PERSONAL HISTORY
No known drug allergies. Cardiovascular risk factors: arterial hypertension (HT). Dyslipidaemia (LD). Never smoker.
Cardiological history of interest: chronic ischaemic heart disease. Coronary artery disease of the left coronary trunk (LMCA) and 3 vessels surgically revascularised in 1992 (AMII-DA and AMID-OM). Admitted for unstable angina in 2010, with 90% disease of LMCA, occlusion of LMAD and occlusion of CXp and CDp; permeable bridges, so it was decided to indicate medical treatment. Last coronary angiography in April/2014 due to stable angina CCS III with positive exercise echocardiogram for extensive global ischaemia, implantation of drug-eluting stents on LMCA was performed with good results (same coronary anatomy, permeable bridges). Persistent atrial fibrillation with controlled ventricular response. CHADSVASc score 4.

Other relevant background: Stable bronchial asthma under follow-up in pulmonology. Spirometry performed in 2014: FVC 3840 (100%), FEV1 2610 (98%), index 71, negative bronchodilator test. Stage 3 chronic renal failure secondary to probable nephroangiosclerosis. Secondary hyperparathyroidism. Secondary chronic anaemia. Hyperuricaemia. Benign prostatic hyperplasia.  Surgical interventions: cholecystectomy. Functional status: dyspnoea NYHA functional class II. Stable angina CCS I. Retired taxi driver, occasionally works as a carpenter.

Usual treatment: fluticasone/salmeterol 50/500, aclidinium bromide 322 mcg, salbutamol if necessary, nitroglycerin transdermal patch 15 mg, atorvastatin 40 mg, dabigatran 110 mg/12h, allopurinol 100 mg, tamsulosin 0.4 mg, calcitriol 0.5 mg, omeprazole 20 mg.

CURRENT ILLNESS
77-year-old patient admitted to the pulmonology department in January/2015 with clinical manifestations of cough with haemoptotic expectoration and increased dyspnoea, afebrile. Initially managed with outpatient levofloxacin. Given the torpid evolution, he was transferred to the emergency department, where a chest X-ray showed cardiomegaly and bilateral pulmonary infiltrates, especially in the upper lobes. After 15 days on antibiotics, oxygen therapy, corticosteroids and diuretics, the clinical symptoms subsided and he was discharged in January 2015. During admission, an autoimmune and infectious study was performed with negative results, and a thoracic CT scan showed ground glass images in the upper lobes suggestive of pulmonary haemorrhage. Bronchoscopy was performed with hyperemic mucosa with no evidence of active bleeding, with bronchoaspirate with haemosiderophages (30% of macrophages with ferric material with positive Perls staining) and on discharge he was diagnosed with alveolar haemorrhage of probable infectious aetiology. He was admitted again in February 2015 from the outpatient pulmonology department as an emergency due to dyspnoea on slight exertion, orthopnoea and a new episode of haemoptysis. A new chest X-ray was performed showing cardiomegaly, data suggestive of heart failure and right basal infiltrate suggestive of pneumonia, afebrile, and a new hospital admission was decided.

PHYSICAL EXAMINATION
Blood pressure (BP) 141/72 mmHg, heart rate (HR) 75 bpm, SatO2 92% with FiO2 30%. Tachypnoea at rest. Good general condition. CBC: minimal IVY at 45 ̊. Cardiac auscultation: arrhythmic, aortic systolic murmur 3/6 with decreased R2; Gallavardin phenomenon. Pulmonary auscultation: bilateral wet crackles. Abdomen: soft, depressible, non-painful. Lower limbs: perimalleolar oedema. No evidence of deep vein thrombosis (DVT).

