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 56-year-old Caucasian man presented from an outlying facility 2 h after acute onset of substernal chest pain at rest with diffuse ST segment depression. Sixteen years ago he had triple vessel CABG with two subsequent cardiac catheterization procedures and percutaneous coronary interventions in the last few years.\nOn presentation, the physical examination was unremarkable. Electrocardiogram had shown diffuse ST segment depression. Laboratory data were unremarkable, including cardiac biomarkers. He underwent cardiac catheterization with coronary and SVG angiography. It revealed severe native vessel coronary artery disease with 100% occlusion of all three native vessels. Left internal mammary artery graft to the left anterior descending artery was patent. SVG to right coronary artery (RCA) angiography revealed two aneurysms, one in the mid-body of the vein graft measuring 3 cm, followed by another 5 cm large aneurysm at the distal segment []. There appeared to be a leak of the contrast into the right atrium (RA) from the distal aneurysm. The aneurysm also had a posterior descending artery (PDA) runoff through the prior placed stent to the PDA at the anastomosis.\nThe patient was hemodynamically stable and reviewing the coronary anatomy we did not find any lesions that were amenable to intervention. He was monitored on the cardiac floor and had further imaging studies for better visualization of the SVG leak. A poorly defined right atrial mass was also appreciated in the subcostal view of the transthoracic echocardiogram for which he underwent a transesophageal echocardiogram (TEE). TEE revealed the aneurysm measuring 5.0 cm × 5.3 cm with Doppler flow within and extending from the structure into the RA []. A chest computed tomographic scan with contrast revealed a partially thrombosed aneurysm measuring 2.8 cm × 3.0 cm about 3.4 cm distal to the RCA graft origin and a large aneurysm measuring 5.0 cm × 4.2 cm distal to the first aneurysm both in the SVG to the RCA. The aneurysm also demonstrated a fistulous connection to the RA [ and ].\nThe cardiovascular surgical consultation was requested regarding further management options given the above findings. Percutaneous treatment including covered stent placement across the aneurysmal segments of the SVG was discussed. After a thorough discussion with the patient, he decided conservative management at the point.