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CASE REPORT |
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| Year : 2006 | Volume
: 22
| Issue : 2 | Page : 156-158 |
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Stroke and myocardial ischemia in a patient of pheochromocytoma: A rare clinical sequele
Vivek Aggarwal, Amit Agarwal, Pradeep Puthenveepil, Ashok K Verma
Department of Endocrine Surgery, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Rae-Bareli Road, Lucknow - 226 014, India
Correspondence Address:
Ashok K Verma
Department of Endocrine Surgery, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Rae-Bareli Road, Lucknow - 226 014
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0970-1591.26578
 Abstract | | |
Pheochromocytoma classically presents with paroxysms of hypertension and adrenergic symptoms including headaches, palpitation, tremor and anxiety. However, these tumors can be clinically silent and occasionally manifest only when catecholamine release is upregulated by exogenous stimuli. In addition, the clinical presentation of pheochromocytoma can mimic a number of other medical conditions including migraine, cardiac arrhythmias, myocardial infarction and stroke, thus, making the diagnosis of pheochromocytoma difficult. We present a case of a 43-year old male patient who presented for evaluation of adrenal mass in the department of endocrine surgery. This patient had a previous history of right side hemiperasis and lateral wall ischemia, with no residual clinical deficit.
Keywords: Myocardial ischemia, pheochromocytoma, reversal, stroke, surgery
How to cite this article:
Aggarwal V, Agarwal A, Puthenveepil P, Verma AK. Stroke and myocardial ischemia in a patient of pheochromocytoma: A rare clinical sequele. Indian J Urol 2006;22:156-8 |
How to cite this URL:
Aggarwal V, Agarwal A, Puthenveepil P, Verma AK. Stroke and myocardial ischemia in a patient of pheochromocytoma: A rare clinical sequele. Indian J Urol [serial online] 2006 [cited 2020 Oct 30];22:156-8. Available from: https://www.indianjurol.com/text.asp?2006/22/2/156/26578 |
| Case Report | |  |
A 43-year male was referred for evalution of right adrenal mass. This mass was incidentally detected on ultrasonography, during evaluation of hypertension following myocardial infarction.
Two years back, the patient developed right hemiparesis, for which he was conservatively treated. CT scan done at that time, revealed a small ischemic infarct in the left capsular region [Figure - 1]. The patient recovered without any permanent deficit. One year later, the patient had lateral wall myocardial infarction. At that time, he was found to be hypertensive for the first time. Ultrasound of abdomen done for evaluation of hypertension revealed a suprarenal mass of heterogeneous echo texture, measuring 6.7 x 7.5 x 8.7 cm [Figure - 2]. Left adrenal and both kidneys were normal. The patient was then referred to us for evaluation of the mass lesion.
At this time, his blood pressure was controlled on two drugs. Investigation revealed raised 24 hour urinary metanephrine value of 13.33 mg /day (normal range: < 8 mg/day). Renal function tests and serum electrolytes were normal. Electrocardiogram (ECG) showed left ventricular strain pattern. Doppler neck did not reveal any thrombus. Treadmill test was negative for inducible angina and echocardiography was normal.
With a clinical diagnosis of adrenal pheochromocytoma, he was taken up for transperitoneal laparoscopic adrenalectomy, which later had to be converted to open approach due to uncontrolled bleeding. A right adrenal mass weighing 210 gm, measuring 10 x 8 x 5 cm was removed. No local infiltration or lymphadenopathy was noted.
Histopathology revealed adrenal pheochromocytoma.
The postoperative course was uneventful and the patient became normotensive. He was discharged on the 8th postoperative day.
| Discussion | | |
Pheochromocytoma is known to have varied clinical presentation. However, presence of myocardial infarction and stroke in a patient with pheochromocytoma with good recovery, has rarely been reported in medical literature.
