HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

A 79-year-old woman attended the emergency department due to gait instability.

History
Cardiovascular risk factors (CVRF): hypertension. Dyslipidaemia treated with diet. No previous cardiological history. Cardiology assessment in another centre in 2017, at that time normal electrocardiogram (ECG). Other history: depression: recent start of sertraline. Phakectomy. Traumatic brain injury (TBI) secondary to a fall at home (no syncope). Previous medication: acetylsalicylic acid 100 mg (0-1-0), hydroferol (1 ampoule every 15 days), hydrochlorothiazide/amiloride 5/50 mg (1-0-0), sertraline 50 mg (1-0-0).

Present illness
He reports gait instability of a week's duration prior to admission, which he relates to the initiation of sertraline due to depressive mood. Denies presyncope/syncope. He has a history of a fall with secondary cranioencephalic trauma, assessed in a private centre by means of a CAT scan and laboratory tests, which were normal. He denies chest pain at all times. No dyspnoea, orthopnoea or paroxysmal nocturnal dyspnoea. No other cardiovascular symptoms. No fever or infectious, respiratory or gastrointestinal symptoms.

We were alerted by elevated markers of myocardial damage and electrocardiogram alterations.

Physical examination
Blood pressure (BP) 117/70 mmHg, heart rate (HR) 85 bpm, temperature 36 oC. Conscious and oriented, good general condition. Eupneic in decubitus, no respiratory work. Cardiac auscultation: rhythmic, systolic murmur in low left sternal border. Pulmonary auscultation: preserved vesicular murmur without added noises. Lower limbs: no oedema. Normal neurological examination.

COMPLEMENTARY TESTS
ECG on admission: sinus rhythm at 90 bpm. Normal PR. Narrow QRS with normal axis, anterior QS, ST elevation of 1-2 mm in precordial and submillimetric in inferior face, negative T in I-aVL. ECG at 48 hours: ST elevation in V2-V6 up to 3 mm in V3 with negative T wave in all precordial leads. Rest unchanged. ECG at discharge: sinus rhythm at 60 bpm, normal PR, narrow QRS, deep and symmetrical negative T wave in inferior face, I and aVL and V2-V6. Ambulatory blood test (day of TBI): sodium 142 mmol/l, potassium 4.0 mmol/l, troponin 1.4 ng/l. Blood tests: haemoglobin 10.8 g/dl, MCV 81, platelets 310000, leucocytes 21700 (neu19800, lin 500). INR 1.02, dim ero D 223, pH 7.49, pCO2 32, bicarbonate 24, lactate 2.8, sodium 104 mmol/l, potassium 3 mmol/l, glucose 109 mg/dl, ALT 23 IU/l, bilirubin 1 mg/dl, GGT 13 IU/l, FA 72 IU/l, LDH 330 IU/l, creatinine 0.78 mg/dl, glomerular filtration rate > 60 ml/min/1.73 m2, magnesium 1.2 mmol/l, CRP 1.4, procalcitonin 0.07. Cardiac markers: ultrasensitive troponin I 8517-->8410 --> 319 ng/l, NT-proBNP 2981 - -> 25000 --> 11500 ng/l. Urinalysis: Sediment: erythrocytes 5-10/field, leukocytes 40-60/field, esterase +, Hb +, protein +. Biochemistry: single micturition osmolality 492 mOsm/kg, single micturition sodium 28 mmol/l, single micturition potassium 51.2 mmol/l. PCR SARS-CoV-2: negative. Chest X-ray: favourable radiological evolution of heart failure data. Cranial CT scan: no evidence of acute intracranial pathology in the post-traumatic context of the patient. Right frontal epicranial contusion/hematoma without bone fractures.

Echocardiogram: left ventricle not dilated, with normal wall thickness. Akinesia of middle and distal segments of all faces and apex. Hyperkinesia of the basal segments. Moderately depressed global systolic function. LVEF 30-35%. Pseudonormalised transmitral filling pattern. Slightly dilated left atrium. Right atrium not dilated. Aneurysm of the interatrial septum displaced towards the right atrium as an indirect sign of increased left atrial pressure. Right ventricle not dilated, with normal global systolic function. Rest normal. Cardiac magnetic resonance (CMR): left ventricle: a) size and function: normal size, with normal thickness. Hypokinesia of the distal segments of all faces and apex. Basal segments are hypercontractile. Global left ventricular function at the lower limit of normality (LVEF 52%). b) T2-STIR: a hyperintense transmural zone affecting the middle and distal segments of all the faces is observed. c) First-pass perfusion: no alterations. d) Late enhancement: no alterations. Right ventricle: a) Size and function: normal size, not hypertrophic, normocontractile. b) T2-STIR: hyperintensity is observed at the level of the apical segment. c) Late enhancement: no alterations. Left atrium not dilated. Right atrium of normal size. Mitral valve with thin leaflets, normal opening. Aortic valve trivalve, functionally normal. Bilateral pleural effusion. Perihilar opacities more suggestive of heart failure. Conclusions: study compatible with stress cardiomyopathy (tako-tsubo syndrome). Data compatible with myocardial oedema affecting the middle and distal segments of the left ventricle, without evidence of late enhancement or segmental perfusion alterations. Global systolic function at the lower limit of normal (LVEF 52%). Coronary angiography: smooth coronary arteries.

CLINICAL EVOLUTION
The patient presented with instability in the context of severe hypoosmolar hyponatraemia (sodium 104 mml/l on admission) euvolaemic with normal urine osmolarity in the probable context of recent initiation of sertraline and potentiated by the concomitant use of hydrochlorothiazide/amiloride. Cranial CT scan with no acute findings. There was also associated hypomagnesaemia and hypokalaemia. In this context, he had an elevated troponin plateau (8500-->8400 ng/l), ECG with anterior QS and residual ST elevation and echocardiogram with previously unknown LVEF 35% and alterations in segmental contraction compatible with takotsubo syndrome/stress cardiomyopathy. Admission to cardiology for monitoring was decided. Sertraline was discontinued and intravenous sodium replacement with serotherapy was started, as well as oral potassium and magnesium replacement, with progressive improvement in natraemia without residual neurological focality. Coronary angiography ruled out obstructive coronary disease. Cardiopathy study was completed with findings compatible with stress cardiomyopathy with LVEF 30-35% on admission, which recovered to near normal (50-55%) on discharge. As the probable origin of the hydroelectrolytic disorder, the use of drugs (thiazides + SSRIs) + SIADH secondary to TCE (Na levels tested in September 2020, normal) is proposed. As a cause of the tako-tsubo syndrome, the main option is severe hyponatraemia present on admission associated with creaneoencephalic trauma.

At discharge asymptomatic, afebrile, haemodynamically stable, with sodium of 139 mmol/l. Follow-up in the cardiology day hospital, with normalisation of ventricular function and asymptomatic.

DIAGNOSIS
Stress cardiomyopathy secondary to severe hyponatremia. Coronary arteries without lesions.
Ventricular function severely depressed, recovered.
Severe hypoosmolar euvolaemic hyponatraemia of probable pharmacological cause + SIADH to TBI.
Cranioencephalic trauma. Arterial hypertension. Dyslipidaemia.
Depressive syndrome in treatment with sertraline.
