Rapid anticalcification treatment for glutaraldehyde-fixed autologous tissue in cardiovascular surgery.


Journal

Journal of cardiothoracic surgery
ISSN: 1749-8090
Titre abrégé: J Cardiothorac Surg
Pays: England
ID NLM: 101265113

Informations de publication

Date de publication:
31 May 2022
Historique:
received: 06 01 2022
accepted: 19 05 2022
entrez: 1 6 2022
pubmed: 2 6 2022
medline: 3 6 2022
Statut: epublish

Résumé

Glutaraldehyde (GA)-fixed autologous tissues, including the pericardium, are widely used as patches and valve substitutes in cardiovascular surgery. However, GA treatment causes tissue calcification. No rapid anticalcification method has been established for use during surgery. Here, we aimed to establish a rapid anticalcification method using ethanol, as has already been demonstrated for bioprosthetic valves. Thoracic aorta tissues were first fixed with GA for 3 min and then treated with ethanol for 0 (group 2), 10 (group 3), 20 (group 4), and 30 (group 5) min; untreated tissues (group 1) served as the control. The treated tissues were subdermally implanted into 3-week-old male Wistar rats and kept in place for 28 days. The calcification in each explant was semiquantitatively evaluated by annotating and measuring the area using virtual slides, and the data obtained were statistically analyzed. Semiquantitative analysis revealed that calcification of the implants from the untreated group (group 1; P = 0.0014) and groups 4 (P = 0.0014) and 5 (P = 0.0031) was significantly lower than that of implants from group 2. Moreover, implants from group 3 showed a tendency toward decreased calcification, although it was not significant (P = 0.0503). A rapid ethanol treatment prevents calcification of GA-fixed tissues in a rat model of subdermal implantation. This method may facilitate effective and rapid anticalcification of autologous tissues for use during cardiovascular surgery.

Sections du résumé

BACKGROUND BACKGROUND
Glutaraldehyde (GA)-fixed autologous tissues, including the pericardium, are widely used as patches and valve substitutes in cardiovascular surgery. However, GA treatment causes tissue calcification. No rapid anticalcification method has been established for use during surgery. Here, we aimed to establish a rapid anticalcification method using ethanol, as has already been demonstrated for bioprosthetic valves.
METHODS METHODS
Thoracic aorta tissues were first fixed with GA for 3 min and then treated with ethanol for 0 (group 2), 10 (group 3), 20 (group 4), and 30 (group 5) min; untreated tissues (group 1) served as the control. The treated tissues were subdermally implanted into 3-week-old male Wistar rats and kept in place for 28 days. The calcification in each explant was semiquantitatively evaluated by annotating and measuring the area using virtual slides, and the data obtained were statistically analyzed.
RESULTS RESULTS
Semiquantitative analysis revealed that calcification of the implants from the untreated group (group 1; P = 0.0014) and groups 4 (P = 0.0014) and 5 (P = 0.0031) was significantly lower than that of implants from group 2. Moreover, implants from group 3 showed a tendency toward decreased calcification, although it was not significant (P = 0.0503).
CONCLUSIONS CONCLUSIONS
A rapid ethanol treatment prevents calcification of GA-fixed tissues in a rat model of subdermal implantation. This method may facilitate effective and rapid anticalcification of autologous tissues for use during cardiovascular surgery.

Identifiants

pubmed: 35642062
doi: 10.1186/s13019-022-01895-7
pii: 10.1186/s13019-022-01895-7
pmc: PMC9158145
doi:

Substances chimiques

Ethanol 3K9958V90M
Glutaral T3C89M417N

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

138

Informations de copyright

© 2022. The Author(s).

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Auteurs

Shotaro Kaneko (S)

Department of Surgery, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan. kaneko.shotaro.903@gmail.com.

Susumu Isoda (S)

Department of Surgery, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.

Toru Aoyama (T)

Department of Surgery, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.

Motohiko Goda (M)

Department of Surgery, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.

Shota Yasuda (S)

Cardiovascular Center, Yokohama City University Medical Center, Yokohama, Japan.

Taisuke Shibuya (T)

Department of Surgery, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.

Mai Matsumura (M)

Department of Pathology, Yokohama City University, School of Medicine, Yokohama, Japan.

Hideaki Mitsui (H)

Department of Pathology, Yokohama City University, School of Medicine, Yokohama, Japan.

Koji Okudela (K)

Department of Pathology, Yokohama City University, School of Medicine, Yokohama, Japan.

Shinichi Suzuki (S)

Department of Surgery, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.

Daisuke Machida (D)

Department of Surgery, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.

Munetaka Masuda (M)

Department of Cardiovascular Surgery, Fukuoka Wajiro Hospital, Fukuoka, Japan.

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Classifications MeSH