restenosis

Restenosis is the re-narrowing of a blood vessel after it has been treated to relieve a prior obstruction. It most commonly occurs after percutaneous coronary intervention (PCI) or peripheral vascular interventions, but can occur in any vascular bed. Restenosis is typically defined as a 50% or greater reduction in luminal diameter at the treated segment on follow-up imaging, or by the return of ischemic symptoms referable to the treated territory.

The principal mechanism is neointimal hyperplasia, in which smooth muscle cells proliferate and extracellular matrix accumulates in the intima in response to vascular injury from angioplasty or stent placement. Early restenosis (within months) is mainly due to neointimal hyperplasia. Late restenosis can involve progressive atherosclerosis, late stent malapposition, or remodeling of the vessel wall.

Incidence and risk factors vary by vessel and intervention. After balloon angioplasty alone, restenosis rates are relatively high; after bare-metal stents they decrease but remain a concern. Risk factors include diabetes mellitus, smoking, hypertension, dyslipidemia, obesity, renal disease, and inadequate control of risk factors, as well as procedural factors such as focal injury or stent length.

Clinical presentation depends on the affected bed and may include recurrent chest pain or angina, shortness of breath, or limb claudication. Diagnosis is made by follow-up angiography or noninvasive imaging that shows significant luminal narrowing; symptom recurrence also prompts evaluation.

Management focuses on risk-factor modification, antiplatelet therapy, and timely revascularization if symptoms or imaging show significant stenosis. Techniques to reduce restenosis include drug-eluting stents and drug-coated balloons; choice depends on clinical context and vessel involved. Preventive strategies emphasize optimal device selection and aggressive risk-factor management.