HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION
An 81-year-old woman, dyslipidaemic, hypertensive, obese, with DDD pacemaker due to complete atrioventricular block (AVB), chronic venous insufficiency, hypothyroidism and spondyloarthrosis.
She attended the emergency department for a single episode of oppressive central thoracic pain, which did not change with palpation, deep inspiration or movement, not radiating or associated with vegetative cortex, onset at rest, after a situation of family stress, of undetermined duration. There was no evidence of orthopnoea, paroxysmal nocturnal dyspnoea, palpitations, dyspnoea at rest or on exertion, malleolar oedema or reduced diuresis. No dietary transgression or modification of his usual medication. No respiratory, abdominal or genitourinary infections.
The patient presented cardiologically stable, with a heart rate of 94 bpm, blood pressure 200/110 mmHg, afebrile and baseline oxygen saturation 95%. She was conscious and oriented, in good general condition, eupneic at rest, normohydrated, normal colour and normal depth. Carotid pulses were rhythmic and symmetrical and we did not detect jugular ingurgitation.
Cardiopulmonary auscultation was rhythmic and without murmurs, with preserved vesicular murmur. Abdominal examination revealed a soft and depressible abdomen, no pain on superficial or deep palpation, no masses or megaliths, generalised tympanism, no peritonism and positive hydro-aerial sounds. The lower extremities showed no malleolar oedema, with symmetrical posterior pedial and tibial pulses present and no stigmata of venous insufficiency or deep vein thrombosis.

COMPLEMENTARY TESTS
Blood tests showed haemoglobin 11.4 g/dl, hcto 35.1%, MCH 29.2 pg, MCV 90 fl, normal leukocytes, normal platelets, normal biochemistry, normal CPK, peak troponin-I 6 ng/ml, normal renal function, normal ions and normal coagulation.
The portable anteroposterior chest X-ray showed an increased cardiothoracic index, no alterations of the bronchovascular tract, no alveolar or interstitial infiltrates, with free costodiaphragmatic angles.
Electrocardiogram (ECG) revealed sinus rhythm at 81 bpm, PR 200 msec, right bundle branch block (RBBB) and HMAIHH, QRS axis at -60o, isodiphasic T waves from V3-V4 and symmetric negative waves from V5-V6 (dynamic changes from baseline ECG) and QTc 394 msec.

CLINICAL EVOLUTION
The patient was admitted to the coronary care unit, where enzyme seriation and ECG were completed, and antianginal treatment was started. The transthoracic echocardiogram showed a left ventricle at the upper limit of normality, not hypertrophied, with strict anteroapical, inferoapical and apical akinesia and compensatory contractility of basal and middle segments, diastolic pattern of impaired relaxation and moderately depressed systolic function (LVEF 40% by Simpson biplane). The right ventricle was neither dilated nor hypertrophied, with normal systolic function (TAPSE > 18 mm), while the right and left atria were normal in size. The mitral valve had discrete thickening of the valve leaflets, with calcification of the posterior annulus, good opening and a regurgitant jet that was suggestive of mild mitral regurgitation (MR). The aortic valve had trivalve morphology, with good opening and a regurgitant jet, leading to mild aortic insufficiency (AIo), with no apparent dilatation of the aortic root. Morphologically normal tricuspid valve, with good opening and mild insufficiency, which allowed estimation of pulmonary arterial systolic pressure (PSAP) 50 mmHg. The pericardium had normal thickness and refractoriness, without effusion, and the inferior vena cava was not dilated, and collapsed adequately (>50%) with inspiration.
During his stay in the unit he remained cardiologically stable, with a tendency to hypertension, requiring high doses of beta-blockers, angiotensin-converting enzyme inhibitors (ACE inhibitors) and nitroglycerin perfusion. He had no new episodes of angina at rest or on slight exertion, palpitations or dyspnoea. Preferential catheterisation confirmed anteroapical and apical cap dyskinesia, with moderately depressed systolic function, and showed coronary arteries without angiographically significant lesions. Given the clinical and haemodynamic stability, the patient was discharged to the cardiology ward, where she remained asymptomatic, with a tendency to hypertension. After adjustment of treatment with beta-blockers and angiotensin II receptor antagonist (ARAII), blood pressure normalised. No periprocedural complications were reported and the patient was discharged with hygienic-dietary recommendations, double antiplatelet therapy, beta-blockers, ARA-II and statins. Three months later the patient remains clinically asymptomatic, and a follow-up echocardiography has revealed full recovery of the segmental alterations described in the acute event.

DIAGNOSIS
Non ST-segment elevation myocardial infarction (NSTEMI) with normal coronary arteries.
Hypertensive emergency.
Stress cardiomyopathy (tako-tsubo syndrome).
