A 60-year-old man with poorly controlled hypertension and a history of cigarette smoking suffered a witnessed out-of-hospital cardiac arrest. The initial rhythm was ventricular fibrillation requiring CPR and multiple defibrillations, with ROSC after ~40 minutes. On arrival, he was intubated and in cardiogenic shock with pulmonary edema. He was stabilized with VA-ECMO, IABP, and mechanical ventilation before coronary angiography.

ECG showed sinus rhythm with ST-segment elevation in V1–V3 and aVL, consistent with anterior STEMI. Brain CT excluded intracranial hemorrhage. Chest CT ruled out aortic pathology but revealed diffuse ground-glass opacities suggesting pulmonary edema. Echocardiography showed severe LV dysfunction with EF 18% and diffuse hypokinesis. Cardiac enzymes were markedly elevated.

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The left main was patent. The LCX had a diffuse long lesion with up to 95% stenosis. The LAD showed a proximal CTO with a blunt stump and well-developed collaterals supplying the distal vessel, giving TIMI 2 flow. The RCA demonstrated TIMI 1 flow with distal critical stenosis, haziness suggesting thrombus, and poor collaterals, identifying it as the culprit for ST elevation and shock.
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Inrefractory VT/VF arrest and cardiogenic shock, emergent culprit RCA PCI wasperformed under VA-ECMO and IABP. A Conquest Pro 12 GW crossed the distal RCACTO after failed attempts with Fielder FC and Gaia 2nd. Sequential POBA wasdone, followed by three BMS from RCA-M to RCA-PL, achieving TIMI 3 flow. Abrief attempt to wire LAD-P CTO with a Fielder XT-R failed, suggesting achronic occlusion, and the procedure was stopped due to instability.Afterneurological recovery, staged LAD CTO PCI was performed. Angiography confirmedLAD-P CTO with a blunt stump, severe LCX disease, and patent RCA stents.Antegrade wiring was initiated with an XB 3.5/7Fr GC. A Gaia 2nd entered aseptal branch using a Trek 1.2×6 mm OTW BC. With APT 1.9Fr and Sasuke MCs,multiple GWs (XT-A, UB3, Conquest Pro 12) attempted proximal cap penetrationbut tracked into false lumens. IVUS from septal and D1 branches was used forcap clarification but remained inconclusive.Usingan IVUS-guided parallel-wire approach, a Progress 200T achieved true–false–truecrossing into distal LAD. Sequential 1.0–2.5 mm BC dilatation prepared thevessel. Given a Medina 1,1,1 LAD–D1 bifurcation, a DK-Crush technique waschosen. A Synergy 2.5×48 mm DES was deployed from LAD-M to LAD-D, crushed,rewired, and optimized. A second 2.5×48 mm DES was placed from LAD-P to D1,followed by kissing balloons and final POT. Final angiography showed TIMI 3flow with good expansion.

Earlyrecognition of the true culprit vessel in cardiogenic shock enabled timely RCArevascularization and hemodynamic stabilization. Staged LAD CTO PCI wassubsequently performed using an image-assisted strategy, incorporating IVUSinterrogation from both septal and diagonal branches to clarify the complexproximal cap and employing an IVUS-guided parallel-wire technique to achievetrue-lumen crossing. These imaging-directed decisions, combined with meticulousbifurcation optimization, were essential to achieving complete and saferevascularization in this extreme-risk clinical scenario.