HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

PERSONAL HISTORY
No allergic drug reactions.
No hypertension or diabetes mellitus. Dyslipidaemia. Ex-smoker for more than 20 years. No alcoholism. Obesity.
Cardiological history: not reported.
Other history:
Last admission to neurology (one year ago): cortical cerebral venous thrombosis with associated parietal subarachnoid haemorrhage. Negative thrombophilia study. ANA Positive 1/160, no apparent autoimmune symptoms.
G3 P3 C0 A0. Hypermenorrhoea due to uterine myoma.
Previous surgical interventions: cholecystectomy 20 years ago.
Usual treatment: atorvastatin 20 mg (0-0-1), citicoline 1g (1-0-0). On treatment with acenocoumarol until 10 days before the current event. As there were no pathological findings requiring indefinite maintenance of anticoagulation, anticoagulation treatment was discontinued.

CURRENT DISEASE
A 44-year-old woman came to the emergency department with oppressive chest pain of 24 hours' duration.
She reported moderate intensity epigastralgia with subsequent irradiation to the central thoracic region and neck associated with vegetative cramping, which did not subside after taking several tablets of non-steroidal anti-inflammatory drugs. No dyspnoea or presyncope. She denied previous episodes of chest pain. Given the persistence of the pain, she decided to go to the emergency department.
On arrival, an electrocardiogram (ECG) was performed showing a subepicardial lesion current in the inferolateral and anterior face (V3-V6 and II, III and aVF). A haemodynamic alert was activated and emergent catheterisation was performed via the left radial route according to the usual technique with a 6F introducer. Right dominance. Evidence of thrombosis at the level of the ostial anterior descending (AD) artery. Thromboaspiration was performed with extraction of scarce white thrombus but recovering distal flow TIMI 2-3. The lesion was predilated with a balloon, a drug-eluting stent was implanted and the proximal segment of the stent was post-dilated with a balloon with good results.
However, there was later evidence of TIMI 1 distal mid-distal LAD flow that did not improve despite multiple doses of intracoronary nitroglycerin (icNTG) or percutaneous coronary intervention (PCI) balloon/guidewire manipulation (no-reflow effect). Periprocedural complications included ventricular fibrillation with haemodynamic instability requiring electrical cardioversion and vasoactive support.
Given the patient's history of cavernous sinus thrombosis and subsequent subarachnoid haemorrhage (SAH), it was decided not to administer potent antiplatelet therapy or abciximab, so acetylsalicylic acid (ASA) 250 mg and clopidogrel 600 mg were administered. After transfer to the coronary unit, a portable transthoracic echocardiography showed severe ventricular dysfunction and an image suggestive of apical thrombus. Given the suspicion of apical thrombus, enoxaparin is maintained at anticoagulant doses.
Two hours after the percutaneous procedure, the pain recurred and a new ST-segment elevation was observed, so it was decided to activate a second haemodynamic alert. Emergent coronary angiography was performed. Acute thrombosis of the stent in the LAD was evidenced and balloon predilatation was performed, restoring TIMI 3 flow with good expansion of the stent, with no images of dissection of the distal edge of the stent; however, there was still a large mobile thrombotic cast. Tirofiban is administered. After several minutes the thrombotic component persists with TIMI 3 flow, so thromboaspiration is performed with a good final angiographic result. He was transferred to the coronary unit.

PHYSICAL EXAMINATION
Blood pressure (BP) 90/50 mmHg, heart rate (HR) 120 bpm, SatO2 97% with Ventimask with FiO2 50%. Rhythmic heart tones, at 120 bpm, with 3R and 4R. Bladder murmur preserved with no over-additions. Lower extremities without oedema, peripheral pulses preserved and symmetrical, no signs of phlebitis.

