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Year : 2016  |  Volume : 4  |  Issue : 3  |  Page : 110-113

Recurrent non-st elevation myocardial infarction: An unusual cause

1 Department of Cardiology, Iqraa Hospital, Kozhikode, Kerala, India
2 Department of Cardiology, Ahalia Hospital, Abudhabi, United Arab Emirates
3 Department of Cardiology, Government Medical College, Kozhikode, Kerala, India

Date of Web Publication16-Sep-2016

Correspondence Address:
M P Ranjith
Bhavatharini, P. O. Pantheerankave, Kozhikode - 673 019, Kerala
United Arab Emirates
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2321-449x.190753

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Pheochromocytoma is a rare, catecholamine-secreting tumor derived from chromaffin cells. It usually presents with palpitations, diaphoresis, headache, and paroxysmal hypertension. Rarely, it may associate with acute myocardial infarction (MI) and other cardiovascular complications. Here, we are reporting a case of a 40-year-old male with adrenal pheochromocytoma presented with a history of repeated episodes of acute pulmonary edema along with electrocardiographic changes and serum cardiac marker elevation, suggestive of MI, with complete reversal of these abnormalities after surgical removal of the tumor.

Keywords: Non-ST elevation myocardial infarction, pheochromocytoma, pulmonary edema

How to cite this article:
Rajesh K F, Ranjith M P, Muneer K. Recurrent non-st elevation myocardial infarction: An unusual cause. Heart India 2016;4:110-3

How to cite this URL:
Rajesh K F, Ranjith M P, Muneer K. Recurrent non-st elevation myocardial infarction: An unusual cause. Heart India [serial online] 2016 [cited 2021 Dec 2];4:110-3. Available from: https://www.heartindia.net/text.asp?2016/4/3/110/190753

  Introduction Top

Pheochromocytoma is a rare tumor with chromaffin cell origin and has varied clinical presentation. [1],[2] Because of excessive catecholamine secretion, it precipitates life-threatening hypertension or cardiac arrhythmias. Other rare cardiovascular manifestations include shock, myocarditis, dilated cardiomyopathy, heart failure, transient left ventricular (LV) apical ballooning, aortic dissection, and prolongation of the Q-T interval. However, pheochromocytoma rarely presents as acute coronary syndrome. Once pheochromocytoma is diagnosed, it is potentially curable. In this case report, we describe a 40-year-old male with pheochromocytoma who presented with retrosternal discomfort and electrocardiographic changes, suggestive of acute myocardial ischemia.

  Case report Top

A 40-year-old male presented to our emergency department with acute onset of retrosternal chest discomfort and breathlessness. He was hospitalized elsewhere 3 months back with similar complaints and was diagnosed to have pulmonary edema, diabetes, and hypertension. On examination, he was orthopneic with a pulse rate of 124/min, regular, and a blood pressure of 210/110 mm Hg. There was basal lung crepitation. Cardiovascular system examination was normal except for a third heart sound. The rest of the examination was unremarkable. Blood investigation revealed elevated troponin I level. Electrocardiogram (ECG) showed sinus rhythm with deep T-wave inversion in inferior and lateral leads [Figure 1]. Echocardiogram was showing concentric LV hypertrophy and impaired LV diastolic function with preserved systolic function. There was no regional wall motion abnormality. Ultrasonogram of the abdomen showed mildly increased renal parenchymal echotexture with normal renal Doppler indices.
Figure 1: First presentation of electrocardiogram showing sinus rhythm with deep T-wave inversion in inferior and lateral leads

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In view of clinical evidence of pulmonary edema in a diabetic and hypertensive man with ECG changes and positive troponin I, a possibility of non-ST elevation myocardial infarction (MI) was considered. In view of MI, a coronary artery angiogram (CAG), right and left heart catheterization study was performed. CAG revealed normal coronaries [Figure 2]a and b. Right and left heart catheterization study did not show any abnormal finding other than high blood pressure. A renal angiogram was performed in view of persistent high blood pressure. Surprisingly, his left renal angiogram revealed a circular contrast-enhancing lesion in suprarenal region [Figure 2]c.
Figure 2: (a-c) Coronary artery angiogram showing normal coronaries and left renal angiogram showing a circular contrast-enhancing lesion in suprarenal region

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A 24 h urine metanephrine assay was subsequently done and it was 1.2 mg/24 h (normal <1). Computed tomography abdomen with contrast revealed left adrenal mass of size 4.1 × 3.7 × 4.5 cm, possibly a pheochromocytoma [Figure 3]. The patient was referred for resection of mass which was accomplished 2 weeks later after controlling blood pressure. Histopathology showed nests of tumor cells surrounded by a discontinuous layer of sustentacular cells and fibrovascular stroma suggesting pheochromocytoma [Figure 4]. Urine 24 h metanephrine assay was repeated 2 weeks after surgery and was normal. During 1-month follow-up after surgery, he is asymptomatic and his ECG changes were normalized [Figure 5].
Figure 3: Computed tomography abdomen with contrast film revealing left adrenal mass of size 4.1 cm × 3.7 cm × 4.5 cm

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Figure 4: Histopathology specimen showing nests of tumor cells surrounded by a discontinuous layer of sustentacular cells and fibrovascular stroma suggesting pheochromocytoma

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Figure 5: Normal electrocardiogram during 1-month follow-up after surgery

