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We report the case of an abscess complication of infective endocarditis detected by electrocardiogram (ECG). A 51-year-old man was admitted to the Emergency Department for fever (39 C°) and asthenia from few days. About 2 months earlier he had undergone cardiac surgery for aortic valve replacement with biological valve for severe aortic stenosis. Vital signs included low blood pressure and high respiratory rate; he was also pyretic. On cardiac auscultation he had a systolic murmur on aortic focus. He underwent blood gas analysis, which showed an increase in serum lactate, ECG, which detected a I grade atrioventricular block, and blood sampling, which showed severe increases in white blood cells, C-reactive protein and procalcitonin. Chest x-ray was normal. An echocardiogram was therefore performed: thickened and hyperechogenic cusps of the aortic biological prosthesis were detected; masses, with character of mobility at the level of the left coronary cusp (maximum size of 1.4×1cm) were also described; there was also a slight increase in transprosthetic gradients and mild valve insufficiency. The first diagnostic hypothesis was therefore that of infective endocarditis (IE), further supported by a recent odontogenic procedure for dental abscesses to which the patient would have undergone a few weeks after heart surgery (possible IE according to the Duke modified criteria). Blood cultures were performed on three samples and empirical antibiotic therapy was initiated until Streptococcus mitis was isolated (definite IE according to the Duke modified criteria) and thus Ceftriaxone was started. During hospitalization in the cardiology ward the patient presented dysarthria and left hemiplegia. A cerebral angio-computed tomography and neurological consultation were conducted and an ischemic stroke of thromboembolic origin from biological valve endocarditis was diagnosed. However, in view of the extensive ischemic hypodensity, acute reperfusion treatment was not indicated. The patient therefore underwent cardiac surgery consultancy but, due to his severe comorbidities and expired clinical conditions, there was no indication for cardiac surgery. After few days, during daily ECG recording, left main coronary artery (LMCA) stenosis-like ECG modifications were detected, with ST elevation in lead aVR in addition to marked ST depression in leads V3 through V6 and in peripherals leads (Fig.). A troponin sample was immediately taken, which would have been increased. He immediately underwent new echocardiogram which revealed a new periprosthetic abscess across left coronary cusp. Given the course of LMCA through the abscess, we believe that the acute coronary syndrome that has occurred to the patient may be due either to a compression of the LMCA by the periprosthetic abscess or to embolization of abscess material in the le LMCA. It was not possible to perform coronary angiography neither to perform cardiac surgery as the patient died a few hours later due to septic shock.

A 65-year-old man was admitted to the emergency department for abdominal pain begun 4 days before. Past medical history consisted of ischemic stroke and diabetes mellitus. Of note, he was not taking any medication. Vital signs: blood pressure 90/50 mmHg, heart rate 50/minute, respiratory rate 18/minute, body temperature 36.5°C; saturation oxygen level 93%. High-sensitivity cardiac troponin was mildly elevated (121 pg/mL). Electrocardiogram showed sinus bradycardia, Q waves with ST elevation in antero-lateral leads consistent with subacute STEMI. Transthoracic echocardiogram (TTE) revealed aneurysmatic expansion of apical left ventricular (LV) walls (ejection fraction 30%) with a large apical thrombus (35×15 mm). Coronary angiography showed complete occlusion of proximal left anterior descending artery and a critical stenosis of right coronary artery; percutaneous coronary intervention with stent implantation on right coronary artery was performed. He received triple antithrombotic therapy with aspirin, clopidogrel, intravenous heparin first and then oral anticoagulation with warfarin. During coronary care unit stay, the patient was asymptomatic and hemodynamically stable. However, a control TTE (day 6) in cardiology ward revealed the presence of pseudoaneurysm with an oval out-pouching (23 × 13 mm) from the apical aspect of LV septum, communicating with the LV chamber through a passage measuring 1.6 cm. Partially organized pericardial effusion was evident around right ventricular free wall (Figure 1). Thus, the patient was immediately transferred to the cardiac surgery department for urgent surgical repair. The LV anterior wall rupture with pseudoaneurysm was then treated with endoaneurysmectomy of the LV with dacron patch and freewall reconstruction with prolene sutures and teflon felt stripes. The patient was finally discharged 3 weeks after surgery with betablockers, ace- inhibitors, diuretics, statins and dual antiplatelet therapy with aspirin and clopidogrel. At one month follow-up visit, the patient was hemodynamically stable with acceptable functional capacity. Figure 1Modified five chamber view (a, b) and three chamber view (c, d) showing apical LV pseudoaneurysm (arrows) with moderate pericardial effusion (arrowhead); color Doppler through the passage (arrow) in 3 chamber view (d). LV, left ventricular.