COMPLEMENTARY TESTS
ECG: Emergency ECG (image 1): sinus tachycardia at 140 bpm, normal PR. Narrow QRS. Q wave in II, III and aVF, V3-6 with ST rise in these leads and fall in I, aVL V1-2. ECG 2 hours after catheterisation with recurrence of pain: sinus tachycardia at 125 bpm, normal PR. Narrow QRS. ST elevation in II, III and aVF as well as in V4-6 with Q wave in II, III and aVF and ST descent in I, aVL, V1-V2.
ECG at discharge OCU: ECG. Sinus rhythm at 100 bpm, normal PR. Narrow QRS. Anteroseptal necrosis.
Chest X-ray on admission (image 3): CTI within normality, no costophrenic sinus pinching; image of vascular redistribution.
CBC: Haemoglobin * 10.2 g/dl, haematocrit * 31.2%, MCV 83.8 fl, MCH 27.3 pg, MCHC 32.6 g/dl, ADE * 16.7%, leucocytes 7.9 10*9/l, neutrophils 59.4%, platelets * 531 10*9/l. Biochemistry: sodium 138 mEq/l, potassium 4.4 mEq/l, chlorine 103 mEq/l, haemostasis: Quick index 88%. INR 1.08 TTPA 30.3 sec. Peak hsTnI: 21,000ng/dl [limits of normality 0.0 - 11.6]. NT-ProBNP: 6300ng/dl. Lipid profile: total cholesterol * 214 mg/dl, triglycerides * 164 mg/dl, HDL cholesterol 47 mg/dl, LDL cholesterol * 134. Glycaemic-metabolic profile: glycosylated haemoglobin (US) 5.2%, thyrotropin (TSH) 1.05 uIU/ml. Iron profile: ferritin 31 ng/l, iron * 23 ng/dl, total Fe-binding capacity * 381 ug/dl, transferrin saturation index * 6%, latent Fe-binding capacity * 357.6 ug/dl. Thrombophilia profile: antithrombin 119%, protein C (functional) * 153%, protein S (Functional) * 115.1%, lupus anticoagulant negative. lupus anticoagulant (TVVRd) 0.9, lupus anticoagulant (SCT) 0.96, anti-cardiolipin IgG negative, anti-cardiolipin IgM negative, anti-cardiolipin IgM negative, anti-cardiolipin IgM negative. anticardiolipin IgM negative, beta 2-glycoprotein-I IgG negative, beta 2-glycoprotein-I IgM negative, activated protein C resistance 2.8, factor V Leiden negative, factor II (G20210A mutation) negative.
Tumour markers: CEA 1.5 ng/ml, carbohydrate ag. 15.3 (CA15.3) 9.1 IU/ml. Ag. carbohydrate 19.9 (CA19.9) 3.3 IU/ml. Ag. carbohydrate 125 (CA125) * 42 IU/ml. Alpha fetoprotein AFP 1.9 ng/ml.
Immunological profile: immunoglobulin IgG 1060 mg/dl, immunoglobulin IgA * 351 mg/dl, immunoglobulin IgM 81 mg/dl, ANA immunofluorescence positive 1/160 dsDNA, antibodies < 9.8 IU/ml, homogeneous IFA pattern ENA screening negative.
Albumin * 52.4%. Alpha 1 globulin * 9%. Alpha 2 globulin 11.1%. Beta globulin 12.2%.
Gamma globulin 15.3%. Albumin/globulin ratio * 1.1%.
Echocardiogram: First day in coronary unit: akinesia of all apical, anterior and mid-lateral segments. Contractility more preserved in bases. Estimated LVEF 30%. RV of normal size with preserved contractility. Mitral pattern with E minor A. Mild TR with estimated PAPs 45 mmHg. IVC 17 mm without respiratory variations. Possible apical thrombus. At discharge: severe left ventricular dysfunction (LVEF 34%) secondary to apical aneurysm and marked hypokinesia of anterior, lateral and septal mid segments. Absence of apical thrombus. Mild to moderate mitral regurgitation (grade II/IV) secondary to posterior leaflet retraction. Filling pattern compatible with increased end-diastolic pressures. Normal right ventricle with indirect signs of increased PAP.
Cardiac magnetic resonance (CMR): LV with normal volumes (VTD 78 ml/m2, VTS 52 ml/m2, IMVI 54 g/m2) without significant hypertrophy of its walls, with anterior and anteroseptal akinesia basal and medial and anterior and apical septal and strict apex with hypercontractility of the remaining segments and severe depression of global systolic function at rest (LVEF 33%). STIR sequences show myocardial oedema in the akinetic segments. Non-dilated RV (RVOT 37 ml/m2, STV 14 ml/m2) with preserved global systolic function (RVEF 64%). Aorta and great vessels of normal diameter and morphology. Atria of normal dimensions. Perfusion study (video 10): Gadoteric acid (0.15 mm/kg) is administered and well tolerated by the patient. Resting perfusion defects are detected in the akinetic segments. Necrosis and viability detection study: presence of myocardial LGE suggestive of transmural necrosis at the anterior and anteroseptal basal and mid and anterior and apical septal level and strict apex with presence of microvascular obstruction in these segments (absence of viability in 7 segments out of 17, DA-dependent). Presence of minimal pericardial and pleural effusion. Conclusion: acute ischaemic LV heart disease with preserved volumes and severe depression of GSF (LVEF 33%) with contractile alteration, oedema, perfusion defect and transmural necrosis with MVO at the level of 7 proximal LAD-dependent segments. Absence of intraventricular thrombus.
Total Body CT: Thoracic CT: centred mediastinum with no evidence of ganglionic formations of significant size. No pulmonary nodules or condensations are observed. No pleural or pericardial effusion is observed. Abdominopelvic CT scan: heterogeneous uterus, enlarged probably due to the presence of myomas. Nodular image of 17 mm with peripheral contrast uptake in left dense topography theoretically suggestive of corpus luteum. Liver of normal size and morphology with no evidence of focal lesions or dilatation of the intra- or extrahepatic bile duct. Cholecystectomy. Spleen, pancreas, adrenal glands and both kidneys were normal. No lymph node formations of significant size were observed in the abdominopelvic chains. Normal calibre and distribution of intestinal loops. No signs of metastatic bone involvement were observed by this technique.

