Sakai H, Kunichika H, Murata K, Seki K, Katayama K, Hiro T, Miura T, Matsuzaki M
Second Department of Internal Medicine, Yamaguchi University School of Medicine, Japan.
J Am Coll Cardiol. 2001 Jan;37(1):270-7. doi: 10.1016/s0735-1097(00)01060-3.
The objective of this study was to examine the hypothesis that a positive inotropic agent improves left ventricular (LV) filling during left atrial (LA) contraction in the presence of markedly elevated LV filling pressure.
In patients with old myocardial infarction (MI), an increase in the operational LV chamber stiffness reduces LV filling during the LA contraction, resulting from an "afterload mismatch" of the LA booster pump function.
We investigated the effect of dobutamine infusion (3 microg/kg/min) on the LA pump function in the presence of elevated LV filling pressure induced by aortic constriction (Aoc) during acute MI in 10 dogs. Transmitral flow velocity was determined by transesophageal echocardiography, LV pressure by a micromanometer and LV volume by a conductance catheter. We measured the early (E) and late (A) diastolic peak transmitral flow velocities (cm/s) and LV chamber stiffness (deltaP/deltaV: mm Hg/ml; where deltaP is developed pressure and deltaV is the absolute filling volume during LA contraction).
When the deltaP/deltaV was increased by Aoc during MI (from 1.1 +/- 0.8 to 3.1 +/- 2.6 mm Hg/ml, p < 0.01), A decreased significantly (from 30 +/- 5 to 22 +/- 8 cm/s, p < 0.01), and the ratio of E to A increased (from 1.0 +/- 0.3 to 1.4 +/- 0.8, p < 0.05) compared with MI without Aoc, showing the pseudonormal transmitral flow pattern, the so called "LA afterload mismatch." Dobutamine under this condition significantly reduced the deltaP/deltaV (to 1.7 +/- 1.2 mm Hg/ml, p < 0.05), resulting in an increase in A (to 31 +/- 8 cm/s, p < 0.01) and a decrease in E/A (to 1.0 +/- 0.3, p < 0.05), and the transmitral flow became a prolonged relaxation pattern as in MI without Aoc in all dogs. There was an inverse correlation between the deltaP/deltaV and the time-velocity integral of A (r = -0.70, p < 0.01).
Dobutamine improved the afterload mismatch of the LA booster pump function. This effect may have been due to the reduction in LV operational chamber stiffness, resulting in an increase in the LA forward ejection into the LV.
本研究的目的是检验这样一个假设，即在左心室（LV）充盈压显著升高的情况下，一种正性肌力药物可改善左心房（LA）收缩期间的左心室充盈。
在陈旧性心肌梗死（MI）患者中，左心室腔操作硬度增加会降低左心房收缩期间的左心室充盈，这是由于左心房增压泵功能的“后负荷不匹配”所致。
我们在10只犬急性心肌梗死期间，研究了多巴酚丁胺输注（3微克/千克/分钟）对主动脉缩窄（Aoc）诱导的左心室充盈压升高时左心房泵功能的影响。经食管超声心动图测定二尖瓣血流速度，微测压计测定左心室压力，电导导管测定左心室容积。我们测量了舒张早期（E）和晚期（A）二尖瓣血流峰值速度（厘米/秒）以及左心室腔硬度（ΔP/ΔV：毫米汞柱/毫升；其中ΔP是产生的压力，ΔV是左心房收缩期间的绝对充盈容积）。
在心肌梗死期间，当Aoc使ΔP/ΔV增加时（从1.1±0.8增加到3.1±2.6毫米汞柱/毫升，p<0.01），与无Aoc的心肌梗死相比，A显著降低（从30±5降低到22±8厘米/秒，p<0.01），E/A比值增加（从1.0±0.3增加到1.4±0.8，p<0.05），呈现伪正常二尖瓣血流模式，即所谓的“左心房后负荷不匹配”。在此条件下，多巴酚丁胺显著降低了ΔP/ΔV（降至1.7±1.2毫米汞柱/毫升，p<0.05），导致A增加（至31±8厘米/秒，p<0.01），E/A降低（至1.0±0.3，p<0.05），并且所有犬的二尖瓣血流都变为与无Aoc的心肌梗死时一样的延长舒张模式。ΔP/ΔV与A的时间-速度积分之间存在负相关（r=-0.70，p<0.01）。
多巴酚丁胺改善了左心房增压泵功能的后负荷不匹配。这种作用可能是由于左心室操作腔硬度降低，导致左心房向左心室的前向射血增加。
