Stent failure remains the major drawback to the use of coronary stents as a revascularization strategy.
It generates significant health care cost and is associated with an increased risk of death and rehospitalization.
Emphasis is placed on frequent use of intracoronary imaging and assessment of timing to determine the precise etiology because that information is crucial to guide selection of the best treatment option
SCAI recommends image-guided coronary stenting at the time of initial implantation to minimize the occurrence of stent failure.
When in-stent restenosis and stent thrombosis are encountered, imaging should be strongly considered to optimize the subsequent approach.
Coronary stenting has transformed revascularization strategy, producing excellent procedural and clinical outcomes in myriad clinical settings. Despite proven short and long-term benefits, in-stent restenosis (ISR) and stent thrombosis (ST) continue to be limitations. There remains no definitive management approach for either condition despite a greater understanding of the underlying mechanisms ensuing from advances in intracoronary imaging
ISR remains a common clinical problem despite numerous improvements in-stent design and polymer coatings over the past 2 decades
The incidence of ISR is 10%; 25% of ISR cases present with acute myocardial infarction (MI) with a 30-day mortality rate of 10% to 25%.1, 2, 3, 4
Recurrent ISR is not unusual in contemporary practice
The failure to appreciate and address the original mechanism of ISR underlies refractory cases of recurrence.
Recurrent ISR occurs in approximately 20% of all ISR cases
The 1-year MACE (43.1%) and target lesion revascularization (41.2%) rates were significantly higher in the ≥3 stent layer group than in the 1-stent-layer and 2-stent-layer groups.
A third layer of metal is almost always associated with underexpansion and should be avoided.
The primary biologic mechanism of ISR is neointimal tissue proliferation or hyperplasia, an exaggerated homeostatic healing response to arterial wall damage sustained during stent implantation
The distribution of neointimal tissue proliferation may be focal or diffuse along the length of the stent
Causative factors are local inflammation resulting from mechanical disruption of the intima/media leading to aggressive neointimal hyperplasia/proliferation that consists of smooth muscle cells and extracellular matrix. Hypersensitivity reactions to the metal and/or the polymer of early-generation DES are also recognized mechanisms of neointimal hyperplasia
Neoatherosclerosis is an increasingly recognized mechanism of stent failure seen with current generation DES. It is characterized by accumulation of lipid-laden foamy macrophages sometimes with necrotic core formation within stented segments
Injury to the vessel by balloon inflation and stent deployment stimulates neointima formation
Suboptimal minimal stent area (MSA) is a major predictor of stent failure, and an IVUS optimized MSA of >5.0 mm2 or OCT optimized MSA of >4.5 mm2 are optimal goals
Another useful criterion is to achieve a target MSA >90% of the closest proximal or distal reference segment.
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