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  Discussion Top

Pheochromocytoma is an uncommon neoplasm occurring in about 1-2 per 100,000 adults. [3] It is a catecholamine-secreting tumor derived from chromaffin cells. [1] Most patients with pheochromocytoma have hypertension. Hypertension can be intermittent, remittent, or persistent. Episodes of high blood pressure can occur in about 50% of the patients having this tumor. Severe and prolonged episodes of hypertension can lead to shock in some of the patients. Low plasma volume, arrhythmias, cardiac damage, or loss of vascular tone due to stimulation of α2 receptors are the suggested reasons for shock in pheochromocytoma. Long-standing hypertension can cause concentric LV hypertrophy and rarely asymmetrical septal hypertrophy. High catecholamine levels can lead to cardiac tachyarrhythmias in about 20% of the patients with catecholamine-secreting tumors. [4] Persistent and prolonged exposure to high levels of catecholamines can result in dilated cardiomyopathy [5] or catecholamine myocarditis, which is characterized by foci of myocardial cellular necrosis. Pheochromocytoma has been reported to mimic an acute MI in rare instances. ECG changes, including T-wave inversion and ST segment elevation, are seen in such cases. Segmental or global myocardial dysfunction may lead to pulmonary edema in some of the cases. [6] Prolongations of Q-T interval, as well as deep and wide symmetrically inverted T-waves are observed in 15% of the patients with pheochromocytoma. [6],[7] The mechanism of QT prolongation is not clear. Alpha adrenergic stimulation can prolong the Q-T interval by prolonging the action potential duration, which is a possible reason for QT prolongation. [8] Polymorphic VT occurs in pheochromocytoma due to adrenergic excess. The diverse manifestations of this tumor reflect variations in the hormones it releases, their patterns of hormone release, and in the individual-to-individual differences in catecholamine sensitivities. [1] The occurrence of non-ST elevation MI along with pulmonary edema in pheochromocytoma is rare, only a few case reports are available in literature. [9],[10],[11],[12] The pathophysiology of myocardial dysfunction associated with pheochromocytoma has been linked to either a direct toxic effect induced by catecholamines or myocardial stunning caused by coronary spasm. [13] During a pheochromocytoma crisis, a myocardial oxygen demand-supply mismatch can occur due to an increased afterload (vasoconstriction), catecholamine-driven tachycardia, and catecholamine-driven coronary vasospasms. This can precipitate myocardial ischemia with concomitant electrocardiographic abnormalities, even in the absence of coronary atherosclerosis. We describe an uncommon presentation of a pheochromocytoma, mimicking a MI and its detection during angiogram.

  Conclusions Top

Pheochromocytoma is a difficult condition to diagnose clinically. A high index of suspicion is required to diagnose it clinically because of its pleomorphic presentations. Non-ST elevation MI along with pulmonary edema is a rare presentation of pheochromocytoma. It would be advisable to evaluate patients with unexplained arrhythmia and high blood pressure to exclude secondary causes of hypertension.

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Conflicts of interest

There are no conflicts of interest.

  References Top

World Health Organization. WHO classification of tumors 2004. In: De-Lellis RA, Lloyd RV, Heitz PV, Eng C, editors. Pathology and Genetics of Tumors of Endocrine Organs. France: IARC Press: 2004. p. 151.  Back to cited text no. 1
Pacak K, Lenders JW, Eisenhofer G, editors. Pheochromocytoma: Diagnosis, Localisation, and Treatment. 1 st ed. Malden: Blackwell Publishing; 2007. p. 8-29.  Back to cited text no. 2
Bravo EL, Tagle R. Pheochromocytoma: State-of-the-art and future prospects. Endocr Rev 2003;24:539-53.  Back to cited text no. 3
Schürmeyer TH, Engeroff B, Dralle H, von zur Mühlen A. Cardiological effects of catecholamine-secreting tumours. Eur J Clin Invest 1997;27:189-95.  Back to cited text no. 4
Mootha VK, Feldman J, Mannting F, Winters GL, Johnson W. Pheochromocytoma-induced cardiomyopathy. Circulation 2000;102:E11-3  Back to cited text no. 5
Sardesai SH, Mourant AJ, Sivathandon Y, Farrow R, Gibbons DO. Phaeochromocytoma and catecholamine induced cardiomyopathy presenting as heart failure. Br Heart J 1990;63:234-7.  Back to cited text no. 6
Liao WB, Chiang CW, Kung CE, Lee CW. Cardiovascular manifestations of pheochromocytoma. Am J Emerg Med; 18:622-5.  Back to cited text no. 7
Viskin S, Fish R, Roth A, Schwartz PJ, Belhassen B. Clinical problem-solving. QT or not QT. N Engl J Med 2000;343:352-6.  Back to cited text no. 8
Koracevic GP. Does pheochromocytoma mimic or cause acute myocardial infarction? Cardiol J 2010;17:215-6.  Back to cited text no. 9
Coroleu SF, Muñoz-Camacho JF, Fernández-Gómez C, Tarroch-Sarasa X. Acute myocardial infarction probably related to severe coronary vasospasm during pheochromocytoma crisis. Rev Esp Cardiol 2011;64:244-6.  Back to cited text no. 10
Darzé ES, Von Sohsten RL. Pheochromocytoma-induced segmental myocardial dysfunction mimicking an acute myocardial infarction in a patient with normal coronary arteries. Arq Bras Cardiol 2004;82:178-80.  Back to cited text no. 11
Menke-van der Houven van Oordt CW, Twickler TB, van Asperdt FG, Ackermans P, Timmers HJ, Hermus AR. Pheochromocytoma mimicking an acute myocardial infarction. Neth Heart J 2007;15:248-51.  Back to cited text no. 12
Sheikhzadeh A, Fatourechi V, Paydar D, Nazarian I. Unusual cardiovascular manifestations in a case of pheochromocytoma. Clin Cardiol 1983;6:136-42.  Back to cited text no. 13


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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