An 81-year-old functionally independent woman with Type 2 Diabetes, Hypertension, and Atrial Fibrillation presented with central chest pain and shortness of breath. Diagnosed with acute anterolateral STEMI, Killip I, she underwent fibrinolysis at a district hospital and referred to our PCI center due to persistent symptoms. Upon examination, she was hemodynamically stable with BP 125/60 mmHg, HR 89 bpm, and SpO2 100% on room air. Cardiopulmonary examination was unremarkable.

High-sensitive Troponin I during admission: 1890.6 ng/LCreatinine 156 umol/L, eGFR27 mL/min/1.73 m²LDL Cholesterol 2.8 mmol/LHbA1c: 6.4 mmol/LEchocardiogram: Poor left ventricular ejection fraction of 30 - 35%, mildly dilated left atrium and ventricle; global mild hypokinesia, functional all valve with mild mitral regurgitation.Chest x-ray: Mild cardiomegalyECG on presentation: ST elevation anterolateral leads, Q waves anterior leads; post-fibrinolysis: >50% resolution of ST-elevation.

CAG revealed a normal LM, mild disease in the proximal LAD, and severe diffuse calcification, 99% stenosis in the mid-LAD, extending to the distal wrap-around LAD. The LCx was recessive with 80% stenosis in the mid LCx, and the dominant RCA showed 80% stenosis at the proximal PDA. SYNTAX score was 18, with a PCI SYNTAX II score of 63 (4-year mortality 68.4%) vs. CABG 41 (16.3%). After heart team and family discussions, PCI to LAD under IVUS guidance was chosen due to age and persistent symptoms.

Access & Guide: 6F Radial EBU 3.0
LAD wired with a workhorse wire. Due to the tight mLAD stenosis, lesion was prepared with  2.0 x 15 mm balloon at 6atm, followed by IVUS. IVUS showed severe 360° calcification from the mid to pLAD, with MLA of 2.88 mm² after pre-dilatation. The total calcified length was 26mm, with calcium score of 3.After weighing the risks of rotablation, IVL was chosen. A 3.0 x 12 mm C2+IVL balloon was used in a 1:1 ratio with the LAD. IVL was delivered to the mLAD (3atm for 10 pulses x 2 and 4atm for 10 pulses x 2) and to the pLAD (6atm for 10 pulses and 8atm for 10 pulses). While treating the pLAD near the diagonal branch, contrast "sipping" was noted in the SB, suspected to be micro-dissection or plaque fissuring without perforation (confirmed by IVUS and angiogram).With 60 pulses remaining, additional IVL pulses were delivered at 6atm to mLAD, causing sudden contrast extravasation, indicating Ellis Type III coronary perforation. IVL was halted, and the perforation was occluded with the IVL balloon immediately. As she developed severe chest pain, hypotension, and ST-elevation, we decided to deploy a 2.5 x 20 mm Papyrus covered stent and post-dilated with a 3.0mm NC balloon. The pLAD was treated with a 3.0 x 30 mm DCB for 60 seconds. Final IVUS confirmed good stent apposition and acceptable expansion, with TIMI III flow to all vessels. 
She was monitored in CCU, and repeat echo showed no effusion progression. She was discharged well after two days.

This case highlights the balance between resource utilization and procedural safety during IVL-guided PCI in heavily calcified lesions. While attempting to maximize the remaining IVL pulses in an elderly patient with symptomatic CAD, an Ellis Type III coronary perforation occurred. Rapid identification and deployment of a covered stent restored vessel integrity and stabilized the patient. This case emphasizes the importance of adherence to IVL protocols and prompt management of complications to achieve favorable outcomes, even in high-risk interventions.