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(a) De novo lesion in LCx (arrow). (b) Successful PCI to LCx lesion-Flow in LAD (arrow) to be noted. (c) Patent LCx prior to OPCAB with flow limiting lesion in LAD (arrow) 12 years back.
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CAG done revealed de novo culprit lesion in proximal circumflex territory (LCx) which was treated by percutaneous coronary intervention (PCI) with drug eluting stent (DES), with resolution of symptoms (Fig. 1(a)-(c)).
(a) RCA disease prior to OPCAB. (b) Patent RSVG graft with progression to CTO of RCA lesions.
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RSVG to PDA was patent with progression of the lesions in RCA to chronic total occlusion (CTO) (Fig. 2(a) and (b)).
Stringed LIMA (arrow).
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LIMA angiography revealed stringing of the arterial graft (Fig. 3).
(a) Critically diseased proximal LAD prior to OPCAB (arrow). (b) Plaque regression in LAD (arrow) with increased flow in the septal arteries. (c) CTCA demonstrating free flowing LIMA graft with no stringing at 9 years follow-up (arrow).
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Interestingly, a regression of the original lesion in the proximal LAD was noted with re-establishment of an unobstructed antegrade flow (TIMI 3) in the artery which explained the competitive flow related stringing of LIMA graft (Fig. 4(a) and (b)). This observation was further corroborated by a computed tomography coronary angiography (CTCA) performed 9 years after the surgery prior to an inguinal hernia repair demonstrating a patent and free flowing LIMA-LAD graft (Fig. 4(c)).