Stugaard M, Risöe C, Ihlen H, Smiseth O A
Institute for Surgical Research, National Hospital, Oslo, Norway.
J Am Coll Cardiol. 1994 Sep;24(3):663-70. doi: 10.1016/0735-1097(94)90012-4.
The present study aimed to investigate the mechanism of intracavitary changes in filling pattern during acute ischemic left ventricular failure and during beta-adrenergic blockade.
Recent clinical studies with color M-mode Doppler imaging have shown abnormal intracavitary filling patterns in the diseased ventricle.
In open chest anesthetized dogs with intracardiac micromanometers and myocardial segment-length crystals, global ischemic left ventricular failure was induced (n = 8) by coronary microembolization. In nonischemic ventricles inotropy was decreased (n = 6) by intravenous propranolol and increased (n = 6) by intravenous isoproterenol. From color M-mode Doppler images we calculated the time difference between peak early diastolic filling velocity at the mitral tip and apex using computer analysis. The time difference of peak velocity was used as an index of the timing of apical filling.
There was marked retardation of apical filling with microembolization and propranolol. Time difference of peak velocity increased from 20 +/- 6 (mean +/- SEM) to 101 +/- 17 ms (p < 0.05) and from 21 +/- 8 to 80 +/- 18 ms (p < 0.05), respectively. Time constant of isovolumic relaxation increased from 34 +/- 3 to 43 +/- 5 ms (p < 0.05) and from 31 +/- 1 to 39 +/- 3 ms (p < 0.05) during microembolization and beta-blockade, respectively. Isoproterenol tended to cause the opposite changes. Time difference of peak velocity showed a positive correlation with time constant of isovolumic relaxation (r = 0.89, p < 0.01) and a negative correlation with peak early transmitral pressure gradient (r = 0.88, p < 0.01). In the intact left ventricle, peak apical filling velocity coincided with peak early transmitral pressure gradient. During ischemic failure however, peak apical filling velocity occurred 53 +/- 14 ms after peak early transmitral pressure gradient had decreased to zero and at a time when transmitral flow had ceased, suggesting a change in intraventricular flow distribution.
Color M-mode Doppler imaging revealed retarded apical filling during depression of myocardial function by global myocardial ischemia or beta-blockade. The abnormal filling pattern may be a sign of impaired left ventricular relaxation.
本研究旨在探究急性缺血性左心室衰竭及β-肾上腺素能阻滞剂作用期间心腔内充盈模式的腔内变化机制。
近期采用彩色M型多普勒成像的临床研究显示，病变心室的心腔内充盈模式异常。
在开胸麻醉的犬身上植入心内微测压计和心肌节段长度晶体，通过冠状动脉微栓塞诱导全心缺血性左心室衰竭（n = 8）。在非缺血心室中，静脉注射普萘洛尔降低心肌收缩力（n = 6），静脉注射异丙肾上腺素增强心肌收缩力（n = 6）。利用计算机分析彩色M型多普勒图像，计算二尖瓣尖部和心尖处舒张早期充盈峰值速度之间的时间差。峰值速度的时间差用作心尖充盈时间的指标。
微栓塞和普萘洛尔导致心尖充盈明显延迟。峰值速度的时间差分别从20±6（均值±标准误）增加到101±17毫秒（p < 0.05），以及从21±8增加到80±18毫秒（p < 0.05）。等容舒张时间常数在微栓塞和β受体阻滞剂作用期间分别从34±3增加到43±5毫秒（p < 0.05），以及从31±1增加到39±3毫秒（p < 0.05）。异丙肾上腺素倾向于引起相反的变化。峰值速度的时间差与等容舒张时间常数呈正相关（r = 0.89，p < 0.01），与二尖瓣早期压力阶差峰值呈负相关（r = 0.88，p < 0.01）。在完整的左心室中，心尖充盈峰值速度与二尖瓣早期压力阶差峰值一致。然而，在缺血性衰竭期间，心尖充盈峰值速度在二尖瓣早期压力阶差峰值降至零后53±14毫秒出现，且此时二尖瓣血流已停止，提示心室内血流分布发生改变。
彩色M型多普勒成像显示，在全心缺血或β受体阻滞剂导致心肌功能抑制期间，心尖充盈延迟。异常的充盈模式可能是左心室舒张功能受损的迹象。
