A hypertensive and diabetic 72-year-old man with 3-vessel CABG surgery, SVG to the first diagonal branch of the left anterior descending artery (LAD) and to the obtuse marginal branch of the left circumflex artery (sequential grafting) and the left internal mammary artery (LIMA) to the distal LAD, performed 25 years earlier, presented at our hospital complaining of recurrent chest tightness over the past week. On physical examination, there were no remarkable findings. An electrocardiography showed a normal sinus rhythm at a rate of 78/min with a complete right bundle branch block, but no significant ST-T change was found compared with the findings of his previous electrocardiography. Regional hypokinesis of the post-lateral wall with moderate left ventricular dysfunction, which had not been previously confirmed, was also observed. Cardiac enzymes were not elevated. Coronary angiography showed the obstruction of SVG with a large thrombus burden (Fig. , Movie 1). Although LAD was chronically occluded from the ostium, there was no significant change compared with his condition 3 years ago. LIMA to LAD was patent, and other natives were the same as they had been 3 years ago. He was diagnosed with unstable angina due to acute SVG thrombosis. Instead of PCI, he was treated with apixaban 5 mg twice a day for 3 weeks in addition to aspirin 100 mg once a day, which was already being taken. We added only apixaban and not a P2Y12 inhibitor considering the high risk of bleeding and the mechanism of thrombotic occlusion. After coronary angiography had been performed and PCI was selected, we planned to load a P2Y12 inhibitor. The angiography 3 weeks after starting apixaban showed a considerable resolution of the thrombus and an opening SVG (Figure , Movie 2). The coronary flow of the final angiography almost reached TIMI grade 3 flow, and there was no significant stenosis in SVG. Therefore, we did not move on to PCI due to the fear of distal embolization. The rest of the patient’s stay in the hospital was uneventful, and he was discharged 1 week after the procedure.
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 ().