61 year old male with underlying dyslipidemia poor adherents to statin. He presents with chest pain on exertion and NYHA class II.He underwent CT coronaries that showed severe stenosis in the LAD with severe calcification.

Hbaic 5.4% LDL 1.4mmol/l

Coronary angiogram shows severe disease ostio-proximal LAD with severe calcification/calcium nodule , mild disease left circumflexsevere stenosis proximal and mid RCA -recessive


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Right Radial approach, Slender 6/7Fr , EBU 3.5 7FR changedto EBU 3.0 7FR Sion blue to LCX, Run-through floppy to LAD IVUS run to LAD Fibro calcified lesion ostial LAD - calcium arc 180 degrees with calcium nodule, ostial LAD 3.48mm2 , tightest proximal LAD 2.31mm2 distallumen size 3.0mm and proximal 3.5mm and ostial 4.0mm ostial LM MLA 10.8mm Used microcatheter fine cross to LAD , Exchange with balloon trapping withRotaWireRotablator 1.5burr introduced- 2 runs high speed 180kph and2 runs at 80kph IVUS done post Rotablator - tightest proximal LAD 2.31mm2 -->3.22mm2 , ostial LAD 3.48mm2 -->4.51mm2Predilate further NC 3.5x15mm up to 16atmStented Synergy monorail 3.0x32mm body LM to proximal LAD at11atm with guide plus 6FRpost dilated NC 3.5x12mm up to 20atm Guiding catheter slipped out and lost the system, tried to reengage but challenging thus decided to change to right femoral puncture to use EBU3.5/7fr ,post dilate LM-LAD NC 4.0/12mm 6atmOstial LCX pinched - decided for Kissing balloon inflation and DCB LCX ostiumpredilated Ostial LCX 2.75x15mm up to 8atmKissing inflation performed with NC emerge 3.5X15mm LAD, NC2.75x12mm in LCX 8atmDCB AGENT MONORAIL 2.75X15 MM 8atm 60seconds to ostial LCXlast POT with NC 4.0x12mm up to 16atm IVUS done stent well opposed, Ostial LAD MSA 8.25mm2Proximal MSA 5.64mm2TIMI III flow 



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In summary, this was a complex PCI for a severely fibro-calcified ostial and proximal LAD lesion with significant calcium arc and a calcium nodule confirmed on IVUS. Despite initial right radial access with a Slender 6/7 Fr system, guide support with EBU 3.5 and later EBU 3.0 remained suboptimal, ultimately necessitating conversion to a right femoral 7 Fr approach for adequate support. Overall, the case highlights the importance of adaptive access strategy, aggressive plaque modification, IVUS-guided optimization, and bifurcation management to achieve an excellent final physiological and angiographic result in a heavily calcified LM–LAD lesion.