Catecholamine-induced cardiomyopathy

To review the pathogenesis as well as the clinical and laboratory features of catecholamine-induced cardiomyopathy associated with pheochromocytoma and other disorders and discuss the various treatment options available.

Materials used for this article were identified through MEDLINE, PubMed, and Google Scholar searches of the relevant literature from 1955 to the present.

Catecholamines and their oxidation products cause a direct toxic effect on the myocardium. Catecholamines also exert a receptor-mediated effect on the myocardium. Catecholamine-mediated myocardial stunning has been implicated in the pathogenesis of stress-induced cardiomyopathy. Biopsy of the myocardium in patients with pheochromocytoma or those with stress-induced cardiomyopathy shows similar pathologic findings. The clinical features in pheochromocytoma-related cardiomyopathy include hypertension, dilated or hypertrophic cardiomyopathy, pulmonary edema due to cardiogenic and noncardiogenic factors, cardiac arrhythmias, and even cardiac arrest. Stress-related cardiomyopathy such as takotsubo cardiomyopathy occurs primarily in postmenopausal women. These patients may present with clinical features suggestive of an acute myocardial infarction or a hemodynamically compromised state. The definitive management of cardiomyopathy associated with pheochromocytoma includes medical treatment with alpha-adrenergic blockade, possibly along with angiotensin converting enzyme blockers and beta1-adrenergic receptor blockers, followed by excision of the tumor. Stress-induced cardiomyopathy is usually self-limiting; patients may require support with nonadrenergic inotropes.

Recognition of catecholamine-induced cardiomyopathy, especially in patients with pheochromocytoma, before surgical treatment is important to minimize morbidity and mortality.