Key result
LAA thrombus in nonparoxysmal AF linked to ~86% greater LAA fibrosis burden.
Why the study?
Although echocardiographic studies suggest left atrial appendage remodeling contributes to thrombus development, histological evidence is lacking.
Is left atrial appendage fibrosis burden associated with thrombus formation in patients undergoing LAA excision?
Observational (n=64)
Is left atrial appendage fibrosis burden associated with thrombus formation in patients undergoing LAA excision?
Absolute Event Rate: 23.8% vs 12.8%
p-value: p=0.004
Histological evidence confirms that increased left atrial appendage fibrosis burden is significantly associated with LAA thrombus formation, particularly in patients with nonparoxysmal AF.
LAA fibrosis assessment may refine thrombus risk stratification in nonparoxysmal AF; leaves open causal role and therapeutic implications.
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.
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Miyauchi et al. (2022) conducted an observational in Left atrial appendage thrombus and atrial fibrillation (n=64). Left atrial appendage fibrosis burden vs. Patients without left atrial appendage thrombus was evaluated on Left atrial appendage fibrosis burden (%) in excised sections (p=0.004). Left atrial appendage fibrosis burden was significantly higher in nonparoxysmal atrial fibrillation patients with an LAA thrombus compared to those without (23.8% vs. 12.8%, p=0.004).
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