HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

BACKGROUND:
No known drug allergies.
Smoker of 6 cigarettes a day since the age of 17.
Cardiovascular risk factors (CVRF): hypertension (HT), dyslipidaemia on dietary treatment, no diabetes mellitus (DM).
Recurrent bladder tumour in follow-up by urology with annual cystoscopy.
Prostatic neoplasia with metastatic involvement in hormonal treatment.
Surgical history: bladder TUR in 2013 and 2014.
Usual treatment: amlodipine 5 mg/day, enalapril/hydrochlorothiazide 20/12.5 mg/day, iron (ferrous sulphate) 105 mg/day, bicalutamide 50 mg/day.

CURRENT ILLNESS:
72-year-old male patient brought to the emergency department of our centre for progressive dyspnoea over the previous 3-4 days until becoming minimal effort, together with accompanying asthenia.
He denied chest pain. No cough or expectoration, no fever or dysthermic sensation.

PHYSICAL EXAMINATION:
Regular general condition, mucocutaneous pallor, normohydrated. Eupneic at rest without use of accessory muscles. Conscious, oriented and cooperative without apparent neurological focality.
Blood pressure (BP) 81/56 -> 103/66 mmHg, heart rate (HR) 100 bpm, oxygen saturation (SatO2) 94% (ambient air). Cardiac auscultation: rhythmic tones without audible murmurs. Pulmonary auscultation: preserved vesicular murmur without added sounds. No oedema in the lower limbs.

COMPLEMENTARY TESTS
ELECTROCARDIOGRAM (ECG) on admission: sinus rhythm at 60 bpm, 60o axis, PR 160 msec, narrow QRS, ST-segment depression of 1.5 mm in II, III and aVF with minimal Q wave, ST-segment depression with a maximum of 2 mm in V2-V4.
ANALYSIS: creatinine 1.49 mg/dl (baseline around 1 mg/dl), CRP 130.6 mg/l, haemoglobin 8.0 g/dl and ultrasensitive troponin T 4,669 pg/ml.
THORAX RADIOGRAPHY: severe changes due to chronic obstructive pulmonary disease (COPD). No pneumothorax was identified. Cardiomegaly. Calcified aortic atheromatosis. No consolidation or pleural effusion.
CORONARYGRAPHY: left coronary trunk (LMCA): of good calibre, without lesions. Anterior descending artery (ADA): good calibre and development, irregularities without significant angiographic lesions. Circumflex artery (ACX): good calibre and scarce development, without significant angiographic lesions. Right coronary artery (RCA): dominant, tortuous, with diffuse disease in the proximal and middle segment and thrombotic occlusion in the middle segment. No clear collateral flow (slight homocoronary).
Transthoracic echocardiography: ventricular septal defect due to rupture of the interventricular septum in the lower medial area where there is a solution of continuity and an anfractuous trajectory. A maximum gradient between LV and RV of 51 mmHg is determined and the width of the jet between both ventricles is 16 mm. A Qp/Qs of 2.2 is calculated. Dilatation of the right chambers and the left ventricle was observed and a left ventricular ejection fraction of 38% was estimated using Simpson's method. There is akinesia of the posterior wall and the basal and medial inferior septum. The aortic valve is slightly sclerosed, with a normal gradient. The mitral valve shows signs of annular fibrosis, preserved opening and grade II/IV, central insufficiency, probably related to the altered mobility of the ventricular wall. Mild tricuspid insufficiency (TI) is observed, which allows estimating a systolic pulmonary artery pressure (PAP) of 49 mmHg. No significant pericardial effusion was observed.

CLINICAL EVOLUTION
The patient was initially admitted to the intensive care unit with a diagnosis of acute myocardial infarction of probably inferior location. Coronary angiography showed thrombotic occlusion in the middle segment of the RCA, but given the chronology of the condition, the infarction was considered to be subacute, and therefore intervention was ruled out.
Subsequently, the patient presented symptoms and signs of heart failure, and transthoracic echocardiography showed ventricular septal rupture with a maximum size of 16 mm, left-right shunt with a maximum gradient of 58 mmHg, overload of the right cavities, Qp/Qs of 2.2 and LVEF by Simpson of 38% with alterations in contractility in the RCA territory. The case was discussed with cardiac surgery and conservative management was decided jointly given the poor prognosis and comorbidity of the patient. The patient was transferred to the hospital ward on the third day and required occasional morphine rescue due to dyspnoea. Finally, given the situation of refractory heart failure, exclusively symptomatic treatment was established and the patient died on the eighth day of admission.

DIAGNOSIS
Advanced acute inferior myocardial infarction.
Thrombotic occlusion of non-revascularised middle right coronary artery.
Ventricular septal rupture.
Refractory heart failure.
Death.
