Spatial and temporal variability in the pattern of recovery of ventricular geometry and function after acute occlusion and reperfusion.
Spatial and temporal variability in the pattern of recovery of ventricular geometry and function after acute occlusion and reperfusion.
复制标题
急性闭塞和再灌注后心室几何形状和功能恢复模式的空间和时间变异性。
DOI：
10.1016/0002-8703(94)90041-8
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发表时间：
1994
影响因子：
4.8
通讯作者：
Weyman,AE
中科院分区：
文献类型：
--
作者：
Davidoff,R;Picard,MH;Force,T;Thomas,JD;Guerrero,JL;McGlew,S;Weyman,AE
已知心肌缺血和梗死会引起心室形状和功能的改变。短暂性心肌缺血后心室几何形状的恢复及其与功能恢复的关系尚不清楚。为了研究短暂冠状动脉闭塞后心室几何形状的恢复模式，并评估其与收缩功能恢复的关系，我们使用超声心动图研究了13只犬左前降支冠状动脉闭塞15分钟后的情况。在缺血期间，总内皮细胞表面积（ESA）从32.55 ± 1.77增加到45.36 ± 3.18 cm 2（p= 0.001）。最显著的增加是在心尖部，此处周长从基线时的5.04 ± 0.24 cm增加到闭塞结束时的7.86 ± 0.43 cm（p= 0.0001），增加了58%。在再灌注期间，心室几何形状迅速恢复正常（基线），再灌注15分钟时ESA明显恢复80%。收缩功能的恢复明显较慢（在再灌注2小时期间的所有观察期，p< 0.005）。在再灌注过程中，心室几何形状和功能的恢复在整个缺血床是不均匀的。心尖部恢复最慢，异常收缩区的中心沿左心室长轴沿着逐渐向心尖部移动。功能障碍区域的半径也逐渐降低，从闭塞结束时的2.0 ± 0.15 cm降至再灌注120分钟时的0.13 ± 0.07 cm（p= 0.0001）。在缺血或再灌注期间，心尖段和眼前段之间的血流量没有差异。在主动收缩功能恢复和几何恢复之前，再灌注有利地减少了缺血区扩张，因此在确定最终功能恢复方面可能是重要的。此外，功能的恢复是向缺血区域的中心向内进行的，并且是从基底部到心尖部的波前。这种不均匀和不对称的恢复表明，在缺血区内的一个点取样可能不能反映恢复的真实时间模式。
Myocardial ischemia and infarction are known to cause changes in both ventricular shape and function. Little is known about the recovery of ventricular geometry after transient myocardial ischemia and its relationship to recovery of function. To examine the pattern of recovery of ventricular geometry following transient coronary artery occlusion and to assess the relationship of this to the return of systolic function, we used echocardiography to study 13 dogs following 15-minute occlusion of the left anterior descending coronary artery. During ischemia, total endocardial surface area (ESA) increased from 32.55 ± 1.77 to 45.36 ± 3.18 cm2(p= 0.001). The most striking increase was at the apex, where circumference increased from 5.04 ± 0.24 at baseline to 7.86 ± 0.43 cm at the end of occlusion (p= 0.0001), an increase of 58%. During reperfusion, ventricular geometry rapidly returned toward normal (baseline), with recovery of 80% of the increase in ESA evident by 15 minutes of reperfusion. Recovery of systolic function was substantially slower (p< 0.005 for all periods of observation during the 2 hours of reperfusion). During reperfusion, recovery of ventricular geometry and function was not uniform throughout the ischemic bed. The apex recovered most slowly, with the centroid of the area of abnormal contraction progressively moving along the long axis of the left ventricle toward the apex. There was also a progressive decrease in the radius of the area of dysfunction, from 2.0 ± 0.15 at end occlusion to 0.13 ± 0.07 cm at 120 minutes of reperfusion (p= 0.0001). There was no difference in blood flow between the apical and anterior segments during ischemia or reperfusion. Reperfusion favorably reduced the ischemic zone dilation before recovery of active systolic function and geometric recovery thus may be important in determining ultimate functional recovery. In addition, recovery of function proceeded inward towards the center of the ischemic territory and in a wavefront from the base to apex. This heterogeneous and asymmetric recovery suggests that sampling at one point within the ischemic zone may not reflect the true temporal pattern of recovery.