Barnes E, Baker C S, Dutka D P, Rimoldi O, Rinaldi C A, Nihoyannopoulos P, Camici P G, Hall R J
Department of Cardiology, Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN, UK.
Heart. 2000 Mar;83(3):283-9. doi: 10.1136/heart.83.3.283.
To determine whether pharmacological stress leads to prolonged but reversible left ventricular dysfunction in patients with coronary artery disease, similar to that seen after exercise.
A randomised crossover study of recovery time of systolic and diastolic left ventricular function after exercise and dobutamine induced ischaemia.
10 patients with stable angina, angiographically proven coronary artery disease, and normal left ventricular function.
Treadmill exercise and dobutamine stress were performed on different days. Quantitative assessment of systolic and diastolic left ventricular function was performed using transthoracic echocardiography at baseline and at regular intervals after each test.
Both forms of stress led to prolonged but reversible systolic and diastolic dysfunction. There was no difference in the maximum double product (p = 0.53) or ST depression (p = 0.63) with either form of stress. After exercise, ejection fraction was reduced at 15 and 30 minutes compared with baseline (mean (SEM), -5.6 (1.5)%, p < 0.05; and -6.1 (2.2)%, p < 0. 01), and at 30 and 45 minutes after dobutamine (-10.8 (1.8)% and -5. 5 (1.8)%, both p < 0.01). Regional analysis showed a reduction in the worst affected segment 15 and 30 minutes after exercise (-27.9 (7.2)% and -28.6 (5.7)%, both p < 0.01), and at 30 minutes after dobutamine (-32 (5.3)%, p < 0.01). The isovolumic relaxation period was prolonged 45 minutes after each form of stress (p < 0.05).
In patients with coronary artery disease, dobutamine induced ischaemia results in prolonged reversible left ventricular dysfunction, presumed to be myocardial stunning, similar to that seen after exercise. Dobutamine induced ischaemia could therefore be used to study the pathophysiology of this phenomenon further in patients with coronary artery disease.
确定药物负荷是否会导致冠心病患者出现与运动后类似的、持续时间延长但可逆的左心室功能障碍。
一项关于运动和多巴酚丁胺诱发心肌缺血后左心室收缩和舒张功能恢复时间的随机交叉研究。
10例稳定型心绞痛患者,经血管造影证实患有冠心病,左心室功能正常。
在不同日期进行跑步机运动和多巴酚丁胺负荷试验。在每次试验前的基线水平以及试验后的定期时间点,使用经胸超声心动图对左心室收缩和舒张功能进行定量评估。
两种负荷形式均导致收缩和舒张功能障碍持续时间延长但可逆。两种负荷形式下的最大心率收缩压乘积(p = 0.53)或ST段压低(p = 0.63)均无差异。运动后,与基线相比,射血分数在15分钟和30分钟时降低(平均值(标准误),-5.6(1.5)%,p < 0.05;以及-6.1(2.2)%,p < 0.01),多巴酚丁胺试验后30分钟和45分钟时降低(-10.8(1.8)%和-5.5(1.8)%,均p < 0.01)。区域分析显示,运动后15分钟和30分钟时,受影响最严重节段的功能降低(-27.9(7.2)%和-28.6(5.7)%,均p < 0.01),多巴酚丁胺试验后30分钟时降低(-32(5.3)%,p < 0.01)。每种负荷形式后45分钟等容舒张期均延长(p < 0.05)。
在冠心病患者中,多巴酚丁胺诱发心肌缺血会导致持续时间延长的可逆性左心室功能障碍,推测为心肌顿抑,与运动后所见相似。因此,多巴酚丁胺诱发心肌缺血可用于进一步研究冠心病患者这一现象的病理生理学。