[Diastolic left ventricular pressure-mitral valve flow velocity curve: influence of heart rate change induced by atrial pacing].

Journal of cardiography Pub Date : 1986-06-01
S Nakaya, Y Arakaki, H Tomita, N Takeuchi, T Kamiya
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Abstract

To assess the left ventricular (LV) diastolic properties, the influence of heart rate change induced by atrial pacing on LV pressure-mitral valve (MV) flow velocity curves was studied. Simultaneous recording of MV flow velocity using pulsed Doppler echocardiography and LV pressure via a catheter-tip micromanometer was performed in 12 cases with past history of Kawasaki disease. Heart rates were increased in gradations of 10 beats from rest to 180 beat/min, or to the time when A-V block occurred. Diastolic LV pressures and MV flow velocities were plotted manually every 10 msec to establish pressure-velocity relationships at each heart rate. The relationship of LV pressure and MV flow velocity was non-linear, and formed a loop. At rest, this loop showed counterclockwise rotation (CCR) in all cases. By increasing heart rate, rotation changed from CCR to clockwise rotation (CR), except in two cases. With much greater increase in heart rate, CCR reappeared in five cases (second CCR). CCR may indicate that the increment of MV flow is smaller than the fall in LV pressure in the early diastolic filling period, suggesting the existence of inflow resistance. This is thought to be physiologic, and it is suspected that it is produced mainly by the MV and subvalvular structures. CR indicates that the MV flow velocity increases more rapidly than the fall in LV pressure, demonstrating that the resistance to inflow is reduced by increasing heart rate, and the increment of left atrial (LA) driving pressure plays a main role. In a case with simultaneous recording of LA and LV pressures, LA pressure became elevated and the LA-LV pressure gradient increased with an increasing heart rate. This suggests that the increment of LA pressure relates to a decrease of inflow resistance. The second CCR suggests that a resistance is produced beyond a capacity to compensate for elevated LA pressure. It can be speculated that this resistance is related to visco-elasticity of the LV, in addition to the MV and subvalvular structures.

[舒张期左室压力-二尖瓣血流速度曲线:心房起搏引起的心率变化的影响]。
为了评价左室舒张特性,研究了心房起搏引起的心率变化对左室压力-二尖瓣血流速度曲线的影响。对12例有川崎病病史的患者,采用脉冲多普勒超声心动图同时记录中压流速和导管尖端微压计同时记录左室压。心率从静止到180次/分,或到发生A-V传导阻滞时,以10次/分的速度递增。每10毫秒手动绘制左室舒张压和中室血流速度,以建立各心率下的压速关系。低压压力与中压流速呈非线性关系,并形成回路。静止时,该环在所有情况下均显示逆时针旋转(CCR)。除了两种情况外,通过增加心率,旋转从CCR变为顺时针旋转(CR)。5例再次出现CCR(第二次CCR),心率增加幅度更大。CCR可能提示舒张早期充盈期中压流量的增加小于左室压的下降,提示存在流入阻力。这被认为是生理性的,怀疑它主要是由中压和瓣下结构产生的。CR表明中压流速的增加快于左室压的下降,说明心率的增加降低了流入阻力,左房驱动压的增加起主要作用。在同时记录左室和左室压的病例中,左室压随着心率的增加而升高,左室-左室压梯度增大。这说明LA压力的增加与流入阻力的减小有关。第二个CCR表明,电阻的产生超出了补偿LA压力升高的能力。可以推测,这种阻力除了与中压和瓣下结构有关外,还与左室的粘弹性有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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