HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
50-year-old male patient, independent for basic activities of daily living and without cognitive impairment. Single, lives alone in a small town in our autonomous community. Cardiovascular risk factors: ex-smoker for 2 years, with an accumulated consumption of 30 packets/year, ex-drinker for 6 months with a previous daily consumption of 5-6 UBE/d. No known metabolic disorders. Cardiological history: no cardiological history of interest. No family history of heart disease or sudden death. Other history: no personal history of note. Treatment: no chronic home treatment. Occasional use of NSAIDs.

Current illness
The patient consulted his regional referral hospital due to a fever and general malaise of 15 days' duration accompanied by inflammatory pain in the lumbar region. He also presented with slightly localised abdominal discomfort, with an accompanying feeling of nausea. No other infectious symptoms at any other level. No chest pain, dyspnoea, palpitations or other cardiological symptoms. During her stay in the emergency department, tests were started with laboratory tests and abdominal ultrasound. The biochemistry showed elevated inflammatory markers, the haemogram showed leukocytosis with left shift and the abdominal ultrasound showed splenomegaly measuring 18 cm with multiple cystic formations inside. For this reason, a thoracoabdominal CT scan was requested which confirmed the presence of multiple splenic and renal infarctions. Finally, following these findings, a transthoracic echocardiogram was performed which revealed the presence of severe aortic insufficiency of uncertain origin, without being able to confirm the presence of warts. On the basis of these studies, and given the suspicion of infective endocarditis, empirical antibiotic treatment was started with ceftriaxone and ampicillin. After 24 h of admission, and following the growth of Enterococcus faecalis in the blood cultures, it was decided to discuss the case with the cardiology department of our hospital in order to perform a transesophageal echocardiogram, as well as to complete the studies and assess definitive treatment. The patient arrived at our hospital haemodynamically stable, with very mild respiratory work, and with basal crackles, as well as petechiae in the lower limbs as the most relevant findings of the examination. A repeat transthoracic echocardiogram was performed with a result similar to that obtained at his regional hospital, and it was decided to complete the cardiological studies.

Physical examination
Vitals: heart rate (HR) 92 bpm; respiratory rate (RR) 29 rpm; blood pressure (BP) 95/48; oxygen saturation 97%. Patient conscious, oriented and cooperative. Good hydration status. Slight skin pallor. No pain gesture. Mild tachypnoea at rest, no intercostal tugging. Head and neck: no jugular ingurgitation and negative hepatojugular reflux. Carotid pulse symmetrical and no murmurs. Pulmonary auscultation: preserved vesicular murmur with crepitant rales in the right base. Cardiac auscultation: rhythmic heart sounds. Aortic systolic murmur II/VI with preserved 2nd sound followed by a protodiastolic murmur II/IV. Abdomen: no skin lesions or scars. Preserved hydro-aerial sounds. Soft and depressible, without discomfort on palpation or rebound. Palpable splenomegaly. Lower extremities: extremities warm and with good capillary filling. Petechial lesions on both legs. Radial and pedial pulses present and symmetrical. No signs of chronic venous insufficiency, no oedema and no signs suggestive of deep vein thrombosis (DVT).