CLINICAL EVOLUTION
After readmission to the coronary unit, he presented haemodynamic lability requiring increased vasoactive support with noradrenaline and dobutamine, so it was decided to implant an intra-aortic balloon counterpulsation device. Progressive weaning of haemodynamic support was achieved, with withdrawal of balloon counterpulsation and dobutamine on the third day. On the fourth day, despite noradrenaline support, levosimendan was started due to sustained hypotension. Norepinephrine was withdrawn on the sixth day. No ventricular arrhythmias were observed on monitoring. Spontaneous diuresis greater than 1500 ml per day with accumulated negative balance.
An MRI was performed which confirmed severe ventricular dysfunction and ruled out the presence of intracavitary thrombus. Discharge to the cardiology ward was decided to continue the study. During his stay on the ward he remained stable from the cardiovascular point of view, with no new episodes of chest pain. He began to ambulate with dyspnoea on moderate exertion (NYHA III/IV) with no other signs of heart failure; he also reported no palpitations, syncopal or presyncopal episodes. Pharmacological titration was carried out, verifying progressive tolerance (bisoprolol 5 mg/12h, enalapril 2.5 mg/12h, eplerenone 50 mg/24h, ivabradine 10 mg/12h).
Given that the patient had presented two thromboembolic events in different vascular territories, the last of which coincided with withdrawal of acenocoumarol, it was decided to perform a complete thrombophilia study. A CT scan of the abdomen and abdomen and pelvis was performed to rule out tumours and a complete blood analysis was performed. No relevant findings were observed in any of them.
The patient was discharged home with follow-up in the heart failure unit with the following treatment regimen:
Enoxaparin 80 mg one subcutaneous injection at breakfast and dinner, as a bridge to acenocoumarol. acenocoumarol 1 mg two tablets at lunch.
ASA 100 mg one tablet at breakfast.
Ticagrelol 90 mg one tablet at breakfast and dinner.
Atorvastatin 40 mg one tablet at dinner.
Bisoprolol 5 mg one tablet at breakfast and dinner.
Ivabradine 5 mg one tablet at breakfast and dinner.
Eplerenone 50 mg one tablet at lunch.
Enalapril 2.5 mg one tablet at dinner.
Furosemide 40 mg one tablet at breakfast.
Omeprazole 20 mg one tablet at breakfast.

DIAGNOSIS
KILLIP IV STEMI: acute thrombotic occlusion of the ostial LAD. Primary angioplasty with DES implantation in complicated LAD with no-reflow phenomenon and subsequent acute stent thrombosis.


Secondary diagnoses:
Severe systolic ventricular dysfunction. Apical aneurysm.
Dyslipidaemia.
