HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History

Male, 73 years old, independent, with an active life. No known drug allergies.
Cardiovascular risk factors: ex-smoker until 30 years ago of about 30 packs/year. High blood pressure (HBP) under pharmacological treatment with good control. Type 2 diabetes mellitus (DM) treated with oral medication with good control. Dyslipidaemia under pharmacological treatment. No alcohol habit.
Previous cardiological history: diagnosed in October 2017 due to episode of oppressive chest pain of degenerative aortic valve disease with double lesion (severe aortic stenosis and moderate aortic insufficiency), ascending aortic aneurysm (52 mm) and 1-vessel coronary artery disease (diffusely diseased DC with poor distal bed). In February 2018, valve replacement was performed, with a number 21 Magna Ease biological aortic prosthesis and a Hemashield No 28 supracoronary tube.

Other history:
Duodenal ulcus requiring Billroth II gastrectomy.
Synchronous lower rectal and pulmonary neoplasia in 2016. Received radio and chemotherapy; subsequently pulmonary lobectomy and rectal resection.
Grade II chronic lower limb ischaemia due to femoropopliteal obstruction in MID and distal popliteal stenosis in MMII.
Neurinoma of the left acoustic nerve causing hypoacusis in the left ear, therapeutic attitude pending decision.

Usual treatment: rosuvastatin 10 mg (0-0-1), clopidogrel 75 mg (0-1-0), omeprazole 20 mg (1-0-0), oxycodone 5 mg 1 cp c/4h sp, paracetamol sp and lactulose sp.

Present illness
73-year-old patient admitted to neurology in April 2019 for diplopia and gait instability. In the previous month, he had presented with a general syndrome with weight loss and asthenia, accompanied by febrile fever.
Twenty-four hours after admission to neurology to complete studies, having previously been asymptomatic from the cardiological point of view, he began with oppressive central thoracic pain with electrocardiographic changes: right bundle branch block (RBBB) not previously seen and ST elevation on the anterolateral side. The infarction code was activated and loading doses of antithrombotic treatment were administered.
A few minutes later, he presented complete atrioventricular block with bouts of prolonged asystole and haemodynamic instability, so orotracheal intubation and connection to mechanical ventilation was performed. He required noradrenaline to maintain blood pressure.
On arrival at the haemodynamics ward, a transient pacemaker was placed via the right femoral vein and a coronary angiography was performed showing 100% stenosis of the anterior descending artery as the vessel responsible for the infarction. Primary angioplasty and pharmacoactive destent implantation was performed with good angiographic results. He was then admitted to the cardiac intensive care unit.

Physical examination
On admission to neurology:
Neurological examination: unstable gait with lateropulsion to the right, right palpebral ptosis and diplopia in various gaze positions.
Blood pressure (BP) 135/73 mmHg. Oxygen saturation (SatO2) 97% basal. Temperature 37.4 oC. Pulmonary auscultation: preserved vesicular murmur, without added noises. Cardiac auscultation: rhythmic with systolic murmur II/VI in aortic focus. Abdomen soft, depressible and non-painful. No oedema in the lower limbs.

On admission to the cardiac ICU:
SAPS-3 (Simplified Acute Physiology Score-3): 76 points (67.4% probability of death on admission). BP 115/56 mmHg with noradrenaline perfusion at 0.7 μg/kg/min. Heart rate (HR) 70 bpm. Temperature 36o C. SatO2 100% (FiO2 0.5). Respiratory rate (RR) 19 rpm.
Under sedoanalgesia, pupils half reactive. Upper limb flexion (MMSS) to algesic stimulus. Pulmonary auscultation: preserved vesicular murmur, without added noises. Cardiac auscultation: rhythmic with systolic murmur II/VI in aortic focus. Abdomen soft and depressible, not painful on palpation with preserved peristalsis, with no signs of peritoneal irritation. No masses or megaliths were palpable. The lower extremities were well perfused, with preserved and symmetrical pulses, with no signs of deep vein thrombosis.


COMPLEMENTARY TESTS
Cranial CT scan without contrast: no signs of bleeding, compressions or displacements in the endocranial structures visualised. Hypodense lesions in the periventricular white matter with a subacute ischaemic appearance.
Laboratory tests: blood biochemistry: glucose 255 mg/dl, urea 49 mg/dL, creatinine 0.95 mg/dl, CK 5,955 U/l, TnT 14,890 ng/l. Haemoglobin 9.3 g/dl, haematocrit 27.4%, leucocytes 14,550/mm (neutrophils 91.9%), platelets 149,000/mm. Coagulation: PT 61%, TTPa 15.9 s, fibrinogen 432 mg/dl.
Electrocardiogram (ECG) with chest pain: sinus rhythm at 97 bpm. BRDHH. ST elevation on the anterolateral side.
Emergent coronary angiography:
Implantation of a transient balloon pacemaker via right femoral vein.
Left main coronary artery: no stenosis. Anterior descending: 100% stenosis, TIMI 0 flow in proximal segment. Circumflex: no stenosis. Right coronary artery: severe stenosis of 99% in its distal segment and 100% stenosis in its middle segment, with impression of chronic occlusion, with bad distal bed.
Primary angioplasty: via the right femoral artery, with JL4 guidewire, guidefloppy is advanced to the distal LAD, recovering arterial flow. Subsequently, direct implantation of a Resolute Onyx 3.5 x 22 mm drug-eluting device was performed in the proximal segment with success and without complications. Good angiographic result and final TIMI 3 flow.
Transesophageal echocardiography:
Study performed in ICU with patient on mechanical ventilation.
Biological prosthesis in aortic position with a large wart (about 24 mm), multilobulated and irregular, which moves from LVOT to aorta with the cardiac cycle. Mild valvular insufficiency. Peak gradient of 43 and mean of 30 mmHg (previous 14 and 6 mmHg) with VTI ratio 0.26. Perivalvular aortic abscess extending to mitro-aortic junction.
Moderate-severe mitral insufficiency due to de-structuring of the valvular annulus in relation to abscess in the mitro-aortic junction.
Severe systolic dysfunction due to extensive akinesia of all apical segments, anterior face and mid-septal and basal segment of anterior septum.
No pericardial effusion.
Blood cultures: taken on admission. Multisensitive Staphylococcus epidermidis.

CLINICAL EVOLUTION
The patient was admitted to the cardiac ICU in shock with high suspicion of infective endocarditis due to febrile fever, being a biological prosthesis holder and the characteristics of the lesion of the anterior descending artery suggesting embolic origin. Transthoracic echocardiography was performed on admission and progressed to transesophageal echocardiography which confirmed the diagnosis of late prosthetic infective endocarditis. In addition, the results of the blood cultures taken on admission were positive for multisensitive Staphylococcus epidermidis.
Joint assessment with cardiac surgery. Given the situation of cardiogenic shock, emergency surgery was ruled out. Despite antibiotic treatment, inotropes at increasing doses and intra-aortic balloon counterpulsation implantation, the patient was unable to overcome the shock situation. Acute renal failure, in anuria. Haemofiltration was performed, without improvement. He developed multi-organ failure and finally died.

DIAGNOSIS
Death due to late prosthetic infective endocarditis caused by Staphylococcus epidermidis, complicated by:
Previous STEMI in haemodynamic Killip-Kimball IVs(cardiogenic hock). 2-vessel coronary artery disease. Chronic right middle coronary artery occlusion. Embolic occlusion of proximal anterior descending artery, primary angioplasty with drug-eluting stent implantation. Severely impaired left ventricular systolic function.
Shock of mixed origin, cardiogenic and septic.
