HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
70-year-old woman.

Personal history
No known allergies.
No toxic habits.
No cardiovascular risk factors.
Pulmonary thromboembolism in 2006.
OI haemianopsia since 2010 due to anterior ischaemic neuropathy.
Undifferentiated connective tissue disease with ANA+, under control by Rheumatology. Secondary hyperparathyroidism.
Right renal lithiasis.
Depressive syndrome.
IQ: appendectomy, cholecystectomy.

Usual treatment: omeprazole, ASA, leflunomide, hydroxychloroquine, denosumab, duloxetine. ʟʟ Baseline functional status: active life, independent in basic activities of daily living. Preserved higher functions.

Current illness
She came to the emergency department for 24 hours of progressive dyspnoea until she became resting, together with palpitations and intermittent episodes of oppressive, non-radiating precordial pain, without vegetative cortex and self-limited in a few minutes. She did not report oliguria or oedema in the previous days.

Physical examination
BP: 136/84mmHg.
HR: 124lpm; SatO2 with O2 at 3L: 95%.
Afebrile.
Conscious and oriented. Impression of gravity. Prostrate and sweating, but with good peripheral perfusion. Tachypnoea at 26 rpm at rest.
Head and neck: no jugular plethora.
AC: rhythmic tachycardia, systolic murmur II/IV in aortic and mitral focus.
PA: crackles up to bilateral midfields, no other superimposed sounds.
Abdomen: soft, not painful on palpation, without signs of peritonism. Bowel sounds present.
Extremities: no oedema or signs of DVT. Femoral and pedial pulses present.


COMPLEMENTARY TESTS
ECG: sinus tachycardia at 114 bpm, QRS axis at 0o. Symmetrical negative T waves in III and avF.
Chest X-ray: bilateral alveolar infiltrates, predominantly perihilar, more marked in the right hemithorax. Pinching of both costophrenic sinuses.
Blood tests: arterial blood gases: pO2 64mmHg, pCO2 32 mmHg, pH 7.27, HCO3 18. Biochemistry: glucose 142mg/dL, urea 110 mg/dL, creatinine 0.96 mg/dL, albumin 3.56 g/dL, CK 159 U/L, ultrasensitive TnT 418. GPT 63 U/l. Na 142 mmol/L, K 4.7 mmol/L. Haemocytometry: Hb 12.6 g/dL, MCV 93 fL, Hcto 31.9%. Platelets 170,000. Leukocytes 12,100 (82% polymoronuclear). Coagulation: Prothrombin index 72%, INR 1.15, activated partial thromboplastin time 38 sec.
Angio-CT of pulmonary arteries: no repletion defects in pulmonary arteries and their branches suggestive of PTE. Aorta of normal calibre and morphology along its thoracic course. Extensive alveolar infiltrates in the right upper lobe and middle lobe. Bilateral pleural effusion, larger in the right hemithorax. Signs of right heart failure with contrast reflux to the inferior cava and suprahepatic arteries, and rectification of the interventricular septum.
Transthoracic echocardiogram: LV not dilated or hypertrophic, with hypokinesia of mediobasal segments of inferior and posterior (inferolateral) face and good global and segmental systolic function. Trivalve aortic valve, normofunctioning. Prolapse of the posterior leaflet of the mitral valve due to rupture of the chordae tendineae, causing a massive eccentric mitral flail directed towards the interatrial septum. Non-dilated left atrium. Non-dilated RV with moderate dysfunction. No pericardial effusion.
Coronary angiography: the common trunk shows mild atheromatosis. The anterior descending artery shows diffuse irregularities with a moderate lesion in the middle segment affecting the origin of the first diagonal, with moderate stenosis. The circumflex artery is of medium development, destined to two obtuse marginal branches with mild atheromatosis, without significant lesions. The right coronary artery is the dominant vessel, of great development. In its middle segment there is a very angulated lesion with severe stenosis. Good distal bed.

EVOLUTION
The patient was assessed in the emergency department and was found to have acute pulmonary oedema with haemodynamic stability initially. Echocardioscopy performed in the emergency department revealed severe mitral insufficiency due to posterior mitral prolapse and possible rupture of the chordae tendineae, so it was decided to transfer her to the coronary care unit, while Cardiac Surgery on duty was contacted to assess urgent surgery, and the haemodynamicist on duty to perform coronary angiography, with the findings described above. On arrival at the coronary unit, oxygen therapy was administered with 100% oxygen reservoir, intravenous diuretic and low-dose ACE inhibitors, despite which he continued to worsen both from the respiratory and haemodynamic point of view, and was admitted to the operating theatre as an emergency patient. Under extracorporeal circulation, aortocoronary saphenous bypass is performed to the middle right coronary artery, with good vessel quality. Subsequently, access was gained to the left atrium, where a rupture of a chordae tendineae was observed at the level of the head of one belly of the posteromedial papillary muscle and a moderately unstructured mitral valve, for which reason it was decided to replace the mitral valve, implanting a biological prosthesis of no. 27. The patient was transferred back to the coronary unit. In the postoperative evolution, the patient presented severe pump failure in the first hours, requiring, in addition to inotropic support, intra-aortic balloon counterpulsation, which could be removed after 24 hours, with subsequent haemodynamic stabilisation. He also presented complete atrioventricular block, recovered in less than 48 hours, and perioperative atrial fibrillation, which was managed with a course of intravenous amiodarone. Once on the hospital ward, he presented septic symptoms of probable respiratory origin, requiring prolonged treatment with intravenous meropenem and vancomycin for 3 weeks. After a prolonged admission with slow physical rehabilitation due to the significant loss of muscle mass, the patient was finally discharged from hospital, with monitoring by Cardiology and Cardiac Surgery.

DIAGNOSIS
Acute pulmonary oedema
Severe mitral insufficiency due to partial rupture of the papillary muscle
Ischaemic heart disease with severe 1-vessel disease: medium CD
