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Thromb Haemost 2000; 84(02): 204-209
DOI: 10.1055/s-0037-1613997
DOI: 10.1055/s-0037-1613997
Review Article
Plasma Concentration of von Willebrand Factor in Acute Myocardial Infarction
This work was supported by a grant-in-aid for Scientific Research in Japan (09770506 and 11770367); by Tokai University School of Medicine Research Aid in 1996, 1997, 1998, and 1999; by grant JSPS-RFTF97I00201 from the Japanese Society for the Promotion of Science; by grant from 1998 Takeda Science Foundation, by the research fund of the Mitsukoshi Health and Warfare Foundation 1999, and by the Suzuken Memorial Fund 1999.
Weitere Informationen
Publikationsverlauf
Received
27. Mai 1999
Accepted after resubmission
16. März 2000
Publikationsdatum:
14. Dezember 2017 (online)
Summary
Recent investigations have revealed the crucial role of von Willebrand factor (vWF) in platelet thrombus formation under flow conditions. The plasma concentrations of vWF were measured together with various hemodynamic and hemostatic parameters in 51 cases of acute myocardial infarction. In 10 randomly selected cases, the plasma concentrations and distribution of multimers vWF were serially determined after reperfusion therapy by percutaneous transluminal coronary angioplasty (PTCA). The vWF concentration at the onset of the acute myocardial infarction was significantly higher than in an age-matched control group (vWF AG: 18.7 ± 1.2 µg/ml vs. 10.3 ± 0.5 µg/ml, p = 8.43×10− (12), mean ± SE). Simultaneous determination of hemodynamic and hemostatic parameters revealed that the only two parameters that were significantly correlated with the patients` plasma vWF concentrations were their pulmonary capillary wedge pressure (PCWP) and heart rate, suggesting a relationship between hemodynamic changes induced by the onset of myocardial infarction and the vWF plasma concentrations. Serial determinations revealed that the vWF concentrations had not changed 1 h after reperfusion therapy, but that they significantly increased by 24 to 72 h. The distribution of the larger multimers of vWF also increased in the acute and subacute phase. The vWF concentration and multimer distribution normalized 14 days after the onset of the myocardial infarction. Our findings suggest that the vWF concentration increased in acute myocardial infarction patients, possibly in association with the hemodynamic deterioration that occurs in acute myocardial infarction.
* The contribution of S.G. on this manuscript is equivalent to that of H.S.
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