HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

PERSONAL HISTORY
41-year-old woman. No drug allergies.
Medical history: migraines. Early menopause at the age of 37, no other known illnesses. Abortion at the age of 21. No family history of heart disease. Active smoking.
When asked about other toxic habits, she did not mention them.

CURRENT ILLNESS
On 10/02/2019 she was referred to the hospital emergency room from her health centre, accompanied by her brother, for presenting progressive dyspnoea of one month's evolution until becoming minimal effort accompanied by cough and orthopnoea on two pillows in the last 3 days. Cough without productive expectoration, on one occasion with haematic strands. There was no concomitant infectious semiology. In the last three days he also reported central thoracic discomfort on exertion and deep inspiration.

PHYSICAL EXAMINATION
Blood pressure (BP) 140/95 mmHg. Conscious and oriented, slightly tachypnoeic at rest (24 breaths per minute). Jugular venous pulse elevated.
Cardiac auscultation: rhythmic tones at 105 bpm with audible third sound.
Pulmonary auscultation: semiology of bilateral pleural effusion, more marked on the left.
No oedema in the extremities or decubitus.
The on-call cardiology department was contacted at that time. We performed portable echocardioscopy: we observed dilated left ventricle with systolic dysfunction at the expense of global hypocontractility, mitral valve with dilation of the mitral annulus and functional central insufficiency that appears to be of moderate degree and bilateral pleural effusion.
It was decided to admit the patient to the cardiology ward as the first episode of heart failure in a patient with no personal cardiological history and, a priori, without a definite aetiology, in order to study the systolic dysfunction and decompensation.
On arrival at the ward and once the patient was in the room, her brother approached us to tell us something important that the patient had been hiding from us: it turns out that our patient, although she had previously denied it, is a regular user of amphetamines.

COMPLEMENTARY TESTS
Electrocardiogram (ECG): sinus rhythm with negative T waves in V2-V6 and inferior face.
Blood tests:
Biochemistry: glucose 96 mg/dl, urea 0.37 g/l, creatinine 1.06 mg/dl, troponin Tus 41.73 ng/l, sodium 142 mEq/l, potassium 4.67 mEq/l, NT-proBNP 5993 pg/ml.
Arterial blood gases: pH 7.43, pO2 104mmHg, pCO2 32mmHg, sPO 298.2%, CO3H 21.4mmol/l.
Blood count: Hb 11.8 g/dl, Hct 34.6%, leukocytes 8l3 mil/mm3 with 55% neutrophils, platelets 172 mil/mm3.
Coagulation: no alterations, fibrinogen 378 mg/dl.
Urine toxicity: positive for amphetamines.
Chest X-ray: signs of interstitial oedema together with cardiomegaly, left costophrenic sinus impingement.
Transthoracic echocardiogram: left ventricle (LV) dilated and hypertrabeculated at apical level with moderate dysfunction (Simpson biplane 33%) at the expense of global hypocontractility. Increased filling pressures (mean E/e" 17 cm/sec). Left atrial dilatation (volume 94 ml) with atrial septal aneurysm without shunt. Mild functional mitral insufficiency. Right ventricle (RV) equally hypertrabeculated with normal size and contractility. Dilated IVC. Normal pericardium.
Coronary angiography: left dominance. Non-significant stenosis in the first obtuse marginal. Rest of the coronary tree without angiographic lesions.
Cardiac MRI: severely dilated LV (LVEDV 240 ml, LVESV 144 ml) hypertrabeculated at apical and lateral level, with discrete improvement of ventricular function (LVEF 40%) with global hypokinesia and akinesia at mid inferolateral, apical and mid inferior septal level. RV of normal size, hypertrabeculated at the free wall level and with RVEF 67%. There was also evidence of a small apical thrombus (6 x 9 mm). In the T1-weighted sequences, two foci of subendocardial enhancement are observed at the mid and apical inferolateral level and mid and apical septo-inferior septal level.

CLINICAL EVOLUTION
The patient had a very good response to depletive treatment with improvement of the congestive signs. Treatment was started for heart failure with systolic dysfunction using beta-blockers, ACE inhibitors and antialdosterone.
The study was completed with a regular echocardiogram and coronary angiography. The diuretic dose was titrated during admission and the patient was discharged a few days later with functional class I, maintaining treatment of the systolic dysfunction. Cardiac MRI was performed on an outpatient basis once the patient was discharged one month after the echocardiogram.
After hospital discharge, the patient has ceased the consumption of toxic substances, remains in New York Heart Association (NYHA) functional class I-II, and has not presented new episodes of decompensation.

DIAGNOSIS
Acute congestive heart failure, first episode of decompensation.
Dilated cardiomyopathy with moderate systolic dysfunction secondary to chronic amphetamine use.
Ejection fraction slightly recovered at follow-up.
Amphetamine abuse.
