Stefanadis C, Dernellis J, Tsiamis E, Toutouzas P
Department of Cardiology, Hippokration Hospital, University of Athens, Greece.
J Am Coll Cardiol. 1999 Mar;33(3):687-96. doi: 10.1016/s0735-1097(98)00623-8.
The aim of this study was to compare left atrial (LA) function in 16 patients with distal left anterior descending (LAD) and in 16 patients with proximal left circumflex (LCx) coronary artery stenosis at rest and immediately after pacing-induced tachycardia (LAD-pacing [P] and LCx-P) or coronary occlusion (LAD-CO and LCx-CO).
During left ventricular (LV) ischemia, compensatory augmentation of LA contraction enhances LV filling and performance. The left atrium is supplied predominantly by branches arising from the LCx. Therefore, we hypothesized that one mechanism for the loss of atrial contraction may be ischemic LA dysfunction.
Left ventricular and LA pressure-area relations were derived from simultaneous double-tip micromanometer pressure recordings and automatic boundary detection echocardiograms.
Immediately after pacing or after coronary occlusion, LV end-diastolic pressure, LV relaxation, LA mean pressure and LV stiffness significantly increased in all patients. However, the area of the A loop of the LA pressure-area relation, representing the LA pump function, significantly decreased in groups LCx-P and LCx-CO (from 14+/-3 to 9+/-2, and from 16+/-4 to 9+/-2 mm Hg.cm2, respectively, p < 0.05), whereas it increased in groups LAD-P and LAD-CO (from 12+/-3 to 54+/-10, and from 16+/-3 to 49+/-8 mm Hg.cm2, respectively, p < 0.001).
In patients with LAD stenosis, LV supply or demand ischemia is associated with enhanced LA pump function. However, in patients with proximal LCx stenosis who develop the same type and degree of ischemia, LA branches might have been affected, rendering the LA ischemic and unable to increase its booster pump function.
本研究旨在比较16例左前降支(LAD)远端狭窄患者和16例左旋支(LCx)近端冠状动脉狭窄患者在静息状态下以及起搏诱发心动过速(LAD起搏[P]和LCx - P)或冠状动脉闭塞(LAD - CO和LCx - CO)后即刻的左心房(LA)功能。
在左心室(LV)缺血期间,左心房收缩的代偿性增强可增强左心室充盈和功能。左心房主要由左旋支发出的分支供血。因此,我们推测心房收缩丧失的一种机制可能是缺血性左心房功能障碍。
左心室和左心房压力 - 面积关系通过同步双尖端微测压压力记录和自动边界检测超声心动图得出。
起搏或冠状动脉闭塞后即刻,所有患者的左心室舒张末期压力、左心室舒张功能、左心房平均压力和左心室僵硬度均显著增加。然而,代表左心房泵功能的左心房压力 - 面积关系A环面积在LCx - P组和LCx - CO组显著减小(分别从14±3降至9±2,以及从16±4降至9±2 mmHg·cm²,p < 0.05),而在LAD - P组和LAD - CO组增加(分别从12±3增至54±10,以及从16±3增至49±8 mmHg·cm²,p < 0.001)。
在LAD狭窄患者中,左心室供血或需求性缺血与增强的左心房泵功能相关。然而,在发生相同类型和程度缺血的近端LCx狭窄患者中,左心房分支可能已受影响,致使左心房缺血且无法增强其辅助泵功能。