Histopathological Characterization of Radiofrequency Ablation in Ventricular Scar Tissue.


Journal

JACC. Clinical electrophysiology
ISSN: 2405-5018
Titre abrégé: JACC Clin Electrophysiol
Pays: United States
ID NLM: 101656995

Informations de publication

Date de publication:
08 2019
Historique:
received: 06 03 2019
revised: 09 05 2019
accepted: 13 05 2019
entrez: 24 8 2019
pubmed: 24 8 2019
medline: 24 10 2020
Statut: ppublish

Résumé

This study sought to characterize the histopathological features of radiofrequency ablation (RFA) in heterogeneous ventricular scar in comparison to those in healthy myocardium. The histopathological features of RFA have been studied largely in normal myocardium. However, its effect on clinically relevant heterogeneous scar is not well understood. Five swine with chronic infarction underwent RFA using 35-W, 45-s, 10-20 g (Biosense Webster, Irwindale, California) in heterogenous scar tissue (voltage ≤1.5 mV) and healthy myocardium (≥3.0 mV). The location of each application was marked using the electroanatomical mapping system. Histological sections at intervals of 0.5 mm with hematoxylin and eosin and Masson's trichrome stained intervals were created. A pathologist blinded to the myocardium type characterized the extent of RF injury in cellular, extracellular, and vascular structures. In healthy myocardium, 23 of 23 lesions (100%) were well demarcated and could be precisely measured (width: 11.3 ± 3.3 mm; depth: 7.3 ± 2.0 mm). In scar tissue, only 3 of 30 lesions (10%) were identified, and none could be measured due to a lack of defined borders. Lesions in healthy myocardium had a distinctive architecture showing a coagulative necrosis core surrounded by an outer rim of contraction band necrosis. Lesions in scar had ill-defined tissue injury without a distinct architecture. In all ablated regions, viable myocytes remained interspersed between necrotic myocytes exhibiting characteristics of both coagulative and contraction band necrosis. Connective tissue was more resistant to thermal injury in comparison to cardiomyocytes. RFA in scarred myocardium results in irregular tissue injury and unpredictable effect on surviving cardiomyocytes. This may be related to biophysical differences between healthy and scarred myocardium.

Sections du résumé

OBJECTIVES
This study sought to characterize the histopathological features of radiofrequency ablation (RFA) in heterogeneous ventricular scar in comparison to those in healthy myocardium.
BACKGROUND
The histopathological features of RFA have been studied largely in normal myocardium. However, its effect on clinically relevant heterogeneous scar is not well understood.
METHODS
Five swine with chronic infarction underwent RFA using 35-W, 45-s, 10-20 g (Biosense Webster, Irwindale, California) in heterogenous scar tissue (voltage ≤1.5 mV) and healthy myocardium (≥3.0 mV). The location of each application was marked using the electroanatomical mapping system. Histological sections at intervals of 0.5 mm with hematoxylin and eosin and Masson's trichrome stained intervals were created. A pathologist blinded to the myocardium type characterized the extent of RF injury in cellular, extracellular, and vascular structures.
RESULTS
In healthy myocardium, 23 of 23 lesions (100%) were well demarcated and could be precisely measured (width: 11.3 ± 3.3 mm; depth: 7.3 ± 2.0 mm). In scar tissue, only 3 of 30 lesions (10%) were identified, and none could be measured due to a lack of defined borders. Lesions in healthy myocardium had a distinctive architecture showing a coagulative necrosis core surrounded by an outer rim of contraction band necrosis. Lesions in scar had ill-defined tissue injury without a distinct architecture. In all ablated regions, viable myocytes remained interspersed between necrotic myocytes exhibiting characteristics of both coagulative and contraction band necrosis. Connective tissue was more resistant to thermal injury in comparison to cardiomyocytes.
CONCLUSIONS
RFA in scarred myocardium results in irregular tissue injury and unpredictable effect on surviving cardiomyocytes. This may be related to biophysical differences between healthy and scarred myocardium.

Identifiants

pubmed: 31439293
pii: S2405-500X(19)30383-4
doi: 10.1016/j.jacep.2019.05.011
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

920-931

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Auteurs

Michael Barkagan (M)

Division of Cardiovascular Medicine, Department of Medicine, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Eran Leshem (E)

Division of Cardiovascular Medicine, Department of Medicine, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Ayelet Shapira-Daniels (A)

Division of Cardiovascular Medicine, Department of Medicine, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Jakub Sroubek (J)

Division of Cardiovascular Medicine, Department of Medicine, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Alfred E Buxton (AE)

Division of Cardiovascular Medicine, Department of Medicine, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Jeffrey E Saffitz (JE)

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Elad Anter (E)

Division of Cardiovascular Medicine, Department of Medicine, Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. Electronic address: eanter@bidmc.harvard.edu.

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Classifications MeSH