PERSONAL HISTORY
Urological examination for elevated PSA, transrectal biopsy with result of low-grade prostate adenocarcinoma. Cardiovascular risk factors (CVRF): type 2 diabetes mellitus (DM) on treatment with oral antidiabetics (HbA1c 7.3%). Hypercholesterolemia. Ex-smoker for 4 months (IPA 30 paq/year).
Cardiovascular history: November 2017: evolved anterior infarction KK IV, performing emergent coronary angiography, and percutaneous transluminal coronary angioplasty (PTCA) to proximal anterior descending artery (LAD) with implantation of drug-eluting stent, with no other angiographically significant lesions. The patient was admitted to the coronary unit in cardiogenic shock, requiring occasional doses of IV noradrenaline. Treatment with angiotensin-converting enzyme inhibitors (ACE inhibitors) and beta-blockers was not started due to a tendency to hypotension, and ivabradine was started due to a tendency to tachycardia. On discharge echocardiogram, the presence of an apical aneurysm with apical thrombus was documented. As well as apical akinesia, anterior septal and middle segments of the inferior, anterior and posteroseptal walls. LVEF 27%. Mild-moderate mitral insufficiency.
Usual treatment: adiro 100 mg c/24 hours, clopidogrel 75 mg c/24 hours, pantoprazole 40 mg c/24 hours, ivabradine 5 mg c/12 hours, atorvastatin 80 mg c/24 hours, metformin 850 mg c/12 hours, sintrom according to guideline.

CURRENT ILLNESS
The patient presented 2 months after his infarction with clinical symptoms consisting of anorexia, asthenia and continuous pain in the right hypochondrium unrelated to ingestion, referred to as a feeling of fullness. The patient reports nausea, vomiting, choluria and acholia, with no clear dysthermic sensation; he also denies intestinal transit disorders. He has two dogs, vaccinated and dewormed. She has not made any recent trips to foreign countries or outings to the countryside, she denies the consumption of toxic substances, herbal products and alcohol. No recent changes in treatment. He has no relatives or people in his environment with similar symptoms. From the cardiovascular point of view, the patient has evolved favourably, being asymptomatic since discharge (he walks 6 km/day without dyspnoea or angina).

PHYSICAL EXAMINATION
Blood pressure (BP) 107/62 mmHg. Heart rate (HR) 92 bpm. Temperature 37.2 ̊C. Height 170 cm. Weight 63 kg. Waist circumference 86 cm. Body mass index (BMI) 22 kg/m2. Patient in good general condition. Well hydrated, nourished and perfused. Eupneic at rest. Head and neck: jaundiced conjunctiva. Jugular venous pulse (PVY) normal. Cardiac auscultation: rhythmic without murmurs. Pulmonary auscultation: preserved vesicular murmur, no extra sounds. Abdominal auscultation: hydro-aerial sounds present, normal tone, abdomen soft and depressible, not painful to superficial or deep abdominal palpation, no signs of peritoneal irritation. PPR negative bilaterally. Lower extremities: no signs of deep vein thrombosis (DVT). No oedema. Preserved paedial pulses.

