**4. Discussion**

474 Aneurysm

**Figure 3.** Echocardiography showing shunt flow through atrial septal defect. The multiple direction of

**Figure 4.** Figure 4. Atrial septum with numerous small pinholes and cribriform atrial septal defect

the flow suggested the presence of a number of holes in the atrial septum.

The incidence of ASA has been found to be higher after a cerebral ischemic event in patients evaluated with transesophageal echocardiogram. A meta-analysis of case-control studies found that the presence of a PFO, ASA, or both was significantly associated with ischemic stroke in subjects less than 55 years of age [2, 3]. It is reported from PFO-ASA study that the presence of PFO together with ASA is a significant predictor of recurrent stroke [4]. Aggressive therapy such as warfarin or surgical repair may be the best option in such patients, but this question needs to be assessed in randomized clinical trials. The 2004 American Academy of Neurology practice parameter concluded that the combination of PFO and ASA increases the risk of subsequent stroke in medically treated patients below age 55 compared with other cryptogenic stroke patients without atrial abnormalities. It also concluded that there is insufficient evidence to evaluate the efficacy of surgical or endovascular closure [5].

The pathological mechanisms that lead to the development of ASA have not yet been clarified. To explain the association between ASA and cryptogenic stroke, two mechanisms have been proposed. Because of the frequency of intraatrial shunt, paradoxical embolism may occur. In patients with ASA without intracardiac shunt, it has been hypothesized that direct thrombi form within the aneurysm or as a result of atrial fibrillation, causing embolism [6].

Surgery is seldom performed for ASA patients. Shinohara and colleagues reported on a three-year follow-up of ASA [7], while Aoyagi and colleagues reported on a case of ASA and stenotic mitral valve [8]. In these two cases ASA was successfully removed and the atrial septum repaired with a pericardial patch. The reports concluded that surgery may be considered as an alternative therapy for patients with atrial arrhythmia and ASA.

The present cases occurred in patients without history of stroke, but who had numerous strong predictors of cryptogenic stroke, including ASA, PFO, ASD, and AF. The right ventricle was mildly dilated and right ventricular pressure mildly elevated in one case. Although the indications for surgical treatment of ASA and PFO remain undetermined, we considered that the symptoms were unlikely to resolve and that surgical intervention was the only curative treatment available. We reported in the above on cases of ASA. We believe surgical repair should be considered for giant ASA to reduce the future risk of cerebral embolism or heart failure.
