We report an 62-year-old gentleman with history of hypertension, diabetes mellitus, dyslipidemia and history of PTCA to LAD and RCA with DES in 1997. He underwent a computed tomography coronary angiography (CTCA) examination for stable angina which revealed severe in stent restenosis with multiple calcified plaques. Guideline directed medical therapies were optimized. After family conference for mode of revascularization, committed to high-risk percutaneous coronary intervention (PCI) approach.

EchocardiogramMildly dilated LA, LVEF 33%, hypokinesia over basal to mid anterior, anteroseptum and inferoseptal wall Akinesia over apical anterior and septal and apical region with mildly calcified MV and trileaflet AVMild MR. Trivial AR. No AS. RVSP 22mmHgMild TR and no pericardial effusion

LMS: Calcified. Minor disease.LAD: In-stent restenosis (ISR) with calcification. o-pLAD total occlusion with antegrade supply to diagonal branches, also receiving collaterals from right systemLCX: Calcified. Critical stenosis (80%) over proximal high OM 1, mLCX critical stenosis (90%), ostial OM2 critical stenosis (90%)RCA: Dominant. pRCA stent 40% ISR, dRCA severe stenosis up to 80%, ostial PDA critical stenosis 70%

Contralateral injection approach PCI. Difficulty in wiring occluded LAD segment with Fielder XT-A and Gaia Next 2^nd despite with Corsair Pro XS support. Wiring of LAD was successful after escalation to Gaia Next 3^rd. After failed attempts to deliver microcatheter, 0.9mm excimer coronary laser atherectomy (ELCA) was performed for 12 cycles (60/80, blood medium) followed by predilatation with Sapphire 3 0.85/10 and Sapphire 1.5/10. Delivery of the microcatheter over the lesion was then successful. Gaia Next 3^rd wire then exchanged to NS Runthrough. Predilatation of the lesion with NC Sapphire 2.0/15 and NC Trek 2.5/15, however noted balloon severe underexpansion. Optical Coherent Tomography (OCT) performed with Dragonfly Opstar showed severely calcified neoatherosclerosis. Four runs of 1.5mm burr rotational atherectomy was then performed at 180,000rpm, followed by another three runs of 1.75mm burr rotablation at 180,000rpm. We then deployed DES Xcience Skypoint 2.5/38 to m-dLAD and another DES 3.5/28 Xcience Skypoint to the LM-pLAD region due to dissection flap evident in OCT. Lesion segment between DES was subsequently prepared with intravascular lithotripsy (IVL) 3.0/12 for 80 shocks and NC Pantera Leo 3.0/15 before deploying Xcience Skypoint 3.0/15. DES optimization was then performed under OCT guidance. Finally, DCB 3.0/20 Sequent Please Neo DCB was deployed to mLAD ISR for 60 seconds. Staged PCI to RCA was performed with IVL followed by DES deployment under imaging guidance. 

Despite recent breakthroughs in treatment, ISR remains the most common cause of stent failure, accounting for 5–10% of all PCI procedures in contemporary clinical practice with increasing volume and procedure complexity. In addition to identifying mechanical factors that predispose to ISR, intracoronary imaging; OCT in particular provides unique insights into the tissue (ISR substrate) inside the stent to predict response to different therapeutic approaches. For ISR in the setting of calcification and stent underexpansion, multiple calcium modification techniques may be required to modify calcium and facilitate stent expansion.