Ventricular synchrony is not significantly determined by absolute myocardial perfusion in patients with chronic heart failure: A
Aged
Ammonia
/ chemistry
Body Mass Index
Coronary Angiography
Coronary Circulation
Female
Heart Failure
/ diagnostic imaging
Heart Ventricles
/ physiopathology
Humans
Male
Middle Aged
Myocardial Ischemia
/ physiopathology
Myocardial Perfusion Imaging
/ methods
Nitrogen Radioisotopes
/ chemistry
Perfusion
Positron-Emission Tomography
/ methods
Retrospective Studies
Ventricular Function, Left
Positron emission tomography
heart failure
mechanical synchrony
myocardial perfusion
Journal
Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology
ISSN: 1532-6551
Titre abrégé: J Nucl Cardiol
Pays: United States
ID NLM: 9423534
Informations de publication
Date de publication:
12 2020
12 2020
Historique:
received:
07
08
2018
accepted:
22
10
2018
pubmed:
18
11
2018
medline:
21
12
2021
entrez:
17
11
2018
Statut:
ppublish
Résumé
It is thought that heart failure (HF) patients may benefit from the evaluation of mechanical (dys)synchrony, and an independent inverse relationship between myocardial perfusion and ventricular synchrony has been suggested. We explore the relationship between quantitative myocardial perfusion and synchrony parameters when accounting for the presence and extent of fixed perfusion defects in patients with chronic HF. We studied 98 patients with chronic HF who underwent rest and stress Nitrogen-13 ammonia PET. Multivariate analyses of covariance were performed to determine relevant predictors of synchrony (measured as bandwidth, standard deviation, and entropy). In our population, there were 43 (44%) women and 55 men with a mean age of 71 ± 9.6 years. The SRS was the strongest independent predictor of mechanical synchrony variables (p < .01), among other considered predictors including: age, sex, body mass index, smoking, diabetes mellitus, dyslipidemia, hypertension, rest myocardial blood flow (MBF), and myocardial perfusion reserve (MPR). Results were similar when considering stress MBF instead of MPR. The existence and extent of fixed perfusion defects, but not the quantitative PET myocardial perfusion parameters (sMBF and MPR), constitute a significant independent predictor of ventricular mechanical synchrony in patients with chronic HF.
Sections du résumé
BACKGROUND
It is thought that heart failure (HF) patients may benefit from the evaluation of mechanical (dys)synchrony, and an independent inverse relationship between myocardial perfusion and ventricular synchrony has been suggested. We explore the relationship between quantitative myocardial perfusion and synchrony parameters when accounting for the presence and extent of fixed perfusion defects in patients with chronic HF.
METHODS
We studied 98 patients with chronic HF who underwent rest and stress Nitrogen-13 ammonia PET. Multivariate analyses of covariance were performed to determine relevant predictors of synchrony (measured as bandwidth, standard deviation, and entropy).
RESULTS
In our population, there were 43 (44%) women and 55 men with a mean age of 71 ± 9.6 years. The SRS was the strongest independent predictor of mechanical synchrony variables (p < .01), among other considered predictors including: age, sex, body mass index, smoking, diabetes mellitus, dyslipidemia, hypertension, rest myocardial blood flow (MBF), and myocardial perfusion reserve (MPR). Results were similar when considering stress MBF instead of MPR.
CONCLUSIONS
The existence and extent of fixed perfusion defects, but not the quantitative PET myocardial perfusion parameters (sMBF and MPR), constitute a significant independent predictor of ventricular mechanical synchrony in patients with chronic HF.
Identifiants
pubmed: 30443751
doi: 10.1007/s12350-018-01507-9
pii: 10.1007/s12350-018-01507-9
pmc: PMC7749096
doi:
Substances chimiques
Nitrogen Radioisotopes
0
Nitrogen-13
0
Ammonia
7664-41-7
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2234-2242Commentaires et corrections
Type : CommentIn
Références
J Nucl Cardiol. 2005 Nov-Dec;12(6):687-95
pubmed: 16344231
Eur J Nucl Med Mol Imaging. 2013 Aug;40(8):1148-54
pubmed: 23553081
Europace. 2013 Aug;15(8):1070-118
pubmed: 23801827
JAMA. 2003 May 28;289(20):2685-94
pubmed: 12771115
Eur J Hybrid Imaging. 2018;2(1):11
pubmed: 29951642
J Nucl Cardiol. 2018 Jun;25(3):797-806
pubmed: 27681955
JACC Cardiovasc Imaging. 2014 Mar;7(3):278-87
pubmed: 24560212
J Nucl Cardiol. 2008 May-Jun;15(3):383-91
pubmed: 18513645
J Nucl Cardiol. 2014 Dec;21(6):1048-56
pubmed: 25245950
J Nucl Cardiol. 2014 Dec;21(6):1057-61
pubmed: 25145634
N Engl J Med. 2010 Dec 16;363(25):2385-95
pubmed: 21073365
J Nucl Med. 2011 Jan;52(1):67-71
pubmed: 21149479
N Engl J Med. 2010 Jan 21;362(3):228-38
pubmed: 20089973
Eur Heart J. 2016 Jan 1;37(1):60-2
pubmed: 26324539
Circ Heart Fail. 2016 Jul;9(7):
pubmed: 27413034
J Nucl Cardiol. 2017 Feb;24(1):43-52
pubmed: 26403144
J Am Coll Cardiol. 2014 Apr 1;63(12):1123-1133
pubmed: 24491689
Circulation. 1999 Sep 7;100(10):1035-42
pubmed: 10477527
J Am Heart Assoc. 2016 Nov 23;5(12):
pubmed: 27881426
Eur Heart J Cardiovasc Imaging. 2014 Jun;15(6):659-65
pubmed: 24408930
J Nucl Cardiol. 2011 Oct;18(5):912-9
pubmed: 21717276
Eur J Nucl Med Mol Imaging. 2012 Jun;39(6):1065-9
pubmed: 22410839
Eur Heart J Cardiovasc Imaging. 2018 Oct 1;19(10):1179-1187
pubmed: 29293983
J Am Coll Cardiol. 1990 Apr;15(5):1032-42
pubmed: 2312957
N Engl J Med. 2002 Jun 13;346(24):1845-53
pubmed: 12063368
Circulation. 2002 Jan 29;105(4):539-42
pubmed: 11815441
Eur J Nucl Med Mol Imaging. 2012 Dec;39(12):1904-9
pubmed: 22875446
Microcirculation. 2003 Apr;10(2):113-26
pubmed: 12700580