While anomalous origin of coronary arteries (AOCA) could occur in the presence of atherosclerotic coronary disease, they may lead to angina pectoris, exercise-induced arrhythmia, acute myocardial infarction (MI) and sudden deaths in the absence of atherosclerotic coronary artery disease (1–3). However, the incidence of all AOCA is from 0.3 to 1.2%, the abnormality of right coronary arteries compromise 6–27% of the whole coronary abnormalities (1–3). A 58-year-old male patient without any previous cardiac complaint applied to the emergency unit due to chest pain radiating to the left upper extremity and back, which started 5 h before. In his medical history, no findings except for cigarette smoking existed. In his cardiovascular examination, tension arterial was 120/70 mm Hg, pulse was 88/min. In auscultation heart sounds were normal, and there was apical 1/6 systolic murmur. Other system examinations were normal. In electrocardiography, 2 mm ST elevation, Q-waves and Twave inversion at D2, D3 and VF derivations, existed. In his venous blood sample collected 6h after the initiation of the pain, CK was 402 u/l, CKMB: 84 u/l and troponin I: 27 ng/ml. Lipid panel was normal. The patient with continuous chest pain was admitted to the cathetery unit, assuming that he was acute inferior MI. In his coronary angiography, no lesion was detected on left anterior descending and circumflex arteries. No RCA localization was detected via standard Judkins CA catheter. Aortography was performed via pigtail catheter (Figure 1). The silhouette of right coronary artery (RCA) originating from left sinus Valsalva was detected. Total occlusion was seen on the proximal of the Six F Amplatz catheter and selective angiography of SKA (Figure 2a). By placing Amplatz guiding catheter (7F), the lesion was passed through via guide wire, and percutanous transluminal coronary angioplasty (3.0620 mm) and stenting (3.5623 mm) were performed for total occlusion and TIMI 3 flow was provided (Figure 2b). After the intervention patient was not expressing chest pain. Ejection fraction was about 40–45% in his echocardiography performed 24h after the intervention, and there was first degree mitral disability. During coronary angiography, RCAs originating from left sinus Valsalva are encountered at the rate of 0.05–0.1% (4). According to the path RCAs originating from left sinus Valsalva follow, there are mainly three subtypes: interatrial, retro-aortic and in front of pulmonary trunkus. Since arteries are exposed to pressure, their spasm, kinking and intramural
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