Case ReportsReversible catecholamine-induced cardiomyopathy in a heart transplant candidate without persistent or paroxysmal hypertension
Section snippets
Case report
A 43-year-old Caucasian woman, with no history of cardiac disease or hypertension, presented with a 3-hour history of severe substernal chest pain, dyspnea, diaphoresis, nausea, and vomiting. Her blood pressure was 180/110 mmHg and pulse was 120 beats/minute. Cardiac and lung examinations were unremarkable. Electrocardiography showed a 1 to 2-mm ST segment elevation in leads I and aVL (Figure 2). Cardiac monitoring demonstrated frequent premature ventricular beats and recurrent episodes of
Reversible catecholamine-induced cardiomyopathy
When a patient presents with severe unexplained systolic heart failure and is evaluated for heart transplantation, causes of reversible cardiomyopathy must be excluded. Thyrotoxicosis, renal failure, septic shock, iron overload, sarcoidosis, hypophosphatemia, hypocalcemia, alcoholism, pheochromocytoma and medications (eg, cocaine) have all been reported to cause reversible cardiomyopathy.2
Catecholamine-induced cardiomyopathy is a recognized complication of pheochromocytoma and may be the only
Conclusion
A 43-year-old patient with pheochromocytoma presented with acute myocardial infarction and normal coronary arteries, developed cardiogenic shock, and had recurrent episodes of nonsustained ventricular tachycardia, without developing persistent or paroxysmal hypertension. She had reversible catecholamine-induced cardiomyopathy, that was discovered during evaluation for cardiac transplantation. Routine screening of heart transplantation candidates for occult catecholamine-secreting tumors, even
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Cited by (41)
Clinical Features and Outcome of Pheochromocytoma-Induced Takotsubo Syndrome: Analysis of 80 Published Cases
2016, American Journal of CardiologyCitation Excerpt :It should be acknowledged that the description of LVWMA is not always accurate especially in the cases described before the TS-era. Five of 9 patients published before 2000 were described to have severe left ventricular dysfunction or severe myocardial depression with a clinical course consistent with TS.6–10 The other 4 patients had typical mid-apical or basal TS pattern.11–14
Endocrine Hypertension
2015, Williams Textbook of EndocrinologyAn autopsy case of bilateral adrenal pheochromocytoma-associated cerebral hemorrhage
2013, Legal MedicineCitation Excerpt :Pheochromocytoma is considered to account for 0.1–0.2% of hypertensive patients, being a rare disease [1,2,4]. Reportedly, a massive amount of catecholamine released by pheochromocytoma causes myocardial ischemia, heart failure, cerebral hemorrhage, fever, and metabolic acidosis [1–9], but only a few autopsy cases of cerebral hemorrhage have been reported [10]. In this study, we present the autopsy of a patient who died of cerebral hemorrhage induced by bilateral adrenal pheochromocytoma.
Hypertension in pheochromocytoma: Characteristics and treatment
2011, Endocrinology and Metabolism Clinics of North AmericaCitation Excerpt :The increase in cardiac contractility along with myocardial hypoxia can result in acute or chronic ischemia and myocardial infarction.63 Unlike myocardial infarction caused by heart disease, patients with pheochromocytoma with no medical history of heart disease seem to have normal coronary arteries on angiography along with normal levels of cardiac enzymes.64 Long-standing hypertension, chronic myocardial hypoxia, and metabolic myocarditis of hypercatecholaminemia are known to cause cardiomyopathy that, in the case of pheochromocytoma, can be chronic (hypertrophic, dilated, obstructive) or acute (ischemic, tako-tsubo).
Pheochromocytoma-related cardiomyopathy or stress cardiomyopathy secondary to pheochromocytoma: Is new terminology needed?
2008, Revista Espanola de Cardiologia