Decrease in forces responsible for diastolic suction during acute coronary occlusion.
Decrease in forces responsible for diastolic suction during acute coronary occlusion.
复制标题
急性冠状动脉闭塞期间舒张吸力的减少。
DOI：
10.1161/01.cir.96.7.2348
复制
发表时间：
1997
期刊：
影响因子：
37.8
通讯作者：
LeWinter,MM
中科院分区：
文献类型：
--
作者：
Bell,SP;Fabian,J;Watkins,MW;LeWinter,MM
背景在收缩过程中产生的左心室(LV)恢复力的产生，负责舒张期吸力，依赖于收缩末期容量(ESV)和收缩期跨壁和三维变形。我们验证了急性冠状动脉闭塞会导致吸力丧失的假设。方法和结果10只开胸犬造成10分钟的急性冠状动脉闭塞(冠状动脉近端左前降支)。一个连接到左心房(LA)的伺服运动被用来在收缩期间迅速地将LA压力夹在随后的LV舒张压水平以下，从而导致非充盈舒张期，在此期间LV在ESV时完全松弛。在多个ESV(电导导管)处的LA钳可以描绘完全松弛的LV压力-容量关系(FRPVR)的正负部分。负的完全松弛压力(FRP)表示存在恢复力。急性冠脉闭塞10分钟后，FRPVR上移。因此，例如，在匹配的室上性心动过速在冠脉闭塞前和冠脉闭塞期间，FRP1.1±1.1(±SD)mm Hg与10分钟后的0.2±1.2 mm Hg(P<；0.05)。结论急性冠脉闭塞导致吸引力的迅速减少。这一现象与ESV水平无关，可能与缺血性舒张期功能障碍有关。
BackgroundThe production of left ventricular (LV) restoring forces generated during contraction, which are responsible for diastolic suction, is dependent on end-systolic volume (ESV) and systolic transmural and 3D deformation. We tested the hypothesis that acute coronary occlusion would result in loss of forces that cause suction.Methods and ResultsTen open-chest dogs were subjected to a 10-minute acute coronary occlusion (proximal left anterior descending coronary artery). A servomotor connected to the left atrium (LA) was used to rapidly clamp LA pressure during systole below the level of the succeeding LV diastolic pressure, resulting in nonfilling diastoles during which the LV fully relaxed at its ESV. LA clamps at multiple ESVs (conductance catheter) allowed delineation of positive and negative portions of the fully relaxed LV pressure-volume relation (FRPVR). A negative fully relaxed pressure (FRP) indicates the presence of restoring forces. After 10 minutes of acute coronary occlusion, there was an upward shift of the FRPVR. Thus, for example, at matched ESVs before and during coronary occlusion, FRP was −1.1±1.1 (±SD) mm Hg before versus 0.2±1.2 mm Hg after 10 minutes of coronary occlusion (P<.05).ConclusionsAcute coronary occlusion results in a rapid decrease in forces responsible for suction. This phenomenon is independent of the level of ESV and may contribute to ischemic diastolic dysfunction.