title: Correlation of circulating von Willebrand factor levels with cardiovascular hemodynamics.
abstract: BACKGROUND
  Valvular heart disease is associated with a decreased platelet circulating time and a thrombotic tendency. The possibility that these events are related to changes in von Willebrand factor (vWF), a multimeric glycoprotein released from endothelial cells and platelets that mediates platelet adhesion to the vascular subendothelium, has not been examined.
  
  
  RESULTS
  We measured the vWF antigen (vWF:Ag) concentration in 43 patients undergoing cardiac catheterization for the evaluation of mitral (n = 17) or aortic (n = 10) stenosis or nonvalvular heart disease (n = 16). Mean vWF:Ag concentration was significantly higher in patients with mitral stenosis than in those without (212 +/- 84 versus 150 +/- 79 units/dl, p less than 0.02); this elevation was associated with a significant elevation of pulmonary vascular resistance (PVR) in the patients with mitral stenosis (186 +/- 49 versus 133 +/- 81 dynes-sec-cm-5, p less than 0.02). The vWF:Ag levels in the entire group of patients (regardless of the presence or type of valvular disease) varied directly with PVR (r = 0.72, p less than 0.0001) and with pulmonary artery pressure (r = 0.60, p less than 0.0001) and inversely with cardiac output (r = 0.64, p less than 0.0001). Changes in PVR, pulmonary artery pressure, or cardiac output could not be correlated with circulating levels of fibrinogen or beta-thromboglobulin, which may be released from activated platelets, nor with the endothelial cell product tissue plasminogen activator.
  
  
  CONCLUSIONS
  The association of high vWF:Ag levels with increased PVR and decreased cardiac output in patients both with and without mitral stenosis suggests a hemodynamically induced increase in the endothelial release of vWF, which might contribute to a thrombotic tendency in these patients.
authors.affiliation: Charles A. Dana Research Institute, Beth Israel Hospital, Harvard Medical School, Boston, Mass.
authors.forename: W F
authors.initials: WF
authors.lastname: Penny
authors.forename: M
authors.initials: M
authors.lastname: Weinstein
authors.forename: E W
authors.initials: EW
authors.lastname: Salzman
authors.forename: J A
authors.initials: JA
authors.lastname: Ware
mesh_terms: D002319:Cardiovascular System / Q000503:physiopathology*; D003327:Coronary Disease / Q000097:blood* / Q000503:physiopathology; D006349:Heart Valve Diseases / Q000097:blood* / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D008970:Molecular Weight; D011446:Prospective Studies; D011652:Pulmonary Circulation; D014655:Vascular Resistance; D001620:beta-Thromboglobulin / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis*
chemical_list: D001620:beta-Thromboglobulin; D014841:von Willebrand Factor