COMPLEMENTARY TESTS
Biochemistry: glucose 113 mg/dl, urea 59 mg/dl, creatinine 1.45 mg/dl, glomerular filtration rate 53 ml/min/1.78 m2, sodium ion 137 mmol/l, potassium ion 4.1 mmol/l, C-reactive protein 17.2 mg/dl; procalcitonin 1.56 ng/ml; NT-proBNP 3.280pg/ml, alkaline phosphatase 107 U/l, AST 21 U/l, ALT 24 U/l, GGT 59 U/l, total bilirubin < 1.0 mg/dl, total cholesterol 126 mg/dl, HDL 10 mg/dl, triglycerides 281 mg/dl, calculated LDL cholesterol 47 mg/dl, HbA1C 4.6%, TSH 2.03 mU/l. CBC: haemoglobin 8.1 g/dl, haematocrit %, red blood cells 2.86x106/μl, leukocytes 10,520/μl, neutrophils 8,760/μl, lymphocytes 1,150/μl, monocytes 530/μl, eosinophils 70/μL, basophils 10/μl, platelets 235,000/μl. Coagulation: prothrombin time (PT) 15.10 sec; partial thromboplastin time (PTAT) 33.70 sec; INR 1.33; derived fibrinogen: 491 mg/l. Blood cultures: growth of Gram + cocci in the first 24 hours. At 72 h the presence of Enterococcus faecalis sensitive to ampicillin, vancomycin and ciprofloxacin was confirmed.
12-lead ECG performed on arrival at our hospital: sinus rhythm at 90 bpm. P wave of normal size and morphology. PR interval in range without prolongation. Narrow QRS with axis between 0-90o and transition between V3-V4. ST segment without suprathresholds. Normal T wave. QTc interval in normal range. Chest X-ray performed on arrival at our hospital: cardiac silhouette of normal size. Slight vascular redistribution towards apical lung fields suggestive of incipient pulmonary congestion. No pinching of the costophrenic sinuses suggestive of pleural effusion. No parenchymal condensation or pneumothorax. Abdominal ultrasound performed in a regional hospital prior to transfer to our centre: hepatic steatosis without focal lesions. Biliary tract without lesions. Kidneys normal. Pancreas not assessable. Spleen 18cm with cystic formations inside. Empty bladder not assessable. Thoracoabdominal CT scan performed in a regional hospital prior to transfer to our centre: no pulmonary nodules or thoracic adenopathies in pathological range or appearance were observed. Small tongue of bilateral pleural effusions. Hypodense lesions of triangular splenic morphology suggestive of infarction, as well as right renal lesions also probably related to infarction. Diffuse hepatic steatosis with cystic lesion in the LHI. Pancreas, adrenal glands are normal. Transthoracic echocardiogram performed in a regional hospital prior to transfer to our centre: left ventricle neither dilated (VTD 128 ml, VTS 39 ml) nor hypertrophic, without segmental alterations and with preserved LVEF (LVEF 69% by Simpson biplane). Left atrium slightly dilated (AP diameter 43 mm). Right ventricle of normal size and function (TAPSE 26 mm). Mild tricuspid insufficiency with a velocity of 3.22 m/s (PSAP 44 mmHg). Inferior vena cava not dilated. High probability of pulmonary hypertension. Mitral valve with thin leaflets without prolapse, mild mitral regurgitation. Trivalve aortic valve, leaflets appear thin and there are no images suggestive of endocarditis. Central aortic insufficiency which appears severe (THP 112/m/s, VC 7-8 mm), without being able to determine the mechanism. Aortic root not dilated. No suprasternal or good visualisation of the abdominal aorta to assess the presence of diastolic reverse flow. No pericardial effusion. Transesophageal echocardiogram (TEE): the atrial septum is intact, with no evidence of atrial septal defect. Mitral valve: vegetation in the anterior mitral leaflet, about 6mm long axis; moderate mitral insufficiency is detected. Tricuspid valve normal in structure and function. Trivalve aortic valve; endocarditis on the aortic valve, with a wart of about 11 mm of major axis, with destruction of the non-coronary leaflet, leading to severe aortic insufficiency. No evidence of perivalvular involvement. There is no pericardial effusion. Cardiac CT scan: trivalve aortic valve with focal thickening of the non-coronary leaflet and a 10 mm polypoid image, mobile, close to the implantation point in relation to the clinical suspicion of endocarditis. Rupture of the non-coronary leaflet. No perivalvular complications were identified. Coronary arteries without significant lesions. CT scan of the brain: hyperdense image in the left subcortical sylvian region with discrete surrounding oedema, without significant mass effect, which in the clinical context of the patient suggests a small haemorrhagic embolus, without being able to rule out underlying abscess due to the fact that the study was performed without VSD. No alterations in the density of the brain parenchyma suggestive of subacute ischaemic pathology were observed. Area of encephalomalacia in the right temporal pole with discrete exvacuo dilatation of the homolateral horn, of residual appearance; we do not know the patient's clinical and traumatic history. Discrete signs of chronic small vessel pathology in the base ganglia, no bone lesions of interest are observed. Positron emission tomography with 18F-deoxyglucose (PETTC): head and neck without pathological alterations of the glycemic metabolism. A focus of mild glycemic hypermetabolism is observed adjacent to the aortic valve area (SUVmax 2.83), which could be related to known endocarditis (the low degree of uptake could be explained by response to antibiotic treatment). No other hypermetabolic foci were detected in the valvular heart area suggestive of endocarditis. Splenomegaly with the presence of several extensive ametabolic lesions, which show increased glycemic metabolism in their periphery (SUVmax 8.27), with fairly homogeneous characteristics, related to known splenic infarcts, without clear signs suggestive of their superinfection. The hypermetabolism could be explained, at least in part, by extramedullary haematopoiesis secondary to known anaemia. Liver, pancreas, adrenal glands and mesentery without pathological alterations of glycemic metabolism. Kidneys not assessable due to physiological excretion of radiotracer. Diffuse and homogeneous increase in metabolism in the bone marrow, probably related to anaemia. Rest of the study with no findings of interest. Cerebral angio-MRI: in the FLAIR sequence, multiple patchy hyperintensities of bilateral subcortical cortical location and in the right cerebellar hemisphere are observed, with a more extensive area in the right temporal pole, which show late enhancement after contrast. They are compatible with infarcts of cardioembolic origin, several of them with signs of petechial microbleeding, in a subacute-late phase evolving to chronicity. A 10 mm haematoma in the left sylvian region with discrete perilesional oedema, which has not increased with respect to previous CT studies. In the magnetic susceptibility sequence at least 3 millimetric formations are identified in convexity grooves (bilateral frontal and right occipital), not assessable in the angio-MRI, not being able to rule out distal mycotic aneurysms. No significant alterations were seen at the level of the polygon of Willis. No lesions suggestive of abscesses are identified. Cerebral arteriography: identified by arteriography from the left ICA as a pseudoaneurysm in M2 branch, embolised using a sandwich technique with coils distal and proximal to the neck of the pseudoaneurysm. Good final angiographic result.

