HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History

Social and family history:
22-year-old male patient, medical student.
Thin. Smoker of 1 cigarette a day for 3 years. Occasional cannabis user.
Maternal grandfather with heart attack at the age of 60.
Mother diagnosed with familial hypercholesterolemia with positive genetic study.

Personal history:
Cardiovascular risk factors (CVRF): no known arterial hypertension (AHT), diabetes mellitus (DM) or dyslipidaemia (DL).
No cardiological history of interest.
Other history:
Irritable colon. Migraine.
Usual medication:
Does not take any medication.

Present illness
The patient came to the emergency department due to oppressive chest pain of great intensity, which started at rest, radiating to the left arm, unchanged with inspiratory movements, accompanying vegetative symptoms. On arrival at the emergency department, the patient had been in pain for more than an hour, with no improvement since onset. He reported symptoms of precordial oppression with exercise since 3 months earlier. No symptoms suggestive of catecholaminergic release.

Physical examination
On arrival at the ED he was afebrile, normoperfused, with chest pain. SatO2 96% on room air, blood pressure 123/84 mm/Hg, heart rate 92 l/min.
Neck: symmetrical, no jugular ingurgitation or hepatojugular reflux. No murmurs on carotid auscultation.
Cardiac auscultation: regular heart sounds without murmurs or extratonos.
Pulmonary auscultation: vesicular murmur present, well ventilated fields, no extra sounds.
Abdominal examination: nondescript.
Lower limbs: symmetrical, no signs of DVT or oedema.

COMPLEMENTARY TESTS

Blood count: haemoglobin 17.2 g/dl, haematocrit 49.5%, red blood cells 5.66x10 , leukocytes 21,800, neutrophils 11,570, lymphocytes 8,270, eosinophils 520, platelets 429,000.
Biochemistry: glucose 124 mg/dl, urea 37 mg/dl, creatinine 1.19 mg/dl, glomerular filtrate > 90 ml/min/1.78 m , sodium ion 142 mmol/l, potassium ion 3.2 mmol/l, troponin T 7 ng/l, creatine kinase 225 U/l, urate 6.8 mg/dl, alkaline phosphatase 121 U/l, AST 37 U/l, ALT 59 U/l, GGT 45 U/l, total bilirubin < 1.0 mg/dl, total cholesterol 98 md/dl, HDL 41 mg/dl, triglycerides 43 mg/dl, calculated LDL cholesterol 49 mg/dl, HbA1C 5.6%, TSH 2.33 mU/l.
Coagulation: normal in all parameters.
Urine toxicity: benzodiazepines, opiates, cocaine, cannabinoids and methamphetamines negative.
Electrocardiogram: sinus rhythm at 80 L/min, normal PR interval, narrow QRS, normal axis at +40, ST-segment elevation up to 3 mm on the anterolateral side with mirror image on the inferior side.
Coronary angiography: CD artery without angiographic lesions. Cx artery without angiographic lesions. DA artery with thrombotic occlusion in its middle third, immediately distal to the exit of the first diagonal.
Angioplasty: with XB 3.5 Sion is advanced to distal DA recovering flow. Due to abundant thrombotic content, tirofiban is administered i.v. (bolus + perfusion). Direct implantation of a Synergy 4 x 20 mm drug-eluting stent was performed in the mid-proximal segment. Due to an image of under-expansion at mid-stent level, post-dilatation with a 4.5 mm NC balloon was performed, achieving adequate expansion. A thrombus floating distal to the stent was found floating intra-arterially, so it was decided to perform thromboaspiration with a Pronto device, extracting a large red thrombus. Excellent angiographic result after thromboaspiration and final TIMI 3 flow.
Echocardiogram: non-dilated left ventricle (LV) with extensive anterior, anteroseptal and lateral akinesia (middle segments and apical cap) with normal contractility of the inferior territory, infero-lateral and basal inferior septum.


Extended CBC:
Serial myocardial damage markers (on admission, at 3 hours, 12 hours and 36 hours, respectively):
Ultrasensitive troponin T (ng/l): 7 -> 7.611 -> 9.234 -> 3.215
Creatinine kinase (U/l): 225 -> 3.764 -> 3.546 -> 912
Genetic study for familial hypercholesterolemia: negative. Liporpotein A: 90.7 mg/dl (normal < 30 mg/dl).
Chromatography and electrophoresis: acid diuresis: 1.850. Collection time (chromatography): metanephrine 24 hours: 198,7 μg/24 hours. Normetanephrine 24 hours: 377.4 μg/24 hours.
Toxicology: metanephrine 30. Normetanephrine 122
Serology antiphospholipid syndrome: anti-cardiolipin IgG and IgM negative (< 1.6 GPL U/ml and 0.8 MPL-U/ml, respectively), anti-beta2 glycoprotein IgM and IgG negative (< 1.4 U/ml and 1.5 U/ml, respectively).
Endocrinology consultation: metanephrine and metanephrine levels in urine were normal and plasma levels were only slightly elevated in normetanephrine, which, together with the absence of compatible clinical manifestations, makes the presence of pheochromocytoma or parnaganglioma highly improbable.

CLINICAL EVOLUTION
We present the case of a very young 23-year-old patient admitted to cardiology for an acute coronary syndrome with ST-segment elevation (STEACS) in extensive anterior face, for which the heart code is activated. An emergent coronary angiography showed coronary artery disease in one vessel, with thrombotic occlusion of the middle LAD coronary artery, and angioplasty was performed with implantation of a drug-eluting stent, perfusion of tirofiban and aspiration of the remains of the thrombotic material.
During his stay on the hospital ward, the patient remained asymptomatic, and the causal study of this acute coronary syndrome was carried out. It is noteworthy that the patient's cardiovascular risk factors were that he was a smoker with a cumulative consumption of less than 1 packet/year, with no other known metabolic disorders. There is a maternal history of ischaemic heart disease and his mother is diagnosed with familial hypercholesterolaemia.
The patient underwent a lipid profile analysis which did not show any markedly elevated total cholesterol or LDL values, but rather a low CV risk profile. Urine toxins were requested and were negative, and a study of coagulopathies was carried out, also negative. Serum and urine metanephrines were requested and the patient was referred to endocrinology, who considered that there was a low probability of pheochromocytoma. Finally, it was decided to expand the lipid profile with a lipoprotein A (Lp(a)), which was found to be elevated for cardiovascular risk with a value 3 times the upper limit of normal.
The patient evolved satisfactorily, with no clinical signs of heart failure, although on discharge he presented moderate LV dysfunction, due to extensive anterior, anteroseptal and lateral akinesia (middle segments and apical cap).


DIAGNOSIS
Extensive anterior STEACS. Haemodynamic status KK1.
Single vessel coronary artery disease (SCAD). Percutaneous total revascularisation using a drug-eluting stent.
Moderate LV dysfunction (LVEF 44%).
Hyperlipoproteinaemia A.
