Copyright © 2006, The European Society of Cardiology
Reply to the Letter to the Editor: Comments on "Atrial septal aneurysm and spontaneous echo contrast: An association with higher embolic risk?" by K.M. Krishnamoorthy and N. Namboodiri
Echocardiography Laboratory, Clinica Bazterrica, Cardiology, Juncal 3002 (C1425AYN) Capital Federal, Buenos Aires, Argentina
Received 19 August 2006; accepted after revision 19 August 2006.
* Corresponding author. Tel.: +54 11 4801 5510; fax: +54 11 4801 4157. tcianciulli{at}fibertel.com.ar
We thank Drs. Krishnamoorthy and Namboodiri for their interest in our report.1 We agree with their comment but as they mention in their report, their patient had a small atrial septal aneurysm (ASA) and spontaneous echo contrast (SEC) in a different clinical settings,2 with two additional risk factors for thromboembolism such as mitral stenosis and atrial fibrillation, that could explain the finding of a clot inside the aneurysmal sac with transesophageal echocardiography.
In contrast, our patient with a large ASA and intense SEC, was in sinus rhythm and had no other cardiac abnormalities, no history of hypertension or coronary artery disease; the likely aetiology was a congenital malformation of the atrial septum.
Several authors have related the presence of ASA with cerebrovascular ischemic events,3–5 but the exact nature of this relation is unclear. Patients with mitral stenosis, mitral prostheses, atrial fibrillation or who have undergone cardiothoracic surgery involving the atrial septum, should be excluded from studies assessing the possible link between ASA and cardiogenic embolism in patients with otherwise unexplained ischemic stroke.
A "lone ASA" is an infrequent finding in adult patients. The incidence of ASA, as diagnosed by transthoracic echocardiography (TTE), has been reported to range between 1.0 and 1.7%. The TTE shows a typical phasic excursion during the cardiorespiratory cycle equal or greater than 10mm, associated with a base of the aneurysm equal or greater than 15mm. In such cases of "lone ASA", the condition could be considered benign. However, when transesophageal echocardiography (TEE) shows the aneurysmal sac with reduced motion and protruding only into the right atrium, with intense SEC in the left side of the ASA, it could be considered as a risk factor for systemic thromboembolism; such was the case of our reported patient, who was defined as having a "high risk ASA".1
Embolic events have been attributed to thrombus formation in the left side of the aneurysmal sac,6–8 but thrombi attached to the ASA as detected by TEE are apparently rare.
However, the associated patent foramen ovale (PFO) resulting in paradoxical embolism from a right-to-left shunting, is the most frequent cause of stroke in patient with a "high risk" ASA, defined as ASA and PFO with associated mitral stenosis, atrial fibrillation, deep venous thrombosis or thrombophilia.
We agree with Krishnamoorthy and Namboodiri that SEC adds incremental embolic risk in patients with ASA, when associated with any of the cardiovascular or clinical conditions mentioned above. However, we have proposed a novel association consisting of a large size and/or reduced motion "lone ASA" and intense SEC, which could entail a higher embolic risk, because clot formation can occur on the concave side of the aneurysmal sac, as a result of blood stasis in this low-velocity chamber.
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