Local Delivery of a Tissue Factor Antibody Reduces Early Leukocyte Infiltration but Fails to Limit Intimal Hyperplasia in Experimental Vein Grafts1

Annex, Brian H.; Fulton, Gregory J.; Huynh, Thi Thanh Tam; Channon, Keith M.; Ezekowitz, Michael D.; Hagen, Per Otto

doi:10.1006/jsre.1998.5438

Cited by 13 publications

(5 citation statements)

References 30 publications

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“…In fact, the most popular experimental model of vein graft neointimal hyperplasia, the external jugular vein graft of the New Zealand White rabbit, rarely develops more than about 100 µm of thickening after 4 weeks, which essentially translates to less than 5% luminal stenosis. 4,7,[27][28][29][30][31][32] Furthermore, the proposed relationship between low τ and NIT does little to explain how occlusive lesions develop in failing vein grafts. Reductions in blood flow of 50% to 80% have generally led to only a doubling of NIT, 14 which still does not result in any discernible encroachment on the lumen.…”

Section: Discussionmentioning

confidence: 99%

The effects of extremely low shear stress on cellular proliferation and neointimal thickening in the failing bypass graft

Meyerson¹,

Skelly²,

Curi³

et al. 2001

Journal of Vascular Surgery

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Extremely low tau (< 2 dyne/cm(2)) stimulates high rates of smooth muscle cellular proliferation in arterialized vein patches. NIT is accelerated in these regions of low tau far beyond that predicted by a simple linear model. The nonlinear nature of the cellular proliferative response and NIT at tau less than 2 dyne/cm(2) may explain the rapid progression of neointimal lesions in failing bypass grafts.

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Section: Discussionmentioning

confidence: 99%

The effects of extremely low shear stress on cellular proliferation and neointimal thickening in the failing bypass graft

Meyerson¹,

Skelly²,

Curi³

et al. 2001

Journal of Vascular Surgery

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“…The FXa inhibitors, LMWH (adjusted equivalent anti-FXa), 209 enoxaparin 209 or DX 9065a 213 markedly inhibit P-selectin expression and platelet aggregation in whole blood. Moreover, the validation of such an operational thrombosis-inflammation circuit in vivo comes from the further demonstrations that leukocyte activation/proliferation 214 and leukocyte adhesion to EC 215 are depressed by anti-TF Ab and DX-9065a, respectively.…”

Section: Thrombosis-inflammation Circuitmentioning

confidence: 98%

Tissue factor upregulation drives a thrombosis–inflammation circuit in relation to cardiovascular complications

Chu

2006

Cell Biochem. Funct.

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The extrinsic coagulation is recognized as an 'inducible' signalling cascade resulting from tissue factor (TF) upregulation by exposure to clotting zymogen FVII upon inflammation or tissue injury. Following the substantial initiation, an array of proteolytic activation generates mediating signals (active serine proteases: FVIIa, FXa and FIIa) that lead to hypercoagulation with fibrin overproduction manifesting thrombosis. In addition, TF upregulation plays a central role in driving a thrombosis-inflammation circuit. Coagulant mediators (FVIIa, FXa and FIIa) and endproduct (fibrin) are proinflammatory, eliciting tissue necrosis factor, interleukins, adhesion molecules and many other intracellular signals in different cell types. Such resulting inflammation could ensure 'fibrin' thrombosis via feedback upregulation of TF. Alternatively, the resulting inflammation triggers platelet/leukocyte/polymononuclear cell activation thus contributing to 'cellular' thrombosis. TF is very vulnerable to upregulation resulting in hypercoagulability and subsequent thrombosis and inflammation, either of which presents cardiovascular risks. The prevention and intervention of TF hypercoagulability are of importance in cardioprotection. Blockade of inflammation reception and its intracellular signalling prevents TF expression from upregulation. Natural (activated protein C, tissue factor pathway inhibitor, or antithrombin III) or pharmacological anticoagulants readily offset the extrinsic hypercoagulation mainly through FVIIa, FXa or FIIa inhibition. Therefore, anticoagulants turn off the thrombosis-inflammation circuit, offering not only antithrombotic but anti-inflammatory significance in the prevention of cardiovascular complications.

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“…The same group, how- ever, noticed no benefit of locally applied antitissue factor antibody regarding the development of NIH. 36 Both local and systemic treatment with aspirin reduced thrombus formation and NIH in animal experiments of vein graft disease. 33,37 C-type natriuretic peptide inhibits vascular smooth muscle cell (VSMC) proliferation and shows antiinflammatory and antithrombotic effects.…”

Section: Special Sites Of Pharmacologic Intervention To Prevent Neointimal Hyperplasia Thrombosismentioning

confidence: 99%

Pharmacologic inhibition of vein graft neointimal hyperplasia

Schachner

2006

The Journal of Thoracic and Cardiovascular Surgery

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Although arterial conduits are widely used and have improved the long-term results of coronary artery bypass grafting, vein grafts remain important additional conduits in coronary surgery. Newer studies show a saphenous vein graft patency of 60% or more at 10 years postoperatively. The pathology of vein graft disease consists of thrombosis, neointimal hyperplasia, and vein graft atherosclerosis, which limit graft longevity. Therapeutic strategies to prevent vein graft disease include external stenting, pharmacotherapy, and gene therapy. The potential benefits of a pharmacologic approach are as follows: (1) Drugs with a broad clinical experience can be used; (2) side effects of systemic application can be minimized by local therapy; and (3) no vascular injury, such as pressurizing the vein for a viral transfection approach, is necessary. The different sites for pharmacotherapy in vein graft disease are reviewed in this article.

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Local Delivery of a Tissue Factor Antibody Reduces Early Leukocyte Infiltration but Fails to Limit Intimal Hyperplasia in Experimental Vein Grafts1

Cited by 13 publications

References 30 publications

The effects of extremely low shear stress on cellular proliferation and neointimal thickening in the failing bypass graft

The effects of extremely low shear stress on cellular proliferation and neointimal thickening in the failing bypass graft

Tissue factor upregulation drives a thrombosis–inflammation circuit in relation to cardiovascular complications

Pharmacologic inhibition of vein graft neointimal hyperplasia

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