A 48-year-old male presented at our hospital with typical chest pain. His past medical history was unremarkable. His coronary risk factors only included "current smoker". On physical examination, he had a systolic blood pressure of 120 mmHg and a heart rate of 62 beats per minute. An initial electrocardiogram (ECG) showed no definite ST segment change and sinus rhythm (). Initial creatine kinase-MB and cardiac troponin I levels were in the normal range. Transthoracic echocardiography showed no regional wall motion abnormality and normal left ventricular function. We administered aspirin 300 mg for 1 day. CAG revealed a filling defect of the distal left anterior descending artery (dLAD), distal left circumflex artery (dLCX) and LMA (). We decided to aspirate the LMA thrombus and to do PCI at the dLAD and dLCX. A guiding catheter was positioned in the left coronary artery ostium. At that time, he complained of aggravating chest pain. On CAG, the distal region of the 1st diagonal branch (D1) and the obtuse marginal branch (OM) were not visualized (). We thought that this event had developed due to coronary embolization that resulted from the migration of thrombi into the LMA during CAG. Intravascular ultrasonography showed the LMA thrombus (). We tried to aspirate the thrombus in the LMA using a guiding catheter and to do balloon angioplasty in the dLAD and dLCX. Balloon angioplasty was successful only for D1 (). However, the dLAD, dLCX and OM had Thrombolysis In Myocardial Infarction (TIMI) grade 1 flow in spite of repeated balloon angioplasty. Applied platelet glycoprotein IIb/IIIa receptor antagonist (Abcimixab, Reopro®) and balloon angioplasty of the dLAD, OM and dLCX were done sequentially. However, filling defects in the dLAD, OM and dLCX remained ().\nWe cared for the patient in the cardiovascular care unit. Creatine kinase-MB and cardiac troponin I levels were elevated to 349.4 ng/mL and 40.91 ng/mL, respectively. Follow up ECG showed a 3 mm ST segment elevation at leads II, III, aVF and V3-5 after angiography (). We thought that the AMI developed due to distal embolization of the LMA thrombus during angiography. Laboratory profiles associated with hypercoaguability such as lupus anticoagulant, protein C activity 102% (NL 70-130%), protein S activity 74% (NL 73.7-146.3%), D-dimer 0.36 µg/mL (NL 0.0-0.4 µg/mL), antithrombin III 91% (NL 80-120%) and homocysteine 12.2 µmol/L (NL 5.0-15.0 µmol/L) were in the normal range.\nAfter 3 days of intravenous unfractionated heparin (25,000 IU/day), follow-up CAG showed only slight resolution of the filling defect and only in the dLAD, not in the OM and dLCX (). He had no chest pain and was discharged on triple antiplatelet agent. After 1 year of this treatment, he experienced no chest pain and, on follow up CAG, had no significant stenosis or intracoronary filling defects ().
A 52-year-old male patient presented to the emergency department with a typical acute chest pain of 1 hour’s duration. The patient was sweaty and anxious on the physical examination and had a systolic blood pressure of 90 mmHg and a diastolic blood pressure of 50 mmHg. Electrocardiography showed ST-segment elevations in DII, DIII, and aVF leads, as well as ST-segment depressions in V1–V3 leads (). His medical history showed double-vessel coronary artery bypass graft surgery (CABG) 2 months earlier due to stable angina pectoris, for which he regularly took diltiazem, acetylsalicylic acid, and atorvastatin. Additionally, there were no cardiovascular risk factors except for family history. The patient’s coronary angiography and bypass reports were, however, not available.\nPrimary PCI was performed based on a diagnosis of acute inferoposterior myocardial infarction within the first hour of chest pain. Coronary angiography showed that the SVG to the right coronary artery (RCA) was occluded with a thrombus (). The left internal mammary artery graft was open and raced with the left anterior descending coronary artery. Additionally, the mid-portion of the circumflex (Cx) obtuse marginalis was 80% stenotic and the Cx and the RCA were totally occluded (Video 1). The lesion on the SVG was passed with a floppy wire and aspirated via manual thrombectomy (Export Catheter, Medtronic Inc., Minneapolis, Minnesota) (). The huge thrombus content was also aspirated (). Tirofiban, a glycoprotein IIb/IIIa inhibitor, at an intracoronary dose of 10 μg/kg was administered. Moreover, severe stenosis was detected in the SVG to RCA anastomosis, and a 2.75×38-mm XIENCE PRO drug-eluting stent (Abbott Vascular, California, USA) was implanted. Post-dilatation with a 3.5×15-mm Emerge NC balloon (Boston Scientific, USA) was performed, and a distal thrombolysis in myocardial infarction (TIMI) flow grade III was provided (/Video 2). An intravenous infusion of 0.15 μg/kg/min of tirofiban was given for 18 hours. After the procedure, the chest pain was relieved and the ST-segment elevation was improved (). The angiographic imaging of the coronary arteries before the surgery was evaluated, and the Syntax Score was calculated to be 30.5 (Video 3). The patient underwent echocardiography, which showed an ejection fraction of 40%, hypokinesia in the inferior and posterior walls, and mild mitral regurgitation. Atorvastatin, nebivolol, prasugrel, acetylsalicylic acid, and ramipril were prescribed, and the patient was discharged without any complications.\nControl angiography and PCI on the 80% mid-portion stenosis of the Cx obtuse marginalis were planned. One month later, a 2.75×24-mm XIENCE PRO drug-eluting stent (Abbott Vascular, California, USA) was implanted in the stenotic region. The stent patency of the SVG to RCA anastomosis was optimal (Video 4). One month later, stress myocardial perfusion scintigraphy was performed and no sign of ischemia was detected. The patient has been followed without any symptoms for 10 months.