Reduced response to regadenoson with increased weight: an artificial intelligence based quantitative myocardial perfusion study.

Cardiovascular magnetic resonance adenosine quantitative perfusion regadenoson weight

Journal

Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance
ISSN: 1532-429X
Titre abrégé: J Cardiovasc Magn Reson
Pays: England
ID NLM: 9815616

Informations de publication

Date de publication:
25 Jul 2024
Historique:
received: 14 11 2023
revised: 31 05 2024
accepted: 22 07 2024
medline: 28 7 2024
pubmed: 28 7 2024
entrez: 27 7 2024
Statut: aheadofprint

Résumé

There is conflicting evidence regarding the response to a fixed dose of regadenoson in patients with high body weight. The aim of this study was to evaluate the effectiveness of regadenoson in patients with varying body weights using novel quantitative CMR perfusion parameters in addition to standard clinical markers. Consecutive patients with typical angina and/or risk factors for coronary artery disease (N=217) underwent regadenoson stress CMR perfusion imaging using a dual-sequence quantitative protocol with perfusion parameters generated from an artificial intelligence (AI) based algorithm. CMR was performed on 1.5T scanners using a standard 0.4mg injection of regadenoson. A cohort of consecutive patients undergoing adenosine stress perfusion (N=218) was used as a control group. An inverse association of myocardial perfusion reserve and weight (mean decrease -0.05 per 10Kg increase, 95% CI -0.009/-0.0001, P=0.045) was noted in the regadenoson group but not in patients stressed with adenosine (P=0.77). Adjusted logistic regression analysis revealed a 10Kg increase resulted in 36% increased odds for inadequate stress response (OR= 1.36, 95% CI 1.10-1.69, P=0.005). Moreover, a significant interaction (OR=1.09, 95% CI 1.02-1.16, P=0.012) between stressor type (regadenoson vs adenosine) and weight was noted. This was also confirmed in the propensity matched subgroup (P=0.024) and was not attenuated after adjustment (P=0.041). BSA (P=0.006) but not BMI (P=0.055) was differentially associated with inadequate response conditional to the stressor used, and this association remained significant after adjustment for confounders (P=0.025). Patients in the highest quartile of weight (>93Kg) or BSA (>2.06m Using quantitative perfusion CMR in patients undergoing pharmacological stress with regadenoson, we found an inverse relationship between patient weight and both clinical response and myocardial perfusion parameters. A fixed-dose bolus approach may not be adequate to induce maximal hyperemia in patients with increased weight. Weight-adjusted stressors like adenosine may be considered instead in patients with body weight > 93Kg and BSA > 2.06m

Sections du résumé

BACKGROUND BACKGROUND
There is conflicting evidence regarding the response to a fixed dose of regadenoson in patients with high body weight. The aim of this study was to evaluate the effectiveness of regadenoson in patients with varying body weights using novel quantitative CMR perfusion parameters in addition to standard clinical markers.
METHODS METHODS
Consecutive patients with typical angina and/or risk factors for coronary artery disease (N=217) underwent regadenoson stress CMR perfusion imaging using a dual-sequence quantitative protocol with perfusion parameters generated from an artificial intelligence (AI) based algorithm. CMR was performed on 1.5T scanners using a standard 0.4mg injection of regadenoson. A cohort of consecutive patients undergoing adenosine stress perfusion (N=218) was used as a control group.
RESULTS RESULTS
An inverse association of myocardial perfusion reserve and weight (mean decrease -0.05 per 10Kg increase, 95% CI -0.009/-0.0001, P=0.045) was noted in the regadenoson group but not in patients stressed with adenosine (P=0.77). Adjusted logistic regression analysis revealed a 10Kg increase resulted in 36% increased odds for inadequate stress response (OR= 1.36, 95% CI 1.10-1.69, P=0.005). Moreover, a significant interaction (OR=1.09, 95% CI 1.02-1.16, P=0.012) between stressor type (regadenoson vs adenosine) and weight was noted. This was also confirmed in the propensity matched subgroup (P=0.024) and was not attenuated after adjustment (P=0.041). BSA (P=0.006) but not BMI (P=0.055) was differentially associated with inadequate response conditional to the stressor used, and this association remained significant after adjustment for confounders (P=0.025). Patients in the highest quartile of weight (>93Kg) or BSA (>2.06m
CONCLUSIONS CONCLUSIONS
Using quantitative perfusion CMR in patients undergoing pharmacological stress with regadenoson, we found an inverse relationship between patient weight and both clinical response and myocardial perfusion parameters. A fixed-dose bolus approach may not be adequate to induce maximal hyperemia in patients with increased weight. Weight-adjusted stressors like adenosine may be considered instead in patients with body weight > 93Kg and BSA > 2.06m

Identifiants

pubmed: 39067701
pii: S1097-6647(24)01093-7
doi: 10.1016/j.jocmr.2024.101066
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

101066

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper Competing interests No competing interests.

Auteurs

E Androulakis (E)

Royal Brompton and Harefield Hospitals, Guy's & St Thomas' NHS Foundation Trust; National Heart and Lung Institute, Imperial College London, UK.

G Georgiopoulos (G)

School of Biomedical Engineering and Imaging Sciences, Kings College London, London, UK.

A Azzu (A)

Royal Brompton and Harefield Hospitals, Guy's & St Thomas' NHS Foundation Trust; National Heart and Lung Institute, Imperial College London, UK.

E Surkova (E)

Royal Brompton and Harefield Hospitals, Guy's & St Thomas' NHS Foundation Trust; National Heart and Lung Institute, Imperial College London, UK.

A Bakula (A)

Royal Brompton and Harefield Hospitals, Guy's & St Thomas' NHS Foundation Trust; National Heart and Lung Institute, Imperial College London, UK.

P Papagkikas (P)

Royal Brompton and Harefield Hospitals, Guy's & St Thomas' NHS Foundation Trust; National Heart and Lung Institute, Imperial College London, UK.

A Briasoulis (A)

Department of Clinical Therapeutics, School of Medicine, Alexandra General Hospital, National and Kapodistrian University of Athens, Athens, Greece.

R De Silva (R)

Royal Brompton and Harefield Hospitals, Guy's & St Thomas' NHS Foundation Trust; National Heart and Lung Institute, Imperial College London, UK.

P Kellman (P)

National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.

D J Pennell (DJ)

Royal Brompton and Harefield Hospitals, Guy's & St Thomas' NHS Foundation Trust; National Heart and Lung Institute, Imperial College London, UK.

F Alpendurada (F)

Royal Brompton and Harefield Hospitals, Guy's & St Thomas' NHS Foundation Trust; National Heart and Lung Institute, Imperial College London, UK. Electronic address: f.alpendurada@rbht.nhs.uk.

Classifications MeSH