Θεματική ενότητα: Stenting

Μ. Ματσάγκας, MD, PhD, FEBVSΣάββατο 1 Φεβρουαρίου

2014

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

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

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

Mode of action

The balloon The balloon catheter lies catheter lies within an within an eccentriceccentric arterial lesionarterial 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