HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
Patient aged 43 years with no personal or family cardiological history. Active smoking of 1 pack/day, no other toxic habits. No recent trips. No regular medication.

Current illness
Patient referred from the emergency department of a regional hospital for an abrupt picture of language alteration, with subtle nominative difficulties, paraphasia and fragmented and incoherent speech together with a tendency to somnolence of 12 hours of evolution. The previous day the patient had been skiing, without incident. A cranial computerised axial tomography (CAT) scan was performed, showing only an old left subthalamic infarction, and a lumbar puncture, with normal biochemistry (according to protocol, PCR for viruses was not indicated). On suspicion of an evolving cerebrovascular accident (CVA), he was referred to our hospital.
On arrival he was assessed by the emergency department. In the anamnesis, the family commented that they had had a mild upper respiratory catarrh two months ago, which had resolved. However, our patient had presented with a persistent non-productive cough for the last 30 days, which she did not attach particular importance to. In addition, in the last week, intolerance to decubitus together with slight oedematisation of the extremities, all compatible with cardiac decompensation.
A joint assessment by neurology and cardiology was requested.

Physical examination
Initially, the patient was assessed neurologically. Of note:
Hypofluent language, with subtle nominative disorder, isolated phonetic paraphasia, with preserved repetition and execution of complex commands. Emotional lability with a tendency to cry, fluctuating. Slightly reduced attentional spaming with alteration of working memory and minimal tendency to pronation without claudication of the right upper extremity.
MIS 0/8. The rest of the neurological examination was normal.
Subsequently, the cardiology examination was performed:
Blood pressure (BP) 152/100 mmHg, tendency to sinus tachycardia, oxygen saturation with nasal goggles at 3 bpm 95%.
Cardiac auscultation: rhythmic at 95 bpm, third sound, systolic murmur in mitral focus. Pulmonary auscultation: crackles to right midfield and left base. Abdomen without semiology of ascites, hepatomegaly of medial predominance of two traverses. Jugular ingurgitation +.
Slight bimalleolar oedema in decubitus.
Urine toxins, enterovirus, RSV and influenza serology were requested, all negative. Admission to cardiology with joint management by both specialties.

