Is there an association of atrial septal aneurysm with arrhythmias?

Citation
B. Schneider et al., Is there an association of atrial septal aneurysm with arrhythmias?, CARDIOLOGY, 91(2), 1999, pp. 87-91
Citations number
30
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOLOGY
ISSN journal
0008-6312 → ACNP
Volume
91
Issue
2
Year of publication
1999
Pages
87 - 91
Database
ISI
SICI code
0008-6312(1999)91:2<87:ITAAOA>2.0.ZU;2-X
Abstract
An association of atrial septal aneurysm (ASA) with cardiac arrhythmias has been described, and it has been suggested that undulating movements of the aneurysm initiate these arrhythmias, thereby causing arterial embolism. In this prospective study, all available electrocardiograms were reviewed and Hotter monitoring was performed in 50 consecutive patients with echocardio graphic diagnosis of ASA in order to assess the relationship between the oc currence of arrhythmias, morphologic characteristics of ASA and arterial em bolism, Significant arrhythmias were identified in 26 (52%) patients (supra ventricular n = 15, ventricular n = 6, both n= 5), Patients with arrhythmia s were older (65 +/- 12 vs. 54 +/- 13 years, p = 0.005), frequently had pal pitations (21/26 vs. 1/24, p < 0.0001) and an abnormal resting electrocardi ogram (18/26 vs. 5/24, p < 0.001). By echocardiography, patients with arrhy thmias had a larger left atrial (42.8 +/- 7.4 vs. 35.3 +/- 4.6 mm, p < 0.00 01) and left ventricular enddiastolic diameter (53.8 +/- 5.6 vs. 49.7 +/- 4 .1, p < 0.01) and a higher prevalence of associated mitral valve prolapse ( 12/26 vs, 4/24, p = 0.05). Potential cardiovascular causes for arrhythmia o ther than ASA were present in the great majority of patients with documente d arrhythmias (24/26 vs. 7/24, p < 0.0001). The base diameter of ASA was la rger in patients with arrhythmias (25.5 +/- 6.2 vs. 21.4 +/- 3.4, p < 0.01) and correlated with a larger left atrial diameter (r = 0.72, p < 0.0001), Concerning the mobility of ASA (maximal protrusion or phasic excursion), th ere was no significant difference between the two patient groups. Arterial embolism, however, predominantly occurred in ASA patients without arrhythmi as (16/24 vs. 9/26, p < 0.05). In conclusion, the majority of patients with ASA and arrhythmias has underlying structural heart disease other than ASA which may be responsible for the arrhythmias observed. Arrhythmias in asso ciation with ASA do not play a major role as a mechanism for arterial embol ism.