Weissman N J, Rose G A, Foster G P, Picard M H
Division of Cardiology, Georgetown University Medical Center, Washington, D.C. 20007, USA.
J Am Coll Cardiol. 1997 Mar 1;29(3):526-30. doi: 10.1016/s0735-1097(96)00558-x.
This study sought to test whether the physiologic advantage of a prolonged dobutamine stage during stress echocardiography can be effectively combined with a clinically practical infusion protocol.
Dobutamine has a half-life of 2 min and requires up to 10 min to achieve steady state. Despite these known pharmacodynamics, dobutamine stress echocardiography is routinely performed by advancing doses at 3-min intervals. Canine studies have shown that dobutamine stress echocardiography end points will occur at a lower dose if each stage is prolonged, but these findings have yet to be used in the clinical setting.
The standard 3-min dobutamine dose stage during stress echocardiography was modified by extending the peak dose (40 micrograms/kg body weight per min) for an additional 2 min. Consecutive patients underwent this modified protocol to test whether the requirement for atropine could be reduced. According to this modified protocol, if a dobutamine stress echocardiographic end point (85% of maximal predicted heart rate, new wall motion abnormalities, hypotension, arrhythmia or intolerable symptoms) was not reached at 3 min of the peak dose, this dose was prolonged for an additional 2 min. If a doubtamine stress echocardiographic end point was still not attained, atropine (up to 1.0 mg intravenously) was administered.
The study included 84 patients, 22 of whom (26.2%) achieved a dobutamine stress echocardiographic end point using the standard 3-min stage. Of the 62 patients who did not reach an end point in the initial 3 min of peak dobutamine dose, the additional 2 min of dobutamine increased heart rate (from 99.6 +/- 23.8 to 107.2 +/- 23.2 beats/min, p < 0.01) and allowed 20 patients (32.3%, p < 0.01) to attain an end point. Of the remaining 42 patients, 23 never achieved a stress echocardiographic end point, despite 1.0 mg of atropine. One patient developed supraventricular tachycardia during the additional 2 min of dobutamine, and one developed nonsustained ventricular tachycardia after receiving atropine.
These data demonstrate that a significant number of patients (32%) who do not reach a dobutamine stress echocardiographic end point with the standard protocol can safely attain an end point solely by extending the duration of the peak dose. Adoption of this strategy may reduce the need for supplemental atropine and its potential adverse effects.
本研究旨在测试在负荷超声心动图检查中延长多巴酚丁胺阶段的生理优势是否能与临床实用的输注方案有效结合。
多巴酚丁胺半衰期为2分钟，达到稳态需要长达10分钟。尽管有这些已知的药效学特点，但多巴酚丁胺负荷超声心动图检查通常仍按3分钟间隔递增剂量进行。犬类研究表明，如果每个阶段延长，多巴酚丁胺负荷超声心动图检查终点将在较低剂量时出现，但这些发现尚未应用于临床环境。
在负荷超声心动图检查中，通过将峰值剂量（40微克/千克体重每分钟）再延长2分钟，对标准的3分钟多巴酚丁胺剂量阶段进行了修改。连续的患者接受了这种修改后的方案，以测试是否可以减少对阿托品的需求。根据这个修改后的方案，如果在峰值剂量3分钟时未达到多巴酚丁胺负荷超声心动图检查终点（最大预测心率的85%、新的室壁运动异常、低血压、心律失常或无法耐受的症状），则将该剂量再延长2分钟。如果仍未达到多巴酚丁胺负荷超声心动图检查终点，则给予阿托品（静脉注射剂量最高可达1.0毫克）。
该研究纳入了84例患者，其中22例（26.2%）使用标准的3分钟阶段达到了多巴酚丁胺负荷超声心动图检查终点。在62例在多巴酚丁胺峰值剂量初始3分钟内未达到终点的患者中，额外2分钟的多巴酚丁胺增加了心率（从99.6±23.8次/分钟增至107.2±23.2次/分钟，p<0.01），并使20例患者（32.3%，p<0.01）达到了终点。在其余42例患者中，23例尽管使用了1.0毫克阿托品，但从未达到负荷超声心动图检查终点。1例患者在多巴酚丁胺额外2分钟期间发生了室上性心动过速，1例在接受阿托品后发生了非持续性室性心动过速。
这些数据表明，相当一部分（32%）使用标准方案未达到多巴酚丁胺负荷超声心动图检查终点的患者，仅通过延长峰值剂量的持续时间就可以安全地达到终点。采用这种策略可能会减少对补充阿托品的需求及其潜在的不良反应。
