Excerpt

A 78-year-old man was admitted with sudden onset chest pain presenting as ST-segment elevation myocardial infarction. He had insulin-treated diabetes and underwent hemodialysis for 2 years because of end-stage diabetic nephropathy. Five months previously, he was treated for effort angina. Everolimus-eluting coronary stents were implanted following scoring-balloon dilatation with excellent expansion under intravascular ultrasound (IVUS) guidance for diffuse stenosis with calcified nodules (CN) and platy calcification in the proximal right coronary artery (Fig. 1A, B). He took prasugrel and aspirin regularly. The emergent coronary angiogram showed a thrombus originating from a large filling defect in the proximal in-stent segment with TIMI flow grade 1. Neither stent deformity nor fracture was seen under fluoroscopy. IVUS showed a convex surface with protruding lumpy, superficial calcification accompanied by acoustic shadow, indicating CN. A floating thrombus originated from the proximal segment (Fig. 1C). After aspirating the thrombus, 1.5-mm balloon dilatation restored the coronary flow. The optical coherence tomography scan showed large protruding high-backscattering lesions with signal attenuation characterized by CN. Neither malapposed nor uncovered stent struts were detected  (Fig. 1D). Finally, 4.0-mm scoring-balloon dilatation provided acceptable expansion of the lumen area. The CN treated with new-generation drug-eluting stents (DESs) recurred in the in-stent lumen and caused stent thrombosis. The protruding CN in the stented lumen from underlying previously stented calcified plaque led to stent thrombosis [1]. A stent for CN in patient on hemodialysis barely expands, and implanted stent struts are covered with minimal neointima [2]. The incidence of coronary stent thrombosis has dramatically decreased in the new-generation DES with dual antiplatelet therapy (DAPT) era. Mechanisms of stent thrombosis have been clarified and solved to avoid early discontinuation of DAPT, stent underexpansion, uncovered struts, malapposition, late positive remodeling, and neoatherosclerosis. Although the mechanism of in-stent CN is unclear, implantation of DES for CN may exaggerate the progression of protruding CN as the cause of stent thrombosis, especially in patients on dialysis.

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