A 56-year-old man with a history of hyperlipidemia and gout was admitted with chest pain and diagnosed with non–ST-elevation myocardial infarction (NSTEMI), with a peak troponin level of 205 ng/L. Coronary angiography demonstrated acute thrombotic occlusion of the left circumflex artery (LCx) with left-to-left collaterals, chronic total occlusion (CTO) of the mid-left anterior descending artery (mLAD), and mild right coronary artery disease.
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Successful percutaneous coronary intervention (PCI) to the LCx was performed, with plans for a staged PCI to the LAD CTO.On readmission for staged PCI, repeat angiography showed a patent LCx stent. The mLAD CTO was long (>50 mm) with distal vessel supplied by left-to-left collaterals of reasonable size, and significant calcification was noted. The lesion carried a J-CTO score of 3, and there had been a previous failed attempt at recanalization.

The procedure was performed via right radial artery access using a 7 Fr EBU 3.5 guiding catheter. Initial antegrade wire escalation with a Gaia Next 2 wire failed to cross the occlusion, and parallel wiring with a GN3 over a Sasuke microcatheter entered the subintimal space. Intravascular ultrasound (IVUS) confirmed true lumen entry at the proximal cap, but subsequent advancement was subintimal, and further passage was prevented by heavy calcification.
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The strategy was switched to antegrade dissection re-entry using a knuckle wire technique with Gladius MG14, Fielder XTA, and Gladius EX, but the wires repeatedly tracked into septal and diagonal branches. During this process, contrast extravasation was noted. The patient remained hemodynamically stable without tachycardia, and echocardiography excluded pericardial effusion at that stage. Balloon tamponade was performed with a 2.0 mm semi-compliant balloon inflated in the proximal LAD for 10 minutes, which appeared to reduce extravasation. Protamine (30 mg) was administered to reverse heparin after removal of all devices.
 However, repeat angiography five minutes later showed worsening extravasation, coinciding with dyspnoea, tachycardia, and hypotension (80/50 mmHg). Echocardiography now revealed pericardial effusion with early right ventricular compression. Emergent pericardiocentesis was performed, yielding fresh blood, but extravasation persisted. Attempts at fat embolization were unsuccessful, and therefore a suture-based approach was employed. Five short segments of 2-0 Vicryl suture were delivered via a Finecross microcatheter near the proximal cap, effectively sealing the entry site and achieving hemostasis.
The patient’s hemodynamics stabilized post-procedure. Hemoglobin dropped by 1 g/dL but did not require transfusion. He remained clinically stable and was discharged after two days of monitoring.
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This case highlights that knuckle wire techniques are not invariably safe, underscoring the importance of careful attention to wire behavior and position during CTO PCI. Operators should be familiar with systematic algorithms for the management of wire-induced coronary perforation and cardiac tamponade. When conventional strategies fail, intracoronary suture embolization may serve as a feasible and effective bailout option for sealing coronary perforations.