Catecholamine-Induced Myocarditis in Pheochromocytoma

Miguel, Valeria de; Arias, Aníbal; Paissan, Andrea; Arenaza, Diego Pérez de; Pietrani, Marcelo; Jurado, Alberto; Jaén, Ana; Day, Patricia

doi:10.1161/circulationaha.113.002762

Cited by 36 publications

(18 citation statements)

References 4 publications

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“…While improper or delayed PPGL diagnosis has long been associated with the destructive results of a sudden release in catecholamines resulting in adverse cardiovascular events (6, 7), Ferreira et al performed the first prospective study on the extent of cardiac involvement in PPGL patients (8). Unlike previous reports detailing the reversal of catecholamine-induced myocarditis following removal of the unsuspected tumor (9), Ferreira discovered persistence of subclinical systolic and diastolic dysfunction in addition to markers for focal and diffuse fibrosis, as well as cardiac abnormalities distinct from the hypertensive control subjects used throughout the study{Ferreira, 2016 #11021}. In the future, early identification of cardiac catecholamine toxicity could be used to predict potentially disastrous cardiovascular events and prevent longterm myocardial alterations (8).…”

Section: Introductionmentioning

confidence: 99%

Pheochromocytoma: A Genetic And Diagnostic Update

et al. 2018

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ATRX = ATRX chromatin remodeler; ccRCC = clear cell renal cell carcinoma; c-MYC = MYC proto oncognene; CT = computed tomography; DOTATATE = DOTA-octreotate; EGLN1/2 = egl-9 family hypoxia inducible factor 1/2; EGLN2/PHD1 = egl-9 family hypoxia inducible factor 2; EPAS1/HIF2A = endothelial PAS domain protein 2/hypoxia-inducible factor 2α; ERK = extracellular signal-regulated kinase; HIFs = hypoxia-inducible factors; HIF-α = hypoxia-inducible factor alpha; HNPGLs = head and neck paragangliomas; Lu-DOTATATE = lutetium octreotate; MAX = myc-associated factor X; MDH2 = malate dehydrogenase; MIBG = metaiodobenzylguanidine; MN = metanephrine; MRI = magnetic resonance imaging; mTOR = mammalian target of rapamycin; NETs = neuroendocrine tumors; NF1 = neurofibromin 1; NMN = normetanephrine; PHD = prolyl hydroxylase domain protein; PI3K = phosphoinositide 3-kinase; PPGLs = pheochromocytoma and paragangliomas; PRRT = peptide receptor radionuclide therapy; Pvhl = von Hippel-Lindau protein; RAS = rat sarcoma oncogene; RET = rearranged during transfection proto-oncogene; SDH = succinate dehydrogenase; SDHA, -B, -C, -D = succinate dehydrogenase subunits A, B, C, D; SDHAF2 = succinate dehydrogenase complex assembly factor 2; SDHB, C, D = succinate dehydrogenase subunits B, C, D; SDHx = succinate dehydrogenase subunits; SSTRs = somatostatin receptors; VHL = von Hippel-Lindau.

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Section: Introductionmentioning

confidence: 99%

Pheochromocytoma: A Genetic And Diagnostic Update

et al. 2018

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“…Common features of DCM as seen by 2-dimensional (2-D) echocardiogram or cardiac MRI include enlarged left ventricle (LV), eccentric hypertrophy with global systolic dysfunction that is not attributable to ischemic or valvular heart disease. The echocardiogram may also show dilated left atrium, elevated end diastolic pressure, and upper normal range or modestly elevated pulmonary artery pressure[10,[45][46][47][48][49].…”

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confidence: 99%

Catecholamine-Induced Cardiomyopathy in Pheochromocytoma: How to Manage a Rare Complication in a Rare Disease?

et al. 2018

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Pheochromocytomas and paragangliomas (PHEOs) are rare neuroendocrine tumors. Clinical manifestations include different cardiovascular signs and symptoms, which are related to excessive secretion of catecholamines. Catecholamine-induced cardiomyopathy in PHEO (CICMPP) is a rare but dreaded complication of PHEO. Once patient is diagnosed with this condition, the prognosis is worse and a surgical risk is much higher than expected. This article focuses on how catecholamines affect the heart and the pathophysiologic mechanism of CICMPP. The cardiovascular responses to catecholamine depend mostly on which catecholamine is released as well as the amount of catecholamine that is released. The acute release of norepinephrine and epinephrine from PHEO increases heart rate, systemic vascular resistance, myocardial contractility, and reduces venous compliance. The excessive adrenergic stimulation by catecholamine results in severe vasoconstriction and coronary vasospasm, myocardial ischemia, and subsequently damage, and necrosis. Chronically elevated catecholamine levels lead to significant desensitization of cardiac β-adrenoceptors. The increased levels of the enzyme β-adrenoceptors kinase (βARK) in the heart seems to mediate these biochemical and physiological changes that are consistently correlated with attenuated responsiveness to catecholamine stimulation. Through these mechanisms different types of cardiomyopathy (CMP) can be formed. This review discusses extensively the 3 types of cardiomyopathies that can be present in a PHEO patient. It also provides the clinical presentation and diagnostic and therapeutic algorithm in managing patients with CICMPP.

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“…3 To the best of our knowledge, this case is unique case because the progressive myocardial injury by catecholamines is shown with serial cardiac MRIs.…”

Section: De Lazzari Et Al Catecolaminergic Cardiotoxicity Seen By Mrimentioning

confidence: 80%