Arteriosclerosis in normal and von Willebrand pigs: long-term prospective study and aortic transplantation study.

Fuster, Valentı́n; Fass, David N.; Kaye, Michael P.; Josa, Miguel; Zinsmeister, A. R.; Bowie, E. J. W.

doi:10.1161/01.res.51.5.587

Cited by 79 publications

(34 citation statements)

References 45 publications

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“…Less atherosclerosis was found in pigs and mice that had a complete deficiency of vWF. [5][6][7][8][9] The goal of the present study was to examine whether vWF plays a role in atherogenesis. Atherosclerotic vessel wall changes were determined in patients with a complete deficiency of vWF (ie, type 3 von Willebrand disease [vWD]) and in individuals with a normal coagulation profile.…”

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Patients With Type 3 Severe von Willebrand Disease Are Not Protected Against Atherosclerosis

et al. 2004

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Background-The results of a number of studies in pigs and mice suggest that absence of von Willebrand factor (vWF) protects against the development of atherosclerosis. We studied whether patients with a complete deficiency of vWF (type 3 von Willebrand disease [vWD]) develop fewer atherosclerotic vessel wall changes than healthy controls. Methods and Results-This study included 47 individuals with type 3 vWD and 84 healthy controls. Early atherosclerotic changes were assessed by measuring the thickness of the intima-media in the carotid and femoral arteries by B-mode ultrasonography. Advanced atherosclerotic changes were quantified by summing the maximal thickness of atherosclerotic plaques in the carotid and femoral arteries and were expressed as a plaque score. Established risk factors were determined to adjust for possible differences between the groups. We found no substantial difference in intima-media thickness between vWD patients and controls (adjusted difference for carotid artery 0.007 mm, 95% CI Ϫ0.022 to 0.036 mm; femoral artery 0.069 mm, 95% CI Ϫ0.056 to 0.19 mm). Similar proportions of patients and controls had atherosclerotic plaques (19% and 17%, respectively). No difference was found in the plaque score between groups (adjusted difference Ϫ0.22 mm, 95% CI Ϫ0.69 to 0.26). Among vWD patients, we found no effect of treatment with vWF concentrates on intima-media thickness or plaque score. Conclusions-The results of this study indicate that vWF does not play a substantial role in human atherogenesis.

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Patients With Type 3 Severe von Willebrand Disease Are Not Protected Against Atherosclerosis

et al. 2004

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“…We used pigs because of their similarity to humans in terms of vascular physiology and coagulation cascade (Bowie et al 1973, Andre et al 1996. Furthermore, the neointimal response to arterial injury histologically resembles human restenotic lesions after balloon angioplasty (Fuster et al 1982, Lam et al 1987, Badimon et al 1988, Schwartz & Holmes 1994.…”

Section: Discussionmentioning

confidence: 99%

“…The pig seems to be the ideal model in terms of disposition to neointimal hyperplasia formation (Fuster et al 1982, Kantor et al 1999) and assessment of novel stent materials. Therefore, the purpose of the study was to evaluate the feasibility of anastomotic stent application in a porcine aortoiliac graft model, in which the downstream anastomosis was sutured with irregularities.…”

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Anastomotic stenting in a porcine aortoiliac graft model

et al. 2007

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SummaryThe purpose of the study was to evaluate the feasibility of anastomotic stent application in a porcine aortoiliac graft model. In a total of 10 pigs, a polytetrafluoroethylene aortobi-iliac graft was implanted through a midline abdominal incision. The lower edge of the iliac vessel was graft-inverted about 1 mm to produce irregularities at the downstream anastomosis. After transverse graft incision, six stainless-steel stents, six poly-L-lactic acid (PLLA) stents and four PLLA stents with 10% polycaprolactone (PCL) were implanted at the iliac anastomotic site using a 6 mm balloon dilatation catheter. Four anastomotic sites were left untreated. After two weeks, the patency of graft limbs was evaluated by contrast-enhanced computed tomography (CT). Both metal and polymeric stent designs provided adequate flexibility to manoeuvre across the anastomotic site for expansion in the chosen position. After deployment, the stent-arterial wall contact was complete on a macroscopic view. On CT scan, all metal and PLLA-stented graft limbs were free of stenosis, whereas all PLLA/PCL stents were occluded. The non-stented graft limbs showed a stenosis of 50-70%. In summary, this model is feasible to assess preclinically the deployment and patency rate of an anastomotic stent and to test future stent developments.

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“…15,16,[18][19][20] Table 1 shows the hemostatic parameters of the normal and vW D pigs used in this study. Platelet number and hematocrit were evaluated by our previously described methods21 (Table 2).…”

Section: Determination Of Hemostatic and Lipid Parametersmentioning

confidence: 99%

Platelet thrombus formation on collagen type I. A model of deep vessel injury. Influence of blood rheology, von Willebrand factor, and blood coagulation.

et al. 1988

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Collagen type I is a major component of atherosclerotic vessel wall that is exposed on deep vessel injury, such as in balloon angioplasty or plaque rupture. Collagen type I from pig Achilles tendon was mounted in a tubular perfusion chamber placed within an extracorporeal circuit (carotid artery to jugular vein). The material was exposed to blood from normal pigs (n= 13), severe homozygous von Willebrand factor (vWF)-deficient pigs (vWF<3%) (n=6), and heterozygous vWF-deficient pigs (vWF=24%) (n=2). Thrombus formation was measured by autologous "'In-platelet labeling and by ultrastructural morphology. Heparinized and native blood from these pigs was perfused over the substrate for 3 and 5 minutes at local shear rates from 212 to 3,380/sec. On collagen type I exposed to nonanticoagulated blood, for all exposure times studied, thrombus formation in the absence of vWF was significantly reduced at high shear rate typical of stenotic areas but not at low shear rate typical of unobstructed medium-size arteries. A similar inhibition in thrombus formation due to vWF deficiency was observed in both heparinized and native blood; however, thrombus formation was significantly more reduced (p<0.05) in the presence of heparin, presumably due to the lack of stability of the accumulated platelets in the absence of fibrin formation. Intermediate levels of vWF, as in heterozygous von Willebrand's disease (vWD), support platelet deposition to extents not significantly different from normal conditions. Therefore, on collagen type I, both the activation of blood coagulation proteins and the presence of vWF contribute significantly to the platelet-platelet interactions necessary for thrombus formation. The efrect of vWF occurs primarily at high shear conditions typical intravascularly of flow at the apex of advanced stenotic lesions; thus, these findings may suggest that the absence of vWF may be protective against the development of acute thrombosis in these regions. (Circulation 1988;78:1431-1442 T hrombosis is a process that involves various blood cells and proteins, the nature of the blood flow, and surface characteristics. In vivo, all blood-surface interactions are dynamic in nature; that is, they occur in the presence of flowing blood. Therefore, blood elements are exposed to fluid transport rates and local shear forces that differ substantially from those that occur in stagnant

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Arteriosclerosis in normal and von Willebrand pigs: long-term prospective study and aortic transplantation study.

Cited by 79 publications

References 45 publications

Patients With Type 3 Severe von Willebrand Disease Are Not Protected Against Atherosclerosis

Patients With Type 3 Severe von Willebrand Disease Are Not Protected Against Atherosclerosis

Anastomotic stenting in a porcine aortoiliac graft model

Platelet thrombus formation on collagen type I. A model of deep vessel injury. Influence of blood rheology, von Willebrand factor, and blood coagulation.

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