Effects of airway obstruction and hyperinflation on electrocardiographic axes in COPD.
Airway obstruction
COPD
Electrocardiographic axis
Hyperinflation
P wave axis
QRS axis
T wave axis
Journal
Respiratory research
ISSN: 1465-993X
Titre abrégé: Respir Res
Pays: England
ID NLM: 101090633
Informations de publication
Date de publication:
27 Mar 2019
27 Mar 2019
Historique:
received:
05
11
2018
accepted:
12
03
2019
entrez:
29
3
2019
pubmed:
29
3
2019
medline:
6
8
2019
Statut:
epublish
Résumé
COPD influences cardiac function and morphology. Changes of the electrical heart axes have been largely attributed to a supposed increased right heart load in the past, whereas a potential involvement of the left heart has not been sufficiently addressed. It is not known to which extent these alterations are due to changes in lung function parameters. We therefore quantified the relationship between airway obstruction, lung hyperinflation, several echo- and electrocardiographic parameters on the orientation of the electrocardiographic (ECG) P, QRS and T wave axis in COPD. Data from the COPD cohort COSYCONET were analyzed, using forced expiratory volume in 1 s (FEV One thousand, one hundred and ninety-five patients fulfilled the inclusion criteria (mean ± SD age: 63.9 ± 8.4 years; GOLD 0-4: 175/107/468/363/82). Left ventricular (LV) mass decreased from GOLD grades 1-4 (p = 0.002), whereas no differences in right ventricular wall thickness were observed. All three ECG axes were significantly associated with FEV Significant clockwise rotations of the electrical axes as a function of airway obstruction and lung hyperinflation were shown. The changes are likely to result from both a change of the anatomical orientation of the heart within the thoracic cavity and a reduced LV mass in COPD. The influences on the electrical axes reach an extent that could bias the ECG interpretation. The magnitude of lung function impairment should be taken into account to uncover other cardiac disease and to prevent misdiagnosis.
Sections du résumé
BACKGROUND
BACKGROUND
COPD influences cardiac function and morphology. Changes of the electrical heart axes have been largely attributed to a supposed increased right heart load in the past, whereas a potential involvement of the left heart has not been sufficiently addressed. It is not known to which extent these alterations are due to changes in lung function parameters. We therefore quantified the relationship between airway obstruction, lung hyperinflation, several echo- and electrocardiographic parameters on the orientation of the electrocardiographic (ECG) P, QRS and T wave axis in COPD.
METHODS
METHODS
Data from the COPD cohort COSYCONET were analyzed, using forced expiratory volume in 1 s (FEV
RESULTS
RESULTS
One thousand, one hundred and ninety-five patients fulfilled the inclusion criteria (mean ± SD age: 63.9 ± 8.4 years; GOLD 0-4: 175/107/468/363/82). Left ventricular (LV) mass decreased from GOLD grades 1-4 (p = 0.002), whereas no differences in right ventricular wall thickness were observed. All three ECG axes were significantly associated with FEV
CONCLUSION
CONCLUSIONS
Significant clockwise rotations of the electrical axes as a function of airway obstruction and lung hyperinflation were shown. The changes are likely to result from both a change of the anatomical orientation of the heart within the thoracic cavity and a reduced LV mass in COPD. The influences on the electrical axes reach an extent that could bias the ECG interpretation. The magnitude of lung function impairment should be taken into account to uncover other cardiac disease and to prevent misdiagnosis.
Identifiants
pubmed: 30917825
doi: 10.1186/s12931-019-1025-y
pii: 10.1186/s12931-019-1025-y
pmc: PMC6437876
doi:
Types de publication
Journal Article
Multicenter Study
Observational Study
Langues
eng
Pagination
61Références
J Appl Physiol (1985). 2004 May;96(5):1920-7
pubmed: 14729724
Pneumologie. 2007 May;61(5):e1-40
pubmed: 17436190
N Engl J Med. 2010 Jan 21;362(3):217-27
pubmed: 20089972
Chest. 2010 Jul;138(1):32-8
pubmed: 20190002
Am J Cardiol. 2011 Apr 1;107(7):1090-2
pubmed: 21306694
Respir Med. 2011 Jul;105(7):959-71
pubmed: 21356587
Am J Cardiol. 2012 Apr 1;109(7):1046-9
pubmed: 22221942
Indian Heart J. 2012 Jan-Feb;64(1):40-2
pubmed: 22572424
Eur Respir J. 2012 Dec;40(6):1324-43
pubmed: 22743675
Eur Respir J. 2013 Aug;42(2):341-9
pubmed: 23143550
Chest. 2013 Oct;144(4):1163-1178
pubmed: 23722528
Chest. 2013 Oct;144(4):1143-1151
pubmed: 23764937
Respir Med. 2013 Sep;107(9):1376-84
pubmed: 23791463
Pneumologie. 2015 Mar;69(3):147-64
pubmed: 25750095
Ann Intern Med. 2015 Mar 17;162(6):438-47
pubmed: 25775317
Am J Respir Crit Care Med. 2015 Apr 1;191(7):e4-e27
pubmed: 25830527
Lancet Respir Med. 2015 Aug;3(8):631-9
pubmed: 26208998
Int J Cardiol. 2016 Jan 1;202:80
pubmed: 26397397
J Am Soc Echocardiogr. 2016 Apr;29(4):277-314
pubmed: 27037982
Respir Med. 2016 May;114:27-37
pubmed: 27109808
Eur Respir J. 2017 Mar 6;49(3):
pubmed: 28182564
PLoS One. 2017 May 15;12(5):e0177501
pubmed: 28505167
Am J Cardiol. 2017 Oct 15;120(8):1399-1404
pubmed: 28826898
Respir Med. 2018 Jan;134:79-85
pubmed: 29413512
Pneumologie. 2018 Apr;72(4):253-308
pubmed: 29523017
Respir Med. 2018 Apr;137:14-22
pubmed: 29605197
Int J Cardiol. 2018 Jun 15;261:172-178
pubmed: 29657040
Respir Res. 2018 Jun 4;19(1):110
pubmed: 29866121
Int J Chron Obstruct Pulmon Dis. 2018 Aug 23;13:2551-2555
pubmed: 30197511
Eur Respir J Suppl. 1993 Mar;16:5-40
pubmed: 8499054