To understand restenosis formation, a differentiation to thrombus can be distinquishing. Restenosis occurs when a stent is placed in a blood vessel, new tissue grows inside the stent, covering the struts of the stent. Initially, this new tissue consists of healthy cells from the lining of the arterial wall (endothelium). This is a favorable effect because development of normal lining over the stent allows blood to flow smoothly over the stented area without clotting. Later, scar tissue may form underneath the new healthy lining. In about 25% of patients, the growth of scar tissue underneath the lining of the artery may be so thick that it can obstruct the blood flow and produce an important blockage. In-stent restenosis is typically seen 3 to 6 months after the procedure; after 12 months have passed uneventfully, it is rare. Restenosis is the result scar tissue, sometimes inflammation. The more extensive the scar tissue growth and the pattern of growth the greater the blockage.
DES appears to be more effective to prevent restenosis when compared to bare metal stents, but there appears to be some risk for clots (thrombus) for up to about a year so plavix is recommended with aspirin (dual therapy).
A cath directed thrombolysis (clot dissoving agent) that is directly delivered to clot site will dissolve a clot. Blood thinners and anticoagulant medication will inhibit thrombus growth and prevent new clots.
Thanks for the reply and the great explanation. I was under the impression that restonisis is due to plaque.
Regarding my fathers case, the Cardiologist has diagnosed the blockage as thrombosis at this time.
Judging by the fact that he was on Plavix and aspirin all the time, is this a mis-diagnosis? OR is the difference between a thrombus and restenosis really very obvious during an angiography
Perhaps its a guess since the BMS is fine while the DES has clogged.
Also since my father is feeling better after all the blood thinners he was given, What could have happened? Do you think the clot (if it was thrombus) can dissolve only with blood thinners.
OR is his blockage unaffected, but the angina symptoms have gone away because of thin blood (at this time)
Plague buildup generally requires more time that "in-stent restenosis". I was referring to what is medically termed and referred to as "in-stent restenois" phenomonon.
Generally, a clot would be obvious during an angiography by a competent interventional cardiologist, and I have found no information that a clot can be disolved without intervention, but who are we to disagree with a cardiologist!? The risk, it seems to me, for a high dose to break up a clot without directly injecting the drug with a cath into the clot may be due the high risk of bleeding.
The cause of angina is almost always due to a lack adequate blood supply to the heart tissues. The blood flow blockage isn't overcome by a change in viscosity otherwise a blood thinner could treat angina. Aspirin makes the platelets flow more smoothly so they will not stick to the walls of the artheries. I was informed by my MD that Aspirin does not thin blood, but blood thinning (aspirin and such) is a characteristic attributed to aspirin and other anticoagulants.