A 74-year-old man with history of prior MI, type 2 DM, HTN, DLP, and CKD presented with dyspnea on exertion and orthopnea for 3 days. Previous CAG at the time of MI in 2020 showed severe RCA disease and borderline distal LM lesion with nodular calcification. PCI of RCA was performed and FFR of LM-LAD at that time was negative. Physical examination revealed fine crepitation in both lower lungs and cardiovascular exam showed regular pulse, normal s1s2, no murmur.

EKG revealed sinus rhythm with diffuse ST depressed in V4-6,I,II, and aVL and ST elevated in aVR. Echocardiogram showed concentric LVH with normal LVEF of 53% without regional wall motion abnormalities and no significant valvular heart disease. Laboratory showed hs-Trop T of 2,350 ng/L. The diagnosis was NSTE-ACS with heart failure.

CAG showed three-vessel disease with LM.LM : 90% stenosis at distal LMbifurcation (Medina 1,1,1) with nodular calcification.LAD : Calcified vessel with 90% stenosis atostial LAD followed by 70% stenosis at proximal to mid LAD, and 70% stenosis D2.LCx : 60-70% stenosis proximal LCx with CTO of distal LCx.RCA:  Patent RCA stents.

Right radial access was obtained with 7Fr sheath. LCA was engaged with EBU3.5, 7Fr catheter and Runthrough NS guidewire crossed LAD lesion in Finecross microcatheter. The IVUS catheter couldn’t pass through the mid LAD lesion. IVUS showed nodular calcification at distal LM and circumferential calcified plaque at proximal LAD. Given nodular calcification, we opted to perform rotational atherectomy at both LAD and LCx. Wire was exchanged to Rotawire Extra support. Rotational atherectomy was performed using Rota Burr 1.75 mm at 180,000 rpm for 2 rounds at proximal LAD. Proximal LCx was treated with Rota Burr 1.75 mm at 180,000 rpm for 4 rounds. IVUS post rotablation showed thinning of nodular calcification in the figure of 8 pattern but there was no evidence of calcium fracture. We then further treated the lesion with Wolverine cutting balloon 3.25 x 10 mm at both LM- ostial LAD and LM-ostial LCx. Repeated IVUS showed large luminal area with multiple calcium fractures and obliteration of LM nodular calcification.After lesion preparation, we performed PCI with Double Kissing Culotte technique using EES 3.5 x 32 mm at LM-LCx and EES 3.5 x 38 mm at LM-LAD. KBI was done with a 3.5 mm and 3.5 mm balloons. Final POT was done using a 4.5 mm NC balloon. Final angiogram showed excellent angiographic results. Final IVUS showed round shaped, and well apposed stents with great expansion. 

PCI of the LM lesion with nodular calcification is very challenging as it causes inadequate lesion preparation and a very high risk of stent underexpansion. In our case, optimal calcium modification was obtained using the combination of:- Rotablation of both LAD and LCx using proper Burr size of 1.75 mm.- The use of rotawire extrasupport to achieve optimal wire bias for ablation.- Further treatment of Wolverine cutting balloon to crack the calcium and gain additional luminal area.- IVUS guidance to confirm adequate lesion preparation and the presence of calcium fracture.- Double Kissing Culotte technique as the final stenting strategy.