HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

A 73-year-old woman attended the emergency department of our centre due to dyspnoea.

History
The patient had the following medical history:
Cardiovascular risk factors: dyslipidaemia in treatment with a lipid-lowering drug in monotherapy, with last LDL-C of 80 mg/dl.
Cardiological history: medical records show detection of a heart murmur more than 20 years ago in check-ups by a primary care doctor, never studied.
Other relevant medical history: locally advanced adenocarcinoma of the left breast at the age of 38, treated with radical mastectomy, lymphadenectomy and chemoradiotherapy, free of disease since then with no recurrences.
Usual treatment: simvastatin 20 mg every 24 hours.

Present illness
On arrival at the emergency department, the patient reported a clinical picture of approximately 4 weeks of progressive deterioration of functional class to the point of presenting dyspnoea at rest (NYHA IV), as well as orthopnoea that forced her to sleep in a sitting position. She also reported a subjective decrease in the volume of diuresis, without associated swelling of the lower limbs. She had no anginal chest pain either at rest or on exertion. He denied any infectious symptoms when questioned by apparatus.

Physical examination
Blood pressure (BP) 122/70 mmHg, heart rate (HR) 100 bpm, O2 Sat 95% with FiO2 35%. Jugular venous pressure increased (15 cm). Cardiac auscultation: rhythmic, with systolic murmur in aortic focus radiating to IV/VI carotid arteries, with abolition of the second sound. Systolic murmur in mitral focus radiating to axilla III/VI. Pulmonary auscultation: mediobasal crackles. Abdomen: soft and depressible, not painful on deep palpation, no masses or megaliths, Blumberg and Murphy negative. Positive hepatojugular reflux. Extremities: no oedema in the lower extremities, peripheral pulses preserved and symmetrical, no signs of phlebitis.
Echoscopy was performed at the bedside in the emergency department, which showed calcification of the aortic valve with severely limited opening, as well as calcification of the mitral valve apparatus with significant regurgitation, so it was decided to admit the patient to the cardiology ward for stabilisation, complete the study and assess therapeutic options.

COMPLEMENTARY TESTS
Portable chest X-ray on admission: cardiomediastinal silhouette not assessable. Left costophrenic sinus impingement. Prominent pulmonary hilarity with a vascular appearance. Signs of vascular redistribution.
Electrocardiogram: sinus tachycardia at 110 bpm. Normal PR. Normal axis. Voltage criteria of left ventricular hypertrophy. QRS 120 ms with intraventricular conduction disturbance type BRI. Signs of systolic overload.

Laboratory tests on admission:
Haemoglobin 16.2 g/dl, no leukocytosis or left shift, platelets 232 x 10^9/l.
Haemostasis: INR 1.2, APTT 30.1 sec.
Biochemistry: glucose 127 mg/dl, creatinine 1.00 mg/dl, GFR 55.8 ml/min/1.72 m, sodium 137 mEq/l, potassium 3.5 mEq/l, total bilirubin 1.2 mg/dl, GOT 45 IU/l, GPT 35 IU/l, C-reactive protein 0.1 mg/dl.
Blood tests after clinical deterioration:
Haemoglobin 15.4 g/dl, no leukocytosis or left shift, platelets 195 x 10^9/l.
Haemostasis: INR 1.9, aPTT 40 sec.
Biochemistry: glucose 150 mg/dl, creatinine 1.94 mg/dl, GFR 25.1 ml/min/1.72 m, sodium 143 mEq/l, potassium 4.2 mEq/l, total bilirubin 2.7 mg/dl, GOT 150 IU/l, GPT 263 IU/l, C-reactive protein 2.3 mg/dl.
Echocardiogram: non-dilated left ventricle (LV) with mild concentric hypertrophy. Global hypokinesia of septal and anterior predominance with severely depressed GSF (LVEF 25%). Dilated left atrium. Double aortic lesion on severely calcified valve: severe stenosis (planimetry 0.5 c,mGm 52 mmHg). Moderate regurgitation (THP 260 ms). Moderate mitral regurgitation (II-III/VI) on sclerodegenerative valve (ERO by PISA 0.25 cm2). RV with non-enlarged diameters and preserved GSF (TAPSE 18 mm). Moderate tricuspid regurgitation that allows estimating PsAP at 70 mmHg. Inferior vena cava (IVC) plethoric.
Coronary angiography 1: calcification of ascending aorta, intensely calcified sigmoid arteries with reduced opening, severe stenosis (peak gradient 55 mmHg). Coronary arteries: normal trunk. Anterior descending artery with 80% lesion in the middle segment. Circumflex artery with irregularities without stenosis. Right coronary artery with 90% lesion in proximal segment.
Thoracic CT without contrast: marked calcified atheromatosis in the thoracic aorta, especially in the location of the aortic button. Calcification of the aortic valve, tricuspid valve and right coronary artery.
Coronary angiography 2: percutaneous transluminal coronary angioplasty (PTCA) was performed on the LAD and RCA lesions with implantation of everolimus-eluting drug-eluting stents, with good angiographic results.
TAVI implantation: after balloon valvuloplasty, a 23 mm SAPIEN ULTRA prosthesis was implanted. After implantation, electromechanical dissociation without identifying coronary occlusion, contrast extravasation to the pericardium, aortic rupture or prosthetic embolisation.

