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 49-year-old man presented to our hospital complaining of dull, central chest pain after 1 week of subjective fever. Fourteen years prior to this presentation, the patient underwent coronary artery bypass grafting, and 10 years prior suffered right knee septic arthritis due to Methicillin-sensitive Staphylococcus aureus (MSSA) which was complicated by a mycotic right femoral pseudoaneurysm. The patient had no immunosuppressive medications or medical conditions.\nIn the week prior to presentation, the patient had taken non-steroidal anti-inflammatory drugs for right knee pain after a mechanical injury and had ceased aspirin due to concerns about gastrointestinal haemorrhage. The patient had experienced subjective fevers and knee pain, however, had full range of movement with no tenderness, warmth, or erythaema.\nOn arrival, his electrocardiogram (ECG) showed sinus tachycardia with inferior ST elevation (). Physical examination revealed a blood pressure of 128/88 mmHg, heart rate of 112 b.p.m. and temperature of 36.7°C. Cardiovascular examination was unremarkable and examination of the right knee demonstrated normal range of motion without pain and no effusion. An urgent coronary angiogram was performed demonstrating severe native triple vessel disease, a patent left internal mammary artery graft and an aneurysmal but patent saphenous vein graft from the posterolateral branch to posterior descending branch of the right coronary artery (PDA) (). The Saphenous vein graft skip to the PDA was believed to be the infarct-related artery. No intervention was performed and the patient was managed with aspirin, clopidogrel, beta-blockade, angiotensin receptor antagonist, spironolactone, and intravenous nitrate infusion. Pathology is available in .\nSix hours later, the patient developed fever (38.4°C) with no localizing signs of infection identified; a septic screen was performed. Leucocytosis on the urinalysis led to commencement of IV augmentin (1000 mg + 200 mg QID) and gentamicin (320 mg), which were then changed to flucloxacillin (2 g QID) after blood and urine cultures grew MSSA.\nDue to ongoing chest pain, intervention with covered stents to the aneurysmal graft was considered but decided against because of the persistent bacteraemia and fever. Without revascularization, the patient developed inferior hypokinesis on echocardiogram and Q waves in the inferior leads on ECG. He remained persistently febrile until Day 5 of IV flucloxacillin.\nThere were no other symptoms or signs to suggest another source of infection. The abdomen was soft and non-tender. As MSSA was detected in urine during the initial work up a renal tract US was performed which revealed echogenic kidneys, and the treating cardiology and infectious disease teams attributed this to the systemic sepsis.\nTransthoracic echocardiography (TTE) and transoesophageal echocardiography (TOE) showed no evidence of infective endocarditis. Vasculitis and rheumatological screens were negative. Given the strong suspicion of a mycotic aneurysm, a labelled white cell scan was performed on Day 7 post-presentation, which failed to demonstrate an infective focus, or infection within the aneurysm.\nThe patient was discharged on IV flucloxacillin for 6 weeks, and dual antiplatelet therapy with a view to cardiology and infectious disease follow-up for consideration of treatment of aneurysm with percutaneous treatment in the future.\nFour days after discharge, the patient represented with left-sided pleuritic chest pain. Blood cultures were persistently negative. His repeat echocardiogram demonstrated moderately reduced left ventricular (LV) function, with thin walled, akinetic inferior and posterior walls consistent with a completed inferior infarct. The expanding aneurysm of the saphenous vein graft was now visible (on TTE and TOE) as a large pulsatile chamber along the posterior and inferior wall, with flow principally seen in diastole, and compressing the inferoposterior LV wall during diastole consistent with expanding aneurysm of the saphenous vein graft ().\nThe cardiothoracic surgery team performed a redo coronary artery bypass grafting with successful identification and resection of the mycotic aneurysm. Cultures of the operative specimen were negative, though the histological microscopic appearance confirmed the presence of the mycotic aneurysm.\nThe patient’s post-operative recovery was complicated by one admission for management of heart failure, after which he has remained stable and independent in the community as of August 2019. The most recent echocardiograph revealed normal LV systolic function with infarcted inferior and posterior walls, severe left atrial enlargement, and mild mitral regurgitation.