Absolute coronary flow and microvascular resistance reserve in patients with severe aortic stenosis.


Journal

Heart (British Cardiac Society)
ISSN: 1468-201X
Titre abrégé: Heart
Pays: England
ID NLM: 9602087

Informations de publication

Date de publication:
13 12 2022
Historique:
received: 06 05 2022
accepted: 29 07 2022
pubmed: 18 8 2022
medline: 6 1 2023
entrez: 17 8 2022
Statut: epublish

Résumé

Development of left ventricle (LV) hypertrophy in aortic stenosis (AS) is accompanied by adaptive coronary flow regulation. We aimed to assess absolute coronary flow, microvascular resistance, coronary flow reverse (CFR) and microvascular resistance reserve (MRR) in patients with and without AS. Absolute coronary flow and microvascular resistance were measured by continuous thermodilution in 29 patients with AS and 29 controls, without AS, matched for age, gender, diabetes and functional severity of epicardial coronary lesions. Myocardial work, total myocardial mass and left anterior descending artery (LAD)-specific mass were quantified by echocardiography and cardiac-CT. Patients with AS presented a significantly positive LV remodelling with lower global longitudinal strain and global work efficacy compared with controls. Total LV myocardial mass and LAD-specific myocardial mass were significantly higher in patients with AS (p=0.001). Compared with matched controls, absolute resting flow in the LAD was significantly higher in the AS cohort (p=0.009), resulting into lower CFR and MRR in the AS cohort compared with controls (p In patients with severe AS and non-obstructive coronary artery disease, with the progression of LV hypertrophy, the compensatory mechanism of increased resting flow maintains adequate perfusion at rest, but not during hyperaemia. As a consequence, both CFR and MRR are significantly impaired.

Sections du résumé

BACKGROUND
Development of left ventricle (LV) hypertrophy in aortic stenosis (AS) is accompanied by adaptive coronary flow regulation. We aimed to assess absolute coronary flow, microvascular resistance, coronary flow reverse (CFR) and microvascular resistance reserve (MRR) in patients with and without AS.
METHODS
Absolute coronary flow and microvascular resistance were measured by continuous thermodilution in 29 patients with AS and 29 controls, without AS, matched for age, gender, diabetes and functional severity of epicardial coronary lesions. Myocardial work, total myocardial mass and left anterior descending artery (LAD)-specific mass were quantified by echocardiography and cardiac-CT.
RESULTS
Patients with AS presented a significantly positive LV remodelling with lower global longitudinal strain and global work efficacy compared with controls. Total LV myocardial mass and LAD-specific myocardial mass were significantly higher in patients with AS (p=0.001). Compared with matched controls, absolute resting flow in the LAD was significantly higher in the AS cohort (p=0.009), resulting into lower CFR and MRR in the AS cohort compared with controls (p
CONCLUSIONS
In patients with severe AS and non-obstructive coronary artery disease, with the progression of LV hypertrophy, the compensatory mechanism of increased resting flow maintains adequate perfusion at rest, but not during hyperaemia. As a consequence, both CFR and MRR are significantly impaired.

Identifiants

pubmed: 35977812
pii: heartjnl-2022-321348
doi: 10.1136/heartjnl-2022-321348
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

47-54

Commentaires et corrections

Type : CommentIn

Informations de copyright

© Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: None declared.

Auteurs

Pasquale Paolisso (P)

Hartcentrum OLV Aalst, Aalst, Belgium.
Department of Advanced Biomedical Sciences, Federico II University Hospital, Napoli, Campania, Italy.

Emanuele Gallinoro (E)

Hartcentrum OLV Aalst, Aalst, Belgium.

Marc Vanderheyden (M)

Hartcentrum OLV Aalst, Aalst, Belgium.

Giuseppe Esposito (G)

Hartcentrum OLV Aalst, Aalst, Belgium.
Department of Advanced Biomedical Sciences, Federico II University Hospital, Napoli, Campania, Italy.

Dario Tino Bertolone (DT)

Hartcentrum OLV Aalst, Aalst, Belgium.
Department of Advanced Biomedical Sciences, Federico II University Hospital, Napoli, Campania, Italy.

Marta Belmonte (M)

Hartcentrum OLV Aalst, Aalst, Belgium.
Centro Cardiologico Monzino Istituto di Ricovero e Cura a Carattere Scientifico, Milano, Lombardia, Italy.

Niya Mileva (N)

Hartcentrum OLV Aalst, Aalst, Belgium.

Konstantinos Bermpeis (K)

Cardiology, Hartcentrum OLV Aalst, Aalst, Flanderen, Belgium.

Cristina De Colle (C)

Hartcentrum OLV Aalst, Aalst, Belgium.
Department of Advanced Biomedical Sciences, Federico II University Hospital, Napoli, Campania, Italy.

Davide Fabbricatore (D)

Hartcentrum OLV Aalst, Aalst, Belgium.
Department of Advanced Biomedical Sciences, Federico II University Hospital, Napoli, Campania, Italy.

Alessandro Candreva (A)

Hartcentrum OLV Aalst, Aalst, Belgium.

Daniel Munhoz (D)

Hartcentrum OLV Aalst, Aalst, Belgium.
Department of Advanced Biomedical Sciences, Federico II University Hospital, Napoli, Campania, Italy.

Ivan Degrieck (I)

Cardiovascular and Thoracic Surgery, Hartcentrum OLV Aalst, Aalst, Belgium.

Filip Casselman (F)

Cardiovascular and Thoracic Surgery, Hartcentrum OLV Aalst, Aalst, Belgium.

Martin Penicka (M)

Cardiology, Hartcentrum OLV Aalst, Aalst, Flanderen, Belgium.

Carlos Collet (C)

Hartcentrum OLV Aalst, Aalst, Belgium.

Jeroen Sonck (J)

Hartcentrum OLV Aalst, Aalst, Belgium.

Fabio Mangiacapra (F)

Campus Bio-Medico University, Roma, Lazio, Italy.

Bernard de Bruyne (B)

Hartcentrum OLV Aalst, Aalst, Belgium.

Emanuele Barbato (E)

Hartcentrum OLV Aalst, Aalst, Belgium barba22@hotmail.com.
Department of Advanced Biomedical Sciences, Federico II University Hospital, Napoli, Campania, Italy.

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