Prevalence and Patterns of Left Ventricular Dysfunction in Patients with Pheochromocytoma

Abstract

BackgroundExcessive catecholamine release in pheochromocytoma is known to cause transient reversible left ventricular (LV) dysfunction, such as in the case of pheochromocytoma-associated catecholamine cardiomyopathy. We investigated patterns of clinical presentation and incidence of LV dysfunction in patients with pheochromocytoma.MethodsFrom January 2004 to April 2011, consecutive patients with pheochromocytoma were retrospectively studied with clinical symptoms, serum catecholamine profiles, and radiologic findings. Patterns of electrocardiography and echocardiography were also analyzed.ResultsDuring the study period, a total of 36 patients (21 males, 49.8 ± 15.8 years, range 14-81 years) with pheochromocytoma were included. In the electrocardiographic examinations, normal findings were the most common findings (19, 52.8%). LV hypertrophy in 12 cases (33.3%), sinus tachycardia in 3 (8.3%), ischemic pattern in 1 (2.8%) and supraventricular tachycardia in 1 (2.8%). Echocardiographic exam was done in 29 patients (80.6%). Eighteen patients (62.1%) showed normal finding, 8 (27.6%) revealed concentric LV hypertrophy with normal LV systolic function, and 3 (10.3%) demonstrate LV systolic dysfunction (LV ejection fraction < 50%). Three showed transient LV dysfunction (2 with inverted Takotsubo-type cardiomyopathy and 1 with a diffuse hypokinesia pattern). Common presenting symptoms in the 3 cases were new onset chest discomfort and dyspnea which were not common in the other patients. Their echocardiographic abnormalities were normalized with conventional treatment within 3 days.ConclusionOut of total 36 patients with pheochromocytoma, 3 showed transient LV systolic dysfunction (catecholamine cardiomyopathy). Pheochromocytoma should be included as one of possible causes of transient LV systolic dysfunction.

Acute catecholamine cardiomyopathy in patients with phaeochromocytoma or functional paraganglioma

“…Based on this definition, the prevalence of ACC was 11%, with a takotsubo-like pattern observed in six patients. A previous, smaller series reported three cases of takotsubo-like cardiomyopathy in 36 patients with PPGL 20. In a series of 145 patients with PPGL, Zelinka et al 21 reported cardiovascular complications in 28 cases.…”

“…ACC in PPGL may be associated with segmental wall motion abnormalities suggestive of takotsubo cardiomyopathy, also known as stress induced cardiomyopathy or apical ballooning 9 20. In this study, we defined ACC as an acute and life-threatening cardiac condition combining chest pain and/or heart failure, evidence of acute myocardial ischaemia, left ventricular systolic dysfunction, and an absence of significant coronary stenosis.…”

Stress-induced cardiomyopathy in a patient with chronic spinal cord transection at the level of C5: Endocrinologically mediated catecholamine toxicity

“…Significantly elevated levels of plasma norepinephrine have already been observed in SIC patients compared to patients with acute myocardial infarction [1]. Furthermore, SIC is prevalent among patients with pheochromocytoma [2] and has been iatrogenically induced by administration of beta adrenergic agonists [3]. All these observations point to circulating catecholamines as the inductors of SIC.…”

No evidence for increased mortality in SDHD variant carriers compared with the general population

“…5 Because of their ability to hypersecrete catecholamines, PCC and sPGLs can give rise to severe cardiovascular complications, such as shock, myocardial infarction, dissecting aortic aneurysms or heart failure due to toxic cardiomyopathy. [9][10][11][12] In order to avoid these potentially lethal complications, adrenalectomy is indicated for PCC, 13 and with implementation of appropriate preoperative care to modulate the effects of catecholamine release, perioperative mortality is nil. [14][15][16] The pooled incidence of malignant PGL, defined as the presence of metastases, [17][18][19] in populations comprising both unaffected SDHD variant carriers and SDHD variant carriers with manifest nonmalignant PGL is about 8%.…”