CLINICAL EVOLUTION
After admission to the cardiology ward, the patient initially evolved favourably, but subsequently presented clinical deterioration due to a new increase in dyspnoea associated with a marked decrease in the volume of diuresis (< 10 ml/kg/h) and hypotension (BP 73/35 mmHg), so that in view of the situation of cardiogenic shock it was decided to admit her to the coronary unit for stabilisation.
Vasoactive support was started with noradrenaline at 12 mcg/min and inotropic support with dobutamine at 10 mcg/kg/min, as well as intensive diuretic therapy with iv perfusion of furosemide at 20 mg/h, with an initial favourable response that allowed negative balances to be maintained without the need to start ultrafiltration therapy.
The echocardiographic study confirmed the presence of severe ventricular dysfunction and severe aortic stenosis (and moderate aortic regurgitation) and diagnostic coronary angiography detected severe two-vessel coronary artery disease, as well as significant calcification of the ascending aorta, which was confirmed by non-contrast thoracic CT.
With these findings, the case was presented at the medical-surgical session, and surgical valve replacement by the HEART Team was rejected given the patient's clinical situation, with an excessive surgical risk (EuroSCORE II 80.35%), as well as her anatomical characteristics, with very marked aortic calcification that unacceptably limited the possibilities of cannulation for extracorporeal circulation.
In addition, given the presence of at least moderate aortic regurgitation, aortic balloon valvuloplasty as a bridge to TAVI was ruled out and it was decided to initially stabilise the patient in the OCU and, depending on the evolution, to consider two-stage treatment with percutaneous revascularisation of the coronary lesions and subsequent percutaneous aortic valve replacement.
During his stay in the OCU, the evolution was slowly favourable and, after treatment with IV levosinendan, inotropic support could be withdrawn, requiring only vasopressor support with low doses (0.1 - 0.2 mcg/kg/min) of NA. Percutaneous revascularisation of the AD and DC lesions was performed.
Finally, percutaneous valve replacement via the right femoral artery was attempted, and after expansion of the bioprosthesis, the patient presented cardiac arrest due to electromechanical dissociation, with no immediate complications derived from the technique (coronary occlusion, pericardial contrast extravasation, aortic rupture, or prosthetic embolisation), so advanced cardiopulmonary resuscitation manoeuvres were started, resulting in exitus after 40 min without achieving recovery of spontaneous circulation.

DIAGNOSIS
Double sclerodegenerative aortic lesion: severe stenosis and moderate regurgitation. Moderate mitral regurgitation on sclerodegenerative valve.
Severe ventricular dysfunction (LVEF 25%).
Ischaemic heart disease: two-vessel disease: CDp 90%, DAm 80%. PCI with implantation of two everolimus-eluting drug-eluting stents.
Porcelain aorta.
Cardiogenic shock.
Failed percutaneous aortic bioprosthesis implantation due to death during the procedure.
