HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION
We present the case of a 42-year-old man who was admitted to cardiology for a first episode of heart failure, with a diagnosis of dilated cardiomyopathy.
His personal history includes abuse of various intoxicants (GHB [gamma-hydroxybutyric acid], mephedrone and methamphetamines on a regular basis; occasional cocaine; smoker of 10 cigarettes a day; occasional testosterone cycles). He is HIV positive with good immunovirological control under treatment with dolutegravir/rilpivirine, and had syphilis which was correctly treated.
He came to the emergency department for one week of progressive dyspnoea until he became resting, associated with orthopnoea and episodes of paroxysmal nocturnal dyspnoea. She also presented with neurological symptoms consisting of dyschromatopsia and retroocular headache. She had not suffered from chest pain, palpitations or other cardiovascular symptoms.
Physical examination revealed the presence of jugular venous engorgement, with a gallop rhythm in the third tone and crackles up to midfield on pulmonary auscultation.

COMPLEMENTARY TESTS
Electrocardiogram (ECG): sinus tachycardia at 125 beats per minute. Narrow QRS, axis deviated to the left. Poor R growth in precordial leads. Flattened T waves with normal QTc interval.
Chest X-ray: increased cardiothoracic index. Signs of pulmonary congestion.
Transthoracic echocardiogram on admission: very dilated left ventricle, with severe systolic dysfunction. LVEF 12%. Mobile images in apex, at least 3, maximum 1.8 x 1.0 cm, hypermobile, compatible with thrombi. Dilated right ventricle, with severe systolic dysfunction. Signs of elevated filling pressures. Moderate mitral insufficiency. Moderate pulmonary hypertension.
Laboratory tests on admission: NT-proBNP 15678 ng/dl. Undetectable HIV load.


Cranial computerised axial tomography (CAT): appearance of cortico-subcortical hypodensity in the right PCA territory, probably related to an ischaemic event of uncertain evolution.
Cranial magnetic resonance imaging (MRI): cortical lesions with contrast uptake and mild diffusion restriction suggesting subacute phase infarcts, the largest right basal occipital with haemorrhagic transformation. There are also three millimetric cortical lesions with intense restriction (right frontal, left frontal and right parietal) that also suggest infarcts but with a shorter evolution time.
Cardiac MRI: severely depressed biventricular systolic function (LVEF 12%, RVEF 14%). Mild-moderate mitral insufficiency. Severe left atrial dilatation. No intracavitary thrombi. Pathological late enhancement in the insertion region of the right ventricular free wall and linear intramyocardial uptake in the basal septum of non-ischaemic aetiology.
Diagnostic coronary angiography: coronary arteries without significant lesions. Genetic study: negative.

CLINICAL EVOLUTION
From the point of view of heart failure, the patient evolved favourably with diuretic treatment until complete resolution of the congestive symptoms. Disease-modifying treatment was started with sacubritril/valsartan, low-dose bisoprolol due to suboptimal tolerance, spironolactone and ivabradine. On monitoring, episodes of paroxysmal atrial fibrillation were detected, as well as episodes of non-sustained monomorphic ventricular tachycardia. Therefore, in view of the negative ventricular remodelling and the presence of late enhancement on MRI, it was decided to implant an implantable cardioverter defibrillator (ICD) for primary prevention.
As a study of ventricular dysfunction, ischaemic aetiology was ruled out by coronary angiography and familial aetiology by genetic study; the possibilities were toxic or HIV-associated cardiomyopathy.
Regarding antithrombotic treatment, anticoagulant treatment was started on admission with low molecular weight heparins due to the presence of intracavitary thrombi and paroxysmal atrial fibrillation. It was discontinued during admission after brain MRI showed haemorrhagic transformation of the cerebral infarction. At discharge, in the absence of new bleedings and once the absence of interactions with antiretroviral treatment had been verified, oral anticoagulation with rivaroxaban was started.

DIAGNOSIS
First episode of heart failure. Severe biventricular dysfunction.
Coronary arteries without significant lesions. Non-sustained monomorphic ventricular tachycardia. Paroxysmal atrial fibrillation.
Intracavitary thrombus (left ventricle), not seen in cardiac MRI after initiation of anticoagulation.
Subacute ischaemic stroke in the right PCA territory of probable cardioembolic aetiology, with subsequent haemorrhagic transformation. HIV infection under treatment with good control. Intake of toxic substances.
