A 70-year-old woman presented to the emergency department of our hospital with retroactive oppressive pain, intensity 10/10, epigastric pain lasting approximately 15 min, associated with profuse sweating.
She reported having had an episode of similar characteristics two days before, which led to consultation in another emergency department, where she was evaluated with electrocardiogram (ECG) and cardiac enzymes, not impressing the picture of coronary origin,
His past medical history included hypertension of unknown date, treated with atenol 50 mg daily, and breast cancer treated 20 years before with surgery and radiotherapy.
The patient was not a smoker and had no family history of coronary heart disease.
On admission, the patient was sweating but without pain.
Her blood pressure was 100/60 mmHg and her heart rate was 87 bpm.
On physical examination, colapable jugular veins stood out during inspiration, cardiac auscultation revealed no murmurs or galloping, and there was sensitivity to epigastric auscultation.
The rest of the examination was not remarkable.
Upon interrogation, the patient reported a history of similar episodes during the last 6 months, with no clear relationship with physical exertion, which were initially sporadic but which during the last week became more frequent, almost daily.
The ECG showed a slight ante-roseptal ST-segment elevation (STSD) with inversion of the T wave from V1 to V3, which was already evident on ECG taken 2 days before and was not evolutionary.
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The chest X-ray showed a cardiac silhouette of normal size and no signs of pulmonary congestion were observed.
The patient was admitted to the coronary care unit with non-ST-segment elevation acute coronary syndrome therapy.
Admission troponin I was determined as pg/ml (normal value < 0.05) and total CK was 117 U/L with a MB fraction of 25.
A few hours after admission the patient developed severe angina pectoris 10/10, associated with dyspnea, hospitalizations, headache, sweating and facial flushing.
Blood pressure increased up to 260/130 mmHg and sinus tachycardia with frequent supraventricular extrasis and ventricular extrasis was observed on the monitor, with a tapering of right bundle branch morphology lasting approximately 5 min.
There were no episodes of hypotension or syncope.
Given the characteristics of the episode, pheochromocytoma was diagnosed.
Heparin was suspended, physiological solution was provided and doxazosin was initiated at a dose of 1 mg every 12 h.
It was measured during the crisis catecholamines plasmatic and metanephrines (previous to the onset of doxazosine), which were markedly elevated.
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An abdominal magnetic resonance was requested, which confirmed the diagnosis, showing a right adrenal mass of 6 cm in diameter.
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The 123-I-metaiodobenzylguanidine scintigraphy (MI) confirmed the uptake in the mass described and showed no metastases.
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Additionally, a transthoracic echocardiogram showed mild left ventricular hypertrophy and mild impairment of global systolic function, with an ejection fraction (EF) estimated by Simpson of 42%, and coronary angiography showed no incidents during the procedure.
Ventricular dysfunction was assumed in the context of myocardial damage caused by catechiae.
The patient was prepared for surgical intervention with α- and β-adrenergic blockade, escalated with doxazosine and, after 2 days, prone position.
Surgery was performed 11 days later, with no significant hemodynamic complications and a favorable postoperative course.
The patient was discharged after 4 days in good condition.
From a clinical point of view, the patient had a good outcome with a progressive decrease in the dose of antihypertensive drugs and normalization of ventricular function in control echocardiography.
