الفهرس 
EXTRA-CRANIAL CAROTID ATHEROSCLEROTIC STENOSIS FUNDEMENTALSOnly 14 pages are availabe for public view
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Abstract
Stroke is the third leading cause of death (164,000 deaths/ year) in the U.S., behind heart disease and cancer. There are approximately 1 million stroke-related events each year, including 500,000 new strokes, 200,000 recurrent strokes, and 240,000 transient ischemic attacks (TIAs), (Kleindorfer, et al. 2005 and Thom, et al. 2006). Patients who suffered a transient ischemic attack had a 13-fold excess risk of stroke during the first year and a sevenfold excess risk over the first 7 years compared with people without transient ischemic attacks (Dennis, et al. 1990). The risk is higher in the first month and highest in patients with hemispheric TIA and carotid stenosis causing more than 70% luminal reduction (Streifler, et al. 1992). However, Carotid occlusive disease amenable to revascularization accounts for 5% to 12% of new strokes (Kleindorfer, et al. 2005 and Thom, et al. 2006). This clarifies the importance of prophylaxis and early interference.
The first balloon angioplasty for carotid stenosis was per¬formed in 1979; reports in the early 1980s (Bockenheimer, et al. 1983), included a balloon occlusion system to reduce embolic complications (Theron, et al. 1990), then the first balloon-expandable stent was deployed in the carotid artery in 1989, these stents were prone to extrinsic compression, and major adverse events occurred in more than 10% of patients at 30 days (Marks, et al. 1994 and Diethrich, et al. 1996). Subsequently, issues about stent deformation were resolved by use of the self-expanding Wallstent (Roubin, et al. 2001), and later by self-expanding nitinol stents. However, risk of embolic stroke was the major concern that limits early enthusiasm for endovascular treatment. Initial strategies focused on neurological rescue which was not always successful. Accordingly, treatment strategies shifted from neurological rescue to neurological protection, utilizing specialized emboli-protection devices (EPDs) to capture and remove embolic debris that were generated during the course of the interventional procedure.
With the evolution and maturation of carotid artery stenting (CAS) equipments and techniques, many nonrandomized and randomized (CAS) clinical trials had compared carotid stenting with the use of an emboli-protection device with carotid endarterectomy (CEA) (American College of Cardiology Foundation, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology and American Society of Interventional & Therapeutic Neuroradiology Clinical Expert Consensus Document on Carotid Stenting. 2007) their results are summarized that; Currently, among patients with severe carotid-artery stenosis (symptomatic stenosis greater than 50% and asymptomatic stenosis greater than 80%) and coexisting conditions, carotid stenting with the use of an emboli-protection device is not inferior to carotid endarterectomy (Jay, et al. 2004).
Although the large number of studies, unfortunately no available studies comparing medical treatment versus CAS in those patients with severe carotid artery stenosis. This emerges an important question, which is superior medical therapy or CAS?
Stroke is the third leading cause of death (164,000 deaths/ year) in the U.S., behind heart disease and cancer. There are approximately 1 million stroke-related events each year, including 500,000 new strokes, 200,000 recurrent strokes, and 240,000 transient ischemic attacks (TIAs), (Kleindorfer, et al. 2005 and Thom, et al. 2006). Patients who suffered a transient ischemic attack had a 13-fold excess risk of stroke during the first year and a sevenfold excess risk over the first 7 years compared with people without transient ischemic attacks (Dennis, et al. 1990). The risk is higher in the first month and highest in patients with hemispheric TIA and carotid stenosis causing more than 70% luminal reduction (Streifler, et al. 1992). However, Carotid occlusive disease amenable to revascularization accounts for 5% to 12% of new strokes (Kleindorfer, et al. 2005 and Thom, et al. 2006). This clarifies the importance of prophylaxis and early interference.
