CTO of the Left Main Coronary Artery with Preserved Ejection Fraction

A 60-year-old postmenopausal woman presented with six months of exertional angina pectoris. Her only cardiovascular risk factor was hypertension; there was no history of smoking, diabetes, prior myocardial infarction, or dyslipidemia. Initial electrocardiography showed left ventricular hypertrophy and left axis deviation — findings consistent with longstanding pressure overload rather than acute ischemia.

Figure 1

12-Lead ECG at Initial Admission

Electrocardiogram demonstrating left ventricular hypertrophy and left axis deviation. The absence of acute ST changes or pathological Q waves belies the hemodynamic severity of the underlying lesion — a classic teaching point in LMCA chronic total occlusion, where collateral flow maintains resting perfusion.

Transthoracic echocardiography demonstrated a preserved ejection fraction of 58.3% with stage 1 diastolic dysfunction and LV hypertrophy. No valvular abnormalities were identified. Troponin was negative, and lipid panel showed LDL-C 89 mg/dL within a near-normal range. This deceptively benign laboratory profile underscored the diagnostic challenge: preserved systolic function, negative biomarkers, and mild symptoms despite a catastrophic anatomic lesion.

Figure 2

Transthoracic Echocardiogram — Preserved LV Systolic Function

Parasternal long-axis view confirming normal left ventricular cavity size and preserved systolic function (EF 58.3%). Maintained function in the setting of LMCA CTO reflects the extraordinary capacity of Rentrop grade 3 collaterals to sustain resting myocardial perfusion.

Multidetector coronary CT (MDCT) raised concern for severe stenosis in both the left main and right coronary artery, prompting diagnostic angiography. Using a transradial approach with a 6F sheath, selective cannulation of the LMCA with a Judkins left catheter immediately revealed 100% occlusion. Subsequent RCA cannulation demonstrated critical proximal stenosis, yet filling of the entire left system was visible through Rentrop grade 3 collaterals connecting the RCA to the LAD and circumflex territories — filling the left system retrogradely all the way to the LMCA ostium.

Figure 3

Multidetector Coronary CT (MDCT) — Pre-Angiography Imaging

Coronary CTA panels A and B demonstrating the occluded left main and concurrent right coronary artery disease. MDCT served as a non-invasive bridge to catheterization, confirming multivessel involvement before the patient committed to an invasive procedure.

Figure 4

Coronary Angiography — LMCA CTO and RCA-to-Left System Collaterals

Panel A: Selective LMCA injection confirming 100% chronic total occlusion. Panels B–D (LAO and RAO cranial/caudal projections): The right coronary artery, despite its own proximal stenosis, supplying the entire left coronary territory through grade 3 collateral circulation. This retrograde filling pattern is the anatomic explanation for the preserved ejection fraction and absence of resting symptoms. LAO = left anterior oblique; RAO = right anterior oblique; CAU = caudal; CRA = cranial.

The patient remained hemodynamically stable throughout catheterization with no angina on the table. A multidisciplinary cardiology and cardiovascular surgery council recommended CABG over PCI given her age, SYNTAX score, and the absence of a protected left system. She underwent uncomplicated bypass grafting and was discharged on aspirin, clopidogrel, metoprolol, atorvastatin, and an ACE inhibitor/indapamide combination.

Discussion

LMCA chronic total occlusion represents one of the most dramatic examples of how the coronary collateral network can mask catastrophic anatomy. With a true prevalence estimated at only 0.04% — and likely underreported because it frequently causes out-of-hospital sudden death before angiography is performed — LMCA CTO survives to clinical presentation only when the RCA is dominant, large, and capable of sustaining Rentrop grade 3 retrograde supply. This patient's case confirms a counterintuitive principle: the slower the atherosclerotic process, the more time the body has to recruit collateral vessels, and the less the clinical presentation correlates with the anatomic severity. Age-related and prolonged plaque evolution, rather than acute rupture, permitted the gradual maturation of this robust collateral network.

The management decision between CABG and PCI in LMCA CTO requires individualised assessment. CABG remains the guideline-preferred revascularisation strategy, but technical innovations in PCI hardware have made percutaneous approaches feasible in carefully selected patients — particularly those with prior bypass grafts protecting the left system, or when a strong collateral network limits ischemic risk during wire manipulation. The absence of a protected left system and the patient's relatively young age pushed the decision firmly toward surgery here. For clinicians, the take-home lesson is that chronic stable angina should never be considered low-risk by default: the differential must include LMCA disease, especially when symptoms persist despite minimal atherosclerotic risk factors and when collateral circulation is well-developed on non-invasive imaging.