HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
77-year-old woman, with no cardiovascular risk factors. Personal history of bronchial asthma with occasional bronchodilator treatment and two episodes of superficial venous thrombosis.
Cardiological history: she consulted the cardiology department for episodes of central thoracic pressure on exertion accompanied by dizziness, sweating and trembling of the limbs. They occurred almost daily, so she has limited her physical activity.

PHYSICAL EXAMINATION:
Notable systolic murmur in aortic focus without erasing second noise. The electrocardiogram showed sinus tachycardia at 110 bpm without acute repolarisation alterations. Echocardioscopy showed a hypertrophic left ventricle (LV), non-dilated, with preserved ejection fraction [LVEF], without alterations in segmental motility or significant valvular heart disease, or pericardial effusion.
On suspicion of ischaemic heart disease, treatment was started with acetylsalicylic acid (ASA), beta-blockers and statins, and an outpatient study with exercise echocardiogram was requested.
The exercise echocardiogram showed moderate baseline left ventricular hypertrophy with mitral systolic anterior systolic motion, baseline dynamic gradient of 40 mmHg and akinesia of all apical segments. During exercise the akinesia extended to mid segments of all sides with moderate dysfunction and increased dynamic gradient to 95 mmHg. Preferential catheterisation and routine laboratory tests were requested.
A few days later, the patient visited her primary care physician for worsening functional class with dyspnoea and mild exertional chest pain. Physical examination revealed crackles in the right base and oedema in the ankles. The electrocardiogram (ECG) showed sinus rhythm with negative T waves, symmetrical and deep V3-V6 and negative T waves in the inferior face. In addition, the analysis requested by the cardiologist showed suppressed thyroid stimulating hormone (TSH) with free T4 63.7 (normal reference values 10.6-26).
She was referred to the emergency department of our hospital. On arrival she was haemodynamically stable with blood pressure (BP) 105/50 mmHg; heart rate (HR) 85 bpm. Afebrile. Oxygen saturation (SatO2) 94%. Well perfused and slightly tachypneic (25 rpm) at rest. Physical examination revealed jugular ingurgitation at the base of the neck, systolic murmur in the aortic focus, crackles in the lung bases and discrete oedema in the lower limbs.
While in the emergency department he presented with an episode of precordial pain at rest, with no dynamic changes in the ECG. Suspicion of unstable angina led to admission to the coronary unit.

