Virchow’s Triad Revisited: Abnormal Flow

Lowe, G. D. O.

doi:10.1159/000083845

Cited by 229 publications

(171 citation statements)

References 19 publications

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“…Our study supports our traditional belief in the pathogenesis of venous thromboembolism. According to the Virchow triad, 81 venous stasis resulting from immobilization of a patient is 1 of 3 key elements in the pathogenesis of venous thromboembolism. Studies have shown that IPC of the lower limbs may improve venous blood flow in the venous system and increase fibrinolytic activity.…”

Section: Discussionmentioning

confidence: 99%

Stratified Meta-Analysis of Intermittent Pneumatic Compression of the Lower Limbs to Prevent Venous Thromboembolism in Hospitalized Patients

2013

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Section: Discussionmentioning

confidence: 99%

Stratified Meta-Analysis of Intermittent Pneumatic Compression of the Lower Limbs to Prevent Venous Thromboembolism in Hospitalized Patients

2013

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“…4,46 Although various anticoagulants contribute to the prevention of venous thromboembolism, 2 increased blood flow rate and velocity are usually interpreted as possible mechanisms by which compression stockings prevent DVT. 16,47 However, we hypothesize that shear rate may be a better predictor of initiation of coagulation than volumetric flow rate or flow velocity, because a considerable amount of coagulation is initiated on or near vessel walls, and the flow velocity approaches zero on the vessel walls.…”

Section: Discussionmentioning

confidence: 99%

Threshold Response of Initiation of Blood Coagulation by Tissue Factor in Patterned Microfluidic Capillaries Is Controlled by Shear Rate

Shen

Kastrup

Liu

et al. 2008

ATVB

111

115

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Objective-Blood flow is considered one of the important parameters that contribute to venous thrombosis. We quantitatively test the relationship between initiation of coagulation and shear rate and suggest a biophysical mechanism to understand this relationship. Methods and Results-Flowing human blood and plasma were exposed to cylindrical surfaces patterned with patches of tissue factor (TF) by using microfluidics. Initiation of coagulation of normal pooled plasma depended on shear rate, not volumetric flow rate or flow velocity, and coagulation initiated only at shear rates below a critical value. Initiation of coagulation of platelet-rich plasma and whole blood showed similar behavior. At constant shear rate, coagulation of plasma also showed a threshold response to the size of a patch of TF, consistent with our previous work in the absence of flow. Conclusion-Initiation of coagulation of flowing blood displays a threshold response to shear rate and to the size of a surface patch of TF. Combined with the results of others, these results set the range of shear rates that limit initiation of coagulation by small surface areas of TF and by shear activation of platelets. This range fits the relatively narrow range of physiological shear rates described by Murray's law. T his article analyzes initiation of coagulation of blood flowing over a patch presenting tissue factor (TF) in the regime where platelets are not activated by shear alone. TF is the primary stimulus for initiation of coagulation in vivo. [1][2][3] We demonstrate that initiation of coagulation displays a threshold response to shear rate and to the size of the patch of TF, and we suggest a biophysical mechanism that explains these threshold phenomena. While low blood flow and endothelial damage are known risk factors for coagulation, 4 the precise effects of blood flow on the initiation of coagulation are not fully characterized, possibly because of the difficulty in experimentally decoupling the effects of volumetric flow rate, flow velocity, and shear rate.The effects of flow and shear rate on the activation of coagulation factors have been studied previously, 5-12 but whether high or low shear rates promote initiation of coagulation remains unclear. Intuitively, high blood flow and shear rates may promote coagulation by increasing the rate of delivery of coagulation proenzymes to sites of vascular damage. Indeed, high shear rates have been shown to increase the generation of factor Xa from surfaces coated with the TF and factor VIIa complex (TF-VIIa). 11 Moreover, high shear rates increase the potential for shear activation of platelets. 13,14 On the other hand, numeric simulations have predicted that low blood flow could promote initiation by reducing the removal of activated coagulation factors from surfaces of TF-VIIa, 15 and, clinically, stasis and low blood flow are considered risk factors for deep vein thrombosis (DVT). 16 Low shear rates have also been found to increase fibrin deposition and appearance of fibrin monomers, indicating that l...

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“…Rubanyi (1993) studied the role of endothelial cells in cardiovascular homeostasis and reported that the activation of endothelial cells could feed back on the regulatory mechanisms of blood coagulation within blood vessels. In addition, Lowe (2005) showed that blood flow exerted shear stresses on the endothelial cells to alter their morphology and function. Thus, it is probable that homeostatic control of blood coagulation occurs in concert with changes in blood flow in P. annectens.…”

Section: Molecular Characterization Of F2 and Fgg From P Annectensmentioning

confidence: 99%

Aestivation induces changes in transcription and translation of coagulation factor II and fibrinogen gamma chain in the liver of the African lungfish,Protopterus annectens

Hiong

Tan

Boo

et al. 2015

Journal of Experimental Biology

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This study aimed to sequence and characterize two pro-coagulant genes, coagulation factor II ( f2) and fibrinogen gamma chain ( fgg), from the liver of the African lungfish Protopterus annectens, and to determine their hepatic mRNA expression levels during three phases of aestivation. The protein abundance of F2 and Fgg in the liver and plasma was determined by immunoblotting. The results indicated that F2 and Fgg of P. annectens were phylogenetically closer to those of amphibians than those of teleosts. Three days of aestivation resulted in an up-regulation in the hepatic fgg mRNA expression level, while 6 days of aestivation led to a significant increase (3-fold) in the protein abundance of Fgg in the plasma. Hence, there could be an increase in the blood-clotting ability in P. annectens during the induction phase of aestivation. By contrast, the blood-clotting ability in P. annectens might be reduced in response to decreased blood flow and increased possibility of thrombosis during the maintenance phase of aestivation, as 6 months of aestivation led to significant decreases in mRNA expression levels of f2 and fgg in the liver. There could also be a decrease in the export of F2 and Fgg from the liver to the plasma so as to avert thrombosis. Three to 6 days after arousal from 6 months of aestivation, the protein abundance of F2 and Fgg recovered partially in the plasma of P. annectens; a complete recovery of the transcription and translation of f2/F2 in the liver might occur only after refeeding.

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Virchow’s Triad Revisited: Abnormal Flow

Cited by 229 publications

References 19 publications

Stratified Meta-Analysis of Intermittent Pneumatic Compression of the Lower Limbs to Prevent Venous Thromboembolism in Hospitalized Patients

Stratified Meta-Analysis of Intermittent Pneumatic Compression of the Lower Limbs to Prevent Venous Thromboembolism in Hospitalized Patients

Threshold Response of Initiation of Blood Coagulation by Tissue Factor in Patterned Microfluidic Capillaries Is Controlled by Shear Rate

Aestivation induces changes in transcription and translation of coagulation factor II and fibrinogen gamma chain in the liver of the African lungfish,Protopterus annectens

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