Peripheral arterial disease and Virchow’s triad

Bennett, Philip C.; Silverman, Stanley; Gill, Paramjit; Lip, Gregory Y.H.

doi:10.1160/th08-08-0518

Cited by 43 publications

(31 citation statements)

References 147 publications

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“…• p < 0.05 versus artery; 9 p < 0.05 versus 10W; ‡ p < 0.05 versus vein. The insets in panels a-d show the respective staining patterns of the venous valves (in particular the endothelium); age-associated alterations in blood Xow; and a shift to a hypercoagulable state (Wilkerson and Sane 2002;Bennett et al 2009). However, the functional relationships between ageing endothelium and enhanced risk for venous and arterial thrombosis are not fully understood.…”

Section: Discussionmentioning

confidence: 99%

Effect of ageing on the murine venous circulation

Hemmeryckx

Emmerechts

Bovill

et al. 2012

Histochem Cell Biol

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The effect of ageing on the morphology of veins, venous valves and arteries was investigated in male wild-type mice using an adapted procedure with injection of a silicone polymer Microfil(®) that preserves morphology of the vasculature. Throughout the hind limb the arterial, but not the venous, lumen area and wall thickness were significantly greater in 24-month as compared to 10-week-old C57BL/6 mice. Venous valves were most frequently located at the sapheno-femoral vein junction in the lower extremities, and appeared thicker at the base supported by structurally intact collagen fibers, and thinner towards the proximal end of the valve leaflet, with less organized collagen. Overall, valves were less supported by structurally intact collagen at 24 months as compared to 10 weeks. Endothelial expression of CD31, endothelial protein C receptor or von Willebrand factor (VWF) was not affected by age, while thrombomodulin expression was lower in aged versus young arteries. At both ages, expression of VWF was lower at venous valves versus veins. Evaluation of the blood coagulation profile revealed that aged mice had shortened prothrombin time, elevated plasma levels of factor (F)VII, FVIII and VWF and increased neutrophil and platelet counts. Thus, our data indicate that in mice with ageing, venous valves become more fragile, in association with a procoagulant and inflammatory blood phenotype. Taken together, we found that the procoagulant state in ageing, is accompanied by mild vascular changes.

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Section: Discussionmentioning

confidence: 99%

Effect of ageing on the murine venous circulation

Hemmeryckx

Emmerechts

Bovill

et al. 2012

Histochem Cell Biol

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“…In the classical Virchow's triad on the abnormalities associated with thrombus formation, hypercoagulability and blood stasis have long been considered as mainly involved in the pathogenesis of venous thrombosis, while vascular damage has been considered to be involved mainly in arterial thrombosis (23). Indeed, a damage to the arterial wall (i.e.…”

Section: The Association Between Venous and Arterial Thrombosismentioning

confidence: 99%

Endothelium, venous thromboembolism and ischaemic cardiovascular events

Gresele

Momi

Migliacci³

2010

Thromb Haemost

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SummaryThe association between venous thromboembolism and arterial thrombosis has emerged as consistent clinical observation in the last few years. While several experimental, epidemiological and pharmacologic studies support this association, the initial pathophysiological mechanism linking these two clinical conditions remains to be established. This review discusses the pathophysiological bases and a number of ex- perimental and clinical observations suggesting that the common link between venous thromboembolism and arterial thrombosis is represented by a dysfunctional endothelium.

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“…P eripheral artery disease (PAD) is an important manifestation of atherothrombosis 1,2 in which several proinflammatory cytokines are increased. [3][4][5][6] Cytokine-mediated monocyte recruitment and differentiation into macrophages play a key role in atherothrombotic lesion progression and vulnerability.…”

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confidence: 99%

Peripheral Artery Disease Is Associated With a High CD163/TWEAK Plasma Ratio

Moreno

Dejouvencel

Labreuche

et al. 2010

ATVB

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Objective-In addition to its role in the clearance of haptoglobin-hemoglobin (Hp-Hb) complexes, CD163 is a macrophage scavenger receptor for tumor necrosis factor-like weak inducer of apoptosis (TWEAK). We recently reported that the CD163/TWEAK plasma ratio could be a potential biomarker of atherothrombosis in asymptomatic subjects. In this study, we assessed soluble TWEAK (sTWEAK) and soluble CD163 (sCD163) plasma levels in white males with peripheral artery disease (PAD) and in atherothrombotic femoral plaques to evaluate their relationship with disease. We also analyzed whether Hp-Hb complexes could compete for CD163-mediated TWEAK uptake. Methods and Results-Patients with PAD (nϭ155) showed a trend toward lower sTWEAK (median [interquartile range]:134 [110 -204] [234 -369] ng/mL; PϽ0.001) plasma concentrations than age-matched controls (nϭ251). sCD163 and sTWEAK plasma levels were negatively correlated in both patients and controls. After stratification according to the severity of disease, sCD163/sTWEAK ratio was significantly increased in patients with more severe disease relative to the other groups (Pϭ0.049). Analysis of conditioned medium obtained from cultured human atherothrombotic femoral plaque samples (nϭ36) and healthy aortas (nϭ14) revealed that high amounts of sCD163 were released by the atherothrombotic tissue, whereas sTWEAK presented the opposite trend (PϽ0.05). Finally, we report a potential association between CD163 shedding and oxidative stress. Conclusion-Our results suggest that the sCD163/sTWEAK plasma ratio may be associated with atherothrombosis burden in PAD. We hypothesize that an imbalance between TWEAK and CD163 could reflect the progression of atherothrombosis. Key Words: atherosclerosis Ⅲ cytokines Ⅲ hemoglobin Ⅲ macrophages Ⅲ peripheral arterial disease P eripheral artery disease (PAD) is an important manifestation of atherothrombosis 1,2 in which several proinflammatory cytokines are increased. [3][4][5][6] Cytokine-mediated monocyte recruitment and differentiation into macrophages play a key role in atherothrombotic lesion progression and vulnerability. [7][8][9] However, recent evidence describes atheroprotective properties of a subtype of macrophages (type II) able to scavenge haptoglobin-hemoglobin (Hp-Hb) complexes via the CD163 receptor from lesions with intraplaque hemorrhage. 10,11 Intraplaque hemorrhage is a common event in advanced atherothrombotic lesions. 12 Hemolysis of extravasated red blood cells leads to accumulation of pro-oxidant Hb. 13 CD163 is expressed mainly at the membrane of resident tissue macrophages; however, a soluble form of the protein (sCD163) has also been identified in both human plasma and cell culture supernatants, 14 resulting from a proteolytic cleavage of the cell surface protein. 15 sCD163 plasma levels are increased in diseases associated with macrophage activation, including coronary artery disease. 16 CD163 has been recently described as a scavenger receptor for tumor necrosis factorlike weak inducer of apoptosis (TWEAK); this prov...

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Peripheral arterial disease and Virchow’s triad

Cited by 43 publications

References 147 publications

Effect of ageing on the murine venous circulation

Effect of ageing on the murine venous circulation

Endothelium, venous thromboembolism and ischaemic cardiovascular events

Peripheral Artery Disease Is Associated With a High CD163/TWEAK Plasma Ratio

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