Goch A, Banach M, Piotrowski G, Szadkowska I, Goch J H
Department of Cardiology, 1st Chair of Cardiology and Cardiac Surgery, University Hospital No 3, Medical University of Lodz, Lodz, Poland.
Thorac Cardiovasc Surg. 2007 Sep;55(6):365-70. doi: 10.1055/s-2007-965304.
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.
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.
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.
(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.
我们的研究旨在评估房间隔瘤（ASA）患者的左心房（LA）和左心耳（LAA）功能，并将其与血栓栓塞并发症相关联。
研究组包括25例孤立性ASA患者（I组）和17例临床健康受试者（对照组 = II组）。对所有研究患者进行经胸和经食管超声心动图检查。
在I组中，以下参数显著高于对照组：左心房最小内径（LA（min））为2.13 cm对1.7 cm；左心房收缩前期内径（LA（a））为2.66 cm对2.29 cm，左心房射血前期/左心房射血时间指数（PEP/ETLA）为1.26对0.41（P < 0.05）。两组间P波和PR间期持续时间无统计学显著差异，分别为69 ms对72 ms和167 ms对173 ms。对所有左心耳参数进行了研究，但研究组的左心耳最小面积（LAA（area min））高于对照组：左心耳横向内径（LAA（trans））为1.89 cm对1.32 cm；左心耳纵向内径（LAA（long））为4.24 cm对3.11 cm；左心耳最大面积（LAA（area max））为4.35 cm²对3.1 cm²；左心耳射血分数（EFLAA）为56%对33%；左心耳峰值排空速度（LAAE）为0.64 m/s对0.41 m/s，充盈速度（LAAF）为0.55 m/s对0.42 m/s（P < 0.05）。结果表明，与临床健康受试者相比，ASA患者左心房收缩功能降低，左心耳功能增强。
（1）房间隔瘤损害左心房收缩功能。（2）在房间隔瘤患者中，左心耳功能发生改变；其收缩功能以及储存功能均得到改善。（3）房间隔瘤患者左心耳功能增强可能是左心房收缩功能恶化的一种代偿机制。（4）由于左心耳收缩功能增强，左心耳不太可能是血栓的起源部位，而血栓在房间隔瘤患者中相对频繁发生（根据文献）。血栓似乎形成于房间隔瘤的膨出囊中，即左心房收缩功能降低的部分。
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