Left atrial dysfunction in patients with patent foramen ovale and atrial septal aneurysm: an alternative concurrent mechanism for arterial embolism?
OBJECTIVE
We postulate that, in patients with large patent foramen ovales (PFO) and atrial septal aneurysms (ASA), left atrial (LA) dysfunction simulating "atrial fibrillation (AF)-like" pathophysiology might represent an alternate mechanism in the promotion of arterial embolism.


BACKGROUND
Despite prior reports concerning paradoxical embolism through a PFO, the magnitude of this phenomenon as a risk factor for stroke remains undefined, because deep venous thrombosis is infrequently detected in such patients.


METHODS
To test our hypothesis, we prospectively enrolled 98 consecutive patients with previous stroke (mean age 37 +/- 12.5 years, 58 women) referred to our center for catheter-based PFO closure. Baseline values of LA passive and active emptying, LA conduit function, LA ejection fraction, and spontaneous echocontrast (SEC) in the LA and LA appendage were compared with those of 50 AF patients as well as a sex/age/cardiac risk-matched population of 70 healthy control subjects.


RESULTS
Pre-closure PFO subjects demonstrated significantly greater reservoir function as well as passive and active emptying, with significantly reduced conduit function and LA ejection fraction, when compared with AF and control patients. Furthermore, in PFO patients, 66.3% (65 of 98) had moderate-to-severe ASA and basal shunt; SEC was observed in 52% of PFO plus ASA patients before closure. Multivariate stepwise logistic regression revealed moderate-to-severe ASA (odds ratio: 9.4, 95% confidence interval: 7.0 to 23.2, p < 0.001) as the most powerful predictor of LA dysfunction. After closure, all LA parameters normalized to the levels of control subjects: no SEC, device-related thrombosis, or aortic erosion were observed on follow-up echocardiography.


CONCLUSIONS
This study suggests that moderate-to-severe ASA might be associated with LA dysfunction in patients with PFO. The resultant similarities to the pathophysiology of AF might represent an additional contributing mechanism for arterial embolism in such patients.
Rigatelli
Gianluca
G
Section of Adult Congenital and Adult Heart Disease, Cardiovascular Diagnosis and Endoluminal Interventions, Rovigo General Hospital, Rovigo, Italy. jackyheart@libero.it
Aggio
Silvio
S
Cardaioli
Paolo
P
Braggion
Gabriele
G
Giordan
Massimo
M
Dell'avvocata
Fabio
F
Chinaglia
Mauro
M
Rigatelli
Giorgio
G
Roncon
Loris
L
Chen
Jack P
JP
D000328:Adult; D016279:Atrial Function, Left; D054087:Atrial Septum / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006328:Cardiac Catheterization; D016022:Case-Control Studies; D017548:Echocardiography, Transesophageal; D019320:Embolism, Paradoxical / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D005260:Female; D054092:Foramen Ovale, Patent / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D006322:Heart Aneurysm / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors