Θεματική ενότητα: Stenting Μ. Ματσάγκας, MD, PhD, FEBVS Σάββατο 9 Φεβρουαρίου 2013

Physics  Tensile strength of a material is the maximum amount of stress that the material can be subjected to before failure  Yield strength represents the stress at which material strain changes from elastic deformation to plastic deformation, causing it to deform permanently  Breaking strength is the stress coordinate on the stress–strain curve at the point of rupture

Physics

 Below a certain stress known as the elastic limit, or the yield strength, the blood vessel demonstrates elastic recoil  As transmural pressure exceeds the elastic limit, the vessel demonstrates irreversible deformation  Elastic limit is a function of the lesion  Typically calcified lesions have low elastic limits as the brittle calcifications yield to moderate angioplasty pressures  Collagen-rich areas of myointimal hyperplasia have high elastic limits and require large transmural pressures to overcome the elastic limit. Physics

 Angioplasty involves the dilatation of a vascular stenosis or occlusion with a balloon catheter Angioplasty

Biological response to balloon angioplasty  Initially thought to be the result of compression of atherosclerotic lesion followed by remodeling of the plaque  Predominant effect of balloon angioplasty is stretching the elastic components of the arterial wall  Inelastic portion of the plaque fracture or tear results in a definite but discrete arterial wall dissection  Histologically evident arterial dissection is nearly present in all diseased vessels following balloon angioplasty procedures

Biological response to balloon angioplasty  The injury to the endothelium exposes the subendothelial space and attracts platelets and fibrin that cover the damaged surfaces  All these events favor the local migration and proliferation of the SMC as a healing response, which may ultimately lead to restenosis, or intimal hyperplasia  Most angioplasty-induced dissections will ultimately heal within a month

Stenting

 Within 15 min following stent implantation, there is an accumulation of red blood cells and platelets on the stent surface  At 24 h, this cellular layer is replaced by a layer of fibrin strands oriented in the direction of blood flow  In the third and fourth weeks after stent insertion, SMC proliferation and endothelialization resulted in a neointimal layer of approximately 1 mm in thickness Biological response to stenting

 Finally, several months after stent placement, the formation of the neointimal vessel begins  At 3–6 years, the fibromuscular tissue layer covering the stent surface is almost completely replaced by collagen Biological response to stenting

 The electrical charge of most metals and alloys used for intravascular devices is electropositive in electrolytic solutions, whereas all biologic intravascular substances are negatively charged  The positive electrical potential of the metallic struts attracts the negatively charged circulating proteins to form a thin layer of fibrinogen strands on the stent surface  The proteins neutralize the stent surface and decrease thrombogenicity Biological response to stenting

 Surface tension is another property that influences biological stent interaction  The initial layer of proteins that cover the metal within seconds of implantation helps reduce surface tension and thrombogenicity Biological response to stenting

 The technique of stent implantation itself may affect thrombogenicity and the rate of endothelialization  Stents should be deployed in such a way that the metal struts are embedded deep enough into the vessel wall to produce troughs where the struts are embedded surrounded by intima  If the struts are not properly embedded, the entire stented surface becomes covered with thrombus, preventing early endothelialization and thus predisposing to complete thrombosis and restenosis Biological response to stenting

 Cellular events analogous to a foreign body reaction are also seen, which include the thrombus formation organized around the stent  Following stent-graft implantation, the media of the underlying artery wall is partially replaced by collagen, perhaps due to the pressure from the stent-graft Biological response to stenting

Mode of action  Fracture of the arterial plaque and a localized tear or dissection of the arterial wall  The tear may extend circumferentially or longitudinally in the vessel wall and may extend into the internal elastic lamina or into the media  The adventitial layer remains intact  Balloon dilatation also causes stretching of the medial layer if the balloon diameter is adequately oversized

 Microscopic plaque material may become separated and embolize distally  This is usually asymptomatic in the peripheral circulation  In carotid artery angioplasty, this phenomenon has potentially more severe consequences Mode of action

 Concentric arterial lesions respond well to PTA, because the arterial plaque and the arterial wall layers are dissected in a uniform fashion, which improves the increase in the luminal diameter Mode of action

 The balloon catheter is centered in a concentric arterial lesion

Mode of action  Balloon dilatation results in uniformly controlled wall dissection with adequate luminal gain

 Eccentric arterial lesions may respond less well to balloon dilatation. This is because the wall opposite the plaque is stretched by the balloon rather than the plaque itself  Once the balloon is deflated, the normal elastic wall may recoil, resulting in an unsatisfactory result Mode of action

 The balloon catheter lies within an eccentric arterial lesion

Mode of action  After balloon dilatation the wall opposite to the plaque is stretched

Mode of action  The stent provides an internal scaffold for the arterial lumen with excellent luminal gain

Advantages of stenting  Rapid, reliable and sustained increase in the luminal diameter  Entrapment of vulnerable plaque material that may cause embolization  Elimination of elastic recoil