Appleton C P
Section of Cardiology, Veterans Affairs Hospital, Tucson, Arizona.
J Am Coll Cardiol. 1991 Jan;17(1):227-36. doi: 10.1016/0735-1097(91)90731-n.
To determine the effect of increasing heart rate on mitral flow velocity variables, the time constant of left ventricular isovolumic relaxation and the transmitral pressure gradient, 16 lightly sedated, conscious dogs were studied with Doppler echocardiography during incremental right atrial pacing (n = 16) or the administration of atropine (n = 8) or isoproterenol (n = 8). With increasing heart rate, similar changes were seen with all three interventions and included: 1) mitral flow velocity in early diastole and the early diastolic transmitral pressure gradient either changed minimally or did not change; 2) mitral flow velocity at the start of and as a result of atrial contraction progressively increased; 3) the "absolute" increase in mitral flow velocity and transmitral pressure gradient at atrial contraction demonstrated a biphasic response, initially decreasing as heart rate increased, but then increasing again when atrial contraction occurred in close proximity (less than 70 ms) to mitral valve opening; 3) mitral flow velocity at atrial contraction did not exceed mitral flow velocity in early diastole until atrial contraction was within 70 ms of mitral valve opening and the two velocity peaks were nearly fused; and 4) the largest transmitral pressure gradient and mitral flow velocity occurred at the fastest heart rates, when left atrial contraction preceded mitral valve opening. Major differences among methods included: 1) variable changes in PR interval (+14.2 +- 8.9 ms with atrial pacing versus -74 +/- 26 ms with isoproterenol at peak heart rate compared with baseline); 2) variable changes in the speed of left ventricular relaxation (-2.8 +/- 2.8 ms with pacing versus -7.6 +/- 2.4 ms with isoproterenol at peak rate); and 3) the heart rate at which equalization of mitral flow velocity in early diastole and mitral flow velocity at atrial contraction velocity occurred (128 +/- 12 beats/min with pacing versus 185 +/- 19 beats/min with isoproterenol). These results show that regardless of method, qualitatively similar changes in mitral flow velocity and transmitral pressure gradient occur as heart rate increases. However, for any given heart rate, mitral flow velocity variables and late diastolic pressure gradient can be markedly different, depending on whether atrial pacing, withdrawal of parasympathetic tone or sympathetic stimulation is the cause of the increase in heart rate. These differences among methods appear most related to their effect on PR interval and to a lesser extent the rate of letf ventricular isovolumic relaxation.(ABSTRACT TRUNCATED AT 400 WORDS)
为了确定心率增加对二尖瓣血流速度变量、左心室等容舒张时间常数和跨二尖瓣压力梯度的影响,对16只轻度镇静、清醒的犬进行了研究,在右心房递增起搏(n = 16)、给予阿托品(n = 8)或异丙肾上腺素(n = 8)期间采用多普勒超声心动图检查。随着心率增加,三种干预措施均出现类似变化,包括:1)舒张早期二尖瓣血流速度和舒张早期跨二尖瓣压力梯度变化极小或无变化;2)心房收缩开始时及心房收缩所致的二尖瓣血流速度逐渐增加;3)心房收缩时二尖瓣血流速度和跨二尖瓣压力梯度的“绝对”增加呈双相反应,起初随心率增加而降低,但当心房收缩发生在距二尖瓣开放很近(小于70毫秒)时又再次增加;3)直到心房收缩发生在距二尖瓣开放70毫秒以内且两个速度峰值几乎融合时,心房收缩时的二尖瓣血流速度才超过舒张早期二尖瓣血流速度;4)当左心房收缩先于二尖瓣开放时,跨二尖瓣压力梯度和二尖瓣血流速度在最快心率时最大。方法之间的主要差异包括:1)PR间期变化不定(与基线相比,心房起搏时心率峰值PR间期增加14.2±8.9毫秒,而异丙肾上腺素时为-74±26毫秒);2)左心室舒张速度变化不定(起搏时心率峰值为-2.8±2.8毫秒,异丙肾上腺素时为-7.6±2.4毫秒);3)舒张早期二尖瓣血流速度与心房收缩时二尖瓣血流速度相等时的心率(起搏时为128±12次/分钟,异丙肾上腺素时为185±19次/分钟)。这些结果表明,无论采用何种方法,随着心率增加,二尖瓣血流速度和跨二尖瓣压力梯度在质量上会出现类似变化。然而,对于任何给定心率,二尖瓣血流速度变量和舒张晚期压力梯度可能会明显不同,这取决于心率增加的原因是心房起搏、副交感神经张力降低还是交感神经刺激。这些方法之间的差异似乎主要与其对PR间期的影响有关,在较小程度上与左心室等容舒张速率有关。(摘要截断于400字)