The first balloon angioplasty for carotid stenosis was per¬formed in 1979; reports in the early 1980s (Bockenheimer, et al. 1983), included a balloon occlusion system to reduce embolic complications (Theron, et al. 1990), then the first balloon-expandable stent was deployed in the carotid artery in 1989, these stents were prone to extrinsic compression, and major adverse events occurred in more than 10% of patients at 30 days (Marks, et al. 1994 and Diethrich, et al. 1996). Subsequently, issues about stent deformation were resolved by use of the self-expanding Wallstent (Roubin, et al. 2001), and later by self-expanding nitinol stents. However, risk of embolic stroke was the major concern that limits early enthusiasm for endovascular treatment. Initial strategies focused on neurological rescue which was not always successful. Accordingly, treatment strategies shifted from neurological rescue to neurological protection, utilizing specialized emboli-protection devices (EPDs) to capture and remove embolic debris that were generated during the course of the interventional procedure.
With the evolution and maturation of carotid artery stenting (CAS) equipments and techniques, many nonrandomized and randomized (CAS) clinical trials had compared carotid stenting with the use of an emboli-protection device with carotid endarterectomy (CEA) (American College of Cardiology Foundation, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology and American Society of Interventional & Therapeutic Neuroradiology Clinical Expert Consensus Document on Carotid Stenting. 2007) their results are summarized that; Currently, among patients with severe carotid-artery stenosis (symptomatic stenosis greater than 50% and asymptomatic stenosis greater than 80%) and coexisting conditions, carotid stenting with the use of an emboli-protection device is not inferior to carotid endarterectomy (Jay, et al. 2004).
Although the large number of studies, unfortunately no available studies comparing medical treatment versus CAS in those patients with severe carotid artery stenosis. This emerges an important question, which is superior medical therapy or CAS?
Stroke is the third leading cause of death (164,000 deaths/ year) in the U.S., behind heart disease and cancer. There are approximately 1 million stroke-related events each year, including 500,000 new strokes, 200,000 recurrent strokes, and 240,000 transient ischemic attacks (TIAs), (Kleindorfer, et al. 2005 and Thom, et al. 2006). Patients who suffered a transient ischemic attack had a 13-fold excess risk of stroke during the first year and a sevenfold excess risk over the first 7 years compared with people without transient ischemic attacks (Dennis, et al. 1990). The risk is higher in the first month and highest in patients with hemispheric TIA and carotid stenosis causing more than 70% luminal reduction (Streifler, et al. 1992). However, Carotid occlusive disease amenable to revascularization accounts for 5% to 12% of new strokes (Kleindorfer, et al. 2005 and Thom, et al. 2006). This clarifies the importance of prophylaxis and early interference.
The first balloon angioplasty for carotid stenosis was per¬formed in 1979; reports in the early 1980s (Bockenheimer, et al. 1983), included a balloon occlusion system to reduce embolic complications (Theron, et al. 1990), then the first balloon-expandable stent was deployed in the carotid artery in 1989, these stents were prone to extrinsic compression, and major adverse events occurred in more than 10% of patients at 30 days (Marks, et al. 1994 and Diethrich, et al. 1996). Subsequently, issues about stent deformation were resolved by use of the self-expanding Wallstent (Roubin, et al. 2001), and later by self-expanding nitinol stents. However, risk of embolic stroke was the major concern that limits early enthusiasm for endovascular treatment. Initial strategies focused on neurological rescue which was not always successful. Accordingly, treatment strategies shifted from neurological rescue to neurological protection, utilizing specialized emboli-protection devices (EPDs) to capture and remove embolic debris that were generated during the course of the interventional procedure.
With the evolution and maturation of carotid artery stenting (CAS) equipments and techniques, many nonrandomized and randomized (CAS) clinical trials had compared carotid stenting with the use of an emboli-protection device with carotid endarterectomy (CEA) (American College of Cardiology Foundation, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology and American Society of Interventional & Therapeutic Neuroradiology Clinical Expert Consensus Document on Carotid Stenting. 2007) their results are summarized that; Currently, among patients with severe carotid-artery stenosis (symptomatic stenosis greater than 50% and asymptomatic stenosis greater than 80%) and coexisting conditions, carotid stenting with the use of an emboli-protection device is not inferior to carotid endarterectomy (Jay, et al. 2004).
Although the large number of studies, unfortunately no available studies comparing medical treatment versus CAS in those patients with severe carotid artery stenosis. This emerges an important question, which is superior medical therapy or CAS?