COMPLEMENTARY TESTS
Electrocardiogram: sinus rhythm at 93 bpm, normal PR, QRS 90 ms, QTc 416 ms. Sokolow-Lyon criteria for LVH. Negative T wave in III, AVF, V5-V6.
Chest X-ray: cardiomegaly, signs of vascular redistribution. Pinching of both costophrenic sinuses in relation to small bilateral pleural effusion.
Blood tests: urea 29 mg/dl, creatinine 1.02 mg/dl, calcium 8.2 mEq/l, magnesium 2 mEq/l, chlorine 108 mEq/l, sodium 137 mEq/l, potassium 3.9 mEq/l, GGT 70 U/l, GOT 84 U/l, GPT 111 U/l, total bilirubin 1.58 mg/dl, leukocytes 7300/mm, haemoglobin 12.9 g/dl, haematocrit 37.5%, platelets 173000/mm, prothrombin activity 95%, NT-proBNP 12396 pg/ml, CRP 2.66 mg/dl, ultrasensitive troponin I 1346 ng/l, D-dimer 2511 ng/ml. Negative urine toxins.
Lumbar puncture: biochemistry 5 red blood cells, 0 nucleated cells, chlorine 130, glucose 0.68, protein 0.37. Gram: no microorganisms found. Bacterial culture negative.
Microbiology: nasopharyngeal swab negative for influenza, enterovirus and respiratory syncytial virus. Rectal smear negative for enterovirus.
CT scan of the brain on admission: midline structures centred. Symmetrical ventricular system of normal size and morphology. Cortical sulci, peritroncular cisterns and cranial base without alterations. No haemorrhagic lesions were observed.
Bedside echocardiogram on admission: dilated left ventricle (LV) (LVED 60 mm) with normal wall thickness, severe ventricular dysfunction with estimated LVEF 15-20%. Global hypocontractility with no clear contractile asymmetries. Mitral valve (MV): thickened leaflets, tenting of both leaflets leading to severe secondary or functional mitral regurgitation. Competent aortic valve. Right ventricle (RV) of normal size, good longitudinal function but CAF 25%. Severe PI. Mild TR allowing estimation of RV-RA gradient 35 mmHg. Dilated inferior vena cava with abolished inspiratory collapse, moderate pulmonary hypertension. Minimal pericardial effusion lamina
Magnetic resonance imaging (MRI) of the brain: craniovertebral junction of normal morphology.
No midline abnormalities detected. Posterior fossa of normal configuration. Ventricular system of normal size and morphology. Base cisterns free. Vascular structures of correct configuration, dural venous sinuses permeable. T2 signal alteration in the left thalamic region with a distribution suggesting lacunar infarction by lenticulostriate artery, with almost complete restitution of diffusion. It suggests subacute infarction. A small subcortical T2 hypersignal is detected in the right insula, in the posterior frontal cortex, predominantly in the left hemisphere and in the right occipital juxtacortical white matter. Some small diffusion brightening is observed in the left frontal cortex, indicating acute cortical infarction at present. Conclusion: subacute lacunar infarction in the left thalamic region and acute cortical microinfarcts in the left posterior frontal cortex.
Cardiac MRI: poor image quality and impossibility of completing the study due to the patient's neurological condition. Dilated LV with severely depressed LVEF (20%). Failure of isovolumetric relaxation. Normal myocardial thickness and global hypocontractility. No oedema/swelling in myocardial thickness. Late enhancement not acquired because the patient was unable to complete the examination. Right ventricle of normal size with mild hypocontractility. Atria of normal size. Pericardial effusion 10 mm thick.
Echocardiogram at discharge: moderately dilated left ventricle with normal thickness (DTDVI 60 mm, indexed VTD 94 ml/m2). Moderate LV systolic dysfunction (LVEF estimated by Simpson biplanar 35%). Global hypocontractility. Pseudonormal diastole. Slightly dilated A.I. MV: thickened cusp leaflets (4 mm). Dilated annulus (38 mm). Preserved opening with posterior leaflet restriction. MI of central origin with jet directed towards the posterolateral wall of LA reaching the roof of the same, without reverse systolic flow in PVs with decreased systolic component (VC 6 mm, estimated ORE 0.30 cm2 and RV 51 ml), which by all data is estimated in grade III/IV. Right ventricle of normal size and function. Tricuspid valve normal in structure and function. Mild TR. Non-dilated IVC with preserved inspiratory collapse. Estimated normal PAPs.
Left and right catheterisation: coronary arteries without angiographically significant lesions. Normal pulmonary pressures.
Endomyocardial biopsy (EMB): insufficient material. Myocardial fragments with preserved structure. Interstitial inflammatory infiltrate consisting of neutrophilic polymorphonuclear neutrophils and lymphocytes, without myocyte damage. There were polymorphonuclear cells/mm2 and 3 CD3+ lymphocytes/mm. Viral PCR negative.
Echocardiogram at follow-up 6 months after discharge: LV indexed slightly dilated, normal wall thickness. Global systolic function preserved (LVEF 60%), without regional contractile abnormalities. Both atria of normal size. RV of normal size and function. MV: preserved opening, mild MI. Estimated pulmonary pressure normal. Absence of pericardial effusion.

CLINICAL EVOLUTION
Given the multidisciplinary management during admission, the neurological and cardiological evolution of our patient will be differentiated:

Neurological evolution
MRI was requested on admission showing a lesion compatible with left anterior thalamic infarction and EEG with no findings of interest. She remained alert and cooperative, mild bradypsychia, and showed some despair when faced with cognitive tests when she could not remember. MOCA 16/30, mainly in TE orientation, language fluency and delayed counting. Reads, but does not achieve full comprehension. Maintains some abstract thinking. Pending assessment by neuropsychologist after discharge. Subsequent periodic neuropsychological studies should be carried out in order to determine whether there is an evolutionary recovery of the cognitive disorders or to conclude her diagnosis as thalamic vascular dementia.

Cardiological evolution
Admission with frank heart failure with orthopnoea, bilateral pleural effusion, hepatomegaly and oedema. Treatment was started with levosimendan and furosemide with progressive improvement of congestive signs. Once stabilised, given acute HF of < 3 months of evolution with a history of upper respiratory tract infection, a cardiac MRI was performed which estimated severely depressed ventricular function (LVEF 20%), with no evidence of myocardial oedema, limited by the impossibility of administering gadolinium given the patient's neurological condition. Subsequently, coronary angiography was performed, with no lesions, right catheterisation showing normal pulmonary pressures and PVR and endomyocardial biopsy of the RV. The biopsy showed an interstitial inflammatory infiltrate consisting of polymorphonuclear (6/m) and CD3+ T lymphocytes (3/mm2) but myocytes with preserved structure. Echocardiogram at discharge showed improvement in ventricular function, estimated at 35%. Once stabilised, neurohormonal treatment was started with sacubitril/valsartan, carvedilol and spironolactone, pending a new control echocardiography three months after discharge, which showed complete recovery of ventricular function and normalisation of repolarisation in the patient's ECG.

DIAGNOSIS
Dilated cardiomyopathy with recovered severe ventricular dysfunction; suspected acute myocarditis (borderline).
Congestive heart failure of subacute onset.
Left thalamic stroke of cardioembolic origin: strategic location for cognitive impairment.
