This prospective, long-term study both confirms and extends our previous observation. The risk of cerebrovascular events in patients after cardiac surgery with an incidental ASA is low. If treatment is needed for this condition, aspirin appears to be effective therapy. ASA is a localized saccular deformity of the interatrial septum, generally at the level of the fossa ovalis.[8] It can be either congenital or caused by other cardiac abnormalities. Its prevalence is 0.08% to 1.2% in adults[2,5,9,10] and up to 4.9% in the pediatric population[11] as detected by transthoracic echocardiography. With transesophageal echocardiography, the prevalence ranges from a low of 2% to a high of 10%.[5,12] The variability in the diagnosis of ASA is probably related to the diagnostic criteria used, imaging technique, population studied, and the vigilance of reporting such findings. The 3 most plausible mechanisms for the development of cerebrovascular events are (1) thrombus formation in or around the ASA,[4,5,8] (2) paradoxical embolization through an interatrial communication in the form of patent foramen ovale or atrial septal defect,[13] and (3) mitral valve prolapse and atrial arrhythmias that have been found to be associated with ASA.[14]
All these studies have one major limitation: referral bias. Patients with cerebrovascular events were referred for an echocardiographic study to determine a cardiac source of embolus. Thus these investigations cannot determine the true frequency and embolic potential of ASA and may actually suggest a falsely high prevalence and risk of embolic events.
In previous reports from this institution,[6,18] we demonstrated that in 1626 patients undergoing cardiac surgery, 80 patients with incidental ASA had no cerebrovascular events in the immediate in-hospital postoperative period. In addition, we prospectively monitored 42 patients with incidental ASA for a mean of 25 months. None had evidence of cerebrovascular events. Our current study now extends these findings to a mean 5.8-year follow-up period. Thus the risk of cerebrovascular events with incidental ASA is probably much lower than previous reported trials and actually may not be significantly increased when referral bias and other confounders for embolic strokes are taken into account.
Although the association between ASA and systemic embolization has been reported, the exact relation between these 2 conditions has not been well established. We think that the association between cerebrovascular events and ASA has been exaggerated because of bias in patient selection. The autopsy study done by Silver and Dorsey[8] supports this notion. They describe 16 patients with fossa ovalis aneurysms among 1578 consecutive autopsies of adults aged 43 to 81 years. None of the aneurysms had been diagnosed during life, and all were clinically asymptomatic. Eight subjects had a probe-patent fossa ovalis, 2 had a secundum-type atrial-septal defect, and 2 had tiny perforations (<1 mm in diameter) in the wall of the aneurysm. Furthermore, in a study by Oneglia et al,[19] 38 patients with ASA were found during 4014 consecutive echocardiographic studies over an 18-month period. No patients demonstrated any evidence of embolic events or atrial arrhythmias.Although absolute risk over time is not known, available data suggest that the risk is probably not high enough to warrant long-term anticoagulation for ASA alone; aspirin alone would be reasonable in the absence of other high-risk variables for stroke or cerebrovascular event.[6] The French Study Group on Patent Foramen Ovale and Atrial Septal Aneurysm[20] supports this concept. They evaluated the risk of recurrent cerebrovascular events over a 22-month period in 132 patients with patent foramen ovale, ASA, or both. The authors concluded that these patients appear to have a low risk of recurrent stroke regardless of what prophylactic antithrombotic therapy was used. Our current study supports the premise that aspirin is effective therapy, and interventions such as long-term anticoagulation or surgery may not be required for treatment and management of incidental ASA
This investigation has several limitations. Our study population of patients with coronary artery disease is small. The incidence and significance of asymptomatic ASA in our study cannot necessarily be generalized to other patient populations. Additional prospective, long-term investigations with larger sample sizes are needed. Second, the patency rate was not determined in all subjects. Although it is similar to previous investigations, the determination of patency in all patients would shed additional light on the possible mechanisms of cerebrovascular events in ASA. Third, almost all patients were receiving long-term aspirin therapy. Thus the true embolic potential of ASA cannot be determined. However, if the mechanism of cerebrovascular events with ASA is platelet/thrombus formation at the site of the aneurysm and/or paradoxical embolization, aspirin is a reasonable therapeutic option and may be effective therapy.
In conclusion, our investigation represents the longest prospective study of patients with ASA to date. The risk of cerebrovascular events in patients after cardiac surgery with an incidental ASA over a 6-year follow-up period is low. If treatment is needed for this condition, aspirin appears to be effective therapy. Additional prospective studies are required to document the exact risk of embolic events in patients with ASA and further clarify their clinical management.
Reprint Address
Reprint requests: Andrew Burger, MD, Beth Israel Deaconess Medical Center, Noninvasive Cardiology Laboratory, Baker-3, 1 Deaconess Rd, Boston, MA 02215
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