[MO-52] Presentation Awards
A case of LMT-ACS with shock after EVT for right foot CLI
A 90-years-old man with diabetes mellitus, hypertension, and prior cerebral infarction admitted to our hospital due to right foot CLI (WIfI stage 3). CT revealed AAA, occlusion in right EIA, SFA, and ATA, and severe stenosis in left EIA. His symptom did not improve with intravenous alprostadil for a week, so we performed EVT by bidirectional femoral approach. After expanding left EIA with semi-compliant balloon, CTO of right EIA could pass with 0.035” Radifocus antegradely, and 8 x 80 mm of Smart stent was implanted retrogradely after GW externalization. Then, right SFA CTO could cross with 0.014” Halberd on body surface echo guidance, 6 x 80 mm of Smart stent was implanted. Finally, we performed Assurant 7 x 40 mm stenting to left EIA.
The patient became shock and hypoxia in the next morning. Electrocardiogram showed ST decline in I, II, aVF, V4-6 and ST elevation in aVR leads. Echocardiogram revealed decrease motion in the anteroseptal and inferior walls. NPPV management, volume overload, catecholamine could not maintain blood pressure, and junctional rhythm occurred. Emergent CAG showed 90% stenosis in distal LMT and proximal LAD, and total occlusion in proximal RCA. Under IABP support from right femoral artery, Pt-EES 3.0 x 20 mm stent was implanted LMT to LAD, and followed KBT. In the RCA, balloon expansion could only perform to RV branch, mid RCA was suggested CTO. Blood pressure increased after PCI, we could withdraw IABP after 2 days, catecholamine 4 days later.
Coronary artery disease often accompanies with the lower limb CLI. Our patient had LMT and RCA CTO disease, therefore, hypoxia due to iodine overload and increased myocardial demand for improved lower limb’s flow after EVT likely caused ACS and shock. Careful evaluation of coronary artery disease should be needed before EVT in the patients with CLI.
The patient became shock and hypoxia in the next morning. Electrocardiogram showed ST decline in I, II, aVF, V4-6 and ST elevation in aVR leads. Echocardiogram revealed decrease motion in the anteroseptal and inferior walls. NPPV management, volume overload, catecholamine could not maintain blood pressure, and junctional rhythm occurred. Emergent CAG showed 90% stenosis in distal LMT and proximal LAD, and total occlusion in proximal RCA. Under IABP support from right femoral artery, Pt-EES 3.0 x 20 mm stent was implanted LMT to LAD, and followed KBT. In the RCA, balloon expansion could only perform to RV branch, mid RCA was suggested CTO. Blood pressure increased after PCI, we could withdraw IABP after 2 days, catecholamine 4 days later.
Coronary artery disease often accompanies with the lower limb CLI. Our patient had LMT and RCA CTO disease, therefore, hypoxia due to iodine overload and increased myocardial demand for improved lower limb’s flow after EVT likely caused ACS and shock. Careful evaluation of coronary artery disease should be needed before EVT in the patients with CLI.