Intervention to proximal lesions should be avoided in graft-protected native coronary arteries in general, because there might be a risk for bypass-graft failure. An 81-year-old man with coronary artery bypass grafting surgery due to 3-vessel disease 17 years previously complained of worsening angina. Coronary angiography (CAG) revealed a diseased saphenous vein graft (SVG) and a probable functional occlusion in the mid left anterior descending coronary artery (LAD) concomitant with calcified severe stenosis in the left main (LM)-proximal LAD, and patent right internal thoracic artery (RITA)-LAD graft. After the first percutaneous coronary intervention (PCI) against the SVG lesion, we performed second PCI against the LM-proximal LAD lesions to release angina symptom and prevent LM occlusion. After rotational atherectomy (RA) with 1.5/1.75 mm burrs and balloon dilations, we detected a slight antegrade flow to distal LAD. To preclude possibility of graft failure in the RITA, we did not add further large-balloon dilations and stent implantations, and finally dilated with 3.0-mm drug-coated balloons (DCBs), leading to angina-free condition. Six-month follow-up CAG revealed no further vessel narrowing in both target vessels without RITA-graft failure. Stent-less PCI using relatively small-sized RA/DCB might be feasible for native proximal calcified lesions with patent bypass graft.
Learning objectives: •Full expansion of native proximal lesions should be avoided in internal thoracic artery (ITA) - protected coronary arteries in general, because it might provoke ITA-graft failure due to flow competition.•Stent-less modest dilation using relatively small-sized rotational atherectomy burr and drug-coated balloon might be a revascularization therapy of choice for native proximal calcified lesion with patent ITA bypass graft.
Keywords: Coronary artery bypass grafting; Drug-coated balloon; Internal thoracic artery; Rotational atherectomy; Stent-less percutaneous coronary intervention.
© 2024 Japanese College of Cardiology. Published by Elsevier Ltd.