Association between left atrial appendage fibrosis and thrombus formation: A histological approach.

Introduction: Although recent echocardiographic studies have suggested that left atrial appendage (LAA) remodeling contributes to the development of LAA thrombus (LAAT), histological evidence is absent. The objective of this study was to examine clinical parameters and histological findings to clari...

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Detalles Bibliográficos
Publicado en:Journal of Cardiovascular Electrophysiology Vol. 33; no. 4; pp. 677 - 688
Autores principales: Miyauchi, Shunsuke, Tokuyama, Takehito, Uotani, Yukimi, Miyamoto, Shogo, Ikeuchi, Yoshihiro, Okamura, Sho, Okubo, Yousaku, Katayama, Keijiro, Takasaki, Taiichi, Nakatani, Nobuhiro, Matsudaira, Yorisato, Furusho, Hisako, Miyauchi, Mutsumi, Takahashi, Shinya, Nakano, Yukiko
Formato: diagnostic images pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell Apr2022
Acceso en línea:Ver este registro en EBSCOhost
Descripción
Sumario:Introduction: Although recent echocardiographic studies have suggested that left atrial appendage (LAA) remodeling contributes to the development of LAA thrombus (LAAT), histological evidence is absent. The objective of this study was to examine clinical parameters and histological findings to clarify the factors involved in LAAT formation. Methods: A total of 64 patients (no atrial fibrillation [AF], N = 22; paroxysmal AF, N = 16; nonparoxysmal AF, N = 26) who underwent LAA excision during surgery were enrolled. Transthoracic and transesophageal echocardiography were performed before surgery. We evaluated the fibrosis burden (%) in the excised LAA sections with Azan–Mallory staining in patients with a LAAT compared with those without. Results: Patients with paroxysmal and non‐paroxysmal AF had a higher LAA fibrosis burden than those without AF (p =.005 and p <.0001, respectively). Among the patients enrolled, 16 had a LAAT and 15 of them had nonparoxysmal AF. Among the nonparoxysmal AF patients, those with a LAAT had significantly higher LAA fibrosis burden than those without (23.8% [14.8%–40.3%] vs. 12.8% [7.4%–18.2%], p =.004) and echocardiographic parameters of the left atrial volume index (R = 0.543, p =.01), LAA depth (R = 0.452, p =.02), and LAA flow velocity (R = − 0.487, p =.01) were correlated with the LAA fibrosis burden. Conclusion: This study provided histological evidence that LAA fibrosis is related to LAAT formation. Echocardiographic parameters of LAA remodeling and function were correlated with the LAA fibrosis burden.