Our patient was a 78-year-old male presenting for evaluation of acute-onset, anginal chest pain of six-hour duration. The pain was typical of classic anginal chest pain with radiation to the left neck. The patient had an additional complaint of a diffusely edematous, ecchymotic left lower extremity (LLE); however, he was recently post-operative from a left total knee arthroplasty (TKA) four days prior.\nThe patient was maintained on warfarin for a previously identified SVGA with associated thrombus. His warfarin was discontinued three days before the surgery, and an enoxaparin bridge was started instead. The warfarin was restarted on postoperative day one without a bridging strategy at an initial international normalized ratio of 1.1.\nThe patient was previously well with a past medical history notable for three-vessel CABG in 2017 [LIMA to left anterior descending (LAD), SVG to right coronary artery (RCA), and SVG to first diagonal (D1)], SVG-D1 aneurysm with thrombus, thrombocytopenia, essential hypertension, mixed dyslipidemia, New York Heart Association [] class III/American Heart Association class C heart failure with reduced ejection fraction, IgA-kappa monoclonal gammopathy of undetermined significance, and osteoarthritis. In addition to the CABG, the patient had undergone bilateral TKA, Roux-en-Y gastric bypass, and cervical fusion of C4-C6.\nThe patient presented afebrile with stable vital signs: a pulse of 73 beats per minute and blood pressure of 123/57 mmHg, saturating 94% on room air at 18 breaths per minute. On examination, the patient had a prominent S4 gallop and a markedly ecchymotic LLE with 3+ pitting edema to the mid-thigh without jugular venous distension. Initial laboratory findings were remarkable for anemia with a hemoglobin of 6.9 g/dL (baseline 13.5 g/dL), thrombocytopenia to 127 × 103/µL, and an initial high sensitivity troponin of 27 pg/mL.\nFollowing evaluation by emergency department personnel, the patient was placed for admission for suspected non-ST-segment myocardial infarction (NSTEMI) with presenting electrocardiogram shown in Figure .\nThe high-sensitivity troponin increased steadily peaking at 9,632 pg/mL before downtrending. Acute coronary syndrome (ACS) protocols were enacted and the patient was started on a heparin drip. The patient was transfused with packed red blood cells for his anemia. Computed tomography (CT) angiogram of the chest identified known SVG to D1 disease (Figure ) without the presence of pulmonary embolus. The chest pain improved with the therapies and the patient consented to cardiac catheterization.\nCardiac catheterization revealed severe native vessel CAD involving the proximal LAD, proximal RCA, and ostial D1. The bypass grafts were patent, and the distal SVG-D1 anastomosis was aneurysmal with an organized thrombus without significant change compared to March 2016 (Figure ). Post-catheterization diagnosis was suspected distal embolization of a thrombus fragment resulting in branch vessel occlusion resulting from warfarin. The patient tolerated the procedure without incident. The remainder of his hospital course was uneventful. He was discharged home in a stable condition on hospital day four on guideline-directed medical therapy for his cardiac ailments.
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.