HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
A 50-year-old man came to the emergency department for chest pain. No known allergies. No toxic habits. No habitual treatment. No CVRF. Only previous history of tonsillectomy in childhood and left meniscectomy. Asymptomatic from the cardiological point of view, until the early morning of admission (4:00 a.m.). He started with shooting pains in the jaw. Subsequently, they radiate to the anterior region of the thorax, become oppressive, of moderate intensity, without vegetative cortex. They subside spontaneously one hour later. She had several recurrences, of greater intensity, and so she went to the emergency department. Arrives more than 6 hours after the onset of the symptoms, with slight residual discomfort. She improved after conventional analgesia. On arrival she was haemodynamically stable. BP 119/83 mmHg; HR 68 bpm; SatO2 98 % on room air; Ta 36.1°C. Glasgow Scale: 15/15. Conscious, oriented in all 3 spheres. Eupneic at rest, well hydrated, nourished and perfused. AC: rhythmic without murmurs or extratonos. PA: vesicular murmur preserved in both lung fields with no extra sounds. Abdomen: hydro-aerial sounds present, soft, not painful on deep or superficial palpation. Renal fist percussion (-). Extremities: no oedema, no signs of DVT. Basic neurological examination was normal.

COMPLEMENTARY TESTS
ECG: sinus rhythm at 68 bpm. Poor R wave growth in precordial leads, isolated Q wave in lead III, with no other alterations. No evolutionary changes in subsequent electrocardiograms. Portable echocardiogram (Vscan in the ER): LV not dilated or hypertrophic, with normal global and segmental systolic function. Normal aortic root. RV not dilated. No significant valvulopathies. No pleural effusion.
Haemogram: leucocytes 5,200/uL; neutrophils 61.3 %; lymphocytes 27.2 %; Hb 15.5 gr/dl; Htc 43.4 %; MCV 87.1 fl; platelets 180,000/uL. Haemostasis: APTT 29.3 sec; INR 1. Biochemistry: glucose 112 mg/dl, creatinine 1.07 mg/dl, sodium 141 mmol/l, potassium 4 mmol/l, total protein 6.3g/dl, albumin 3.7g/dl, calcium 8.6mg/dl, phosphorus 3.4 mg/dl, uric acid 7.6 mg/dl, triglycerides 141 mg/dl, cholesterol 163 mg/dl, GOT 114 U/l, GPT 119 U/l, GGT 95 U/l, alkaline phosphatase 63 U/l, LDH 496 U/l, total bilirubin 1.91 mg/dl, direct bilirubin 0.52 mg/dl. Enzyme serology: 1a: CK 766 U/l, troponin I 25.89 ng/ml (normal < 0.06 ). 2a: CK 727 U/I troponin I 36.13 ng/ml. 3a: CK 696 U/I, troponin I 27.52 ng/ml.
Chest X-ray: no signs of CHF or parenchymal infiltrates.
Serology: IgM HAV: negative; IgG anti HBc: negative; Anti HCV: negative; IgM anti CMV: negative; IgM against VCA: negative; Anti HIV: negative; Toxoplasmosis IgG IgM: negative. MRSA culture: negative. Magnetic resonance imaging (MRI) (Image 2): LV with preserved systolic function. Late gadolinium enhancement in basal and medial, anterior, lateral and inferior segments of the left ventricle, respecting only the interventricular septum and apex. The enhancement shows subepicardial distribution without transmural involvement, being compatible with myocarditis.
Coronary angiography: LCT, LAD and DC within normality. Mild stenosis of 20-30% in the middle CX. LVEF preserved in ventriculography. No images suggestive of coronary anomalies, dissection or thrombosis.

EVOLUTION
Given the clinical manifestations of chest pain and enzyme elevation, the initial diagnosis of NSTEACS was established. He was admitted to the ICU and treatment was started with double antiplatelet therapy and anticoagulation, statins and beta-blockers. He remained haemodynamically stable, asymptomatic, with no heart rhythm disturbances or evidence of CHF. Serialisation of markers of myocardial damage showed a clear increase, in addition to continuing with mild chest pain. Coronary angiography was performed and no coronary pathology was found to justify the clinical picture.
Laboratory tests showed an increase in transaminases and bilirubin with no clinical alterations on examination at the digestive level, so a viral serology study was requested. In view of the coronary angiography findings, the patient was questioned again and reported that in the last 2 months he had presented catarrhal symptoms and pharyngitis with clinical symptoms the week prior to admission of general malaise, myalgia and dysthermic sensation with fever of up to 37.4°C, with good response to paracetamol. In the presence of coronary arteries without significant lesions, chest pain after respiratory infection and elevated markers of myocardial damage, myocarditis was suspected. Treatment for NSTEACS was suspended.
The patient remained stable on the ward, with no recurrence of chest pain, heart failure or arrhythmias. An echocardiographic study prior to discharge showed preserved LVEF with no alterations in global or segmental contractility. No evolutionary ECG changes during admission. Clinical evolution was favourable, with treatment with ACE inhibitors. MRI was requested 48 hours later, which confirmed the diagnosis of myocarditis.

DIAGNOSIS
Acute myocarditis of probable viral aetiology.
Preserved LVEF.
