Search In this Thesis
   Search In this Thesis  
العنوان
RESTENOSIS AFTER INFRAINGUINAL ANGIOPLASTY
المؤلف
Elnemr,Mohamed Ragab Saad
هيئة الاعداد
باحث / Mohamed Ragab Saad Elnemr
مشرف / Emad Eldin Ahmed Hussein
مشرف / Wagih Fawzy Abd Elmalek
مشرف / Ahmed Farouk Mohamed
الموضوع
Equipments of angioplasty-
تاريخ النشر
2009
عدد الصفحات
136.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
جراحة
تاريخ الإجازة
1/1/2009
مكان الإجازة
جامعة عين شمس - كلية الطب - General Surgery
الفهرس
Only 14 pages are availabe for public view

from 136

from 136

Abstract

L
ower-extremity arterial occlusive disease is one of the most common manifestations of atherosclerosis. Patients with this condition may present with a wide variety of symptoms ranging from mild claudication to limb- threatening gangrene. As the population ages, the prevalence of chronic occlusive disease of the lower extremity increases significantly influencing lifestyle, morbidity, and mortality. In addition, multiple comorbid conditions increase risks of surgical procedures. Recent advances in endovascular interventions have made this minimally invasive approach an important alternative in the treatment of lower extremity occlusive disease. However, despite rapidly evolving endovascular technology, lower-extremity endovascular intervention continues to be one of the most controversial and challenging areas of therapeutic strategy.
Endovascular interventions initially begin with the desire to avoid the morbidity and operative risk of surgical revascularization. However, interventional techniques have become more common as a result of rapid technologic advances that include smaller catheter and balloon profiles, better balloon and guidewire construction, superior imaging equipment, and the introduction of stents. Both short- and long-term outcomes of PTAs have improved tremendously despite of the problems of restenosis and difficulty in opening diffusely diseased or occluded arteries. Patients also seem to prefer less invasive PTA over surgery.
Percutaneous transluminal angioplasty is sometimes appropriate for strictures or short-segment occlusions of the superficial femoral, popliteal, and, occasionally, infrapopliteal arteries. Angioplasty is performed by passing a guidewire through the lumen of the strictured artery and then advancing a balloon angioplasty catheter over the guidewire. The balloon is inflated to several atmospheres of pressure under angiographic visualization. This effectively disrupts the plaque and provides a wider, patent lumen. Somewhat surprisingly, even if the guidewire cannot negotiate the lumen of a stricture and instead passes through the subintimal plane, subintimal (extraluminal) angioplasty has been quite successful in some centers. This method seems to create a new channel in a virgin plane.
The acute procedural success rate for PTA is 90% and the patency rates are 80% at 1 year, 70% at 3 years, and 60% at 5 years. Stent placement, especially in the iliac arteries, may be associated with higher success rates. The 1-year restenosis rates are less than 5%.
Three mechanisms are responsible for the development of restenosis: elastic recoil, intimal hyperplasia, and late vascular constriction, all grouped under the catch phrase ”negative remodeling”. In the peripheral system, restenosis is seen mainly in small-sized and medium sized arteries. whereas manipulations in larger arteries, such as the iliac system, yield patency rates that are much more promising, manipulations in smaller vessels are plagued by lesion length, degree of stenosis, plaque burden, vessel size, and proximal and distal flow, all factors that seem to contribute to restenosis.
Because of the clinical sequelae of restenosis following endovascular interventions, a wide variety of strategies to prevent neointimal hyperplasia have been proposed as a means to decrease restenosis and improve clinical outcomes. One clinical strategy in particular that has demonstrated a significant efficacy relates to delivering intraluminal stents, which elute pharmacological agents designed to inhibit neointimal hyperplasia.