Hypertension in pheochromocytoma is sustained in only about half of all patients, paroxysmal in about a third and non-existent in approximately a fifth. Dramatic manifestation of cardiovascular complications accompanies the hypertensive crisis. Myocardial infarction is frequently diagnosed in these patients.[1] However, it is more often due to coronary vasospasm, rather than due to coronary artery disease. Both these conditions may cause release of cardiac enzymes and produce electrocardiographic patterns, strongly resembling those of myocardial infarction.[2]
A possible role for catecholamine-induced vasospasm of the coronary arteries at the periphery, is supported by the fact that the most prominent dysfunction is observed at the apex of heart.[3]
It has also been speculated that sudden stimulation of Beta-receptor in the heart might cause infarction in humans.[4] In addition, excess catecholamine also induces increased sarcolemmal membrane permeability and calcium influx.[5] Excess calcium ion has a direct toxic activity on myocytes, leading to necrosis. In our patient, the echocardiography was not suggestive of any ventricular hypertrophy and hence it seems that the myocardial events could have been due to coronary vasospasm as a result of excess circulating catecholamines.
The nature of the cerebrovascular disease that results in stroke, includes possibilities like emboli from a cardiac source, thrombosis in situ and unusual cerebrovascular diseases such as fibro- muscular hyperplasia and complex migraine. Cerebral infarction commonly results from vasospasm due to catecholamine effects. Cerebral vasospasm can be either due to excess catecholamine or secondary to the other secretory products of the adrenal tumor such as nuropeptide -Y.[6] Vascular spasm in peripheral, coronary and cerebral arteries has been induced with sympathomimetic agents, either intentionally as in the treatment of epistaxis or as an unintended complication of use of these agents.[7] In fact, cerebral infarct and gangrene of the extremities, secondary to vasospasm, has been reported in some patients with pheochromocytoma.[8] Since a cerebral angiographic study was not performed in this case, we cannot precisely pinpoint the cause, but even with an angiographic examination, the precise vascular cause of such a stroke can seldom be determined with certainty. In our case, hemiperasis could have been due to vasospasm of the cerebral vessels, since this patient did not have any source of embolus or any history of migraine. This is also supported by the fact that in our case, the patient had a complete recovery after a documented infarct in the watershed area of internal capsule. Spasm is known to cause either transient impairment of circulation or infarcts with reversible dementia. Hypertension per se can also result in infarct in patients with pheochromocytoma. However, such lesions are more widespread, unlike in our case, where the infarct was restricted to the distribution of middle cerebral artery. Moreover, such hypertension is usually of malignant severity, which is difficult to control on drugs.
A clear understanding of etio-pathogenesis and high index of suspicion for pheochromocytoma, is necessary to avoid any catastrophe in cases presenting with history of early onset hypertension, cardiac or cerebro-vascular events.
| References | | |
| 1. | Cohen CD, Dent DM. Pheochromocytoma and acute cardiovascular death (with special reference to myocardial infarction). Postgrad Med J 1984;60:111-5.  [PUBMED] |
| 2. | Bravo EL. Evolving concepts in the pathophysiology, diagnosis and treatment of pheochromocytoma. Endoc Rev 1994;15:356-8. [PUBMED] [FULLTEXT] |
| 3. | Sardesai SH, Mourant AJ, Sivathandon Y, Farrow B, Gibbons DO. Pheochromocytoma and catecholamine induced cardiomyopathy presenting as heart failure. Br Heart J 1990;63:234-7. |
| 4. | Elian D, Harpaz D, Sucher E, Kaplinsky E, Motro M. Reversible catecholamine-induced cardiomyopathy presenting as acute pulmonary edema in a patient with pheochromocytoma. Cardiology 1993;83:118-20. |
| 5. | Bloom S, Davis DL. Calcium as mediator of isoproternol induced myocardial necrosis. Am J Pathol 1972;69:459-70. [PUBMED] |
| 6. | Gray TS, Morley JE. Neuropeptide Y. anatomical distribution and possible function in mammalian nervous system. Life Sci 1986;38:389-401. [PUBMED] |
| 7. | Isner JM, Estes NA 3rd, Thompson PD, Costanzo-Nordin MR, Subramanian R, Miller G, et al . Acute cardiac events temporally related to cocaine abuse. N Eng J Med 1986;315:1438-43. |
| 8. | Samuels MA, Southern JF. A 26-year-old woman with cardiomypathy, multiple strokes and an adrenal mass. N Eng J Med 1988;318:970-81. |
[Figure - 1], [Figure - 2]
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