In-stent restenosis: Neointimal priliferation or neoatherosclerosis

In-stent restenosis, according to the time of occurrence presents itself as: earlywithin 24 hours; subacutewithin the first month; latewithin the first year; and very lateafter the first year. A 72yearold female patient, D.Đ., was referred for rescue PCI (Percutaneous Coronary Intervention) after fibrinolysis for anteriorwall STEMI. Coronary angiography showed subocclusive lesions in the Cx (Circumflex artery) and LAD (Left Anterior Descendent), as well as a significant lesion in the RCA (Right Coronary Artery). A Synergy 3×16 stent at 12 atm was placed in the Cx, and a Synergy 3.5×16 stent at 10 atm in the LAD. After six months, she was re-hospitalized for anterior-wall NSTEMI (Non-ST Elevation Myocardial Infarction). Coronary angiography revealed in-stent restenosis in the Cx and LAD, which were treated with post-dilatation using an NC Mozec 3.5×18 balloon. Four months later, recurrent chest pain occurred. Coronary angiography showed subocclusive restenosis in the Cx. IVUS (Intravascular Ultrasound) demonstrated the presence of calcium behind the stent and neointimal proliferation within the stent. IVL (Intravascular Lithotripsy) was performed with a 3.5×15 balloon for 4 cycles. A DEB (Drug-Eluting Balloon) Elutax 3.5×20 was applied to the stent and proximal Cx for 55 seconds. After eight months, another coronary angiography was performed due to reoccurring chest pain and a subsequent positive exercise stress test. Coronary angiography again showed a subocclusive lesion in the Cx stent, managed with a 3.5×16 NC balloon. Due to recurrent in-stent restenosis despite successful calcium removal with IVL and the presence of neointimal proliferation seen on IVUS, colchicine 0.5 mg daily was added for one year. After one year, control coronary angiography again revealed in-stent restenosis in the Cx. Repeat IVUS this time demonstrated a small thrombus and areas of neoatherosclerosis as the mechanism of restenosis. Due to the neoatherosclerotic changes, the in-stent stenosis was treated with repeated IVL using a 3.5×15 balloon for all 12 cycles, and implantation of a new Synsiro 3.5×15 stent. In-stent restenosis, based on the timing of presentation, may be acute, subacute, late, or very late. Mechanisms of in-stent restenosis, according to the time of onset, may include thrombosis, neointimal proliferation, and neoatherosclerosis. Regardless of timing, therapeutic approaches include balloon dilatation, application of a DEB, or implantation of a DES. Only in cases of proven neointimal proliferation additional oral therapy with colhicine, methotrexate or sirolimus should be considered, or parenteral administration of paclitaxel.