Document Detail

Cardiac sympathetic nerve biology and brain monoamine turnover in panic disorder.
MedLine Citation:
PMID:  15240408     Owner:  NLM     Status:  MEDLINE    
Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.
Murray Esler; Marlies Alvarenga; Gavin Lambert; David Kaye; Jacqui Hastings; Garry Jennings; Margaret Morris; Rosemary Schwarz; Jeff Richards
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Annals of the New York Academy of Sciences     Volume:  1018     ISSN:  0077-8923     ISO Abbreviation:  Ann. N. Y. Acad. Sci.     Publication Date:  2004 Jun 
Date Detail:
Created Date:  2004-07-08     Completed Date:  2004-08-18     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  7506858     Medline TA:  Ann N Y Acad Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  505-14     Citation Subset:  IM    
Baker Heart Research Institute, PO Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia.
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MeSH Terms
Biogenic Monoamines / metabolism*
Brain / metabolism*
Epinephrine / secretion
Heart / innervation*
Panic Disorder / metabolism*,  physiopathology
Sympathetic Nervous System / metabolism*,  physiopathology
Reg. No./Substance:
0/Biogenic Monoamines; 51-43-4/Epinephrine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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