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  • Title: Echocardiographic evaluation of the left atrium and left atrial appendage function in patients with atrial septum aneurysm: implications for thromboembolic complications.
    Author: Goch A, Banach M, Piotrowski G, Szadkowska I, Goch JH.
    Journal: Thorac Cardiovasc Surg; 2007 Sep; 55(6):365-70. PubMed ID: 17721845.
    Abstract:
    BACKGROUND: Our study aimed to assess left atrium (LA) and left atrial appendage (LAA) function in patients with atrial septum aneurysm (ASA) and to relate it to thromboembolic complications. METHODS: The study group comprised 25 patients with isolated ASA (group I) and 17 clinically healthy subjects (control group = group II). Transthoracic and transesophageal echocardiography were performed in all investigated patients. RESULTS: In group I, the following parameters were significantly higher than in the controls: LA minimal dimension (LA (min)) was 2.13 vs. 1.7 cm; LA presystolic dimension (LA (a)) was 2.66 vs. 2.29 cm and LA pre-ejection period/LA ejection time index (PEP/ETLA) was 1.26 vs. 0.41 ( P < 0.05). There were no statistically significant differences between groups as to P wave and PR-interval duration, which were 69 vs. 72 ms and 167 vs. 173 ms, respectively. All LAA parameters were investigated, but LAA minimal areas (LAA (area min)) were higher in the study group than in controls: LAA transversal dimension (LAA (trans)) was 1.89 vs. 1.32 cm; LAA longitudinal dimension (LAA (long)) was 4.24 vs. 3.11 cm; LAA maximal area (LAA (area max)) was 4.35 vs. 3.1 cm (2); LAA ejection fraction (EFLAA) was 56 vs. 33 %; LAA peak emptying (LAAE) was 0.64 vs. 0.41 m/s, and filling velocities (LAAF) was 0.55 vs. 0.42 m/s ( P < 0.05). The results indicate a depression of LA systolic and an enhancement of LAA function in patients with ASA compared with clinically healthy subjects. CONCLUSION: (1) Atrial septum aneurysm impairs left atrium systolic function. (2) In patients with atrial septum aneurysm, left atrium appendage function changes; its systolic as well as a reservoir function improve. (3) The enhancement of LAA function in ASA may be a compensatory mechanism for LA systolic function deterioration. (4) As LAA systolic function is enhanced, it is rather unlikely that LAA is the place of origin of thrombi, which occur relatively frequently (according to the literature) in patients with ASA. The thrombi seem to be formed in the bulging sack of ASA, i.e., in the part of the LA whose systolic function is depressed.
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