COMPLEMENTARY TESTS
Laboratory tests (on admission): Hb 12.4 g/dl. Ht 36.5%. MCV 85 fl. Leukocytes 14,200/mm3 (N 70.2%, L 7.25%, Eo 22.53%). Platelets 409.000/mm3. CRP 12.8 mg/dl. INR 25. Glucose 224 mg/dl. Urea 52 mg/dl. Creatinine 0.95 mg/dl. GFR 86.6 ml/min. Sodium 136 mEq/l. Potassium 4.6 mEq/l. LDH 627 U/l. CK 76. ALT 202 u/l. AST 167 u/l. GGT 897 u/l. FA 546 u/l. BT 3.5 mg/dl (BD 2.11 mg/dl). Lipase 32 u/l. Calcium 10.1 mg/dl. Magnesium 1,6 mg/dl. Total cholesterol 261 mg/dl, triglycerides 130 mg/dl, HDL 60 mg/dl, LDL 174 mg/dl. Lp(a) 160 mg/dl, Apo A 157 mg/dl, Apo B 136 mg/dl. TSH 1.13 μU/ml, T4 11.7 mcg/dl. Glycosylated haemoglobin 7.4%. Ferritin 487 mg/dl. Iron 93 mg/dl. IST 17%. GV (on admission): pH 7.40, pCO2 37 mmHg, pO2 57 mmHg, HCO3 23 mEq/l, lactate 1.2 mmol/l. Electrocardiogram (ECG): RS at 70 bpm, normal PR, narrow QRS, QS on anterolateral side with no progression of R in precordial leads, persistent ST-segment elevation in anterolateral side.
Cardiac MRI: acute myocardial infarction (AMI) in the left anterior descending (LAD) territory with mildly dilated left ventricle (LV), apical aneurysm and akinesia of the anterior face and mid and distal anterior septum and all distal segments. Severe LV systolic dysfunction (LVEF 25%). Late enhancement of ischaemic features with absence of viability in anterior face and mid and distal septum and in all distal segments except lateral face. No intraventricular thrombi are seen. Mild right ventricular (RV) systolic dysfunction (RVEF 45%). Abdominal ultrasound: discrete hepatomegaly without identifying a clear focal lesion. Portal vein permeable. The gallbladder has no clear content inside. No dilatation of the biliary tract. The visible part of the pancreas shows no alterations. There are several lymphadenopathies in the hepatic hilum and the celiac region, the largest of pathological size 10 mm - 11 mm short axis. The trunk of the portal vein is permeable, of normal calibre with hepatopetal flow. Splenic and superior mesenteric veins also patent, not dilated. Suprahepatic veins patent, of normal calibre. Inferior vena cava also of normal calibre. Homogeneous spleen of normal size. Kidneys without pyelocaliceal dilatation or clear lithiasis. Distended bladder without clear alterations. Prostatic calcifications. Volume 21 cc. No free fluid.
Cholangio-MRI: the signal and morphology of the liver are normal. No focal lesions. The bile duct has normal calibre, both intrahepatic and extrahepatic. No content is identified inside the common bile duct. Morphologically there are no notable alterations affecting the pancreas, adrenal glands, kidneys or spleen. Minimal pleural effusion on both sides.
Serology: HAV and HCV negative. Anti-HBs > 30 mIU/ml, negative anti-HBc (compatible with vaccination against HBV), positive IgG against VZV and CMV, negative IgG against EBV. Immunology: anti parietal cell antibodies, anti LC1, antiLKM, anti mitochondrial, anti smooth muscle, anti reticulin, cANCA, anti glomerular basement membrane, pANCA negative. Stool parasites: negative.

CLINICAL COURSE
A 61-year-old man with dilated cardiomyopathy of ischaemic aetiology consulted the emergency department for asthenia, anorexia, jaundice, choluria and acholia of one week's evolution, associated with thermometric fever of up to 37.9 ̊C. Analysis on arrival revealed elevated transaminases and a marked increase in the cholestasis profile with hyperbilirubinaemia at the expense of direct bilirubin, as well as leukocytosis and eosinophilia together with elevated acute phase reactants and coagulopathy, with an INR of 25, requiring the administration of 1 ampoule of vitamin K for correction.
The patient was admitted to the internal medicine department to complete the aetiological study of the condition, and all medication was withdrawn except for aspirin and clopidogrel, replacing acenocoumarol treatment with enoxaparin. To this end, serology for hepatotropic viruses, determination of parasites in faeces and immunology tests were carried out, all of which were negative. Imaging studies were also carried out by abdominal ultrasound and cholangio-MRI, which only revealed the presence of lymphadenopathies in the hepatic hilar and celiac region, without content or dilatation at the level of the biliary tree. Having ruled out an infectious, autoimmune or obstructive aetiology, a systematic review of the literature was carried out and cases of idiosyncratic hepatitis secondary to the administration of statins were found. The allergology and gastroenterology departments were consulted and confirmed the diagnosis of suspected idiosyncratic hepatitis, recommending definitive discontinuation of statin treatment and reintroduction of the rest of the treatment that had been withdrawn on admission.
With regard to the subsequent evolution, the patient presented a resolution of the cytolysis profile and normalisation of eosinophilia within 8 days of withdrawal of atorvastatin; he persisted with a discrete elevation of the cholestasis pattern at discharge. Clinically, the patient experienced a marked improvement, with resolution of abdominal symptoms, as well as resolution of choluria and acholia. In relation to the above, and given that the patient had high LDL cholesterol levels (LDL 174 mg/dl), he was referred to the lipid unit of our centre in order to consider the use of PCSK9 inhibitors, and was assessed 1 month later, with transaminase and cytolysis enzyme levels within normal limits in control analyses. From the cardiovascular point of view, a control echocardiogram and magnetic resonance imaging were performed during admission, showing persistent severe left ventricular dysfunction (LVEF 25%), with anteroseptal akinesia and apical aneurysm. For this reason, treatment for ventricular dysfunction was progressively introduced with enalapril, eplerenone and metoprolol, with adequate tolerance, and ICD implantation was performed as primary prevention 40 days after the acute event.  

DIAGNOSIS
Dilated cardiomyopathy of ischaemic aetiology with severe ventricular dysfunction (LVEF 25%). Idiosyncratic hepatitis secondary to taking atorvastatin. Advanced anterior infarction, with extensive anteroapical aneurysm and intraventricular thrombus. Implantation of ICD in primary prevention. CVRF: type 2 diabetes mellitus, hypercholesterolemia, ex-smoker.
