Central nervous pathways mediating angina pectoris.

Details

Serval ID
serval:BIB_60FA33A3450E
Type
Article: article from journal or magazin.
Collection
Publications
Title
Central nervous pathways mediating angina pectoris.
Journal
Lancet
Author(s)
Rosen S.D., Paulesu E., Frith C.D., Frackowiak R.S., Davies G.J., Jones T., Camici P.G.
ISSN
0140-6736 (Print)
ISSN-L
0140-6736
Publication state
Published
Issued date
1994
Volume
344
Number
8916
Pages
147-150
Language
english
Notes
Publication types: Journal ArticlePublication Status: ppublish
Abstract
The central nervous pathways of angina pectoris have never been identified in vivo in man. We used positron emission tomography to examine the changes in regional cerebral blood flow associated with angina pectoris. Dynamic positron emission tomography with 15O-labelled water was used in 12 patients with angina and angiographically proven coronary artery disease to measure regional cerebral blood flow changes during angina induced by intravenous dobutamine. All subjects had typical retrosternal chest pain accompanied by ischaemic electrocardiographic changes during dobutamine infusion. Compared to the resting state, angina was associated with increased regional cerebral blood flow in the hypothalamus (percentage change in regional cerebral blood flow +6.5 and Z score 7.2) periaquaductal grey (+2.6 and 4.0), bilaterally in the thalamus (left: +2.7 and 4.3; right +3.7 and 4.7) and lateral prefrontal cortex (left +11.5 and 7.6; right +8.5 and 7.8) and left inferior anterocaudal cingulate cortex (+9.4 and 6.6). In contrast, it was reduced bilaterally in the mid-rostrocaudal cingulate cortex (left -3.7 and 6.3; right -4.7 and 4.6) and fusiform gyrus (left -3.2 and 4.0; right -3.3 and 3.7), right posterior cingulate (-3.9 and 5.8) and left parietal cortices (-4.8 and 6.3). Several minutes after stopping dobutamine infusion, when the patients no longer experienced angina and the electrocardiographic changes had resolved, thalamic, but not cortical activation could be seen. We propose that the central structures activated constitute the pathways for perception of anginal pain and that the thalamus may act as a gate to afferent pain signals, with cortical activation being necessary for the sensation of pain. This method of investigation may form a basis for research into anomalies of visceral pain perception such as silent myocardial ischaemia.
Keywords
Adult, Aged, Angina Pectoris/physiopathology, Brain/physiopathology, Brain/radionuclide imaging, Cerebrovascular Circulation, Female, Heart/innervation, Humans, Male, Middle Aged, Neural Pathways, Tomography, Emission-Computed
Pubmed
Web of science
Create date
16/09/2011 20:47
Last modification date
20/08/2019 14:18
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