Arrhythmias & electrophysiology

Relationship Between Fibrosis, Endocardial Endothelial Damage, and Thrombosis of Left Atrial Appendage in Atrial Fibrillation

JACC Clin ElectrophysiolPublished Cross-sectional histological study

Authors' conclusion

These histological findings may be essential in considering the pathophysiology of LAAT and stroke within the atrial cardiomyopathy context.

Study context

Population
Patients with atrial fibrillation (AF) scheduled for left atrial appendage (LAA) excision during surgery
Participants
96 patients
Exposure
Patients with LAAT and/or ischemic stroke history vs those without
Outcome
LAA fibrosis degree and endocardial endothelial damage (CD31 expression)

Main finding

As reported in the abstract

GroupValueCD31 expression
LAAT and/or stroke18.4% (SD 9.9%)0.27 [IQR: 0.05-0.57]
No LAAT or stroke10.4% (SD 7.0%)1.02 [IQR: 0.49-1.65]

Value

LAAT and/or stroke18.4% (SD 9.9%)
No LAAT or stroke10.4% (SD 7.0%)

CD31 expression

LAAT and/or stroke0.27 [IQR: 0.05-0.57]
No LAAT or stroke1.02 [IQR: 0.49-1.65]
  • LAAT and/or stroke vs No LAAT or stroke: P < 0.0001 — fibrosis degree
  • LAAT and/or stroke vs No LAAT or stroke: P < 0.0001 — CD31 expression
Endothelial damage (E4) associated with LAAT and/or stroke history independent of AF type (multivariate logistic regression), OR
3.47
Nonparoxysmal AF: fibrosis (F4) independently associated with LAAT and/or stroke, OR
3.66
Nonparoxysmal AF: endothelial damage (E4), OR
4.62
Nonparoxysmal AF: non-chicken-wing LAA morphology, OR
3.79
Fibrosis degree correlated with endothelial damage, R = −0.38
P = 0.0001

Observational data: associations, not effects.

Original publication

Relationship Between Fibrosis, Endocardial Endothelial Damage, and Thrombosis of Left Atrial Appendage in Atrial Fibrillation. JACC Clin Electrophysiol. Published 22 March 2023. doi:10.1016/j.jacep.2023.01.029

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