Rigatelli Gianluca, Aggio Silvio, Cardaioli Paolo, Braggion Gabriele, Giordan Massimo, Dell'avvocata Fabio, Chinaglia Mauro, Rigatelli Giorgio, Roncon Loris, Chen Jack P
Section of Adult Congenital and Adult Heart Disease, Cardiovascular Diagnosis and Endoluminal Interventions, Rovigo General Hospital, Rovigo, Italy.
JACC Cardiovasc Interv. 2009 Jul;2(7):655-62. doi: 10.1016/j.jcin.2009.05.010.
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.
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.
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.
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.
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.
我们推测，在患有大型卵圆孔未闭（PFO）和房间隔瘤（ASA）的患者中，模拟“房颤（AF）样”病理生理学的左心房（LA）功能障碍可能是促进动脉栓塞的另一种机制。
尽管先前有关于通过PFO发生反常栓塞的报道，但由于在此类患者中很少检测到深静脉血栓形成，因此这种现象作为中风危险因素的程度仍不明确。
为了验证我们的假设，我们前瞻性地纳入了98例连续的既往有中风病史的患者（平均年龄37±12.5岁，58例女性），这些患者因基于导管的PFO封堵术被转诊至我们中心。将LA的被动和主动排空、LA管道功能、LA射血分数以及LA和LA心耳中的自发显影（SEC）的基线值与50例AF患者以及70例健康对照受试者的性别/年龄/心脏风险匹配人群进行比较。
与AF患者和对照患者相比，封堵前PFO患者表现出明显更大的储器功能以及被动和主动排空，管道功能和LA射血分数明显降低。此外，在PFO患者中，66.3%（98例中的65例）有中度至重度ASA和基础分流；封堵前52%的PFO加ASA患者观察到SEC。多因素逐步逻辑回归显示中度至重度ASA（优势比：9.4，95%置信区间：7.0至23.2，p<0.001）是LA功能障碍最有力的预测因素。封堵后，所有LA参数均恢复至对照受试者水平：随访超声心动图未观察到SEC、与装置相关的血栓形成或主动脉侵蚀。
本研究表明，中度至重度ASA可能与PFO患者的LA功能障碍有关。由此产生的与AF病理生理学的相似性可能是此类患者动脉栓塞的另一个促成机制。
