HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
24-year-old male, working in a hardware store, with no known drug allergies or toxic habits. No cardiovascular risk factors (CVRF). Hypothyroidism on replacement therapy.
In June 2008, he consulted for cough and progressive dyspnoea of 6 months' evolution, and was diagnosed by the pulmonology department as having sarcoidosis with grade II pulmonary involvement, with associated bronchial hyperresponsiveness. Immunosuppressive treatment with corticosteroids was started.
In September 2008 he was admitted for sustained monomorphic ventricular tachycardia with haemodynamic instability. During admission, a dilated left ventricle with severe systolic dysfunction was observed. A haemodynamic study showed coronary arteries without stenosis. Cardiac magnetic resonance imaging showed a dilated left ventricle with a maximum telediastolic diameter of 60 mm, apical thinning with apical inferior, anterior and lateral akinesia, medial lateral, medial anterior hypokinesia and medial inferior hypokinesia, with severe systolic dysfunction (LVEF 20%). Late subendocardial enhancement in basal inferior and basal lateral face, with extension to papillary muscles; and transmural in mid and apical lateral, mid and apical inferior, and apical anterior face.
Implantable cardioverter defibrillator (ICD) implantation was performed in October 2008.
He was admitted in December 2008 due to infection of the surgical wound of the ICD, the system was explanted and antibiotics were administered, despite which the infectious clinical symptoms persisted with febrile syndrome, and the studies were extended and tricuspid endocarditis was detected, complicated with pulmonary embolisms. With progressive deterioration of his functional status and refractory heart failure, associated with several episodes of non-sustained and sustained ventricular tachycardia (VT) with poor haemodynamic tolerance. On 9 February 2009, he suffered cardiorespiratory arrest (CRA) due to primary ventricular fibrillation (VF), recovered after 2 shocks, with no sequelae. She was referred to the reference centre for evaluation for cardiac transplant, which was performed on 20/02/2009.
During admission, he presented with complications such as avascular necrosis of both hips, probably related to corticosteroid treatment. Subsequently, in May 2011, he underwent bilateral hip replacement surgery.
During the following years, he was admitted on multiple occasions for infectious complications (lung abscess in 2010, thoracic herpes zoster in 2010, repeated UTI, gastroenteritis).
In January 2013 he presented with an episode of acute grade 3R rejection symptomatic for dizziness, dyspnoea on minimal exertion and complete atrioventricular block (AVB). After treatment with corticosteroid boluses, the condition was reversed, with disappearance of AVB and clinical improvement. In the control biopsy, the acute cellular rejection was in resolution. Prior to discharge, he presented an episode of atrial deflutter, treated with atrial overstimulation. A control biopsy was repeated 6 months later, with no evidence of rejection.
He was admitted on 23/06/2013 for self-limited epigastric pain radiating to the back, associated with a feeling of breathlessness, lasting about 15 minutes, after walking for 10 minutes. Previously, the patient had been suffering from asthenia for a week, with no other associated cardiovascular symptoms. He denied any infectious symptoms or fever. He suffered an episode of alimentary vomiting in the emergency department.
On physical examination, the patient had a good general appearance, was haemodynamically stable, with no congestive symptoms, and was eupneic at baseline. On cardiac auscultation, he was tachycardic, with no murmurs or friction rubs. Abdomen painful on palpation in the right hypochondrium, soft, depressible and with no evidence of peritoneal irritation.

COMPLEMENTARY TESTS
Electrocardiogram (ECG): sinus tachycardia at 135 bpm, normal PR, narrow QRS, ST rectification of V1-V4 and convex ST in inferior face.
ECG: sinus tachycardia at 105 bpm, inferior ST elevation, ST depression of V1-V3, inferior-posterior Q wave.
ECG: complete VAB spells in the context of myocardial ischaemia.
CBC: blood count: leukocytes 13,600/μl (normal leukocyte formula), haemoglobin 13.7 g/dl, haematocrit 43.9%, platelets 206,000/μl. Coagulation: To. T. Partial Activated 29.9 s, INR 1.22, prothrombin rate 77%. Biochemistry: glucose 80 mg/dl, urea 58 mg/dl, creatinine 1.10 mg/dl, GFR 79 ml/min, sodium 142 mEq/l, potassium 4.6 mEq/l, chlorine 109 mEq/l, GOT(AST) 109 U/l, GPT (ALT) 58 U/l, amylase 35 U/l, total bilirubin 1.3 mg/dl. Serialisation of myocardial damage markers: ultrasensitive troponin 1919 ng/l - 1964 ng/l - 1990 ng/l [ 0 - 13].
Coronary angiography: three-vessel coronary artery disease, with poor distal beds and diffuse disease, with thrombotic occlusion of the proximal right coronary artery (RCA). During percutaneous coronary intervention (PCI), multiple dilatations with balloon angioplasty were attempted to recanalise the coronary artery, but no flow was achieved due to severe no reflow phenomenon.


CLINICAL COURSE
The patient was admitted with initial suspicion of acute myocarditis versus acute coronary syndrome type NSTEMI, with flat enzyme mobilisation in the following 12 hours.
The ECG on admission showed sinus tachycardia, with subtle changes in the repolarisation of ST rectification in V1-V4 and convex ST in the inferior face. At 21:00h on the day of admission, the patient began with dyspnoea, tachypnoea and vegetative symptoms.
The ECG showed sinus tachycardia with lower ST elevation, with self-limited spells of complete AVB, and an emergent haemodynamic study was performed.
Catheterisation revealed three-vessel coronary artery disease, with poor distal beds and diffuse disease, with thrombotic occlusion of the proximal DC. During PCI, multiple dilatations with balloon angioplasty were attempted, but no flow was achieved due to no reflow. During the procedure the patient suffered complete AVB with severe haemodynamic deterioration Killip IV, which triggered ventricular fibrillation. Despite multiple shocks at 200J and advanced CPR for a prolonged period, the patient did not respond to these measures and died.

DIAGNOSIS
Acute coronary syndrome with ST-segment elevation (STEACS) lower Killip IV. Complete AVB due to myocardial ischaemia. CRP due to VF.
Graft vascular disease in heart transplant patients. Proximal DC thrombotic occlusion.
Death.

Previous:
Sarcoidosis with pulmonary and cardiac involvement, on corticosteroid treatment. Infiltrative cardiomyopathy in dilated phase due to sarcoidosis, with severe systolic dysfunction, ACC/AHA stage D CHF.
Multiple infectious complications probably related to immunosuppressive treatment. Acute tricuspid infective endocarditis.
Cardiac transplant. Acute rejection resolved.
