Coronary artery restenosis

Principal cause of restenosis after coronary artery stenting is neointimal hyperplasia resulting from the proliferation and migration of smooth-muscle cells and extracellular matrix production.

In-stent restenosis treated with balloon angioplasty, atherectomy, repeat stenting provide a high rate of technical success and low rate of ischemic events but 30-60% of patients require another vessel revascularization in subsequent months.

Hyperplasia reaches its maximum peaks at 6 months after stenting.

Clinical manifestations of in-stent restenosis can occur as long associated 9 months or longer after stent placement.

Clinical manifestations of in-stent restenosis varies from asymptomatic angiographic findings to acute myocardial infarction/angina and complete arterial occlusion.

Polymer based sirolimus-eluting stents reduce the risk of restenosis.

Sirolimus stents reduce angiographic evidence for restenosis and rate of event-free survival in patients at low risk for restenosis and for patients with small coronary arteries.

May be as high as 50% in small coronary arteries suggesting an inverse relationship between vessel size and restenosis.

Neointima proliferation has the major role in restenosis of native coronary blood vessels, while saphenous vein grafts thrombus formation, cellular hyperplasia and progression of atherosclerotic process all play a role depending upon the time interval from the index procedure to the time of examination.

In patients undergoing PCI for de novo saphenous vein graft lesions, drug eluting stents are the pref2242ed treatment with reduced risk of adverse events compared with bare metal stents (Mehilli J et al).

Dual platelet therapy reduces cardiovascular events after PCI by 80%.

Stent thrombosis occurs in 0.5-4% of patients with PCI within the first year.

Majority of stent thromboses after PCI occur in the first month and is ref2242ed to as early stent thrombosis.

Early stent thrombosis has a mortality rate of up to 40%, and up to 80% of survivors have a large myocardial infarction.

Stent thrombosis associated with death in 1 in 5 cases with more than 2/3 of cases associated with clinically significant myocardial infarction.

Premature discontinuance of antiplatelet drugs is a significant independent predictor of stent thrombosis.

Int2242uption of dual antiplatelet therapy is the most important risk factor in early stent thrombosis.

PCI of diffuse long coronary artery lesions is difficult because of the prevalence of in-stent restenosis and stent thrombosis which remains high compared to short length coronary lesions.

Meta-analyses show that intravascular ultrasound is useful for providing information on pre-intervention lesion characteristics, including plaques, lesion severity, lesion length, and lesion morphology.

Intravenous ultrasound guided drug-eluting stent implantation is associated with significant reduction in cardiac events, stent thrombosis, and target lesion revascularization.

Among individuals that require a long coronary stent implantation, the use of intravenous ultrasound-guided drug eluding stent implantation compared with angiography-guided stent implantation, resulted in lower rate of composite major adverse cardiac events at one year, due to low risk due to low risk of target lesion revascularization(IVUS-XPL Investigators).

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