Thrombus formation in vivo

Furie, B

doi:10.1172/jci26987

Cited by 421 publications

(339 citation statements)

References 58 publications

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“…However it embodies a necessary first step, particularly for porcine in vivo studies of ultrasound-enhanced rt-PA thrombolysis. The thrombolytic drug used in this study, rt-PA, may very likely have a different effect on human thrombi in vivo than the efficacy demonstrated in this in vitro porcine clot study [46][47][48]. In addition, the amount of endogenous plasminogen in humans and pigs differs by as much as an order of magnitude.…”

Section: Discussionmentioning

confidence: 93%

Ultrasound-enhanced tissue plasminogen activator thrombolysis in an in vitro porcine clot model

Holland

Vaidya

Datta

et al. 2008

Thrombosis Research

100

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Section: Discussionmentioning

confidence: 93%

Ultrasound-enhanced tissue plasminogen activator thrombolysis in an in vitro porcine clot model

Holland

Vaidya

Datta

et al. 2008

Thrombosis Research

100

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“…Biochemical and hemodynamic factors contribute to thrombus formation at a vulnerable vessel wall (2)(3)(4). Thrombogenic components exposed upon plaque rupture-e.g.…”

mentioning

confidence: 99%

Atherosclerotic geometries exacerbate pathological thrombus formation poststenosis in a von Willebrand factor-dependent manner

Westein

Meer

Kuijpers

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

242

257

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Rupture of a vulnerable atherosclerotic plaque causes thrombus formation and precipitates cardiovascular diseases. In addition to the thrombogenic content of a plaque, also the hemodynamic microenvironment plays a major role in thrombus formation. How the altered hemodynamics around a plaque promote pathological thrombus formation is not well understood. In this study, we provide evidence that plaque geometries result in fluid mechanical conditions that promote platelet aggregation and thrombus formation by increased accumulation and activity of von Willebrand factor (vWF) at poststenotic sites. Resonant-scanning multiphoton microscopy revealed that in vivo arterial stenosis of a damaged carotid artery markedly increased platelet aggregate formation in the stenotic outlet region. Complementary in vitro studies using microfluidic stenotic chambers, designed to mimic the flow conditions in a stenotic artery, showed enhanced platelet aggregation in the stenotic outlet region at 60-80% channel occlusion over a range of input wall shear rates. The poststenotic thrombus formation was critically dependent on bloodborne vWF and autocrine platelet stimulation. In stenotic chambers containing endothelial cells, flow provoked increased endothelial vWF secretion in the stenotic outlet region, contributing to exacerbated platelet aggregation. Taken together, this study identifies a role for the shear-sensitive protein vWF in transducing hemodynamic forces that are present around a stenosis to a prothrombogenic microenvironment resulting in spatially confined and exacerbated platelet aggregation in the stenosis outlet region. The developed stenotic microfluidic chamber offers a realistic platform for in vitro evaluation of shear-dependent thrombus formation in the setting of atherosclerosis.

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“…Once the plug has been assembled, a fibrin chemically crosslinked network is polymerized in-situ through a large network of chemical reactions (for a more detailed description see ref. 13). Interestingly, the propensity for forming a thrombus is highly regulated by fluid flows, increasing as you increase the flow strength for shear rates as high as 10,000 s À 1 (refs 14,15).…”

mentioning

confidence: 99%

Blood-clotting-inspired reversible polymer–colloid composite assembly in flow

et al. 2013

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Blood clotting is a process by which a haemostatic plug is assembled at the site of injury. The formation of such a plug, which is essentially a (bio)polymer-colloid composite, is believed to be driven by shear flow in its initial phase, and contrary to our intuition, its assembly is enhanced under stronger flowing conditions. Here, inspired by blood clotting, we show that polymer-colloid composite assembly in shear flow is a universal process that can be tailored to obtain different types of aggregates including loose and dense aggregates, as well as hydrodynamically induced 'log'-type aggregates. The process is highly controllable and reversible, depending mostly on the shear rate and the strength of the polymer-colloid binding potential. Our results have important implications for the assembly of polymercolloid composites, an important challenge of immense technological relevance. Furthermore, flow-driven reversible composite formation represents a new paradigm in non-equilibrium self-assembly.

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Thrombus formation in vivo

Cited by 421 publications

References 58 publications

Ultrasound-enhanced tissue plasminogen activator thrombolysis in an in vitro porcine clot model

Ultrasound-enhanced tissue plasminogen activator thrombolysis in an in vitro porcine clot model

Atherosclerotic geometries exacerbate pathological thrombus formation poststenosis in a von Willebrand factor-dependent manner

Blood-clotting-inspired reversible polymer–colloid composite assembly in flow

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