HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
We present the case of a 77-year-old man who, after eating fresh fish, developed severe anaphylaxis requiring the administration of intramuscular adrenaline with subsequent chest pain and ST-segment elevation, accompanied by clinical and laboratory data of low cardiac output.

History
No known drug allergies.
Cardiovascular risk factors: ex-smoker, hypertension (HT), type 2 diabetes mellitus (DM2), high blood pressure.
No known heart disease or bronchopathy.
Chronic ischaemia syndrome of both lower extremities, grade IV. Transphalangeal amputation of the second toe of the left lower extremity (IBD) in June 2017. Amputation of the fourth toe of the right lower extremity (EID) in October 2018. Infracondylar amputation of EID on 26/08/2019.
Previous surgical interventions: cataract of right eye.
Usual treatment: insulin glargine, 20 units at dinner; metformin 850 mg, 1 tablet every 12 hours; sitagliptin 50 mg, 1 tablet every 12 hours, repaglinide 1 mg, 1 tablet breakfast, lunch, dinner; acetylsalicylic acid 100 mg, 1 tablet at lunch; enalapril/lercanidipine 20/20 mg, 1 tablet at breakfast; atorvastatin 20 mg, 1 tablet at dinner; allopurinol 300 mg, 1 tablet at breakfast; etoricoxib 120 mg, 1 tablet per day; metamizole 575 mg; paracetamol 1 g, on demand. Baseline functional status: cognitive functions preserved. Wheelchair-bound due to recent infracondylar amputation of DID. No angina or dyspnoea in his usual life.

Present illness
A 77-year-old man, who after having dined on fresh hake and clams, started after 4 hours with generalised erythema, intense palmo-plantar pruritus, genital pruritus and tongue oedema with slight dysphonia. On arrival of basic life support, he was administered intravenous dexchlorpheniramine and Actocortin (i.v.), despite which, on arrival at the emergency department of his hospital of reference, he persisted with slight pruritus and notable tongue oedema, so it was decided to administer adrenaline 0.5 mg intramuscular (i.m.), starting instantly with intense chest pain radiating to the left upper limb. An electrocardiogram (ECG) was performed showing anteroseptal ST elevation with specular decrease in the inferior face, which did not improve after sublingual nitroglycerine, with accompanying signs of low cardiac output (arterial hypotension, acral coldness and obnubilation), so continuous perfusion of dobutamine (DBT) and noradrenaline (NAD) was started. Suspicion of ST-segment elevation acute coronary syndrome (STEMI) anteroseptal Killip IV, the infarction code was activated and the patient was transferred to the haemodynamics ward of our hospital for emergent percutaneous coronary intervention (PCI).
On arrival, the patient was conscious and oriented, affected by pain, under continuous perfusion of NAD (at 0.8 mcg/kg/min) and DBT (at 5 mcg/kg/min) with a tendency to arterial hypotension (blood pressure [BP] 75/50 mmHg) and sinus tachycardia (heart rate [HR] 120 bpm). The ECG showed persistent anteroseptal ST elevation, and on arrival echocardiography, moderate LV dysfunction with akinesia of all mid-apical and anterior segments. He was transferred directly to the haemodynamics ward.
Time of onset of chest pain: 5:15 am.
Time of arrival at the emergency room: 5:30 am.
Time of opening of the artery: 7:08 hours.
TIMI risk scale: 12 points (35.9%).
CRUSADE risk scale: 59 points, 19.5% (high haemorrhagic risk).

Physical examination
On admission to the coronary unit
BP 75/50 mmHg; HR 120 bpm; baseline SatO2 95%; afebrile. Somnolent. Poor distal perfusion with lividity in the lower extremities and acral coldness.
Head and neck: no jugular ingurgitation.
Cardiac auscultation: rhythmic, no clear audible murmurs.
Pulmonary auscultation: bibasal crackles.
Abdomen: soft, depressible, not painful on palpation, normal hydro-aural sounds. Lower extremities: amputation of the DID, no oedema in the lower extremities, palpable left foot.

