Pheochromocytoma: a cause of ST-segment elevation myocardial infarction, transient left ventricular dysfunction, and
Sheela Subramanyam1, Robert A Kreisberg
1Department of Diabetes, Metabolism, Endocrinology and Internal Medicine, Baptist Health System, Birmingham, Alabama 35213, USA. sheela.subramanyam@bhsala.com
Insights
Pheochromocytoma can mimic acute coronary syndrome (ACS) and cause takotsubo cardiomyopathy (TC). Surgical removal of the pheochromocytoma resolved cardiac dysfunction, supporting catecholamine excess as the cause of TC.
Area of Science:
- Cardiology
- Endocrinology
- Oncology
Background:
- Pheochromocytoma, a rare adrenal tumor, secretes catecholamines, potentially causing hypertensive crises.
- Excess catecholamines can lead to cardiovascular complications, including myocardial dysfunction.
- Takotsubo cardiomyopathy (TC) is a form of non-ischemic cardiomyopathy often triggered by stress.
Observation:
- A 60-year-old male presented with symptoms mimicking acute coronary syndrome (ACS).
- Cardiac investigations revealed apical ballooning consistent with TC, but no significant coronary artery obstruction.
- The patient had a history of labile hypertension and palpitations, with an incidentally discovered adrenal mass.
Findings:
- Elevated 24-hour urine catecholamines confirmed pheochromocytoma.
- Surgical resection of the pheochromocytoma led to complete resolution of left ventricular dysfunction.
- This case supports the hypothesis that catecholamine excess from pheochromocytoma can induce TC.
Implications:
- Pheochromocytoma should be considered in the differential diagnosis of ACS, especially with hypertensive episodes.
- Understanding the link between catecholamines and TC is crucial for managing these complex cases.
- Prompt diagnosis and surgical management of pheochromocytoma can reverse catecholamine-induced cardiac dysfunction.
Objective:
To report the case of a patient with a pheochromocytoma and apical left ventricular dysfunction that resolved after surgical resection of the pheochromocytoma, to review the effects of catecholamines on myocyte function and the concept that takotsubo cardiomyopathy (TC) is caused by excess catecholamines, and to illustrate the difficulty in the management of an acute coronary syndrome (ACS) during a hypertensive crisis attributable to a pheochromocytoma.
Methods:
We present the clinical history, physical findings, laboratory results, and imaging studies in a 60-year-old man with an ACS, TC, and an incidentaloma later diagnosed to be a pheochromocytoma. The association with TC and the pertinent literature are reviewed.
Results:
A 60-year-old man was suspected of having myocardial ischemia on the basis of symptoms of paroxysmal chest pain extending to the left shoulder, diaphoresis, ST-segment elevation on an electrocardiogram, and elevated serial levels of cardiac enzymes. Coronary angiography did not reveal substantial coronary artery obstruction but detected ballooning of the apical, anterior, and inferior cardiac walls, consistent with TC. He had a history of labile hypertension and palpitations of 3 months' duration. An adrenal mass detected on a prior computed tomographic scan and increased 24-hour urine catecholamine levels were consistent with a pheochromocytoma. Treatment with phenoxybenzamine was initiated, and he underwent a right adrenalectomy, which confirmed that the tumor was a pheochromocytoma and dramatically improved the patient's condition.
Conclusion:
Pheochromocytomas manifest with labile blood pressures and should be considered in the differential diagnosis of ACS. This case also supports the concept that TC is caused by excess catecholamines.
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