Case 1: A 49 yo, female with a history of hypertension and hyperthyroidism (on propranolol and thiamazole), presented with chest pain since 7-hours prior to admission. ECG: ST elevation at AVR.Case 2: A 45 yo female with known hypertension and type 2 DM, presented with a 5-hour history of burning chest pain prior to admission. ECG: ST elevation at AVR. 

Case 1: Vital signs: BP 120/80 mmHg, HR 100 bpm, RR 20/min, and SpO₂ 98% on room air. Labs: Blood glucose: 140 mg/dL; Serum creatinine: 0.64 mg/dL; hs-Troponin I: 67.6 µg/mL. Echo: EF: 58% ; TAPSE: 2.0 cm.Case 2: vital signs: BP was 155/104 mmHg, HR 91 bpm, RR 20/min, and SpO₂ 97% on room air. Lab: blood sugar of 199 mg/dL; serum creatinine 0.79 mg/dL; and elevated hs-Troponin I at 912.3 µg/mL. Echo: EF 41%, TAPSE 2.3 cm.

In both cases, coronary angiography revealed a critical lesion extending from the ostial LM artery to the proximal LAD artery. The LCx and RCA were angiographically normal. 
Cranial case 2.mp4
Spider Case 2.mp4
Spider Case 1.mp4

Case 1:  a case of a patient with chest pain and stable hemodynamics, with angiographic findings suggestive of critical stenosis from ostial LM to pLAD. IVUS of the LAD revealed a MLA of pLAD: 9.29 mm², osteal LAD: 5.06 mm², and LM: 5.43 mm² without clear evidence of fixed stenosis. Intracoronary nitrate administration led to significant improvement in symptoms and ECG changes. IVUS showed marked improvement: MLA of osteal LAD: 8.67 mm² and LM: 8.34 mm². No intervention was performed. The patient remained symptom-free and hemodynamically stable during follow-up. At one-month post-discharge, the patient was asymptomatic on calcium channel blockers and long-acting nitrates.  Case 2: A patient presented with chest pain and hemodynamic instability. Angiography via right femoral artery using a JL 3.5/6F guiding catheter revealed critical stenosis from the ostial LM to pLAD. The patient was hypotensive (systolic BP 60 mmHg) with ST-segment elevation in lead aVR. Intravenous norepinephrine was administered, leading to partial hemodynamic improvement, although chest pain persisted. PCI was performed with implantation of a DES 3.5/24 mm from the ostial LM to pLAD, overlapped with a 3.5/15 mm DES. POT was done using a 4.5/15 mm NC balloon inflated at 20 atm. Post-PCI IVUS confirmed good stent apposition and expansion, with no edge dissection. Final angiography showed TIMI 3 flow. The patient’s chest pain resolved and hemodynamics stabilized post-procedure.  
IVUS pre nitrat Case 1.mp4
IVUS post nitrat Case 1.mp4
IVUS case 2 post DES.mp4

LM coronary artery spasm can occur spontaneously due to endothelial dysfunction or be induced iatrogenically. It typically responds well to vasodilator therapy. The first case was successfully managed with intracoronary vasodilators (nitrates), without the need for stenting. The second case showed persistent spasm and symptoms despite intracoronary vasodilators. Therefore, PCI with DES implantation was performed. PCI can be a safe and effective treatment option in selected patients with refractory left main spasm. Careful assessment is essential to determine whether conservative or interventional management is appropriate for LM coronary artery spasm.