Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?

Objective: To investigate the possible causes of abnormal blood pressure control in light chain related (primary, AL) amyloidosis. Design: Cardiovascular, autonomic, and respiratory response to passive tilting were investigated in 51 patients with primary amyloidosis (mean (SEM) age 56 (2) years) an...

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Main Authors: Bernardi, L, Passino, C, Porta, C, Anesi, E, Palladini, G, Merlini, G
Formato: Artigo
Idioma:English
Publicado em: Copyright 2002 by Heart 2002
Assuntos:
Cardiovascular Medicine
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC1767452/
https://ncbi.nlm.nih.gov/pubmed/12433892
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spelling pubmed-17674522007-06-20 Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension? Bernardi, L Passino, C Porta, C Anesi, E Palladini, G Merlini, G Heart Cardiovascular Medicine Objective: To investigate the possible causes of abnormal blood pressure control in light chain related (primary, AL) amyloidosis. Design: Cardiovascular, autonomic, and respiratory response to passive tilting were investigated in 51 patients with primary amyloidosis (mean (SEM) age 56 (2) years) and in 20 age matched controls. Spontaneous fluctuations in RR interval, respiration, end tidal carbon dioxide, blood pressure, and skin microcirculation were recorded during supine rest and with tilting. The values were subjected to spectral analysis to assess baroreflex sensitivity and the autonomic modulation of cardiac and vascular responses. Setting: Tertiary referral centre. Results: Autonomic modulation of the heart and blood pressure was nearly absent in the patients with amyloidosis: thus baroreflex sensitivity and the low frequency (0.1 Hz) fluctuations in all cardiovascular signals were severely reduced (p < 0.01 or more), as were respiratory fluctuations in the RR interval, and no change was observed upon tilting. Despite reduced autonomic modulation, blood pressure remained relatively stable in the amyloid group from supine to tilting. End tidal carbon dioxide was reduced in the amyloid patients (p < 0.001) indicating persistent hyperventilation; the breathing rate correlated inversely with the fall in blood pressure on tilting (p < 0.05). Conclusions: In primary amyloidosis, pronounced abnormalities in arterial baroreflexes and cardiovascular autonomic modulation to the heart and the vessels may be partly compensated for by hyperventilation at a slow breathing rate. Copyright 2002 by Heart 2002-12 /pmc/articles/PMC1767452/ /pubmed/12433892 Text en Copyright © Copyright 2002 by Heart
institution US National Library of Medicine
collection PubMed Central
language English
format Article
topic Cardiovascular Medicine
spellingShingle Cardiovascular Medicine
Bernardi, L
Passino, C
Porta, C
Anesi, E
Palladini, G
Merlini, G
Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?
description Objective: To investigate the possible causes of abnormal blood pressure control in light chain related (primary, AL) amyloidosis. Design: Cardiovascular, autonomic, and respiratory response to passive tilting were investigated in 51 patients with primary amyloidosis (mean (SEM) age 56 (2) years) and in 20 age matched controls. Spontaneous fluctuations in RR interval, respiration, end tidal carbon dioxide, blood pressure, and skin microcirculation were recorded during supine rest and with tilting. The values were subjected to spectral analysis to assess baroreflex sensitivity and the autonomic modulation of cardiac and vascular responses. Setting: Tertiary referral centre. Results: Autonomic modulation of the heart and blood pressure was nearly absent in the patients with amyloidosis: thus baroreflex sensitivity and the low frequency (0.1 Hz) fluctuations in all cardiovascular signals were severely reduced (p < 0.01 or more), as were respiratory fluctuations in the RR interval, and no change was observed upon tilting. Despite reduced autonomic modulation, blood pressure remained relatively stable in the amyloid group from supine to tilting. End tidal carbon dioxide was reduced in the amyloid patients (p < 0.001) indicating persistent hyperventilation; the breathing rate correlated inversely with the fall in blood pressure on tilting (p < 0.05). Conclusions: In primary amyloidosis, pronounced abnormalities in arterial baroreflexes and cardiovascular autonomic modulation to the heart and the vessels may be partly compensated for by hyperventilation at a slow breathing rate.
author Bernardi, L
Passino, C
Porta, C
Anesi, E
Palladini, G
Merlini, G
author_facet Bernardi, L
Passino, C
Porta, C
Anesi, E
Palladini, G
Merlini, G
author_sort Bernardi, L
title Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?
title_short Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?
title_full Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?
title_fullStr Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?
title_full_unstemmed Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?
title_sort widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?
publisher Copyright 2002 by Heart
publisher_facet Copyright 2002 by Heart
publishDate 2002
url https://ncbi.nlm.nih.gov/pmc/articles/PMC1767452/
https://ncbi.nlm.nih.gov/pubmed/12433892
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