COMPLEMENTARY TESTS
ECG in the emergency department of the regional hospital: sinus rhythm at 70 bpm, long PR, right bundle branch block (RBBB), ST elevation of V1-V5, I and AVL, maximum of 9 mm in V3, with specular decrease in inferior face.
ECG on admission to the coronary unit: sinus tachycardia at 115 bpm, long PR, persistent ST elevation in precordial leads, maximum of 6 mm in V3.
Chest X-ray: cardiac silhouette not enlarged, vascular redistribution, free costophrenic sinuses, no apparent condensation.
Laboratory tests on admission to the coronary unit:
Arterial blood gas: pH 7.27, PCO2 31 mmHg, PO2 90 mmHg, HCO3 14 mmol/l, lactate 4.5.
Biochemistry: urea 80 mg/dl, creatinine 0.96 mg/dl, GPT 14 U/L, total bilirubin 0.3 mg/dl, sodium 134 mEq/l, potassium 5 mEq/l, CRP 16 mg/l, CK 138 U/l, LDH 450 U/l, ultrasensitive troponin T 118 ng/l (normal < 14).
CBC: haemoglobin 10.5 g/dl, platelets 469,000, leucocytes 31,000 (with 86% neutrophils).
Coagulation: aPTT > 180 sg, INR 1.2.
Enzyme peak: peak CK 779 U/l, peak troponin T 2016 ng/dl.
Other analytical results:
HbA1c: 7.5%. TSH: 1.01 (in range).
Lipid panel: total cholesterol 102, triglycerides 112, HDL 33, LDL 47.
Laboratory tests requested by the allergology department: tryptase curve (9/9/2019): Regional hospital: 24; 4 hours after onset of symptoms: 11; 24 hours: 10; (normal tryptase value undetectable, or < 1.2 mg/l).
IgE: 190.00 kUA/L (elevated); Anisakis Ac.IgE: 36.90 kUA/L (very positive).
Urgent catheterisation: short common trunk with non-significant distal atheromatosis. Anterior descending (AD): subtotal ostial lesion in the AD, with the rest of the vessel with mild atheromatosis, TIMI 2 flow. The 1st and 2nd diagonals present moderate ostial stenosis. Circumflex (Cx): proximal moderate lesion and distal moderate long atheromatosis. Right coronary artery (RC): dominant. Mild proximal-moderate atheromatosis and severe short lesion at the level of the IVP cross-ostium. Primary PCI: the severe lesion of the ostial LAD is pre-dilated with a 3.0 mm balloon and a 3.5/24 mm ANGIOLITE stent is implanted from ostial CT with an optimal result. The most distal LAD at the apical level is occluded and does not recover flow after PTCA at the level of the 2.0 mm balloon occlusion.
Echocardiogram on admission: left ventricle (LV) neither dilated (DTD 45mm) nor hypertrophic (IVS 9mm, PP 9mm) with moderately depressed global systolic function at the expense of akinesia of all mid-apical segments with hypercontractility of the rest. Non-dilated right ventricle (RV), preserved global function with apical akinesia. Sclerosed aortic valve with preserved opening, without functional alterations. Sclerosed mitral valve with slight restriction of the posterior leaflet and moderate mitral insufficiency, directed towards the posterior wall of the left atrium (LA). Normal appearing tricuspid valve with mild mitral insufficiency (MI) and RV-AD gradient 25-30 mmHg. Inferior vena cava (IVC) not dilated with inspiratory collapse (estimated PSAP 30-35 mmHg, no pulmonary hypertension). No pericardial effusion.
ECG at discharge from the coronary unit: sinus rhythm at 100 bpm, long PR, axis at -60a, LBBB + HAIHH.
Second-time catheterisation with PCI to CD: after advancing the guidewires to PL and IVP, a RESOLUTE 2.5 x 15 mm direct drug-eluting stent is implanted in distal Cd-IVP, leaving slight under-expansion, so it is post-dilated with a 2.5 x 8 mm NC balloon with a good final result. The LP was caged, with no ostial lesion. The PVI, distal to the stent, is diffusely atheromatous with severe distal small vessel lesions.

CLINICAL EVOLUTION
The patient is admitted to the coronary unit after emergent catheterisation where severe bivascular coronary artery disease with acute thrombotic lesion of the ostial LAD is detected and treated with a stent in the LAD-CT with good results. Immediate haemodynamic improvement was observed and dobutamine could be discontinued in the haemodynamics room. He was admitted to the coronary unit in a stable condition and was able to completely discontinue noradrenaline 2 hours after admission. On admission, he reported some residual mild chest discomfort that resolved in the first 4 hours.
Suspicion of anaphylaxis (tongue oedema, pruritus, etc.) led to serial tryptase determinations during the first 24 hours, which were positive. He was maintained during his admission to the coronary unit with corticoid and intravenous dexchlorpheniramine (Polaramine) with complete resolution of genital itching and tongue oedema in the first 12 hours, remaining asymptomatic thereafter. He was assessed by the allergology department, which analysed him for specific IgE and found elevated IgE for Anisakis and negative IgE for hake and clams. According to the recommendation of the allergology department, the intravenous glucocorticoid doses were reduced and Polaramine (antiH1) was maintained throughout the hospital stay until 5 days after the acute event. She was also forbidden to eat fish or seafood until further assessment by her after discharge from hospital.
Haemodynamically, he remained stable during the 48 hours of admission with a tendency towards asymptomatic mild hypotension (TAS 90-100 mmHg) and sinus tachycardia (95-110 bpm), without new exploratory or analytical data of low perfusion, with moderate LV dysfunction persisting at discharge, and the introduction of beta-blockers or angiotensin-converting enzyme inhibitors (ACE inhibitors) not being possible due to mild hypotension. Spironolactone is started, with good tolerance.
Respiratory status remained stable, with the appearance on the first day of admission of mild heart failure (bibasal crackles) without dyspnoea or desaturation. A daily dose of oral furosemide was started and was well tolerated. He presented a single febrile peak up to 38.3oC without shivering on the third day of admission (11/9/2019) with no clinical evidence of infection. Samples were taken for culture (blood/urine culture) and empirical amoxicillin/clavulanic acid was prescribed. During his admission, he was assessed by the vascular surgery department for evaluation of the recent surgical wound of amputation of DID, the wounds were found to be in a good state of healing with some necrotic spots but with no evidence of infection, and intradermal suture removal was pending.
Once the condition had stabilised, it was decided to transfer the patient to the ward for evolutionary control and to perform a new catheterisation in the second stage, with PCI to CD-IVP, which was successful. During his stay on the ward, the patient remained haemodynamically and respiratory stable, asymptomatic, and after re-evaluation by the allergology service, the patient was discharged with an outpatient appointment for joint follow-up by allergology and cardiology.

DIAGNOSIS
Main diagnosis:
Killip IV STEACS (Kounis syndrome type II).
Severe Anisakis anaphylaxis (in the context of fresh fish ingestion). Severe two-vessel coronary artery disease: DA and CD.
Acute thrombotic lesion in ostial LAD with severe stenosis.
Primary PCI with drug-eluting stent implantation in TC-DA axis.
Second stage PCI with drug-eluting stent implantation in DC-PVI with moderately depressed LVEF.

Secondary diagnoses:
Cardiovascular risk factors: ex-smoker, AHT, DM2.
Grade IV chronic ischaemia syndrome of the LVES. Recent postoperative infracondylar amputation of DID.
