Increased platelet and coagulatory activity indicate ongoing thrombogenesis in peripheral arterial disease

Reininger, Cornelia; Graf, Johann; Reininger, Armin J.; Spannagl, Michael; Steckmeier, B.; Schweiberer, L.

doi:10.1016/0049-3848(96)00102-8

Cited by 43 publications

(31 citation statements)

References 19 publications

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“…By inspection of Fig. 10, the maximum non-dimensionalised platelet flux occurs at the stagnation point streamline ðR ¼ 0Þ; in contradiction to that found by experiments (Reininger et al, 1993;Affeld et al, 1995;Reininger et al, 1996). Although it is recognised that RBCs can augment the diffusion of platelets, Affeld et al's experiments used platelet-rich plasma and hence contained no RBCs.…”

Section: Discussioncontrasting

confidence: 46%

“…Over the past 20 years, there have been a number of proposed models for platelet adhesion and its relationship to blood flow and vascular geometry (Leonard et al, 1972;Turitto and Baumgartner, 1975;Kratzer and Kinder, 1986;Affeld et al, 1995) as well as a considerable amount of experimental data collected (Petschek et al, 1968;Friedman and Leonard, 1971;Leonard et al, 1972;Turitto and Baumgartner, 1975;Kratzer and Kinder, 1986;Strong et al, 1987;Tippe et al, 1992;Reininger et al, 1993;Schoephoerster et al, 1993;Affeld et al, 1995;Reininger et al, 1996). The models concentrated on both stagnation point flow as well as simple linear shear flow.…”

Section: Introductionmentioning

confidence: 99%

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Boundary‐Layer Type Solutions for Initial Platelet Activation and Deposition

Todem

Groot²,

Walker

2002

Computational and Mathematical Methods in Medicine

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This paper presents, on the basis of high Peclet number, a mathematical model for the activation and initial adhesion of flowing platelets onto a surface. In contrast to past work, the model is applicable to general 2D and axi-symmetric flows where the wall shear stress is known a priori. Results indicate that for high activation reaction rates there exist two layers, one containing only activated platelets and the other both activated and non-activated platelets. Fundamental relationships are proposed between the adhesion rate of platelets to the surface and the characteristic parameters of Peclet number and Reynolds number. Activation in the bulk fluid (blood) is characterised by the Damkohler number, which is a function of activation rate and the free-stream velocity. It is shown that, as the free-stream velocity varies, there exists a maximum of activated platelet flux to the wall for particular values of the velocity. These values, at which the maximum occur, are themselves functions of the platelet activation rate. As the free-stream velocity increases the activation of platelets ceases altogether and adhesion is reduced to a very small value strengthening the hypothesis of the correlation between atherogenesis/thrombogenesis and areas of low shear.

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Section: Discussioncontrasting

confidence: 46%

Section: Introductionmentioning

confidence: 99%

Boundary‐Layer Type Solutions for Initial Platelet Activation and Deposition

Todem

Groot²,

Walker

2002

Computational and Mathematical Methods in Medicine

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“…Many studies have suggested that patients with PAD manifest platelet hyperaggregability, increased levels of soluble platelet activation markers, enhanced thrombin generation and altered fibrinolytic potential (summarised in table 1). [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] These findings, which are consistent across the different stages of PAD, have important ramifications. Individually, many of the markers characterising the prothrombotic environment of PAD are predictive of future cardiovascular events.…”

Section: Pad and Thrombogenesismentioning

confidence: 83%

Antithrombotic treatment for peripheral arterial disease

Hackam

Eikelboom

2007

Heart

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“…Enhanced platelet aggregability 33 has been demonstrated in this disease, suggesting that antiplatelet therapy should be a cornerstone of therapy. While aspirin remains the primary antiplatelet agent for patients with CAD, the FDA has only approved clopidogrel for the reduction of ischemic events in patients with established PAD.…”

Section: Resultsmentioning

confidence: 99%

Masterclass series in peripheral arterial disease

Hiatt

Krantz

2006

Vasc Med

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Peripheral arterial disease (PAD) of the lower extremities is a common and potentially life-threatening manifestation of systemic atherosclerosis. Significant PAD is identified by an ankle brachial index (ABI) Ͻ0.90; its presence is strongly associated with the major modifiable cardiac risk factors. Early detection and treatment of asymptomatic PAD is a current focus of numerous cardiovascular guideline organizations as less than a third of patients report typical claudication symptoms. This has created an ever-increasing treatment gap, whereby millions of eligible patients are inadequately treated. Risk factor management including exercise, smoking cessation, and aggressive treatment of lipids and blood pressure are essential in PAD patients. However, life-long antiplatelet therapy provides additional reductions in vascular events beyond aggressive risk factor management. The use of aspirin as well as more potent antiplatelet therapies such as thienopyridines holds promise for reducing atherothrombosis in this very high-risk population.

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Increased platelet and coagulatory activity indicate ongoing thrombogenesis in peripheral arterial disease

Cited by 43 publications

References 19 publications

Boundary‐Layer Type Solutions for Initial Platelet Activation and Deposition

Boundary‐Layer Type Solutions for Initial Platelet Activation and Deposition

Antithrombotic treatment for peripheral arterial disease

Masterclass series in peripheral arterial disease

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