Takeuchi M, Hanada H, Numata T
Second Department of Internal Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Chest. 1998 Feb;113(2):306-11. doi: 10.1378/chest.113.2.306.
Sinus node deceleration during exercise is a highly specific marker for significant stenosis of the right coronary artery. Prior studies of dobutamine-induced sinus node deceleration have contained relatively few patients, and the purpose of this study was to determine if sinus node deceleration is an accurate marker of right coronary artery disease in a much larger study population.
Dobutamine stress echocardiography was performed in a cohort of patients, and submaximal exercise testing and coronary angiography were performed in most of the patients.
A university hospital.
Dobutamine stress echocardiography was performed in 757 patients, and symptom-limited submaximal treadmill ECG was also performed in 571 of those patients. Sinus node deceleration was defined as a decrease in the heart rate at peak stress compared with that at the previous stage. Coronary angiography was performed in 631 patients, 184 of whom were found to have significant right coronary artery stenosis.
The prevalence of dobutamine-induced sinus node deceleration (54 [7%] of 757 patients) was significantly higher than that induced during treadmill ECG (3 [0.5%] of 571 patients; p<0.001). The prevalence of inferior ischemia by echocardiography did not differ between patients with dobutamine-induced sinus node deceleration (26%) and those without (30%). There was also no significant difference in the prevalence of right coronary artery stenosis between the two groups (27% vs 29%). The specificity of dobutamine-induced sinus node deceleration for detecting significant stenosis of the right coronary artery (92%) was higher than that of echocardiography (84%; p<0.00), but the positive predictive value was lower (28% vs 64%; p<0.001).
Although sinus node deceleration during dobutamine stress echocardiography is a relatively more common finding, it does not always accompany significant stenosis in the right coronary artery. The mechanism for its induction is postulated to be vagal activation caused by multiple factors.
运动期间窦房结减速是右冠状动脉严重狭窄的高度特异性标志物。先前关于多巴酚丁胺诱发窦房结减速的研究纳入的患者相对较少，本研究的目的是在更大的研究人群中确定窦房结减速是否为右冠状动脉疾病的准确标志物。
对一组患者进行多巴酚丁胺负荷超声心动图检查，大多数患者还进行了次极量运动试验和冠状动脉造影。
一家大学医院。
对757例患者进行了多巴酚丁胺负荷超声心动图检查，其中571例患者还进行了症状限制下的次极量平板心电图检查。窦房结减速定义为与前一阶段相比，峰值应激时心率下降。对631例患者进行了冠状动脉造影，其中184例被发现有右冠状动脉严重狭窄。
多巴酚丁胺诱发的窦房结减速的发生率（757例患者中的54例[7%]）显著高于平板心电图检查期间诱发窦房结减速的发生率（571例患者中的3例[0.5%]；p<0.001）。多巴酚丁胺诱发窦房结减速的患者（26%）和未诱发的患者（30%）之间，超声心动图显示下壁缺血的发生率没有差异。两组右冠状动脉狭窄的发生率也没有显著差异（27%对29%）。多巴酚丁胺诱发的窦房结减速检测右冠状动脉严重狭窄的特异性（92%）高于超声心动图（84%；p<0.00），但阳性预测值较低（28%对64%；p<0.001）。
尽管多巴酚丁胺负荷超声心动图检查期间窦房结减速是相对更常见的发现，但它并不总是伴随着右冠状动脉的严重狭窄。推测其诱发机制是多种因素引起的迷走神经激活。
