as a result of hyperlipidaemia, smoking, or hypertension [4, 5]. Tyrosine-842 and methionine-843 bonding is cleaved by ADAMTS13 in the VWF multimers domain A2, resulting in two 140 and 176 kDa portions. e 2 fragments behave less actively in aggregation of platelets than the uncleaved VWF multimers [7, 8]
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