Inline perfusion mapping provides insights into the disease mechanism in hypertrophic cardiomyopathy.
Cardiomyopathy, Hypertrophic
/ diagnosis
Coronary Circulation
/ physiology
Coronary Vessels
/ diagnostic imaging
Female
Follow-Up Studies
Humans
Image Interpretation, Computer-Assisted
Magnetic Resonance Imaging, Cine
/ methods
Male
Microcirculation
/ physiology
Middle Aged
Myocardial Perfusion Imaging
/ methods
Retrospective Studies
Advanced cardiac imaging
Cardiac magnetic resonance (CMR) imaging
Hypertrophic cardiomyopathy
Journal
Heart (British Cardiac Society)
ISSN: 1468-201X
Titre abrégé: Heart
Pays: England
ID NLM: 9602087
Informations de publication
Date de publication:
06 2020
06 2020
Historique:
received:
15
08
2019
revised:
29
10
2019
accepted:
05
11
2019
pubmed:
12
12
2019
medline:
16
2
2021
entrez:
12
12
2019
Statut:
ppublish
Résumé
In patients with hypertrophic cardiomyopathy (HCM), the role of small vessel disease and myocardial perfusion remains incompletely understood and data on absolute myocardial blood flow (MBF, mL/g/min) are scarce. We measured MBF using cardiovascular magnetic resonance fully quantitative perfusion mapping to determine the relationship between perfusion, hypertrophy and late gadolinium enhancement (LGE) in HCM. 101 patients with HCM with unobstructed epicardial coronary arteries and 30 controls (with matched cardiovascular risk factors) underwent pixel-wise perfusion mapping during adenosine stress and rest. Stress, rest MBF and the myocardial perfusion reserve (MPR, ratio of stress to rest) were calculated globally and segmentally and then associated with segmental wall thickness and LGE. In HCM, 79% had a perfusion defect on clinical read. Stress MBF and MPR were reduced compared with controls (mean±SD 1.63±0.60 vs 2.30±0.64 mL/g/min, p<0.0001 and 2.21±0.87 vs 2.90±0.90, p=0.0003, respectively). Globally, stress MBF fell with increasing indexed left ventricle mass (R Microvascular dysfunction is common in HCM and associated with hypertrophy and LGE. Perfusion can fall during vasodilator stress and is abnormal even in apparently normal myocardium suggesting it may be an early disease marker.
Identifiants
pubmed: 31822572
pii: heartjnl-2019-315848
doi: 10.1136/heartjnl-2019-315848
pmc: PMC7282549
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
824-829Subventions
Organisme : British Heart Foundation
ID : SP/20/2/34841
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/T005181/1
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/13/97/30487
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/18/83/34025
Pays : United Kingdom
Informations de copyright
© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: SEP provides consultancy to Circle Cardiovascular Imaging (Calgary, Alberta, Canada).
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