Wagner S, Mohr-Kahaly S, Nixdorff U, Kuntz S, Menzel T, Kölsch B, Meinert R, Meyer J
IL Medizinische Klinik, Johannes-Gutenberg-Universität Mainz.
Z Kardiol. 1997 May;86(5):327-35. doi: 10.1007/s003920050065.
Dobutamine stress echocardiography (DSE) leads to strong hypercontraction, tachycardia, and peripheral vasodilatation. In previous studies systolic obstruction of the left ventricular outflow tract (LVOT) was observed as a result of these factors. To evaluate left ventricular function and morphology in patients (pts) with induced systolic LVOT obstruction, we used continuous wave (CW) doppler registrations in combination with quantitative 2-D-echocardiography in 100 pts during routinely performed DSE (5-40 micrograms/kg/min). In addition left ventricular wall thickness was measured. Symptoms were registered using a standardised questionnaire and cardiac arrhythmias were counted over a two minute interval at rest and during the maximal heart rate of each patient. During DSE dynamic flow acceleration with late systolic peak velocity above 2 m/second (s) was considered to represent LVOT obstruction in pts with normal flow profiles in the LVOT before infusion of dobutamine. For invasive studies pts were investigated with femoral catheterisation by the method of Judkins. A greater than 50% stenosis was judged to be significant.
Examinations in 73 pts provided data of sufficient quality for echocardiographic and Doppler sonographic evaluations. 39 pts, 26 men, 13 women, mean age 64 +/- 8 years, developed late systolic flow velocities above 2 m/s and therefore formed the obstructive group (grp A). Grp B consisted of 34 pts, 26 men and 8 women, mean age 66 +/- 10 years, who showed normal time velocity integrals during DSE. In 41 pts invasive data provided information concerning the existence and severity of coronary artery disease. There were no significant differences in the increase of heart rate, the product of maximal systolic blood pressure and maximal heart rate or the percentage of pts, who reached their age corrected submaximal heart rate during DSE. Obstructive pts (group A) showed late systolic dynamic acceleration of systolic flow with a mean maximal speed of 315.4 +/- 139.8 cm/s, which peaked 0.12 +/- 0.04 s after the R-wave. From the velocities we calculated a mean pressure gradient of 47.5 +/- 39.7 mm Hg using the modified Bernoulli equation. Group B patients showed lower and earlier maximal speeds with a mean value of 158.2 +/- 37.6 cm/s, 0.09 +/- 0.04 s after the R-wave, corresponding to a pressure gradient of 10.6 +/- 4.9 mm Hg (p < 0.001). Ejection fractions were higher (p < 0.001) before the test in grp A: 68.2 +/- 8% compared to 55.7 +/- 10.4% in B. This difference increased during peak stress: 74.1 +/- 7.7% compared to 59.5 +/- 12.8%. End diastolic (EDVI) and end systolic volume indexes (ESVI) were lower in grp A (p < 0.001). During DSE, the decrease in ESVI was somewhat stronger for pts in grp A. Left ventricular hypertrophy was more often seen with obstruction. Septal thickness was increased in A: 1.45 +/- 0.34 cm compared to 1.13 +/- 0.27 cm in B (p < 0.001). Left ventricular posterior wall measured 1.03 +/- 0.28 cm in A and 0.83 +/- 0.23 cm in B (p < 0.01). 27 pts in grp B and only 9 in grp A had a history of previous myocardial infarction. Showing no difference at rest, wall motion score indexes raised under DSE in both groups and developed significantly higher scores in grp B at peak stress: 1.30 (1.0-1.90) compared to 1.18 (1.0-1.75) in A. We observed typical chest pain more often in grp B. Unspecific symptoms and arrhythmogenic complications were not statistically different, with the exception of ventricular bigeminy which was more often observed in grp B. A decline in the diastolic blood pressure was observed in pts with very severe obstruction (> 3.5 m/s, p < 0.05). Sensitivity of DSE was 84%, specificity 79%. No significant differences between pts with and without obstruction were observed.
Intraventricular obstructions during DSE are often observed in pts with normal systolic function at rest and during peak stress, especially in the case of left ventricular hypertrophy. (ABSTRACT TRU
多巴酚丁胺负荷超声心动图（DSE）可导致强烈的心肌过度收缩、心动过速和外周血管扩张。在以往研究中，观察到这些因素可导致左心室流出道（LVOT）收缩期梗阻。为评估诱发收缩期LVOT梗阻患者的左心室功能和形态，我们在100例患者常规进行DSE（5 - 40微克/千克/分钟）期间，采用连续波（CW）多普勒记录结合二维定量超声心动图进行研究。此外，还测量了左心室壁厚度。使用标准化问卷记录症状，并在静息和每位患者最大心率时的两分钟间隔内统计心律失常情况。在多巴酚丁胺输注前LVOT血流形态正常的患者中，DSE期间动态血流加速且收缩晚期峰值速度超过2米/秒被认为代表LVOT梗阻。对于侵入性研究，采用Judkins法通过股动脉插管对患者进行检查。狭窄大于50%被判定为显著狭窄。
73例患者的检查提供了质量足以进行超声心动图和多普勒超声评估的数据。39例患者（26例男性，13例女性，平均年龄64±8岁）出现收缩晚期血流速度超过2米/秒，因此形成梗阻组（A组）。B组由34例患者组成（26例男性和8例女性，平均年龄66±10岁），他们在DSE期间时间速度积分正常。41例患者的侵入性数据提供了有关冠状动脉疾病存在和严重程度的信息。在心率增加、收缩压最大值与心率最大值的乘积或在DSE期间达到年龄校正次最大心率的患者百分比方面，两组之间无显著差异。梗阻患者（A组）表现出收缩期血流的收缩晚期动态加速，平均最大速度为315.4±139.8厘米/秒，在R波后0.12±0.04秒达到峰值。根据速度，使用改良伯努利方程计算平均压力阶差为47.5±39.7毫米汞柱。B组患者的最大速度较低且出现较早，平均值为158.2±37.6厘米/秒，在R波后0.09±0.04秒，对应压力阶差为10.6±4.9毫米汞柱（p<0.001）。A组在试验前的射血分数较高（p<0.001）：68.2±8%，而B组为55.7±10.4%。这种差异在应激峰值时增大：A组为74.1±7.7%，B组为59.5±12.8%。A组的舒张末期（EDVI）和收缩末期容积指数（ESVI）较低（p<0.001）。在DSE期间，A组患者ESVI的降低更为明显。梗阻患者更常出现左心室肥厚。A组的室间隔厚度增加：1.45±0.34厘米，而B组为1.13±0.27厘米（p<0.001）。A组左心室后壁厚度为1.03±0.28厘米，B组为0.83±0.23厘米（p<0.01）。B组27例患者和A组仅9例患者有心肌梗死病史。两组在静息时无差异，DSE期间两组的室壁运动评分指数均升高，且B组在应激峰值时的评分显著更高：1.30（1.0 - 1.90），而A组为1.18（1.0 - 1.75）。我们在B组更常观察到典型胸痛。除了B组更常观察到室性二联律外，非特异性症状和致心律失常并发症在统计学上无差异。在梗阻非常严重（>3.5米/秒）的患者中观察到舒张压下降（p<0.05）。DSE的敏感性为84%，特异性为79%。有梗阻和无梗阻患者之间未观察到显著差异。
在静息和应激峰值时收缩功能正常的患者中，DSE期间常观察到心室内梗阻，尤其是在左心室肥厚的情况下。（摘要正确）
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