CLINICAL EVOLUTION
During the first days of admission, a transesophageal echocardiography was performed, as well as a cardiac CT scan, which confirmed the presence of aortic vegetation with involvement of the non-coronary leaflet, with rupture of the same, leading to severe aortic insufficiency. In addition, data suggestive of a previously undescribed vegetation at the mitral level and coronary arteries without lesions were also observed. With these findings, it was decided to discuss the case in a multidisciplinary endocarditis session, with the participation of the radiology, infectious diseases and cardiac surgery departments, with a view to assessing valve replacement. Given the history of splenic infarction, it was decided to request extension studies prior to surgery to rule out embolisms at other levels and to re-evaluate the state of spleen involvement. On the same day, a cranial CT scan was performed which showed the presence of a haemorrhagic lesion in the region of Sylvius compatible with the rupture of a mycotic aneurysm and a PET-CT scan showed marked splenic involvement, with large necrotic areas. At this point, with the presence of valvular involvement, splenomegaly with multiple areas of large infarction, and intracranial bleeding, it was decided jointly with the neurology, cardiac surgery and general surgery services to establish an order of action to treat the set of complications developed by the patient. Initially, an arteriography with embolisation of the mycotic aneurysm affecting the M2 branch of the left middle cerebral artery was performed (after study with cerebral angio-MRI). The procedure was performed without incident and without secondary neurological sequelae. Subsequently, it was decided to perform a splenectomy. The reason for initially resecting the spleen rather than the heart was to avoid the risk of bleeding that could have been caused by the extracorporeal circulation (ECC) and subsequent heparinisation. One week after embolisation, splenectomy by laparotomy was performed without complications. Finally, three days after the splenectomy, the patient underwent surgery for his valve disease. The aortic valve was resected and a St. Jude No. 23 biological prosthesis was implanted. It is noteworthy that during the operation: both the intraoperative TEE and the visual inspection did not reveal the mitral involvement described in the previous report; only a grade II/IV mitral insufficiency, so it was decided not to operate on it (the same grade was maintained at the discharge control). During admission, the patient was treated with intravenous antibiotics according to the recommendations of the infectious diseases department (ceftriaxone, gentamicin and ampicillin). The patient's evolution during the first weeks of admission was acceptably good. The patient remained practically asymptomatic from the cardiological point of view, with development of mild heart failure (but good clinical tolerance) and improvement in both fever and digestive symptoms. The main complications were marked anaemia, which required repeated transfusions of several red blood cell concentrates. On the other hand, he also had a deterioration of renal function that made it necessary to space contrast studies and maintain adequate hydration. After the two surgeries, the patient remained in hospital for a little over a month, with a very poor evolution due to complications derived from his abdominal surgery. This even necessitated reoperation for drainage of the abdominal abscess and the patient's admission to the chronic wound unit for management of the laparotomy incision. In the end, however, the patient can be discharged home to continue his recovery there.

DIAGNOSIS
Acute E. faecalis endocarditis on native aortic valve.
Non-coronary aortic valve leaflet rupture with secondary severe aortic insufficiency. Aortic valve replacement with St. Jude biological prosthesis no 23.
Acute heart failure with preserved LVEF in the setting of infective endocarditis.
Epicardial arteries without lesions.
Splenic and renal infarcts of embolic mechanism secondary to infective endocarditis. Splenectomy by laparotomy with subsequent drainage of purulent collection.
Mycotic cerebral aneurysm in M2 branch of left middle cerebral artery secondary to infective endocarditis. Embolisation of cerebral mycotic aneurysm by arteriography.
Multifactorial normocytic anaemia (bleeding, hypersplenism, deterioration of renal function...).
Multifactorial acute renal failure (hypotension, iodinated contrast, diuretics...).
