Anomalous Origin of the Right coronary artery from the Left
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A 70-year-old woman presented at the emergency department (ED) with a complaint of exertional dyspnea and a stabbing retrosternal pain radiating between her shoulders, both bothering her intermittently over the past three hours. The patient was overweight, and her medical history included arterial hypertension and hypothyroidism both controlled with medication. The 12-lead ECG revealed a normal sinus rhythm with ST-segment depression of 1mm at the anterior and lateral leads. High sensitivity troponin-I (hs-cTnI) was measured before admission to the coronary care unit (CCU) at 83.2 ng/L, confirming the diagnosis of non-ST elevation myocardial infarction (NSTEMI). The rest of the blood and biochemical panel was within normal limits, including a negative D-dimer assay. Chest X-ray revealed a marginally increased cardiothoracic ratio, and transthoracic echocardiography (TTE) revealed mild concentric left ventricular (LV) wall hypertrophy with a normal left ventricular ejection fraction (LVEF) and no wall motion abnormalities. Before the initiation of antiplatelets and due to the clinical description of the patient's complaint, a computed tomography (CT) angiography of the aorta was performed in order to rule out an acute aortic syndrome. No signs of aortic pathology were detected, but the CT revealed an anomalous origin of the right coronary artery from the left coronary sinus.

The ectopic right coronary artery followed an interarterial course between the trunk of the pulmonary artery and the aorta. It should be noted that the CT scanner used was not technically capable of performing a CT coronary angiography (CTCA) but adequately visualized the anomaly. The patient remained hemodynamically stable during her stay, her symptoms gradually improved, and hs-cTnI was normalized. The patient was referred to a tertiary hospital for coronary angiography which confirmed the anomalous origin of the right coronary artery and did not reveal any atherosclerotic coronary lesions. A CTCA was also performed, after the classical coronary angiography, to accurately visualize the anatomy of the CAA. The CTCA unveiled an eccentric noncalcified plaque at the middle segment of the LAD branch of the LCA, causing luminal stenosis of 25-49%, which we speculate is the culprit lesion of the patient's NSTEMI, probably involving a mechanism of plaque rupture and subsequent fibrinolysis or coronary artery spasm. Finally, a dobutamine stress echocardiography study was negative for segmental wall motion abnormalities. In this case, the CAA was an incidental finding on the initial CT aortic angiography. It is probably a benign finding since the observed ischemic changes of the ECG were not compatible with the supply distribution of the right coronary artery, and the stress echo study was unremarkable.