PERSONAL HISTORY
Toxic habits: smoker of 1 cigarette/day.
No cardiovascular risk factors.
Anxiety-depressive syndrome.
Usual treatment: fluoxetine 20 mg.
CURRENT ILLNESS
A 54-year-old man consulted for chest pain of 8 hours' duration, oppressive, radiating to the left upper limb and jaw. Although the pain started in the early hours of the morning, the patient did not consult his primary care centre until late in the morning. He reported similar symptoms in the previous days, with similar episodes of chest pain that were self-limiting within the first 10 minutes. She denies intercurrent infectious clinical manifestations. No other symptoms.
On arrival at the primary care centre, an electrocardiogram was performed showing sinus rhythm at 85 bpm with ST-segment elevation in inferior leads. Acetylsalicylic acid (ASA) 300 mg and ticagrelor 180 mg were administered and the Infarction Code was activated.
On arrival at our centre, the patient was found to be sweaty, in fair general condition, with persistent chest pain and the electrocardiographic abnormalities described.

PHYSICAL EXAMINATION
Blood pressure (BP) 140/60 mmHg, heart rate (HR) 85 bpm, Sat 95% baseline.
General condition was fair.
Cardiac auscultation: rhythmic, no murmurs.
Pulmonary auscultation: preserved vesicular murmur with no added noises.
The rest of the examination was of no interest.


COMPLEMENTARY TESTS
Electrocardiogram (ECG): sinus rhythm at 90 bpm. PR 200 msg. Narrow QRS. Normal axis.
ST segment elevation II, III, aVF, V5 and V6.
Chest X-ray: CTI at the limit of normality. No pleural effusion.
No radiological congestive data.
Analysis on arrival: haemoglobin 12.4 g/dl. Leukocytes 10.82 Miles/mm3. Urea 49.0 mg/dl. Creatinine 0.85 mg/dl. Sodium 135 mEq/l. Potassium 3.8 mEq/l. Total bilirubin 0.64 mg/dl. GOT/AST 63 U/l. GPT/ALT 134 U/l. GGT 503 U/l. LDH 702 U/l. Alkaline phosphatase 214 U/l. CK 259 U/l. Troponin T (high sensitivity) 2790.00 ng/l.
Coronary angiography: thrombotic occlusion of the circumflex artery (ACx), immediately distal to an aneurysmal segment. The thrombotic lesion was crossed with an angioplasty guidewire, partially recovering distal flow, visualising an intraluminal contrast defect compatible with a large amount of intracoronary thrombus. For this reason it was decided to perform thromboaspiration; abundant red thrombus was removed, thus recovering distal TIMI 3 flow. A marginal branch remained occluded despite repeated attempts at thromboaspiration and balloon angioplasty. Given the high thrombotic content, intracoronary abciximab was added to the double antiplatelet therapy already administered and it was decided to maintain anticoagulation with enoxaparin at therapeutic doses.
Echocardiogram after catheterisation: left ventricle of normal size with inferior akinesia and inferolateral hypokinesia, leading to moderate ventricular dysfunction (LVEF 35%). Normal RVEF. Normal sized atria. Absence of significant valvular heart disease. Trivial tricuspid insufficiency that allows estimating a systolic pressure in the pulmonary artery of 25 mmHg. Mild detachment of pericardial leaflets. Normal sized inferior vena cava with physiological inspiratory collapse.
ECG at discharge: sinus rhythm at 80 bpm. Normal PR. Q wave in II, III and AVF.
Persistence of minimal ST underleveling in these leads and in V5-V6.

CLINICAL EVOLUTION
The patient initially presented a good evolution in the coronary unit, with no new episodes of chest pain or signs of heart failure. Monitoring showed no ventricular arrhythmias.
Two days later, he began to experience chest pain that worsened with inspiration and decubitus, with a clear pericardial profile, accompanied by elevated acute phase reactants in the blood tests (CRP 16, ESR 95).
A new echocardiogram was performed and reported: "Study performed with HR 87 bpm and BP 102/73 mmHg. Left ventricle (LV) without being able to estimate real size, with normal wall thickness, except for the lower basal segment. Severe ventricular dysfunction (LVEF 33%).
Lateral and inferior akinesia and severe hypokinesia of the rest of the segments. Right ventricle (RV) of normal size with mild systolic dysfunction. Normal sized atria, with right atrium with diastolic collapse. Mitral valve of normal appearance and function. Anatomically normal aortic valve with aortic flow recording with inspiratory descent of 20%.
Severe circumferential pericardial effusion: maximum diameter 28 mm in subxiphoid plane, rest of the planes approximately 15-18 mm. Inferior vena cava (IVC) at the limit of dilatation with absence of inspiratory collapse and pattern in suprahepatic veins with inversion of the respiratory sinus Y, compatible with haemodynamic compromise. Contrast was administered to assess extravasation to the pericardial space without contrast passage.
After the echocardiogram, pericardiocentesis was performed with extraction of abundant haematic fluid. Subsequently, the patient evolved satisfactorily without further incidents.


DIAGNOSIS
Acute ST-segment elevation myocardial infarction (STEMI) inferolateral Killip I.
Severe vessel disease: circumflex artery with aneurysm and thrombotic occlusion. Effective thromboaspiration.
Severe ventricular dysfunction.
Epistenocardial pericarditis. Severe pericardial effusion with cardiac tamponade.
Evacuative pericardiocentesis.
