HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

BACKGROUND:
73-year-old patient. Allergies: idiosyncrasy to multiple non-steroidal anti-inflammatory drugs (NSAIDs). Only cardiovascular risk factor: hypertensive. Arthrosis. Cataract surgery. No previous known cardiological history. No family history of heart disease or sudden death. She leads an active life with good functional class. Of interest, her husband had been discharged from our service 15 days ago for acute coronary syndrome with ST-segment elevation (STEACS).

CURRENT ILLNESS:
She came to the emergency department for presenting, after doing household chores, with oppressive central thoracic pain radiating to the neck, lasting about 30 minutes, with progressive spontaneous decrease but without disappearing, for which she took a caffeine sl from her husband, with complete disappearance of the symptoms. No accompanying vegetative cortex. No previous similar episodes. No episodes of syncope or presyncope. Usual New York Heart Association (NYHA) functional class I, although in the last two weeks she reported dyspnoea on moderate exertion.

PHYSICAL EXAMINATION:
Blood pressure (BP) 140/68. Heart rate (HR) 98 bpm. Oxygen saturation 99% baseline.
Afebrile. Eupneic at rest. Cardiac auscultation: rhythmic, systolic murmur in lower left parasternal border that increases after Valsalva. Pulmonary auscultation: normoventilation.
Abdomen: soft and depressible. No masses or megaliths. No oedema in the lower extremities.
No IY. No carotid murmurs.

COMPLEMENTARY TESTS
THORAX RADIOGRAPHY: no pleuroparenchymal findings of acute evolution.
ECG (asymptomatic): sinus rhythm at 83 bpm, narrow QRS with hypertrophy criteria in high lateral face with growth of R, secondary repolarisation alterations in anterolateral face and deep Q waves in V1-3. No dynamic changes.
ANALYTICS: Tn I 0,28 -->2.20-->0,88. Glu 126 mg/dl, urea 38 mg/dl, creat 0.69 mg/dl, Na 142 mEq/l, K 4.3 mEq/l. Leukocytes 9400 mm3 (81% N), Hb 14.4 g/dl, Hto 45.5%, Platelets 155000/mm3. Coagulation: normal. Thyroid function: normal. Iron metabolism: normal. Hb 1AC 5.5%. LDL 80 mg/dl, HDL 33 mg/dl.
Echocardiogram: non-dilated LV, ventricular hypertrophy (LVH) at basal septal level (sigmoid septum, 16 mm), rest of segments mild concentric LVH. Mild LV dysfunction (estimated by Teicholz and Simpson biplanar 49-50%), mid and apical septal akinesia and inferoapical, rest of segments preserved contractility. Acceleration of flow in the left ventricular outflow tract (LVOT) with maximum baseline obstructive gradient 100 mmHg that increases with Valsalva manoeuvres up to 120 mmHg. Mitral filling pattern: impaired relaxation, with current data of elevated left ventricular end-diastolic pressure (LVEDP).
Left atrium (LA) slightly dilated. Right chambers not dilated, right ventricle (RV) normocontractile (TAPSE 19 mm, S' wave in lateral TDI 11.7 cm/sec). Aortic root and visualised portion of proximal ascending aorta normal. Mitral valve (MV) thin leaflets, correct opening. Complete SAM is observed generating MI with eccentric direction directed towards the AIS, reaching the roof of the left atrium (LA) without correctly visualising flow in the pulmonary veins, which appears significant (high Doppler intensity, although E wave < 1.2 cm/sec). Aortic valve (VAo) trivalve, thin leaflets, correct opening, not stenotic (Grad max 18 mmHg), competent. Tricuspid insufficiency (TI). Grad VD-AD 27 mmHg. Inferior vena cava (IVC) not dilated with preserved inspiratory collapse. Estimated normal systolic pulmonary artery pressure (PAPs). Absence of pericardial effusion, without intracavitary masses through this access route.
CORONARYGRAPHY: coronary arteries without significant angiographic lesions. Intramyocardial segment of mid LAD causing extrinsic compression in systole without generating severe milking. Ventriculography: severe hypokinesia of apical and middle segments of diaphragmatic and anterolateral face with hypercontractility of basal segments. Moderate LV dysfunction. MI grade I-II.
CARDIAC MRI: LV of normal size, with normal systolic function (EF 52%). Basal septal hypertrophy of 16 mm maximum thickness with signs of left ventricular outflow tract obstruction. No areas of late enhancement are evident in the myocardial thickness. Signs of MI with mild LA dilatation.
ECHOCARDIOGRAM prior to discharge: the echocardiogram was repeated on the ward after starting the dose of beta-blocker, finding a baseline gradient of 64 mmHg which increased to 100 mmHg with Valsava, with other findings similar to the previous echo, with no clear improvement in contractile asymmetries but with less hyperdynamia of the basal segments and preserved LV systolic function (50-55%).

CLINICAL EVOLUTION
At first it was treated as acute coronary syndrome. However, the patient was allergic to aspirin and trifusal. It was decided to perform a diagnostic cardiac catheterisation under treatment with clopidogrel and, if there were lesions, to subsequently perform aspirin desensitisation prior to performing coronary intervention.
Coronary angiography showed epicardial coronary arteries without lesions and ventriculography showed severe hypokinesia of apical and middle segments of the diaphragmatic and anterolateral face with hypercontractility of basal segments with moderate LV dysfunction.
With these findings, the first clinical suspicion was of tako-tsubo syndrome due to segmental asymmetries, history of stress (recent admission of her husband), elevated necrosis markers and epicardial coronary arteries without lesions.
Treatment with beta-blocker (bisoprolol) was started progressively up to 10 mg/24 hours with good clinical tolerance. The patient did not present heart failure during admission and remained asymptomatic. Platelet antiplatelet therapy was withdrawn.
Given the diagnostic doubt with hypertrophic cardiomyopathy, cardiac magnetic resonance imaging was performed, which showed no areas of late enhancement in the myocardial thickness and no evidence of hypertrophic cardiomyopathy. The septum was 16 mm with normal remaining segments.
At 30 days post-discharge, the patient presented NYHA functional class I and remained asymptomatic. Physical examination showed no congestive signs and no auscultation of a murmur. The ECG showed disappearance of Q waves with negative T waves in inferior and precordial leads. Echocardiogram in consultation showed LVEF 65%, without segmental asymmetries. The LVOT gradient was 10 mmHg and 24 mmHg after Valsalva. MR was mild.
The patient was referred to the cardiology department for follow-up.

DIAGNOSIS
Tako-tsubo syndrome with left ventricular outflow tract obstruction and significant MR due to SAM in a patient with septal LVH.
