Postmortem Intraosseous Phlebography as an Aid in Studies of Venous Thromboembolism

Lund, F; Diener, Lennart; Ericsson, Jan L. E.

doi:10.1177/000331976902000306

Cited by 29 publications

(13 citation statements)

References 17 publications

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“…They are also areas where stasis and hypoxia may occur. Direct evidence from autopsy studies and phlebography have established the venous valvular sinus as a frequent location of thrombosis initiation 5,[7][8][9] . This phenomenon has been attributed to stasis, one of the components of Virchow's triad.…”

Section: A Where Does Venous Thrombosis Begin and Why?mentioning

confidence: 99%

Basic mechanisms and pathogenesis of venous thrombosis

2009

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In 1856 Virchow proposed a triad of causes for venous thrombosis, postulating that stasis, changes in the vessel wall or changes in the blood could lead to thrombosis. We now know that abnormally high levels of some coagulation factors and defects in the natural anticoagulants contribute to thrombotic risk. Among these, factor V Leiden, which renders factor Va resistant to activated protein C, is the most prevalent with approximately 5% of the Caucasian population having this genetic alteration. These genetically controlled variants in coagulation factors work in concert with other risk factors, such as oral contraceptive use, to dramatically increase thrombotic risk. While these abnormalities in the blood coagulation proteins are associated with thrombotic disease propensity, they are less frequent contributors to thrombosis than age or cancer. Cancer increases thrombotic risk by producing tissue factor to initiate coagulation, by shedding procoagulant lipid microparticles or by impairing blood flow. Age is the strongest risk factor for thrombosis. Among possible reasons are fragility of the vessels potentially contributing to stasis, increased coagulation factor levels, impaired function of the venous valves, decreases in the efficacy of natural anticoagulants associated with the vessel wall, increased risk of immobilization and increased risk of severe infection.

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Section: A Where Does Venous Thrombosis Begin and Why?mentioning

confidence: 99%

Basic mechanisms and pathogenesis of venous thrombosis

2009

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“…‘Distal’ thrombosis isolated below the PV occurs in the remainder and rarely produces clinically significant pulmonary embolism . Proximal LEDVT almost invariably exists at the common femoral vein (CFV) or PV, so US of these vessels detects virtually all LEDVT requiring anticoagulation . Repeating this ‘two‐point’ examination also identifies the 10–25% of distal thromboses that propagate proximally .…”

Section: Introductionmentioning

confidence: 99%

Sensitivity and specificity of three‐point compression ultrasonography performed by emergency physicians for proximal lower extremity deep venous thrombosis

Crowhurst

Dunn

2013

Emerg Medicine Australasia

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“…[1][2][3][4] This phenomenon has been attributed to stasis, one of the components of Virchow triad. In the 1960s, contrast media was shown to linger in valve sinuses an average of 27 minutes postvenography.…”

Section: Introductionmentioning

confidence: 99%

Valves of the deep venous system: an overlooked risk factor

Brooks¹,

Trotman²,

Wadsworth³

et al. 2009

Blood

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Deep venous valves are frequent sites of deep venous thrombosis initiation. However, the possible contribution of the valvular sinus endothelium has received little attention in studies of thrombosis risk. We hypothesized that the endothelium of valve sinus differs from that of vein lumen with up-regulation of anticoagulant and down-regulation of procoagulant activities in response to the local environment. In pursuit of this hypothesis, we quantified endothelial protein C receptor (EPCR), thrombomodulin (TM), and von Willebrand factor (VWF) by immunofluorescence in great saphenous veins harvested at cardiac bypass surgery. We found significantly increased expression of EPCR and TM in the valvular sinus endothelium as opposed to the vein lumenal endothelium, and the opposite pattern with VWF (paired t test for TM and EPCR, each P < .001; for VWF, P ‫؍‬ .01). These data support our hypothesis and suggest that variation in valvular sinus thromboresistance may be an important factor in venous thrombogenesis. (Blood. 2009; 114:1276-1279) IntroductionDirect evidence from autopsy studies and phlebography, as well as circumstantial evidence such as the correlation between frequency of deep venous thrombosis and the number of valves in individuals, have established the venous valvular sinus as a frequent location of thrombosis initiation. [1][2][3][4] This phenomenon has been attributed to stasis, one of the components of Virchow triad. In the 1960s, contrast media was shown to linger in valve sinuses an average of 27 minutes postvenography. 5 Valvular sinus stasis has also been associated with hypoxia and increased hematocrit, 6 as well as preventing the efflux of activated clotting factors and influx of clotting factor inhibitors, constituting a potentially hypercoagulable microenvironment, another component of Virchow triad. Stasis alone, however, is not a sufficient explanation for the propensity of thrombi to form in deep venous valve sinuses because, for example, prolonged periods of stasis associated with sleep are not associated with thrombus formation. Accordingly, there must be other factors interacting with stasis in the generation of venous valvular thrombi.In recent years, attention has been focused on the importance of endothelial heterogeneity in different vascular beds. 7,8 Venous endothelium manifests multiple distinct phenotypes in different organs such as the kidney and liver. Gene expression microarray studies have shown that endothelial cells from macro-versus microvascular beds, from arteries versus veins, and from different organs have distinctly different and characteristic gene expression profiles. 9 In response to local changes in flow, shear stress, or oxygenation, endothelial cells often adapt by increasing or decreasing expression of critical cell-surface and cytoplasmic proteins. 10 Thus, we hypothesized that valvular sinus endothelium would maintain a thromboresistant phenotype with the expression of the anticoagulant proteins thrombomodulin (TM) and endothelial protein C receptor (EPCR) u...

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Postmortem Intraosseous Phlebography as an Aid in Studies of Venous Thromboembolism

Cited by 29 publications

References 17 publications

Basic mechanisms and pathogenesis of venous thrombosis

Basic mechanisms and pathogenesis of venous thrombosis

Sensitivity and specificity of three‐point compression ultrasonography performed by emergency physicians for proximal lower extremity deep venous thrombosis

Valves of the deep venous system: an overlooked risk factor

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