HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
59-year-old woman. No known drug allergies.
Toxic habits: smoker since youth of 15 cigarettes a day (30 pack-years).
Cardiovascular risk factors: no arterial hypertension (AHT), no diabetes mellitus (DM). Dyslipidaemia such as hypertriglyceridaemia.
No previous cardiological history.

Other personal history of interest:
Hepatic haemangiomas monitored by abdominal ultrasound annually.
Primary biliary cholangitis being monitored by the digestive system.
Generalised anxiety disorder being monitored by psychiatry.
Usual treatment: Ursodeoxycholic acid 300 mg 2 tablets every 12 hours, bezafibrate 400 mg 1 tablet every 24 hours, quetiapine 100 mg 1.5 tablets at bedtime, lorazepam 1 mg 1 tablet for breakfast, lunch and dinner.

Present illness
For 48 hours prior to attending the emergency department, the patient began with clinical symptoms of central thoracic oppression radiating towards the left scapula of intermittent course, which increased with decubitus and coughing and decreased with sitting. She had suffered a catarrhal episode several weeks earlier, which was self-limiting. On the other hand, she also reported intense emotional distress in the last few days. When asked about cardiovascular symptoms in previous months, the patient reported a non-radiating central thoracic pressure that occurred on exertion, lasting several minutes and which subsided with rest, which had been present for about 6 months but which did not exactly remind her of the current pain. No dyspnoea, syncope or other relevant symptoms in the anamnesis by apparatus.

Physical examination
Blood pressure 123/83 mmHg; heart rate 77 beats per minute; S02 97% room air; temperature 36.6 oC
Conscious and oriented. Well perfused and hydrated. Eupneic at rest.
Head and neck: no jugular ingurgitation.
Cardiac auscultation: rhythmic, with pan-focal systolic murmur and no other pathological sounds (no friction sounds).
Pulmonary auscultation: preserved vesicular murmur.
Abdomen soft, depressible, not painful on palpation. No masses or megaliths palpable.
No signs of peritoneal irritation. Preserved hydro-aerial sounds.
Femoral and radial pulses present and symmetrical.
Lower extremities without oedema or signs of deep vein thrombosis (DVT).

COMPLEMENTARY TESTS
Electrocardiogram (ECG) performed in the emergency department: sinus rhythm at 75 beats per minute. PR of normal duration with a decrease in the PR in the inferior face and an increase in the aVR. Narrow QRS with rSr' morphology in V1. Rectilinear ST elevation of 1 mm in inferolateral face with symmetrical ST descent in precordials. Symmetrical negative T waves V3-V6.
QTc 430 msec.
Laboratory tests performed in the emergency department:
Biochemistry: glucose 84 mg/dl, urea 24 mg/dl, creatinine 0.78 mg/dl, GPT 42 U/l, bilirubin 0.4 mg/dl, amylase 90 U/l, calcium 9.6 mg/dl, albumin 4.1 g/dl, Na 144 mEq/l, K 4.1 mEq/l, Cl 109 mEq/l, CRP 7 mg/l, CK 200 U/l, LDH 233 U/l, TnT 457 ng/l (99th percentile in our hospital: 14 ng/l).
Haemogram: haemoglobin 13.4 g/dl, 8,390 leukocytes/ul with normal leukocyte formula, 192,000 platelets/ul.
Haemostasis: APTT 31 seconds, prothrombin time 100%, INR 1, fibrinogen 283 mg/dl.
Arterial blood gases (Fi02 0.21): pH 7.45, pCO2 31 mmHg, pO2 96 mmHg, bicarbonate 22 mmol/l, lactate 1.1 mmol/l.
Chest X-ray performed in the emergency department: cardiomediastinal silhouette preserved, without pleural effusion or gross condensation in the lung parenchyma.
Echocardiogram performed on admission to the coronary unit: left ventricle neither dilated (DVItd 37mm) nor hypertrophic (SIVtd 8mm and PPtd 8mm) with prominent septal knee. Moderate-severe systolic dysfunction. Mid-apical akinesia of all faces with hypercontractility of the bases leading to a dynamic gradient in the left ventricular outflow tract of up to 42 mmHg and SAM, resulting in moderate-severe mitral regurgitation.
The transmitral flow pattern suggests prolonged relaxation. Trivalve aortic valve with preserved opening and functionally normal. Right ventricle normal in structure and function. Tricuspid valve normal in structure. Mild-moderate tricuspid insufficiency with RV-AD gradient 28 mmHg. No pericardial effusion. Dilated inferior vena cava (22 mm) and inspiratory collapse > 50%. Estimated PSAP 38 mmHg. Aortic root of normal size. Echocardiographic contrast is injected in which the presence of apical thrombus is ruled out by this technique.
Urgent coronary angiography (videos 4, 5 and 6): right radial access. Truncus, anterior descending and circumflex arteries without lesions. Dominant right coronary artery without lesions (mechanical spasm due to proximal cannulation of the catheter, resolved with intracoronary NTG). Non-dilated left ventriculography with midventricular akinesia on all sides. Moderate mitral insufficiency. Intraventricular gradient of 30 mmHg between apex and LV outflow tract. There is an image of contrast repletion defect at inferoapical level (to rule out intracavitary thrombus with echocardiography).
Peak myocardial damage markers: CK 200 U/l, TnT 457 ng/l.
Regulated echocardiogram prior to hospital discharge: left ventricle neither dilated (DVItd 38mm, VTD BP indexed 43.8ml/m2) nor hypertrophic (SIVtd 8mm, PPtd 9mm) with prominent septal knee. Mild-moderately depressed systolic function (Simpson biplane 42.3%).
Mediastinal akinesia of all faces with hypercontractility of the bases, without generating dynamic gradient in the left ventricular outflow tract. Structurally normal mitral valve, without associated SAM. Mild central mitral insufficiency. Trivalve aortic valve with preserved opening and functionally normal. Right ventricle normal in structure and function. Tricuspid valve normal in structure. Tricuspid insufficiency mildly moderate with maximum gradient VD-AD 29 mmHg. Inferior vena cava not dilated (16 mm) and with inspiratory collapse > 50%. Estimated PSAP 34 mmHg. Aortic root of normal size (33mm). Minimal enveloping pericardial effusion.
MRI after several months: no myocardial oedema or pathological late enhancements suggesting myocarditis or previous ischaemic heart disease. Biventricular function preserved without alterations of segmental contractility.

