HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

PERSONAL HISTORY
71-year-old woman, with no known drug allergies, hypertensive, obese, dyslipidemic and diabetic; with a history of hypothyroidism under replacement therapy and left knee replacement surgery 5 years ago. No personal or family history of heart disease or sudden death.
She is on regular treatment with: omeprazole 20 mg/24h, simvastatin 20 mg/24h, olmesartan/amlodipine/hydrochlorothiazide 40/10/12.5 mg/24h, levothyroxine 175 mcg/24h and insulin.

CURRENT ILLNESS
The patient consults because for the last 3 days she has been presenting progressive dyspnoea until minimal effort, together with episodes of orthopnoea and paroxysmal nocturnal dyspnoea; she does not report episodes of angina or other associated symptoms. She presented significant respiratory distress, so the emergency health services were notified and she was transferred to our centre. Prior to admission, the patient was in New York Heart Association (NYHA) functional class I/IV.

PHYSICAL EXAMINATION
General condition was fair. Blood pressure (BP) 140/70 mmHg. Heart rate (HR) 110 bpm. PVY not assessable. O2 saturation with reservoir (FiO2 50%): 80%.
Tachypneic, with significant respiratory work. Conscious and oriented.
Cardiac auscultation: rhythmic heart sounds. Systolic murmur in mitral focus III/VI.
Pulmonary auscultation: fine crackles to upper lung fields and auscultatory silence in the right hemithorax.
Abdomen: globular, non-painful. No masses or megaliths palpable. No ascites.
Lower limbs: pulses present with slight bilateral pretibial oedema.

COMPLEMENTARY TESTS
ECG on admission: sinus rhythm at 70 bpm, PR 220ms, narrow QRS. Inferior Q wave. Poor R wave progression in precordial leads. QTc of 520 ms.
Portable chest X-ray on admission: cardiomegaly. Bilateral alveolar oedema. Right pleural effusion.
Laboratory tests during admission:
Haemogram: 11,100 leukocytes (76% neutrophils), haemoglobin 12.5 g/dl, haematocrit 43%, 388,000 platelets,
Biochemistry: creatinine 1.02 mg/dl (glomerular filtration rate 52 ml/min/m2), urea 46 mg/dl, ions normal. Peak myocardial damage markers: CK 316 U/l (CK MB40), TnUS 332 ng/dl. Hb1AC 6.8%. Total cholesterol 143 g/dl, HDL 41 mg/dl,
Triglycerides 76 mg/dl.
Coagulation: INR 1.06; prothrombin rate 91%. proBNP on admission: 17680 pg/ml.
Transthoracic echocardiogram: dilated left ventricle (DTd 61 mm), with postero-basal and infero-basal akinesia. LVEF calculated by Simpson biplane of 35%.
Right ventricular dysfunction (TAPSE 11 mm). Severe mitral insufficiency by Carpentier mechanism IIIb. Mild tricuspid regurgitation with pulmonary hypertension at rest (50 mmHg).
Transesophageal echocardiogram: mitral valve with calcification of the annulus, fibrosis of the leaflets with restriction of movement of the posterior leaflet leading to severe regurgitation. Posterior leaflet 10-11mm. Mild tricuspid regurgitation. Right ventricular dysfunction. Left atrial appendage free of thrombus.
Haemodynamic study: three-vessel coronary artery disease. Right dominance. Coronary anomaly consisting of origin of all the coronary arteries in the right sinus of Valsalva, with independent ostium. Severe stenosis of the middle anterior descending artery (ADA), severe stenosis in the first obtuse marginal (OM1) and occlusion of chronic appearance in the distal right coronary artery (RCA), whose distal vessel is filled by heterocoronary circulation.
Ventriculography: severely dilated left ventricle (LV), with severe depression of LVEF (31%) at the expense of inferior and posterolateral akinesia and hypokinesia of the remaining segments.
Angioplasty: the OM1 lesion was predilated and a 2.75 x 15 mm drug-eluting stent was implanted to cover the lesion with good angiographic results. The middle LAD lesion is then predilated with a balloon and a 2.25 x 38 mm drug-eluting stent is implanted with a good final angiographic result.

CLINICAL EVOLUTION
On arrival at the emergency department, the patient was found to have acute pulmonary oedema and was admitted to the coronary unit, where ventilatory support was started with non-invasive mechanical ventilation and diuretic and vasodilator treatment with a good response, achieving stabilisation of the clinical picture within a few hours.
An echocardiogram showed severe mitral regurgitation due to restriction of posterior leaflet mobility (mechanism IIIb of Carpentier's classification). Subsequently, a haemodynamic study was performed which revealed a coronary anomaly consisting of the origin of the left coronary tree in the right sinus of Valsalva and severe three-vessel coronary artery disease. After discussing the case with the cardiac surgery department of our centre, percutaneous revascularisation of OM1 and ADA was decided, with subsequent re-evaluation of mitral insufficiency (MI).

After percutaneous revascularisation, the patient showed good clinical evolution, although the heart failure data persisted despite diuretic treatment, so after discussing the therapeutic alternatives with the heart team and in agreement with the patient, percutaneous treatment of her mitral valve pathology was decided using a MitraClip device; this procedure was successfully performed one month after hospital discharge, with a single clip implanted in the mitral position, guided by fluoroscopy and transesophageal echocardiography, with a reduction in regurgitation from grade 4+ to 1+, with no post-implant residual mitral stenosis.
After the procedure, the patient had a good clinical evolution and was discharged two days after the procedure.

DIAGNOSIS
Dilated cardiomyopathy of ischaemic aetiology with moderate left ventricular dysfunction (35%). Old inferior myocardial infarction.
Coronary anomaly (origin of all coronary arteries in the right sinus of Valsalva, with independent ostium).
Severe three-vessel coronary artery disease. Partial percutaneous revascularisation (anterior descending [AD] and circumflex [Cx]).
Severe mitral regurgitation by Carpentier mechanism IIIb. Percutaneous mitral repair by MitraClip device successful and without complications.
