HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION
We present the case of a 38-year-old man with no CVRF, family history or previous cardiological history. Under digestive follow-up for Crohn's disease with enterovesical fistula and recent admission for severe infectious disease of abdominal origin. Clinical judgement at discharge was septic shock secondary to perforation of toxic megacolon with faecaloid peritonitis, requiring urgent surgical intervention (subtotal colectomy + ileostomy).
Three days after discharge from the general surgery department, he consulted for chest pain.
This discomfort was atypical and partially improved with non-steroidal anti-inflammatory drugs (NSAIDs). He also reported progressive dyspnoea that started at the same time and became minimal effort (New York Heart Association functional class III [NYHA III]. There were no other cardiological symptoms in the anamnesis.
On examination, the patient's general condition was acceptable. He is eupneic at rest and tolerates decubitus. Blood pressure (BP) 90/70 mmHg. Tachycardic at 110 bpm. Afebrile. No jugular ingurgitation. Tracheostomy (previous prolonged stay in the intensive care unit [ICU]) without complication data. Cardiopulmonary auscultation was unremarkable. Abdomen soft and depressible, with normofunctioning ileostomy. There was a soft tissue lesion in the left fossa with mucopurulent secretion. Lower limbs without oedema.
The electrocardiogram performed in the consultation room showed sinus tachycardia with generalised flattening of the T wave. The chest X-ray was unremarkable. Blood tests showed haemoglobin (Hb) of 8.6 g/dl and elevated C-reactive protein (CRP) without leukocytosis. D-dimer negative.
Serial ultrasensitive troponin T (TnTus) maintained at around 30 (25-30-29 ng/l), normal CPK.
Urgent echocardiography was performed, showing severe left ventricular dysfunction (LVEF 30%) with global hypokinesia, and the patient was admitted to cardiology.


COMPLEMENTARY TESTS
ANALYTICS: renal function preserved. No leukocytosis or neutrophilia. Hb 8.6 g/dl. Platelets and coagulation in range. D-dimer negative. TNT US 25---30---29.
THORAX RADIOGRAPHY: normal cardiothoracic index. Free costophrenic sinuses. Slight increase of interstitial tissue at the bases. No images of condensation or pleural effusion.
ELECTROCARDIOGRAM (ECG): sinus tachycardia at 100 bpm. Normal PR. Narrow QRS.
Generalised flattening of the T wave. Normal QTc.
Transthoracic echocardiography (TTE): left atrium of normal dimensions (24 mm in AP). Mitral valve with fine leaflets and good mobility (opening and closing preserved).
Left ventricle (LV) of normal dimensions (end-diastolic diameter (EDD) 49 mm and end-systolic diameter (ESD) 43 mm with end-diastolic volume (EDV) and end-systolic volume (ESV) of 136 ml and 97 ml, respectively). Normal myocardial thickness (8 mm septum and 7 mm inferolateral wall). Generalised hypocontractility and ejection fraction (EF) estimated by biplane disc of 29%. Aortic valve with fine leaflets and good opening. Left ventricular outflow tract (LVOT) 21 mm, sinuses of Valsalva 31 mm, UST 23 mm. Right ventricle (RV) of normal dimensions with normal systolic function. Mild (1+) tricuspid insufficiency (TI) jet with suboptimal Doppler to estimate systolic pulmonary artery pressure PAPs. No pericardial effusion.
CORONARYGRAPHY: coronary arteries without angiographic lesions.
CARDIAC MAGNETIC RESONANCE (CMR): generalised hypokinesia, more accentuated in the septum/inferior segment in the middle and apical zones. Severely depressed LVEF (34.6%). RV of normal dimensions and preserved right ventricular ejection fraction (RVEF). Myocardial thickness and tissue signal in T2 and STIR sequences (short TI
Inversion Recovery) normal. No significant valvulopathies. No pericardial effusion.
Conclusion: signs of severe contractile dysfunction of the LV without deriving from this exploration data to guide possible aetiology. The examination was not complete as it was interrupted at the patient's express wish (incomplete sequence/no late gadolinium enhancement).
Control abdominal CT scan: resolution of the previous effusions. 14 mm lesion in segment VI of the liver (haemangioma). Discrete splenomegaly 12.2 x 5.6 cm. Collections in the anterior abdominal wall: one under the laparotomy scar (30 x 7 x 10 mm) and another more caudalsupravesical (12 x 13 x 38 mm). At retroperitoneal level in right anterior pararenal space (56 x 20 x 52 mm) and right posterior pararenal space (60 x 29 x 137 mm) and left anterior pararenal space (38 x 17 x 47 mm). Uncomplicated right vacuum ileostomy. Loops of normal calibre with no mucosal hypercaptation or mural thickening suggestive of current inflammatory bowel disease (IBD). No other striking alterations.

