Author + information
Patient initials or identifier number
Relevant clinical history and physical exam
Mr. HMS was a 65-year-old gentleman who presented with intermittent chest pain for 10 hours. His cardiovascular risk factors were Diabetes Mellitus and 20-pack years of cigarette smoking. BP 152/90 mmHg, pulse rate 72 bpm, SpO2 96% breathing room air and blood glucose 7.4 mmol/l. Cardiovascular examination was unremarkable. Chest auscultation revealed fine basal crackles bilaterally.
Relevant test results prior to catheterization
ECG showed ST segment elevation and pathological Q wave in leads V1-V4. Transthoracic echocardiography revealed moderately impaired LV systolic function, LVEF 40-45% with hypokinesia in the anterior, septal and apical walls. Troponin T level was markedly elevated. A diagnosis of acute anterior STEMI Killip class II was made. He received immediate fibrinolysis with IV Tenecteplase, but rescue PCI was performed later for persistent ST elevation and chest pain.
Relevant catheterization findings
Coronary angiogram was performed via right transfemoral approach:
1. Mild distal left main coronary artery (LMCA) disease. Tight ostial and proximal left anterior descending (LAD) artery stenosis of 80-90%. Intermediate mid LAD disease. TIMI 2 flow to distal LAD.
2. Dominant left circumflex (LCX) artery with intermediate-mid segment disease and 70-90% stenosis of the obtuse marginal (OM) branch.
3. The right coronary artery was recessive, small and diffusely diseased.
The LCA was engaged with 6Fr XB 3.5 guiding catheter. Runthrough NS Hypercoat wire (Terumo) was placed in LCX. PT2 moderate support wire (Boston Scientific) was advanced into distal LAD. Ostial and proximal LAD was predilated with GENOSS 2.5 x 10 mm balloon up to 12 atm. IVUS (Boston Scientific) of mid LAD to LMCA showed heavy plaque burden in proximal LAD with MLA of 3.3 mm2. Xience Prime DES (Abbott) 4.0 x 23 mm was deployed at proximal LAD-mid LMCA at 10 atm. Post-dilatation was performed with NC EUPHORA balloon (Medtronic) 4.0 x 8 mm up to 16 atm. Subsequent cine showed severely pinched ostium of LCX but perfusion remained TIMI 3. Run through wire recrossed into LCX. IVUS of LCX showed MLA of ostium LCX was <4 mm2.Ostial LCX lesion was predilated with the used GENOSS balloon 2.5 x 10mm up to 14 atm. Final kissing balloon inflation was performed (LCX-LM GENOSS 2.5 x 10 mm) & (LAD-LM NC EUPHORA 4.0 x 8 mm) at 10 atm. IVUS of LAD showed well-opposed stent edges with ostial LAD MLA about 6.4 mm2. Unfortunately, we did not have time to repeat IVUS of the LCX as the patient was becoming restless at this point of time but he remained hemodynamically stable. Final cine, showed TIMI 2 flow to distal LAD and TIMI 3 flow to distal LCX. There is about 20-30% residual ostial stenosis but we were happy to accept the final results.
Our initial plan was to proceed with provisional stenting of the proximal LAD up to the LMCA as the ostium/proximal LCX appeared relatively disease-free. However, PCI for an ostial LAD lesion is well known to be associated with plaque shift in LMCA or LCX, and it is not uncommon to end up with a 2-stent bifurcation PCI. Fractional Flow Reserve (FFR) in the non-infarct related LCX can be a useful asset in addition to IVUS in assessing the need for a complex LM bifurcation PCI. If the TIMI flow in LCX was compromised, we would have opted for a TAP bifurcation stenting strategy. Nonetheless, we were happy to have kept a potential complex procedure simple and the patient remains well until today.