COMPLEMENTARY TESTS
ECG: atrial fibrillation at 75 bpm. Lateral ST rectification. CBC: haemogram: white blood cells 6.08 x10^9/l. Haematocrit 27.6%. Haemoglobin 9.1 g/dl. Platelets 289 x10^9/l. Biochemistry: glucose 90 mg/dl. Urea 57 mg/dl. Creatinine 1.33 mg/dl. Sodium 139 mmol/l. Potassium 4.3 mmol/l, ESR 1 hour 65 mm. NT-proBNP 4700 pg/ml. Chest X-ray: increased cardiopericardial silhouette. Vascular redistribution, bilateral perihilar oedema and minimal right pleural effusion. Right basal consolidation. Control chest X-ray: significant radiological improvement, with resolution of the right basal infiltrate. Bilateral alveolar infiltrates persist. Coronary angiography: no changes with respect to the previous study. Aorto-iliac axes not suitable for percutaneous prosthesis implantation (severe tortuosity in the right axis, ulcerated plaque in the left common iliac). Echocardiogram: left ventricle (LV) of normal size. Moderate concentric wall thickening. Preserved LV systolic function (LVEF > 55%). LA moderately dilated (49 mm). RV slightly dilated (45 mm) with preserved RVSF. Normal mitral valve with central 1/4 mitral regurgitation. Normal appearing tricuspid valve, central 2/4 IT with mild pulmonary hypertension (PH). Sclerocalcified aortic valve, with severe aortic stenosis (Vmax 4.5 m/s, mean gradient 40 mmHg, aortic valve area 0.78 cm2, TVI ratio 0.23); aortic regurgitation 2/4 central. Normal sized IVC with collapse > 50%. No pericardial effusion. Transesophageal echocardiogram monitoring transapical TAVI implantation: Baseline TEE: slightly calcified aortic valve with severe stenosis and central insufficiency grade 2/4. Aortic annulus 2.75 cm2 (2D: 18 mm, 3D diameters 17.5x18 mm). Aortic valve annulus-ICD ostium distance 11.8 mm. Mitral valve insufficiency grade 1/4. Tricuspid valve insufficiency grade 2/4. Normal LV systolic function (LVEF > 55%). No pericardial effusion. Intervention: implantation of a 23 mm SAPIEN 3 prosthesis via transapical route. Post-implantation TEE: well-positioned, normofunctioning biological aortic valve prosthesis, with trivial periprosthetic insufficiency. Normal LV systolic function. Rest unchanged with respect to the previous study.

CLINICAL EVOLUTION
This is a patient with repeated admissions for haemoptysis with migratory pulmonary infiltrates and examination data suggestive of decompensation of heart failure, as well as elevated natriuretic peptide levels, with good clinical-radiological evolution in the various admissions with diuretic treatment. The complementary tests performed were suggestive of alveolar haemorrhage (although the bronchoscopy showed no evidence of active bleeding, it was performed in a stable clinical situation after resolution of the haemoptysis, showing haemosiderin-laden macrophages with no evidence of active infection), the substrate of which seems to be decompensation of heart failure in the context of severe aortic stenosis. In view of these findings, the case was discussed with cardiology, and the case was presented at a medical-surgical session, and a decision was made to replace the aortic valve. Given the EuroScore of 7.3%, percutaneous replacement by femoral access was initially considered, but was ruled out after angiography in which inadequate aorto-iliac axes were observed. For this reason, it was decided to implant the prosthesis via transapical access. On 24/02/2015, a 23 mm Edwards SAPIEN 3 biological prosthesis was implanted under echocardiographic monitoring. After the intervention he was transferred to the coronary ICU, being extubated a few hours later without complications. He remained in the CICU for 48 hours with good clinical evolution, requiring transfusion of three red blood cell concentrates and slight deterioration of renal function, and was transferred to the cardiac surgery ward. During his stay on the cardiac surgery ward he evolved favourably without complications and was discharged after 7 days. Since then, the patient has been under active follow-up in cardiology consultations with no new admissions for haemoptysis or decompensation of heart failure, New York Heart Association (NYHA) functional status I-II, with control echocardiograms showing preserved systolic function and a normofunctioning prosthesis with trivial periprosthetic insufficiency.


DIAGNOSIS
Symptomatic severe aortic stenosis with heart failure decompensation. Diffuse alveolar haemorrhage secondary to heart failure. Transapical aortic valve replacement with biological prosthesis Edward Sapien 3 No23. Normofunctioning prosthesis at follow-up. Preserved systolic function. Moderate tricuspid regurgitation. Mild PH. Stable chronic ischaemic heart disease. LMCA and 3-vessel disease revascularised surgically (IAMI-AD, IAMI-OM in 1997) and percutaneously (stent implantation in LMCA-AD in 2013). Permanent atrial fibrillation (AF) anticoagulated with pradaxa. Cardiovascular risk factors: HBP. LD.