CLINICAL EVOLUTION
On arrival of the patient at the emergency department, the on-call cardiology department was contacted. On anamnesis, the patient reported pain compatible in part with pericardial characteristics (changes in intensity with posture and coughing, previous respiratory infection, etc.) but the type of pain was oppressive and she also reported what appeared to be exertional angina in recent months. On the other hand, the patient reported an emotional upset in the days prior to the onset of the pain.
Initial laboratory tests showed elevated markers of myocardial damage (TnT 457 ng/l, CK 200 U/l) and a minimal elevation of CRP (7 mg/l). On the other hand, the ECG showed ST-segment elevation in the inferolateral face with a decrease in the PR and negative T waves in the precordial leads described above. Bedside echocardiography showed the same findings as in the initial echocardiography, i.e. moderate-severe left ventricular systolic dysfunction due to mid-apical akinesia of all segments together with significant mitral regurgitation due to SAM and presence of aliasing in the left ventricular outflow tract.
At that time, we considered several differential diagnoses: inferolateral ST-segment elevation acute coronary syndrome (STEMI), pericarditis, myopericarditis, tako-tsubo syndrome or a mixed picture.
The decision was made to activate the haemodynamics unit to perform an emergent coronary angiography, which did not show coronary lesions that would justify the current picture, so the picture was initially interpreted as a tako-tsubo syndrome that would justify the elevation of the markers of myocardial damage together with the alterations in segmental contractility and associated pericarditis.
During her stay in the coronary unit, the patient remained haemodynamically stable with a tendency to arterial hypotension, and neurohormonal medication could not be introduced.

Control echocardiograms showed a disappearance of the gradient and SAM with improvement of LVEF to mild-moderate dysfunction. The control ECG showed a QTc of up to 500 msec without arrhythmic events in the telemetry with subsequent normalisation of the QTc, with persistent symmetrical negative T waves in anterior precordial leads.
During her stay in the coronary unit and on the hospital ward, she presented chest pain with pericardial characteristics that subsided after initiation of treatment with non-steroidal anti-inflammatory drugs (NSAIDs).
At the time of discharge, the patient was completely asymptomatic in the anamnesis by apparatus. She was discharged with treatment for her pericarditis with anti-inflammatory drugs and subsequent follow-up by local cardiology. Neurohormonal treatment (ACE inhibitors/ARA-II) could not be started due to a tendency to arterial hypotension.
After 3 months, cardiac magnetic resonance imaging (MRI) was performed on an outpatient basis, showing complete recovery of ventricular function with no alterations in segmental contractility and no oedema or late enhancement, thus supporting the diagnosis of tako-tsubo syndrome and ruling out the presence of myocardial damage due to myocarditis or ischaemic heart disease.

DIAGNOSIS
Tako-tsubo syndrome.
Acute pericarditis. No evidence of myocarditis.
Left ventricular outflow tract gradient and moderate to severe mitral regurgitation due to SAM in the context of tako-tsubo syndrome, resolved on discharge.
Moderately-severely depressed left ventricular systolic function on admission in the context of tako-tsubo syndrome, with recovery to mild-moderate on discharge.
Coronary arteries without significant lesions or anomalous origins.
CVRF: active smoker, dyslipidaemia.
