In summary, this discussion has dealt with the current state of restenosis occurring after coronary angioplasty. I have developed the theory that the lesion responsible for cases of restenosis is largely a proliferative lesion composed of activated and proliferating vascular smooth muscle cells. When this uncontrolled process continues it will finally obliterate the lumen, between three and six months after the dilatation. The restenosis process is predicted or at least more likely to occur in patients to have certain risk factors. These risk factors don't appear to be related to the patient per se but instead to the lesion and some procedural factors. Lesions that are proximal, particularly in the left anterior descending and vein grafts are at highest risk to undergo restenosis. Lesions that are long, very severely stenosed, incompletely dilated or in small coronary arteries are also at high-risk for restenosis. Overall, about one-third of all patients who have a successful PTCA will have restenosis. At least one-third of these will have no symptoms that are interpreted as ischemia. Therefore, the definition of restenosis has to be by angiography. There is no other way to make a definition at present. There are no medical treatments that are proven to prevent restenosis. Currently the only acceptable treatment is a repeat dilation or another interventional procedure.
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