HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

The patient was a 21-year-old male, with no known drug allergies. With regard to his toxic habits, he was a social drinker, non-smoker, denying the consumption of other toxic substances. He denied cardiovascular risk factors, cardiological history of interest and did not follow any outpatient treatment. He came to our emergency department with a fever of up to 39oC of three days' evolution. In the last 24 hours he began to experience abdominal pain in the mesogastrium, more accentuated in the right iliac fossa, which did not change with ingestion and was more accentuated when standing upright. There was no loss of appetite. He denied nausea or vomiting, alteration of transit, externalisation of bleeding or urinary symptoms. Blood pressure was 132/89 mmHg, oxygen saturation 100% baseline, temperature 36.4oC, acceptable general condition, conscious, oriented and cooperative, good hydration and perfusion, eupneic at rest and without neurological focality. Cardiac and pulmonary auscultation showed no relevant findings. The abdomen was soft, depressible, with hydro-aerial sounds present, without palpable masses or megaliths, with intense pain on palpation of the right iliac fossa but without signs of peritoneal irritation. Given the suspicion of appendicitis, urgent analysis, abdominal CT scan and PCR for SARSCoV- 2 of the protocol prior to admission, initially in charge of the digestive system, were requested.

COMPLEMENTARY TESTS
With regard to the tests performed in the emergency department: In the urgent analysis, the biochemical analysis showed total bilirubin of 2.58 mg/dl (0.3-1.2) with direct bilirubin of 0.5 mg/dl (0-0.5) and C-reactive protein of 180 mg/l (0-5). The haemogram showed discrete leukocytosis of 11.69 x10^3/μl (4-11) with neutrophilia of 9.68 x10^3/μl. Coagulopathy was present, with prothrombin time of 51% (75-140) and calculated fibrinogen of 841 mg/dl, with normal activated partial thromboplastin time. Urinalysis showed urobilinogen 8 mg/dl and ketone bodies 60 mg/dl. PCR for SARS-CoV-2 was performed and was positive, with gene amplification in late cycles, probably compatible with residual RNA.
Abdominal CT scan without contrast showed normal liver and spleen, with no obvious focal lesions, normal-sized gallbladder, alliasic, with no signs of acute cholecystitis or bile duct dilatation. Pancreas without significant alterations. Normal sized kidneys with no evidence of lithiasis or hydronephrosis. Inflammatory changes were identified in the cecum, ileocecal valve and terminal ileum. The terminal ileum had a thickened wall with marked inflammatory changes in the vicinity. There were also multiple reactive lymphadenopathies in the right iliac fossa. There was an amina of free fluid in the right paracolic gutter. The cecal appendix showed minimal enlargement of its base, probably secondary to the described inflammatory changes and the proximity to the ileum. Distally the appendix was of normal calibre. Therefore, these findings were more suggestive of ileitis with associated inflammatory changes (slightly affecting the base of the appendix) than appendicitis. During admission to the gastrointestinal department and later cardiology: a study of hepatotropic viruses and HIV, anti-transglutaminase and thiopurine methyltransferase antibodies was carried out, which were negative. A determination of orosomucoid acid alpha-1-glycoprotein was requested, which was 198 mg/dl (50-120) and ferritin 940 ng/ml (21-274). A stool culture showed dysbacteriosis due to gram-positive microorganisms. Seventy-two hours after admission, chest pain analysis was requested, with elevated troponin I (high sensitivity) of 522.8 ng/l (5-34) and C-reactive protein 352 mg/l. Subsequent enzyme serum serology showed a troponin I peak of 13,418 ng/l, which subsequently decreased progressively, as well as CK 671 U/l (30-200) and NTproBNP 3405 pg/ml. An electrocardiogram was performed with chest pain, showing sinus tachycardia at 103 bpm. PR 120 ms constant. QRS 90ms, normal electrical axis. No repolarisation alterations. The electrocardiogram on the ninth day of admission showed sinus rhythm at 64 bpm. PR 160 ms constant. QRS 88 ms, normal electrical axis. QTc 429 ms. Negative T wave in III and flattened in aVF. Electrocardiogram prior to discharge showed sinus rhythm at 85 bpm. PR 140 ms constant. QRS 84 ms, normal electrical axis. Biphasic T waves on the inferolateral side. An urgent echocardiogram was performed on suspicion of myocarditis, showing: left atrium (LA) not dilated (21 ml/m2). Left ventricle (LV) not dilated (DTD 49 mm/62 ml/m2) not hypertrophic (septum 7 mm pp 7 mm mass 55 g/m2 RWT 0.29). Global hypokinesia with moderate LV systolic dysfunction (biplane Simpson EF 42%). Normofunctioning mitral valve. Filling pattern with fusion of E and A. Normofunctioning trivalve aortic valve. Aortic root and ascending aorta not dilated. Right chambers of normal size, right ventricular (RV) systolic function at low limit of normality (TAPSE 16 mm S-wave DTI 10 cm/s). Mild tricuspid insufficiency (TI) with V max 2 m/s, estimated normal PAPS. Normal pulmonary acceleration time. Dilated inferior vena cava (IVC) without adequate inspiratory collapse. No pericardial effusion. The control echocardiogram performed 5 days later showed improvement of the previously described global hypokinesia.

CLINICAL EVOLUTION
A new PCR was performed 48 hours after admission, which was negative, and COVID isolation was lifted. Subsequently, serology was performed with positive IgG for SARS-CoV-2. Seventy-two hours after admission, she began to experience repeated episodes of central thoracic pain described as stabbing, radiating to the neck, which increased with deep inspiration. They were accompanied by sweating and, on occasion, vomiting. Following the findings described in the complementary tests (analysis with elevated acute phase reactants and markers of myocardial damage, electrocardiogram with sinus tachycardia and echocardiogram with global hypokinesia), treatment was started with beta-blockers and he was transferred to the coronary unit where he was monitored without arrhythmic events of interest. After 48 hours he was transferred to the cardiology hospital ward to complete the study and treatment. During his stay on the ward he remained asymptomatic, with no evidence of heart failure. Treatment was started with angiotensin-converting enzyme inhibitors (ACE inhibitors) and beta-blockers. A repeat echocardiogram showed normalisation of systolic function, although slight hypokinesia persisted in the basal segments of the septum and anterolateral face. The control electrocardiogram showed sinus rhythm alternating with bouts of nodal rhythm without relevant clinical translation (he did not present syncope or other alarm symptoms), so the beta-blockers were discontinued and he was monitored with telemetry and these episodes were observed during sleep, which could be secondary to vagal hypotonia or be in the context of the evolution of myocarditis. From the digestive point of view, he presented significant clinical improvement, without pain and with normalisation of intestinal transit. He completed empirical antibiotic therapy with ceftriaxone and metronidazole, started on admission. At discharge he had good oral tolerance. After progressive tests showed a clear decrease in myocardial enzymes, practically normalised, and in acute phase reactants, in a stable clinical and haemodynamic situation, he was discharged from hospital after 10 days of hospitalisation.

DIAGNOSIS
Myocarditis and acute ileocolitis in the context of late-stage SARS-CoV-2 infection.
Mild hypokinesia in the basal septum and basal anterolateral septum of the LV.
