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Dive into the research topics where William J. Boyle is active.

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Featured researches published by William J. Boyle.


Heart | 2003

Embolic protection devices

William J. Boyle; David H. Burkett; Andy E. Denison; Benjamin C. Huter; Scott J. Huter; Arkady Kokish; Kent C. B. Stalker; Chicheng Wang; John D. Whitfield

Percutaneous intervention for the treatment of coronary and peripheral atherosclerotic disease has become a well established technique, and has been recently extended also to the carotid arena. However, distal embolisation of particulate matter, including plaque debris such as fibrin, necrotic atheromatous core, foam cells, cholesterol clefts, and thrombus,1 at the time of balloon inflation or stent deployment, complicate percutaneous mechanical interventions more often than had been recognised before. The risk of distal embolisation is now considered significant in carotid arteries,2 degenerated saphenous vein graft, and in thrombotic lesions characterising the patient affected by acute coronary syndromes.3–5 The process of plaque embolisation catalyses a complex interaction also involving microvascular spasm and thrombosis. This often results in diminished blood flow to the distal vascular bed, potentially complicated by periprocedural ischaemia and/or infarction or stroke.6,7 In particular, the risk of distal embolisation is especially high in degenerated saphenous vein grafts, with the “no reflow” phenomenon being reported in up to 31.8% of cases during treatment of thrombotic lesions and in up 7.9% of cases with no thrombus present.8 Although large particles (> 100 μm) may obstruct large, epicardial vessels, very small particles, as little as 15–50 μm, can also obstruct the microvascular bed causing microinfarcts and left ventricular dysfunction. In the setting of acute myocardial infarction, Ito and associates9 detected by myocardial contrast echocardiography a substantial “no reflow” area, potentially related to distal embolisation of atherosclerotic debris in 37% of patients with TIMI-3 flow shortly after reperfusion treatment. Those “infarctlets”, indicated by an increase in periprocedural creatine kinase-MB, have been recently associated with worse outcome at one year follow up, even in patients without any apparent procedure or in-hospital complications.10 Different approaches have been attempted in the past to reduce distal embolisation, including intracoronary …


Archive | 2003

Delivery systems for embolic filter devices

William J. Boyle; Benjamin C. Huter; Scott J. Huter


Archive | 2001

Deployment and recovery control systems for embolic protection devices

William J. Boyle; Benjamin C. Huter; Charles R. Peterson; Donald Schwarten; Richard S. Stack


Archive | 2001

Intraluminal delivery system for an attachable treatment device

William J. Boyle; Benjamin C. Huter; John E. Papp


Archive | 1999

Stent delivery catheter and method of use

Richard S. Stack; Udayan G. Patel; William J. Boyle; Kent C. B. Stalker; Paul F. Muller


Archive | 2001

Delivery and recovery sheaths for medical devices

William J. Boyle; Andy E. Denison; Benjamin C. Huter; Scott J. Huter; John E. Papp; Charles R. Peterson; Kent C. B. Stalker


Archive | 2000

Guide wire with damped force vibration mechanism

William J. Boyle; Paul F. Muller


Archive | 2002

Support structures for embolic filtering devices

William J. Boyle; John E. Papp; Francisco Sanchez; Steven T. Saville


Archive | 2003

Vessel occlusion device for embolic protection system

William J. Boyle; Andy E. Denison; Paul F. Muller


Archive | 2001

Offset proximal cage for embolic filtering devices

William J. Boyle; John E. Papp

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