CLINICAL EVOLUTION
A regular TTE was requested which showed severe left ventricular dysfunction (LVEF by Simpson biplane of 29%) with global hypocontractility (see complete report in complementary tests). Ischaemic aetiology of the systolic dysfunction was ruled out by coronary angiography. To complete the study, CMR was performed, which showed no data suggesting an aetiology (normal T2 and STIR, without being able to administer late enhancement due to the patient's refusal) (see full report in complementary tests).
After reviewing the literature and, taking into account the clinical context of the patient, two diagnostic possibilities are evaluated, which are not mutually exclusive:
Severe ventricular dysfunction in the context of gram-negative sepsis (recent faecaloid peritonitis).
Deficiency cardiomyopathy in a patient with probable nutritional deficit (Crohn's disease with prolonged admission to the ICU).
The patient started treatment for systolic dysfunction during admission: carvedilol 6.25 mg (2-0-1), ramipril 2.5 mg (1⁄2 tablet at breakfast), oral ferrotherapy (1 tablet on an empty stomach) and loop diuretics in initial phases. Treatment with spironolactone was not started due to low blood pressure with a minimum dose of angiotensin-converting enzyme inhibitor (ACE inhibitor).
The possibility of vitamin (vitamin D-thiamine) and trace element (selenium-iron) deficiency was assessed.
Samples were taken for intraerythrocyte trancetolase activity and selenium, iron profile, vitamin D and folic acid. Treatment was started with IV thiamine, polyvitamin complex, polymeric supplements and an optimised oral diet.
The patient's follow-up during admission was multidisciplinary:
Digestive/general surgery: treatment with azathioprine was restarted. A control CAT scan was performed (see complementary tests) and, in view of the patient's good evolution, it was decided to continue with antibibiotherapy (metronidazole), clinical follow-up and re-evaluation by imaging test in two months' time.
Nutrition: supervises treatment during admission, achieving a weight gain of 3 kg.
Otorhinolaryngology: assesses the tracheostomy and proceeds to decannulation. The tracheostomy was closed by second intention.
The patient's evolution was favourable, being discharged without chest pain and in good functional class. Treatment at discharge was as follows: omeprazole 20 mg (1-0-0). carvedilol 6.25 mg (2-0-1), ramipril 2.5 mg (0.5-0-0), metronidazole 250 mg every 8 hours, oral iron (1-0-0), vitamin complex (2 tablets per day), cinitapride (1 mg every 8 hours), thiamine (300 mg every 24 hours), Ca + VitD 1000 U complex (2 tablets per day), calorie shakes, citalopram 20 mg (1 tablet per day), lorazepam 1 mg (at night), fibre-free diet avoiding excess fibre.
At the consultation two months after admission, the patient was asymptomatic and there was no recurrence of chest pain. TTE showed normalisation of LVEF. The patient has regained weight and has had no new Crohn's flares/abdominal complications. The tracheostomy has closed by second intention.
Discharge was decided by the advanced HF and transplant team for periodic follow-up in the local cardiology department.

DIAGNOSIS
Heart failure in a patient with transient severe left ventricular dysfunction in the context of Gram-negative sepsis.
Possibly aggravated by nutritional deficits secondary to his digestive pathology (Crohn's disease) and recent prolonged hospitalisation.
