Bradydysrhythmia‐related presyncope secondary to pheochromocytoma

Zweiker, Robert; Tiemann, Markus; Eber, Bernd; Schumacher, M.; Fruhwald, Friedrich; Lipp, Rainer W.; Lax, Sigurd; Pristautz, H; Klein, W.

doi:10.1046/j.1365-2796.1997.00198.x

Cited by 30 publications

(18 citation statements)

References 7 publications

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“…Some patients who have pheochromocytoma present with bradyarrhythmia or asystolic arrest [10,47,48]. These situations are the result of a reflex mechanism in which sinus slowing occurs at the onset of a sudden rise in blood pressure during a paroxysm [48].…”

Section: Arrhythmiamentioning

confidence: 99%

Emergencies Caused by Pheochromocytoma, Neuroblastoma, or Ganglioneuroma

Brouwers

Eisenhofer

Lenders

et al. 2006

Endocrinology and Metabolism Clinics of North America

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This article reviews emergency situations caused by diseases of the sympathetic nervous system. Pheochromocytoma is discussed first and most extensively, because there are numerous reports in the literature on patients with (unsuspected) pheochromocytoma presenting as an emergency. Two other tumors of the sympathetic nervous system are then discussed that less commonly result in endocrine emergencies: neuroblastoma and ganglioneuroma. PheochromocytomaParagangliomas are rare catecholamine-producing tumors derived from chromaffin cells that can be fatal if left undiagnosed.

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Section: Arrhythmiamentioning

confidence: 99%

Emergencies Caused by Pheochromocytoma, Neuroblastoma, or Ganglioneuroma

Brouwers

Eisenhofer

Lenders

et al. 2006

Endocrinology and Metabolism Clinics of North America

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“…On the other hand, the results of chronic catecholamine elevations observed in patients are more mixed, showing both paroxysmal tachycardia as well as occasional bradyarrhythmias (3,28,39). The elevated bioamine levels observed in the MAO-A/B KO mice since early development could certainly alter their cardiovascular autonomic control; however, it is not immediately apparent how the entire system may (or may not) adapt during the animal's lifespan.…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

Heart rate dynamics in monoamine oxidase-A- and -B-deficient mice

Holschneider

Scremin

Chialvo

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Heart rate (HR) dynamics were investigated in mice deficient in monoamine oxidase A and B, whose phenotype includes elevated tissue levels of norepinephrine, serotonin, dopamine, and phenylethylamine. In their home cages, spectral analysis of R-R intervals revealed more pronounced fluctuations at all frequencies in the mutants compared with wild-type controls, with a particular enhancement at 1-4 Hz. No significant genotypic differences in HR variability (HRV) or entropies calculated from Poincaré plots of the R-R intervals were noted. During exposure to the stress of a novel environment, HR increased and HRV decreased in both genotypes. However, mutants, unlike controls, demonstrated a rapid return to baseline HR during the 10-min exposure. Such modulation may result from an enhanced vagal tone, as suggested by the observation that mutants responded to cholinergic blockade with a decrease in HRV and a prolonged tachycardia greater than controls. Monoamine oxidase-deficient mice may represent a useful experimental model for studying compensatory mechanisms responsible for changes in HR dynamics in chronic states of high sympathetic tone. Keywordsserotonin; norepinephrine; cholinergic; arrhythmia; heart rate variability; vagus nerve; sympathetic; parasympathetic ENZYMATIC DEGRADATION by monoamine oxidase (MAO)-A and -B plays a crucial role in the regulation of tissue levels of serotonin (5-HT), norepinephrine (NE), epinephrine, Address for reprint requests and other correspondence: D. P. Holschneider, Dept. of Psychiatry, Univ. of Southern California, Keck School of Medicine, LAC-USC Hosp., 1200 N. State St., Rm. 10-621, Los Angeles, CA 90089 (holschne@hsc.usc.edu).. NIH Public Access Author ManuscriptAm J Physiol Heart Circ Physiol. Author manuscript; available in PMC 2014 June 30. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript phenylethylamine, and dopamine. Our laboratory has recently identified (29) a natural mutation of MAO-A occurring in mice with targeted deletion of the . These mice doubly deficient in both MAO isoforms [MAO-A/B knockout (KO)] demonstrate brain levels of 5-HT, NE, dopamine, and phenylethylamine that are increased 8.5-, 2.2-, 1.7-, and 15.7-fold above those noted in adult, wild-type (WT) animals, with levels of the 5-HT metabolite 5-hydroxyindoleacetic acid essentially undetectable in both the brain and urine.When these neuroactive compounds are administered acutely, they show cardiac electrophysiological effects, including changes in the dynamics of the sinoatrial node and in the atrioventricular conduction, as well as in the ventricular fibrillation threshold (11,18,27,31,36). On the other hand, the results of chronic catecholamine elevations observed in patients are more mixed, showing both paroxysmal tachycardia as well as occasional bradyarrhythmias (3,28,39). The elevated bioamine levels observed in the MAO-A/B KO mice since early development could certainly alter their cardiovascular autonomic control; however, it is not immediately apparent how t...

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“…4 In congestive heart failure elevation of circulating and ventricular adrenomedullin has been documented, 5 as well as a myocardial stunning-like phenomenon during a crisis of pheochromocytoma. 6 Bradydysrhythmias, for instance sinus node arrest, without systemic hypertension 7 and ventricular arrhythmias, associated with intermittent hypertension 8 can be secondary to pheochromocytoma and disappear after removal of the tumour. Peripheral arterial vasospasm can lead to neurologic deficits and leg ischaemia.…”

Section: Discussionmentioning

confidence: 99%

Cardiac involvement in pheochromocytoma

et al. 2000

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We report the details of a 40-year-old farmer, a cigarette smoker, who was admitted with general malaise, nausea, vomiting, upper abdominal pain, with ST-elevation on ECG suggestive of an acute anterolateral myocardial infarction. He was treated with nitrates, heparin, betablockade and angiotensin-converting enzyme (ACE) inhibitors. Because of the presence of some blood while vomiting no thrombolysis was given and abdominal echography was performed. This revealed a nodular mass at the right adrenal gland. Urinary catecholamines and abdominal magnetic resonance imaging confirmed the suspected diagnosis of pheochromocytoma. Before

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Bradydysrhythmia‐related presyncope secondary to pheochromocytoma

Cited by 30 publications

References 7 publications

Emergencies Caused by Pheochromocytoma, Neuroblastoma, or Ganglioneuroma

Emergencies Caused by Pheochromocytoma, Neuroblastoma, or Ganglioneuroma

Heart rate dynamics in monoamine oxidase-A- and -B-deficient mice

Cardiac involvement in pheochromocytoma

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