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Case Study
Asymptomatic Presentation of a Totally Occluded Left Main Coronary Artery
January 2018
Angiographic findings of atherosclerotic disease and stenosis in the left main coronary artery are not uncommon in both symptomatic and relatively asymptomatic patients. However, the angiographic finding of a completely occluded left main coronary artery is relatively uncommon and most often not compatible with life.1,2 It is even more unusual to have no symptoms related to the complete obstruction of the left main coronary artery.
Case Report
A 56-year-old male presented to outpatient clinic complaining of right lower extremity claudication. He had a history of hypertension, hyperlipidemia, and diabetes mellitus type 2. His family history was significant in that his father had coronary artery disease with reported myocardial infarction. The patient had a long history of one pack per day tobacco abuse, which was ongoing.
A peripheral artery duplex was performed, revealing complete occlusion of the right superficial femoral artery (SFA), and was followed by a pre-op cardiovascular exam with a Lexiscan myocardial perfusion scan (MPS) using a rest thallium/stress technicium-99 protocol. The results of the MPS included non-diagnostic electrocardiogram (EKG) findings due to resting ST segment depression in inferior leads II, III, aVF, and precordial leads V4-V6, as well as ST segment elevation in leads I, aVL, and V1-2. Single-photon emission computed tomography (SPECT) images demonstrated a large perfusion abnormality of severe intensity in the apical myocardial walls on the stress images, as well as rest images consistent with previous myocardial infarction. A large anterolateral defect was present in the stress imaging that was reversible at rest, suggestive of ischemia. Left ventricular ejection fraction was 19%. An echocardiogram was performed, revealing mild mitral regurgitation, moderately dilated left ventricle with a reduced ejection fraction of 30-35%, and that the mid to apical posterior, septum, inferior and anterior segments of the left ventricle were akinetic.
The patient was scheduled for an elective diagnostic left heart catheterization that revealed a total occlusion of the left main coronary artery at the ostium (Figure 1). Angiography of the right coronary arteries revealed mild luminal irregularities of a large dominate artery that collateralized the entire left circumflex (LCx) and obtuse marginal artery (OM) network, as well as the left anterior descending artery (LAD) all the way to its proximal segment (Figure 2). The distal left main artery also appeared patent by retrograde collateral flow to the LAD/LCx/OM (Figure 3).
Following the diagnostic portion of the cardiac catheterization, management options, including percutaneous intervention, bypass surgery and medical management, were discussed with the patient and his family. The patient elected to be evaluated by cardiothoracic surgery for coronary artery bypass surgery.3,4 Viability assessment with cardiac MRI was performed, revealing transmural enhancement involving the mid and apical anterior wall, suggesting nonviable myocardium. Potentially viable non-transmural enhancement was seen in base and apex anterior and anterolateral and anteroseptal segments. The mid and apical anterior wall were akinetic and otherwise generalized hypokinesis was present. A dilated left ventricle was measured at 6 cm, with an end diastolic volume of 226 mL and a calculated ejection fraction of 17%. The patient was scheduled to follow up with cardiothoracic surgery and was discharged from the hospital with a LifeVest (ZOLL Medical).
The patient was evaluated by cardiothoracic surgery for coronary artery bypass surgery and was deemed too high-risk for surgical revascularization due to his poor cardiac function. There was also concern for proceeding with coronary artery bypass surgery due to the unclear benefit that it would provide the patient, based on his poor viability scan. The patient was referred to a quaternary hospital with ventricular assist device capabilities and to be evaluated for cardiac transplantation.
Discussion
Left main coronary artery stenosis to a varying degree is not an uncommon finding on coronary angiography in patients with known and unknown coronary artery disease. Several reports and studies have been published pertaining to clinical presentation and management of left main coronary artery stenosis, but very little is known about the clinical presentation or incidence of left main coronary artery occlusion. This is likely due to total occlusion of the left main coronary artery being incompatible with life. Total occlusion of the left main coronary artery is usually a highly symptomatic event or in many cases, a terminal event. The survival rate and clinical symptoms are likely correlated with the rate of occlusion and the degree of collateralization from the right coronary artery that can supply blood flow to the left coronary arteries when the left main coronary artery becomes totally occluded.
Conclusion
Our patient likely had a subacute presentation of a potentially deadly occlusion in his left main coronary artery that was atypically asymptomatic.
References
- Cohen MV, Gorlin R. Main left coronary artery disease. Clinical experience from 1964-1974. Circulation. 1975; 52(2): 275-285.
- Flugelman MY, Shalit M, Shefer A, Hasin Y, Gotsman MS. Survival after sudden obstruction of the left main coronary artery. Am J Cardiol. 1983; 51(5): 900-901.
- Lee MS, Kapoor N, Jamal F, Czer L, Aragon J, Forrester J, et al. Comparison of coronary artery bypass surgery with percutaneous coronary intervention with drug-eluting stents for unprotected left main coronary artery disease. J Am Coll Cardiol. 2006; 47(4):864-870.
- Palmerini T, Marzocchi A, Marrozzini C, Ortolani P, Saia F, Savini C, et al. Comparison between coronary angioplasty & coronary artery bypass surgery for the treatment of unprotected left main coronary artery stenosis (the Bologna Registry). Am J Cardiol. 2006; 98(1): 54-59.
Disclosure: The authors report no conflicts of interest regarding the content herein.
The authors can be contacted via Robert Tonks, MD, at rtonks@utmck.edu.