Title
Coronary Artery Aneurysm in a Young Adult Presenting with Acute Coronary Syndrome and Cardiac Tamponade
Introduction
Coronary artery ectasia (CAE) is thought to occur in 1.2-8% of the population. The most common cause is atherosclerosis. However, about 17% of cases present as a sequala to Kawasaki Disease (KD) in childhood. Here we present a case of a young female who initially presented with cardiac tamponade and myocardial infarction (MI).
Clinical Case
A 31-year-old female with a past medical history of hypertension, not receiving any medications, presented following a syncopal episode. Patient reported chest pressure four days prior to presentation. She had blood pressure of 60/40 and heart rate of 121. The patient was found to have an inferolateral MI and acute heart failure secondary to cardiac tamponade. She underwent a pericardiocentesis which improved her symptoms and corrected her vitals. Given the concern for an MI, the patient underwent a left heart catheterization (LHC) which demonstrated aneurysmal dilatation of the left main coronary artery (LMCA) and proximal left circumflex artery (LCx) with no atherosclerotic stenosis. There was evidence of aneurysmal changes of the LCx just proximal to the origin of the second marginal branch. There was small amount of contrast extravasation into the aneurysm which is otherwise primarily thrombosed with evidence of peripheral calcifications. There was no evidence of obstructive coronary disease. In order to better visualize the aneurysmal changes seen on LHC, a CTA of the coronary arteries was obtained which revealed aneurysmal LMCA and proximal to mid left LCx. There was a large thrombosed calcified aneurysm originating from the mid left LCx with minimal contrast flow into the periphery of the aneurysm. The patient was ultimately discharged on dual antiplatelet therapy (DAPT) with plans for an outpatient cardiac MRI and follow-up with cardiovascular surgery for a possible repair of the aneurysms.
Discussion
The patient’s pericardial effusion was thought to originate from the large LMCA and LCx aneurysms given the extravasation of the contrast on LHC. The etiology of her LCx-territory infarct is thought to be secondary to embolization from the thrombus found in the LMCA and LCx artery aneurysms. The patient’s aneurysms may be related to an undiagnosed KD in the past. Although less likely, it may have represented congenital coronary aneurysm. Different adverse cardiac events including ACS have been described in association with KD-related CAEs in the literature. KD-associated CAEs differ from atherosclerosis-associated CAEs; they develop through an inflammatory mechanism, are usually single, non-elongated, non-tortuous, do not accelerate arterial stiffness over time, and are often identified in young populations. When a young adult presents with ACS or pericardial effusions, one should have a high-index of suspicion for KD as an antecedent diagnosis as this may affect management. Patients with atherosclerotic CAE may be treated with DAPT or therapeutic anticoagulation. As for KD-related CAE, CABG is preferred to PCI in KD patients with multivessel involvement or involvement of the LAD, whereas PCI is preferred in single-vessel or focal multivessel disease. Cardiac transplantation is considered if PCI or CABG is not feasible.