Therapeutic Ultrasound Improves Myocardial Blood Flow and Reduces Infarct Size in a Canine Model of Coronary Microthromboembolism.


Journal

Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography
ISSN: 1097-6795
Titre abrégé: J Am Soc Echocardiogr
Pays: United States
ID NLM: 8801388

Informations de publication

Date de publication:
02 2020
Historique:
received: 18 04 2019
revised: 18 09 2019
accepted: 19 09 2019
pubmed: 10 12 2019
medline: 28 7 2021
entrez: 9 12 2019
Statut: ppublish

Résumé

Therapeutic ultrasound (TUS) has been used to lyse infarct-related coronary artery thrombus. There has been no study examining the effect of TUS specifically on myocardial microthromboemboli seen in acute myocardial infarction and acute coronary syndromes. The aim of this study was to test the hypothesis that TUS improves myocardial blood flow (MBF) and reduces infarct size (IS) in this situation by dissolving myocardial microthrombi. An open-chest canine model of myocardial microthromboembolism was created by disrupting a thrombus in the left anterior descending coronary artery, and 1.05- and 0.25-MHz TUS (n = 7 each) delivered epicardially for 30 min was compared with control (n = 6). MBF and IS (as a percentage of left anterior descending coronary artery perfusion bed size) were measured 60 min after treatment. In addition, immunohistochemistry was performed to assess microthrombi, and histopathology was performed to define inflammation. Transmural, epicardial, and endocardial myocardial blood volume and MBF (measured using myocardial contrast echocardiography) and percentage wall thickening were significantly higher 60 min after receiving TUS compared with control. The ratio of IS to left anterior descending coronary artery perfusion bed size was significantly smaller (P = .03) in the 1.05-MHz TUS group (0.14 ± 0.04) compared with the control (0.31 ± 0.06, P = .04) and 0.25-MHz (0.36 ± 0.08) groups. MBF versus percentage wall thickening exhibited a linear relation (r = 0.65) in the control and 1.05-MHz TUS groups but not in the 0.25-MHz TUS group (r = 0.29). The presence of myocardial microemboli in vessels >10 μm in diameter was significantly reduced in the 1.05-MHz TUS group compared with the other two groups. The distribution and intensity of inflammation was higher in the 0.25-MHz TUS group compared with the other groups. TUS at 1.05 MHz is effective in restoring myocardial blood volume and MBF, thus reducing IS by clearing the microcirculation of microthrombi. IS reduction is not seen at 0.25 MHz, despite improvement in MBF, which may be related to the increased inflammation noted at this frequency. Because both acute myocardial infarction and acute coronary syndromes are associated with microthromboembolism, these results suggest that TUS could have a potential adjunctive role in the treatment of both conditions.

Sections du résumé

BACKGROUND
Therapeutic ultrasound (TUS) has been used to lyse infarct-related coronary artery thrombus. There has been no study examining the effect of TUS specifically on myocardial microthromboemboli seen in acute myocardial infarction and acute coronary syndromes. The aim of this study was to test the hypothesis that TUS improves myocardial blood flow (MBF) and reduces infarct size (IS) in this situation by dissolving myocardial microthrombi.
METHODS
An open-chest canine model of myocardial microthromboembolism was created by disrupting a thrombus in the left anterior descending coronary artery, and 1.05- and 0.25-MHz TUS (n = 7 each) delivered epicardially for 30 min was compared with control (n = 6). MBF and IS (as a percentage of left anterior descending coronary artery perfusion bed size) were measured 60 min after treatment. In addition, immunohistochemistry was performed to assess microthrombi, and histopathology was performed to define inflammation.
RESULTS
Transmural, epicardial, and endocardial myocardial blood volume and MBF (measured using myocardial contrast echocardiography) and percentage wall thickening were significantly higher 60 min after receiving TUS compared with control. The ratio of IS to left anterior descending coronary artery perfusion bed size was significantly smaller (P = .03) in the 1.05-MHz TUS group (0.14 ± 0.04) compared with the control (0.31 ± 0.06, P = .04) and 0.25-MHz (0.36 ± 0.08) groups. MBF versus percentage wall thickening exhibited a linear relation (r = 0.65) in the control and 1.05-MHz TUS groups but not in the 0.25-MHz TUS group (r = 0.29). The presence of myocardial microemboli in vessels >10 μm in diameter was significantly reduced in the 1.05-MHz TUS group compared with the other two groups. The distribution and intensity of inflammation was higher in the 0.25-MHz TUS group compared with the other groups.
CONCLUSIONS
TUS at 1.05 MHz is effective in restoring myocardial blood volume and MBF, thus reducing IS by clearing the microcirculation of microthrombi. IS reduction is not seen at 0.25 MHz, despite improvement in MBF, which may be related to the increased inflammation noted at this frequency. Because both acute myocardial infarction and acute coronary syndromes are associated with microthromboembolism, these results suggest that TUS could have a potential adjunctive role in the treatment of both conditions.

Identifiants

pubmed: 31812549
pii: S0894-7317(19)30991-5
doi: 10.1016/j.echo.2019.09.011
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

234-246

Informations de copyright

Copyright © 2019 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.

Auteurs

Mrinal Yadava (M)

Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon; Portland Veterans Administration Medical Center, Portland, Oregon.

D Elizabeth Le (DE)

Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon; Portland Veterans Administration Medical Center, Portland, Oregon.

Igor V Dykan (IV)

Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon.

Marjorie R Grafe (MR)

Department of Pathology, Oregon Health and Science University, Portland, Oregon.

Matthew Nugent (M)

Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon; Portland Veterans Administration Medical Center, Portland, Oregon.

Azzdine Y Ammi (AY)

Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon.

David Giraud (D)

Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon.

Yan Zhao (Y)

Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon.

Jessica Minnier (J)

Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon; Department of Biostatistics, Oregon Health and Science University, Portland, Oregon.

Sanjiv Kaul (S)

Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon. Electronic address: kauls@ohsu.edu.

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Classifications MeSH