LAUSR

An asymptomatic 53-year-old male was referred to our hospital to undergo long-term follow-up coronary computed tomography (CT). Approximately 6.5 and 6 years before, based on the diagnosis of silent myocardial ischemia due to probable sequelae of Kawasaki disease (KD), we had performed stent-less percutaneous coronary intervention (PCI) using rotational atherectomy (RA)/conventional balloon and that using RA/drug-coated balloon (DCB) against a de novo lesion and a restenotic lesion, respectively, at the inlet of the aneurysm in the proximal left anterior descending coronary artery (LAD) under optical frequency domain imaging (OFDI) [1, 2]. Although he had no definite history of KD and had been kept free of chest symptom throughout his clinical course, he had experienced 40-day admission due to fever of unknown origin with eruption at the age of 6 months. Coronary CT suggested stenoses at the inlet/outlet of the eggshell-like calcified aneurysm in the proximal LAD (Suppl Fig. 1A). Coronary angiography (CAG) showed an intermediate narrowing from the takeoff to the inlet of the aneurysm (Suppl Fig. 1B, 1C). Subsequent instantaneous wave-free ratio (iFR) and fractional flow reserve measurement at the distal LAD revealed 0.87 (iFR drop of 0.02 at the outlet of the aneurysm; iFR drop of 0.05 between the LAD ostium and the inlet of the aneurysm) and 0.72, respectively (Suppl Fig. 1D). Based on the iFR map, we therefore planned to perform PCI against the proximal LAD lesion from the takeoff to the inlet of the aneurysm. Preprocedural OFDI depicted a high-backscattering protruding mass with signal attenuation and irregular surface connecting with proximal calcified plate, indicating progression of calcified nodule in the nearly ostial segment proximal to the inlet of the aneurysm (Fig. 1A2, A3, B2, B3, C2, C3). The inlet of the aneurysm itself, the target lesion in the previous PCI (Fig. 1D2, D3), as well as the surrounding-calcified aneurysm (Suppl Fig. 1K1, 1L1) including the outlet (Suppl Fig. 1M1) showed no apparent progression on the OFDI. As planned, we performed RA with 2.0/2.25-mm burrs (Suppl Fig. 1E), inflated a 3.25/10-mm cutting balloon, and finally dilated with a 3.5/15-mm DCB (Suppl Fig. 1F) under guidance of OFDI. Final OFDI depicted a lumen enlargement and a relatively smooth luminal border without malignant dissections (Fig. 1C4, D4). Final CAG showed an acceptable result without flow delay (Suppl Fig. 1G). Calcified nodule, one of etiology of acute coronary syndrome, is pathologically composed of multiple calcium fragments with thrombus disrupting the overlying fibrous cap and protruding into the vessel lumen [3]. Even in the new-generation drug-eluting stent (DES) era, the lesions with calcified nodule still remain therapeutic challenge for interventional cardiologists. Simple stenting for calcified nodule tends to result in stent under-expansion, stent recoil, and a tissue protrusion inside the stent, leading to refractory in-stent restenosis, stent thrombosis, and repeat PCI [4]. Thus, it might be appropriate to debulk calcified nodules as much as possible before DES/DCB treatments, irrespective of stent-based or stent-less strategy. Coronary sequelae of KD has a variety of morphological manifestations, such as aneurysm, stenosis, and total occlusion concomitant with post-inflammatory intimal thickening, frequent calcification, organized thrombus, and early atherosclerosis [5]. This is