PubMed · 9554764
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R R Heuser. 1998. Garbage in, garbage out.. https://doi.org/10.1002/(sici)1097-0304(199804)43%3A4%3C402%3A%3Aaid-ccd8%3E3.0.co%3B2-c
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We evaluated the influences of minor edge dissections on late angiographic in-stent restenosis in 327 patients with 348 lesions (281 lesions without edge dissection and 67 lesions [19.3%] with edge dissection); the angiographic restenosis rate was 29.9% in the lesions with edge dissections versus 25.3% without edge dissections (p = 0.540). The minor non-flow-limiting dissections at the edge of stents may not be associated with the development of late angiographic in-stent restenosis.
In 1987, Glagov published a provocative hypothesis that the principal initial response to plaque accumulation was enlargement of the vessel as a whole (remodeling), which preserved luminal diameter until the lesion occupied a substantial proportion of the area within the elastic external membrane (EEM). This model has been confirmed and extended by intravascular ultrasound (IVUS) studies. Remodeling renders most atheromas invisible to angiography. In patients with single-vessel disease, the mean percent of EEM area occupied by atheroma at a segment with an angiographically normal appearance is 39%. IVUS studies further show that the disease progresses in a diffuse manner and that stenotic lesions represent only a small proportion of the total disease burden. We further know that disease can begin as early as the teenage years. Data suggest that up to 25% of individuals < 25 years old may be affected. Atherosclerotic lesions can be effectively targeted with lipid-lowering therapy. Preliminary data suggest that as plaques stabilize and become smaller, a reverse modeling occurs: the EEM area decreases but the lumen size remains unchanged. This may explain why significant reductions in cardiovascular events in clinical trials were accompanied by only modest angiographic evidence of regression. This hypothesis will be tested prospectively in the Reversal of Atherosclerosis with Lipitor (REVERSAL) study.
Atherosclerosis is often asymptomatic, unrecognized, and undertreated. Lumen irregularities are important angiographic findings that should be addressed aggressively through risk factor modification, medical therapy, and coronary revascularization. Both angiographic and clinical benefits have been demonstrated with lipid reduction therapy in randomized clinical trials. Coronary revascularization is indicated for symptom relief and improvement in quality of life in patients with acute coronary syndromes at "intermediate" and "high" risk of subsequent death or myocardial infarction. In patients following percutaneous coronary intervention (PCI), future cardiac events may be related to lumen renarrowing or to progression of atherosclerotic disease at sites remote from the site of coronary revascularization. The time course of restenosis is relatively self-limiting, generally occurring within 6-12 months after the procedure. Clinical events occurring > 1 year after PCI generally relate to new lesions or progression of existing atherosclerotic disease. Patients with diabetes mellitus may be at higher risk for late coronary events than nondiabetic patients. In post-coronary artery bypass surgery (CABG) patients, the majority of late events relate to degeneration of saphenous vein grafts. Lipid lowering therapy after coronary revascularization has been shown to prevent clinical events related to plaque instability and inhibit progression of saphenous vein graft disease. Thus, there are 2 goals in management of patients with symptomatic coronary artery disease: (1) to relieve the flow-limiting stenosis, and (2) to prevent future clinical events with aggressive lipid lowering and modification of other risk factors. Patients, specialists, and primary care physicians each need to take accountability for this risk-factor modification.