Case Presentation: We present the case of a 32-year-old woman with past medical history of anxiety/depression, previous heroin abuse, hepatitis C who presented with tremors, chest pain, and vomiting. In the ER, her vitals were HR 94, RR 22, BP 117/83, SpO2 95% on room air. Initial labs showed elevated troponin 1.38, 4.44, 9.15. EKG in sinus rhythm, ST depression <-0.07mV in anterior/lateral/inferior leads. She was diagnosed with NSTEMI. Echocardiogram revealed ejection fraction of 35-40% with, lateral and apical hypokinesis consistent with TTC. Heart catheterization demonstrated normal coronary arteries. Chest CT angiogram demonstrated no acute cardiopulmonary abnormality, but a heterogeneous right adrenal mass was found. On further questioning, she endorsed long-standing, random, episodic tremors and flushing without alleviating or aggravating factors. Abdominal MRI confirmed 46 mm right adrenal mass without lymphadenopathy or venous invasion. Urine studies showed norepi 248, epinephrine 364, dopamine 174, vanillylmandelic acid 13.2. A clinical diagnosis of pheochromocytoma (pheo) was made and patient started on doxazosin and metoprolol. She underwent surgery for removal of the adrenal mass. Pathology confirmed pheo.
Discussion: Pheo secrete norepinephrine and epinephrine with combined alpha- and beta-adrenergic stimulation, the former usually more prominent and accounting for the rapid onset of labile systemic hypertension. Norepi acts on cardiac beta-adrenergic receptors to cause increased contractility and on alpha receptors in arteries and veins to cause vasoconstriction. The effect is elevated blood pressure, the usual manifestation of predominantly norepi-secreting tumors. Epinephrine has beta-stimulatory effects on the heart and both alpha and beta effects on peripheral vessels. With usual clinical doses, beta effects predominate and total peripheral resistance decreases. Patients with predominantly epinephrine-secreting tumors present with tachycardia, sweating, pallor, abdominal pain, nausea. Occasionally, patients with pheo are normotensive. It has been proposed that patients whose tumors secrete significant amounts of epinephrine may experience alternating hypertension and hypotension with concomitant symptoms due to the predominance of beta-adrenergic over alpha-adrenergic effects. Our patient had epinephrine greater than norepi levels. TTC is a cardiomyopathy related to excess catecholamines and can be precipitated by intense physical or emotional stressors. A typical TTC patient is older (60–70 years) with an identifiable preceding stressor. TTC-pheo patients are younger and rarely have an identifiable stressor. In clinical practice, pheo is rarely expected in normotensive patients. Our case in unique in that our patient did not have hypertension, and her other symptoms were overlooked due to her previous heroin abuse.
Conclusions: Pheo are rare. Symptoms produced by these chromaffin cell tumors are due to catecholamine secretion and classically include the triad of headache, diaphoresis, and palpitations . Hypertension is extremely common, and other, less common symptoms including flushing, fever, nausea, pallor, vision changes, and weight loss may occur. Pheo occasionally present with more serious cardiovascular symptoms including cardiogenic shock, heart failure, and cardiomyopathy, these presentations are associated with poor prognosis. It is advisable to rule out pheo in clinically appropriate patients presenting with TTC.