脊髓刺激对起搏诱发的心绞痛的影响及其可能的作用机制。
Effects of spinal cord stimulation in angina pectoris induced by pacing and possible mechanisms of action.
作者信息
Mannheimer C, Eliasson T, Andersson B, Bergh C H, Augustinsson L E, Emanuelsson H, Waagstein F
机构信息
Department of Medicine, Ostra Hospital, Gothenburg, Sweden.
出版信息
BMJ. 1993 Aug 21;307(6902):477-80. doi: 10.1136/bmj.307.6902.477.
OBJECTIVE
To investigate the effects of spinal cord stimulation on myocardial ischaemia, coronary blood flow, and myocardial oxygen consumption in angina pectoris induced by atrial pacing.
DESIGN
The heart was paced to angina during a control phase and treatment with spinal cord stimulation. Blood samples were drawn from a peripheral artery and the coronary sinus.
SETTING
Multidisciplinary pain centre, department of medicine, Ostra Hospital, and Wallenberg Research Laboratory, Sahlgrenska Hospital, Gothenburg, Sweden.
SUBJECTS
Twenty patients with intractable angina pectoris, all with a spinal cord stimulator implanted before the study.
RESULTS
Spinal cord stimulation increased patients' tolerance to pacing (p < 0.001). At the pacing rate comparable to that producing angina during the control recording, myocardial lactate production during control session turned into extraction (p = 0.003) and, on the electrocardiogram, ST segment depression decreased, time to ST depression increased, and time to recovery from ST depression decreased (p = 0.01; p < 0.05, and p < 0.05, respectively). Spinal cord stimulation also reduced coronary sinus blood flow (p = 0.01) and myocardial oxygen consumption (p = 0.02). At the maximum pacing rate during treatment, all patients experienced anginal pain. Myocardial lactate extraction reverted to production (p < 0.01) and the magnitude and duration of ST segment depression increased to the same values as during control pacing, indicating that myocardial ischaemia during treatment with spinal cord stimulation gives rise to anginal pain.
CONCLUSIONS
Spinal cord stimulation has an anti-anginal and anti-ischaemic effect in severe coronary artery disease. These effects seem to be secondary to a decrease in myocardial oxygen consumption. Furthermore, myocardial ischemia during treatment gives rise to anginal pain. Thus, spinal cord stimulation does not deprive the patient of a warning signal.
目的
研究脊髓刺激对心房起搏诱发的心绞痛患者心肌缺血、冠状动脉血流及心肌耗氧量的影响。
设计
在对照期和脊髓刺激治疗期间，将心脏起搏至诱发心绞痛状态。从外周动脉和冠状窦采集血样。
地点
瑞典哥德堡市奥斯特拉医院医学部多学科疼痛中心及萨尔格伦斯卡医院瓦伦贝格研究实验室。
研究对象
20例顽固性心绞痛患者，均在研究前植入了脊髓刺激器。
结果
脊髓刺激提高了患者对起搏的耐受性（p<0.001）。在与对照记录期间诱发心绞痛的起搏频率相当的情况下，对照期心肌乳酸生成转变为摄取（p=0.003），且心电图上ST段压低程度降低、ST段压低时间延长、ST段压低恢复时间缩短（分别为p=0.01；p<0.05和p<0.05）。脊髓刺激还减少了冠状窦血流（p=0.01）和心肌耗氧量（p=0.02）。在治疗期间的最大起搏频率时，所有患者均出现心绞痛。心肌乳酸摄取又转变为生成（p<0.01），ST段压低的幅度和持续时间增加至与对照起搏时相同的值，表明脊髓刺激治疗期间的心肌缺血会引发心绞痛。
结论
脊髓刺激对严重冠状动脉疾病具有抗心绞痛和抗缺血作用。这些作用似乎继发于心肌耗氧量的降低。此外，治疗期间的心肌缺血会引发心绞痛。因此，脊髓刺激并未使患者失去预警信号。
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