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overhealing?
I had a stent placed back in November. Last weekend I ended up in ER with chest pains. I had two more stents added upstream and downstream of the original stent. The cardiologist mentioned there was "overhealing" with the oringinal stent. I assume something related to restinosis? There was blockage on either side of the original stent. The original stent was coated to avoid restinosis. I am on all kinds of meds for this. Why would the artery clog that quickly and have I now shown that I may likely have the recur?
Are these problems due to cardiologists not removing plaque? In all my stent treatments, plaque has been removed up to the artery lining before ballooning. If a cardiologist simply balloons a high level of hard plaque into an artery lining, surely it's obvious it will cause a lot of damage to the tissue. It would be like me doing pressups on glass and expecting no damage to my hands.
The cardiologist mentioned there was "overhealing" with the oringinal stent. That is another word for vessel injury and inflammatory response and involves the immune system. The immune response is how your body recognizes and defends itself against bacteria, viruses, and substances that appear foreign and harmful to the body.
The inflammatory reaction triggered by the stent insertion is maintained by several concomitant factors. Besides the mechanism of stent expansion with vessel wall rupture, there are the superimposed permanent radial mechanical strain applied to arterial wall, the presence of an intravascular residual metallic foreign material, and ischemic phenomena induced by endothelial dysfunction. The stent struts cause focal deep vascular trauma, and it has been demonstrated that the initial inflammatory reaction is more accentuated at the points of greatest strain of the stent struts on the arterial wall.
For a perspective stents have evolved from the early concept of providing support to prevent vessel recoil and negative remodeling, becoming elaborate devices, and have culminated with the highly sophisticated technology of drug-eluting stents. However, unlike balloon angioplasty, in which elastic recoil and vessel remodeling play an important role for vessel luminal loss in the long term, restenosis after coronary stenting takes place because of neointimal proliferation. It also bears a relationship to the extent of the vessel injury and inflammatory response.
Recent evidence has demonstrated that implant of coronary stents evokes the advent of a local and systemic inflammatory response syndrome , and restenosis comprises only part of the manifestation of the inflammatory reaction. The consequent **endothelial dysfunction and ischemia are connected events that have not been well studied.
**Endothelial dysfunction is characterized by a shift of the actions of the endothelium toward reduced vasodilation, a proinflammatory state, and prothrombic properties. It is associated with most forms of cardiovascular disease, such as hypertension, coronary artery disease, chronic heart failure, peripheral artery disease, diabetes, and chronic renal failure. Endothelium cells line the inner wall and have a very important role regulating hemodynamics.
Occlusion on both sides of the stent may have a different etiology unrelated to the restenosis of the stent implant.
The inflammatory reaction triggered by the stent insertion is maintained by several concomitant factors. Besides the mechanism of stent expansion with vessel wall rupture, there are the superimposed permanent radial mechanical strain applied to arterial wall, the presence of an intravascular residual metallic foreign material, and ischemic phenomena induced by endothelial dysfunction. The stent struts cause focal deep vascular trauma, and it has been demonstrated that the initial inflammatory reaction is more accentuated at the points of greatest strain of the stent struts on the arterial wall.
For a perspective stents have evolved from the early concept of providing support to prevent vessel recoil and negative remodeling, becoming elaborate devices, and have culminated with the highly sophisticated technology of drug-eluting stents. However, unlike balloon angioplasty, in which elastic recoil and vessel remodeling play an important role for vessel luminal loss in the long term, restenosis after coronary stenting takes place because of neointimal proliferation. It also bears a relationship to the extent of the vessel injury and inflammatory response.
Recent evidence has demonstrated that implant of coronary stents evokes the advent of a local and systemic inflammatory response syndrome , and restenosis comprises only part of the manifestation of the inflammatory reaction. The consequent **endothelial dysfunction and ischemia are connected events that have not been well studied.
**Endothelial dysfunction is characterized by a shift of the actions of the endothelium toward reduced vasodilation, a proinflammatory state, and prothrombic properties. It is associated with most forms of cardiovascular disease, such as hypertension, coronary artery disease, chronic heart failure, peripheral artery disease, diabetes, and chronic renal failure. Endothelium cells line the inner wall and have a very important role regulating hemodynamics.
Occlusion on both sides of the stent may have a different etiology unrelated to the restenosis of the stent implant.
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