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首页> 外文期刊>American Journal of Physiology >Role of impaired myocardial relaxation in the production of elevated left ventricular filling pressure.
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Role of impaired myocardial relaxation in the production of elevated left ventricular filling pressure.

机译：心肌舒张受损在左心室充盈压升高中的作用。

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Although present in many patients with heart failure and a normal ejection fraction, the role of isolated impairments in active myocardial relaxation in the genesis of elevated filling pressures is not well characterized. Because of difficulties in determining the effect of prolonged myocardial relaxation in vivo, we used a cardiovascular simulated computer model. The effect of myocardial relaxation, as assessed by tau (exponential time constant of relaxation), on pulmonary vein pressure (PVP) and left ventricular end-diastolic pressure (LVEDP) was investigated over a wide range of tau values (20-100 ms) and heart rate (60-140 beats/min) while keeping end-diastolic volume constant. Cardiac output was recorded over a wide range of tau and heart rate while keeping PVP constant. The effect of systolic intervals was investigated by changing time to end systole at the same heart rate. At a heart rate of 60 beats/min, increases in tau from a baseline to extreme value of 100 ms cause only a minor increase in PVP of 3 mmHg. In contrast, at 120 beats/min, the same increase in tau increases PVP by 23 mmHg. An increase in filling pressures at high heart rates was attributable to incomplete relaxation. The PVP-LVEDP gradient was not constant and increased with increasing tau and heart rate. Prolonged systolic intervals augmented the effects of tau on PVP. Impaired myocardial relaxation is an important determinant of PVP and cardiac output only during rapid heart rate and especially when combined with prolonged systolic intervals. These findings clarify the role of myocardial relaxation in the pathogenesis of elevated filling pressures characteristic of heart failure.
机译：尽管存在于许多患有心力衰竭和射血分数正常的患者中，但在充盈压升高的起源中，孤立性损伤在主动性心肌舒张中的作用尚不十分清楚。由于难以确定体内延长的心肌舒张效果，因此我们使用了心血管模拟计算机模型。通过tau（舒张指数时间常数）评估，在宽范围的tau值（20-100毫秒）内研究了心肌舒张对肺静脉压力（PVP）和左心室舒张末期压力（LVEDP）的影响。和心率（60-140次/分钟），同时保持舒张末期容积恒定。在大范围的tau和心率下记录心脏输出，同时保持PVP恒定。通过改变在相同心率下结束收缩的时间来研究收缩间隔的影响。以60次/分钟的心跳速率，tau从基线增加到100 ms的极值时，只会导致PVP轻微增加3 mmHg。相反，以120次/分钟的速度，tau的相同增加会使PVP增加23 mmHg。高心率时充盈压增加归因于放松不完全。 PVP-LVEDP梯度不是恒定的，并且随着tau和心率的增加而增加。延长的收缩间隔增加了tau对PVP的作用。仅在心律加快时，尤其是与延长的收缩间隔结合时，受损的心肌松弛才是PVP和心输出量的重要决定因素。这些发现阐明了心肌松弛在心力衰竭特征性充盈压升高的发病机理中的作用。

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