COMPLEMENTARY TESTS
STRESS ECOCARDIOGRAM (outpatient):
Baseline echocardiogram: moderate left ventricular hypertrophy. Akinesia of the apical half of the inferior, anterior and posterior septum and of the apical segment of the anterior face and anterior septum. Systolic function preserved but at the lower limit of normal. Left atrium slightly dilated (20-30 cm2). Slightly thickened mitral valve, with SAM leading to mild mitral regurgitation (MR). The right ventricle (RV) is normal in terms of size and systolic function. Mild-moderate tricuspid regurgitation with Vd-Ad gradient of 48 mmHg. Estimated pulmonary artery systolic pressure (PSAP) of 55 mmHg. Trivalve aortic valve, normofunctioning. In the left ventricular outflow tract (LVOT) there is turbulent flow with a dynamic gradient of 40 mmHg. The aortic root is of normal size.
Stress echocardiogram: he performed 55 seconds of the first step, presenting intense dyspnoea that forced the test to be suspended. He reached 100% of the maximum theoretical heart rate (MTHRF). During exercise, akinesia extends to the middle segments of all faces with moderate dysfunction and an increase in the dynamic gradient to 95 mmHg.
ECG on admission: sinus rhythm at 86 bpm, normal PR, narrow QRS with axis at 60o, negative T waves in V3-V6 and inferior face, QTc 433 ms.
ANALYTICS: biochemistry: glucose 106 mg/dl, urea 42 mg/dl, creatinine 0.40 mg/dl, glomerular filtration rate (CKD-EPI) > 90 ml/min/1.73 m2, total cholesterol 114 mg/dl, HDL cholesterol 59 mg/dl, non-HDL cholesterol 55 mg/dl, LDL cholesterol 37 mg/dl, triglycerides 91 mg/dl, albumin 3.64 g/dl, total bilirubin 0.74 mg/dl, GOT 33 U/l, GPT 39 U/l, GGT 74 U/l, alkaline phosphatase 64 U/l, phosphorus 2.55 mg/dl, total calcium 9.32 mg/dl, sodium 143 mmol/l, potassium 4.46 mmol/l, iron 103 μg/dl, C-reactive protein 0.1 mg/dl, ferritin 106 ng/ml, HbA1c 5.8%. TSH < 0.005 μU/ml, free T4 63.7 pmol/l. Myocardial damage marker curve: TnT 17 ng/l [normal 0-14] --> 20 --> 14, CK 34 U/l --> 33 --> 39. Haemogram: haemoglobin 13.1 g/dl, platelets 279 10^3/μl, leucocytes 5.7 10^3/μl, neutrophils 43.4%, lymphocytes 33.3%, monocytes 14.9%, eosinophils 7.5%, basophils 0.9%.
CHEST X-RAY: no cardiomegaly, slight vascular redistribution to upper fields, free costophrenic sinuses.
ECHOCARDIOGRAM on admission: non-dilated LV with moderate concentric hypertrophy. Preserved global systolic function (LVEF 64%) with no abnormalities of segmental contractility.
Tricuspid aortic valve with preserved opening, without significant functional alterations.
Dynamic gradient in LVOT, maximum of 28 mmHg. SAM is observed with mild protosystolic MR. Slightly dilated left atrium. RV not dilated with preserved systolic function. Mild tricuspid insufficiency, with Vd-Ad gradient 22 mmHg. No pericardial effusion.
CARDIAC CATHETERISM: coronary network without lesions.
AL ALTA ECOCARDIOGRAM: small LV with mild concentric parietal hypertrophy and moderate septal hypertrophy. Global systolic function preserved, compared with previous outpatient study, having disappeared the alterations of apical motility and basal hyperdynamics that caused systolic gradient. Diastolic pattern of elongated relaxation. RV is normal with respect to size and function. Slightly dilated left atrium (20-30 cm2). Mild calcification of the posterior mitral annulus with mild MR. Mild tricuspid insufficiency (TI) with Vd-Ad gradient 31 mmHg. Estimated PSAP 36 mmHg. Mild pulmonary hypertension. Sclerosed aortic valve, trivalve, without functional alterations. The aortic root is of normal size. No pericardial effusion.

CLINICAL EVOLUTION
The patient was admitted to the coronary unit with a suspected diagnosis of unstable angina.
During her stay she remained haemodynamically stable with a slight tendency to arterial hypotension. In the echocardiogram on admission, no alterations in segmental contractility were observed, with a dynamic gradient persisting in the LVOT but of a lesser magnitude than in the outpatient echocardiogram. In the first 24 hours of admission, the patient presented several episodes of central thoracic pressure accompanied by intense sweating, nausea and tremor of the extremities. Given the presence of a dynamic gradient in LVOT and the analytical results compatible with thyrotoxicosis, beta-blocker treatment with atenolol was intensified for adequate symptomatic control and the congestive symptoms were resolved with intravenous diuretic treatment.
She was assessed by the endocrinology department where, given the abruptness of the hyperthyroid symptoms, eosinophilia and relative lymphomonocytosis, they suspected Graves-Basedow disease as the first possibility and indicated treatment with methimazole 15 mg/12 hours.
Coronary angiography was performed, revealing a coronary arterial network without lesions.
Given these results, the improvement of the segmental alterations in the echocardiography, the recovery of left ventricular systolic function and the good symptomatic control with the prescribed treatment, the condition was interpreted as tako-tsubo syndrome in the context of the debut of primary hyperthyroidism.
The process was continued in outpatient endocrinology and cardiology consultations. She remained euthyroid and asymptomatic, without dyspnoea or exertional angina, palpitations or other cardiovascular symptoms, and was discharged after 3 months of follow-up.

DIAGNOSIS
Tako-tsubo syndrome secondary to primary hyperthyroidism, suspected Graves-Basedow disease.
