Immediate recruitment of dormant coronary collaterals can provide more than half of normal resting perfusion during coronary occlusion in patients with coronary artery disease.


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:
Dec 2023
Historique:
received: 18 11 2022
accepted: 24 03 2023
medline: 28 11 2023
pubmed: 7 6 2023
entrez: 6 6 2023
Statut: ppublish

Résumé

Dormant coronary collaterals are highly prevalent and clinically beneficial in cases of coronary occlusion. However, the magnitude of myocardial perfusion provided by immediate coronary collateral recruitment during acute occlusion is unknown. We aimed to quantify collateral myocardial perfusion during balloon occlusion in patients with coronary artery disease (CAD). Patients without angiographically visible collaterals undergoing elective percutaneous transluminal coronary angioplasty (PTCA) to a single epicardial vessel underwent two scans with 99mTc-sestamibi myocardial perfusion single-photon emission computed tomography (SPECT). All subjects underwent at least three minutes of angiographically verified complete balloon occlusion, at which time an intravenous injection of the radiotracer was administered, followed by SPECT imaging. A second radiotracer injection followed by SPECT imaging was performed 24 h after PTCA. The study included 22 patients (median [interquartile range] age 68 [54-72] years. The perfusion defect extent was 19 [11-38] % of the LV, and the collateral perfusion at rest was 64 [58-67]% of normal. This is the first study to describe the magnitude of short-term changes in coronary microvascular collateral perfusion in patients with CAD. On average, despite coronary occlusion and an absence of angiographically visible collateral vessels, collaterals provided more than half of the normal perfusion.

Sections du résumé

BACKGROUND BACKGROUND
Dormant coronary collaterals are highly prevalent and clinically beneficial in cases of coronary occlusion. However, the magnitude of myocardial perfusion provided by immediate coronary collateral recruitment during acute occlusion is unknown. We aimed to quantify collateral myocardial perfusion during balloon occlusion in patients with coronary artery disease (CAD).
METHODS METHODS
Patients without angiographically visible collaterals undergoing elective percutaneous transluminal coronary angioplasty (PTCA) to a single epicardial vessel underwent two scans with 99mTc-sestamibi myocardial perfusion single-photon emission computed tomography (SPECT). All subjects underwent at least three minutes of angiographically verified complete balloon occlusion, at which time an intravenous injection of the radiotracer was administered, followed by SPECT imaging. A second radiotracer injection followed by SPECT imaging was performed 24 h after PTCA.
RESULTS RESULTS
The study included 22 patients (median [interquartile range] age 68 [54-72] years. The perfusion defect extent was 19 [11-38] % of the LV, and the collateral perfusion at rest was 64 [58-67]% of normal.
CONCLUSION CONCLUSIONS
This is the first study to describe the magnitude of short-term changes in coronary microvascular collateral perfusion in patients with CAD. On average, despite coronary occlusion and an absence of angiographically visible collateral vessels, collaterals provided more than half of the normal perfusion.

Identifiants

pubmed: 37280387
doi: 10.1007/s12350-023-03271-x
pii: 10.1007/s12350-023-03271-x
pmc: PMC10682227
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2338-2345

Informations de copyright

© 2023. The Author(s).

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Auteurs

Brandon J Reid (BJ)

Kolling Institute, Royal North Shore Hospital, and University of Sydney, Sydney, Australia.

Thomas Lindow (T)

Kolling Institute, Royal North Shore Hospital, and University of Sydney, Sydney, Australia.
Clinical Sciences, Department of Clinical Physiology, Skane University Hospital, Lund University, Lund, Sweden.
Clinical Physiology, Department of Research and Development, Växjö Central Hospital, Kronoberg, Sweden.

Stafford Warren (S)

Department of Medicine, Cardiology Division, Anne Arundel Medical Center, Annapolis, MD, USA.

Eva Persson (E)

Clinical Sciences, Department of Clinical Physiology, Skane University Hospital, Lund University, Lund, Sweden.

Ravinay Bhindi (R)

Department of Cardiology, Royal North Shore Hospital, and University of Sydney, Sydney, Australia.

Michael Ringborn (M)

Thoracic Center, Blekinge County Hospital, Karlskrona, Sweden.

Martin Ugander (M)

Kolling Institute, Royal North Shore Hospital, and University of Sydney, Sydney, Australia. martin.ugander@gmail.com.
Department of Clinical Physiology, Karolinska University Hospital, and Karolinska Institute, Stockholm, Sweden. martin.ugander@gmail.com.

Usaid Allahwala (U)

Department of Cardiology, Royal North Shore Hospital, and University of Sydney, Sydney, Australia.

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