Blood Flow in the Left Atrial Appendage and Embolic Stroke in Nonvalvular Atrial Fibrillation

Abstract

It is unclear if low flow velocity in the left atrial appendage (LAA) is a predisposing factor to stroke in patients with nonvalvular atrial fibrillation (NVAF). We investigated flow velocity in the LAA in NVAF patients in relation to a past history of stroke and other potential embolic sources. We measured and analyzed peak flow velocities into (FV-in) and out of (FV-out) the LAA in a middle portion of the LAA in 35 NVAF patients by transesophageal echocardiography (TEE). We divided the NVAF patients into 3 groups: the Eaf group had a history of embolic stroke without any other potential embolic sources; the Emulti group had other potential embolic sources, and the control group had no embolic history. FV-in and FV-out in the Eaf group (12.3 ± 6.7 and 10.2 ± 7.3 cm/s) were significantly lower than those in the control group (24.3 ± 11.3 and 19.9 ± 8.8 cm/s; multicomparison Scheffé’s test, p = 0.0123 and 0.0395, respectively). The Emulti group varied in those values from less than 5 to above 35. Low flow velocity in the LAA seems to be a predisposing factor for stroke in NVAF patients without any other sources of emboli.

Role of Imaging in Left Atrial Appendage Occlusion

“…In AF patients, LAA structure and function have several characteristics that make LAA a prothrombotic milieu favouring thrombus formation. The elements of the Virchow's triad are found in this setting: blood stasis in this blind-ended pouch with trabeculations and electromechanical dysfunction [36,37], endothelial dysfunction (secondary to fibrosis and inflammation) [38]. and prothrombotic state (linked to the activation of coagulation cascade) [39,40].…”

Noninvasive Surrogate Markers to Predict Thrombogenesis in Patients with Nonvalvular Atrial Fibrillation

“…7) It is well known that the left atrial appendage (LAA) is a major cardioembolic source in patients with AF who have suffered a stroke. [8][9][10][11] We conducted a retrospective study of the relation between LAA thrombus (LAAT) and patient characteristics, transthoracic and transesophageal echocardiographic variables, and blood markers in patients with persistent AF to determine whether thrombogenesis can be predicted in patients with NVAF.…”

Higher Levels of Serum Fibrin-Monomer Reflect Hypercoagulable State and Thrombus Formation in the Left Atrial Appendage in Patients With Acute Ischemic Stroke

“…However, it is sometimes difficult to make a diagnosis because of the splashing and vanishing of the intracardiac source of the emboli. [4][5][6][7][8][9][10][11][12] In patients with cardioembolic stroke it is necessary to carefully examine the intracardiac hypercoagulable state based on echocardiographic findings and/or serum sensitive markers, and then use this information to prevent recurrent attacks.It is well known that the left atrial appendage (LAA) is a major thromboembolic source in cardioembolic stroke. 7,8 Many clinical reports have shown a close relationship between LAA thrombus formation and left atrial mechanical remodeling, based on echocardiographic findings such as the presence of spontaneous echo contrast or a progressive Circulation Journal Vol.70, August 2006 reduction in LAA emptying flow velocity.…”

“…However, it is sometimes difficult to make a diagnosis because of the splashing and vanishing of the intracardiac source of the emboli. [4][5][6][7][8][9][10][11][12] In patients with cardioembolic stroke it is necessary to carefully examine the intracardiac hypercoagulable state based on echocardiographic findings and/or serum sensitive markers, and then use this information to prevent recurrent attacks.…”

“…7,8 Many clinical reports have shown a close relationship between LAA thrombus formation and left atrial mechanical remodeling, based on echocardiographic findings such as the presence of spontaneous echo contrast or a progressive Circulation Journal Vol.70, August 2006 reduction in LAA emptying flow velocity. 6,10,12,13 Serum fibrin monomer (FM) is a precursor of the fibrin polymer that is produced by the thrombin-mediated resolution of fibrinopeptide A from fibrinogen.…”