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A Rabbit Venous Interposition Model Mimicking Revascularization Surgery using Vein Grafts to Assess Intimal Hyperplasia under Arterial Blood Pressure
Published on: May 15, 2020
Circulating inflammatory cells are associated with vein graft stenosis
Katherine Moreno1, Jacqui Murray-Wijelath, Mayumi Yagi
1Division of Vascular Surgery, VA Puget Sound Health Care System and the University of Washington School of Medicine, Seattle, Wash., USA. morenok@u.washington.edu
Platelet-monocyte aggregates (PMA) are key in vascular injury. Elevated spontaneous and stimulated PMA levels, not baseline levels, indicate vein graft stenosis, suggesting a role in its development.
Area of Science:
- Vascular Surgery
- Immunology
- Thrombosis
Background:
- Infrainguinal autogenous vein grafts are susceptible to stenosis and failure.
- Platelets and monocytes are critical thrombo-inflammatory cells at vascular injury sites.
- Interactions between platelets and monocytes amplify thrombotic and inflammatory responses.
Purpose of the Study:
- To investigate if elevated platelet-monocyte aggregates (PMA) correlate with vein graft stenosis.
- To determine if PMA levels can differentiate between patients with and without vein graft stenosis.
Main Methods:
- Studied 36 vascular surgery patients with infrainguinal autogenous vein grafts.
- Quantified baseline, spontaneous, and stimulated PMA levels using two-color flow cytometry.
- Compared PMA levels in 18 patients with significant stenosis versus 18 without stenosis.
Main Results:
- Baseline PMA levels were similar between stenosis and non-stenosis groups.
- Patients with stenosis exhibited significantly higher spontaneous and stimulated PMA levels (P < .001).
- These differences were independent of smoking, diabetes, statin, or antithrombotic therapy.
Conclusions:
- Platelet-monocyte reactivity, particularly aggregation predisposition, may contribute to vein graft stenosis.
- Spontaneous and stimulated PMA measurements reveal pathologic differences not seen in baseline levels.
- Further understanding of these mechanisms could improve prediction and prevention of vein graft stenosis.
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