Carluccio Erberto, Biagioli Paolo, Bentivoglio Maurizio, Mariotti Myriam, Politano Massimo, Savino Ketty, Sardone Mariagrazia, Locati Emanuela H, Ambrosio Giuseppe
Division of Cardiology, University of Perugia School of Medicine, Perugia, Italy.
Am J Cardiol. 2003 Feb 15;91(4):385-90. doi: 10.1016/s0002-9149(02)03230-7.
Increased dispersion of the QT interval has been observed during pacing or exercise stress testing in patients with coronary artery disease (CAD). It has not been established whether this phenomenon is a consequence of ischemia. Therefore, we sought to evaluate whether dipyridamole-induced myocardial ischemia, as directly detected by echocardiographic monitoring of regional contractile function, would affect QT dispersion. Twenty-four patients with nonsignificant and 34 patients with significant CAD but no previous myocardial infarction underwent dipyridamole stress echocardiography while not taking medications. QT dispersion was measured on a 12-lead electrocardiogram at baseline and at various times after dipyridamole infusion. Dipyridamole infusion did not influence QT dispersion in patients without CAD. QT dispersion was similarly unaffected in patients with CAD in whom dipyridamole did not induce wall motion abnormalities. In contrast, in patients with positive dipyridamole stress test findings, QT dispersion increased from 60 +/- 17 ms at baseline to 94 +/- 25 ms during peak infusion (p <0.0001), with a time course mirroring that of development of contractile abnormalities. QT dispersion returned to 63 +/- 25 ms upon relief of ischemia by administration of aminophylline. The increase in QT dispersion was significantly related to the extent of contractile dysfunction induced by dipyridamole. Although ST-segment depression occurred in only 40% of patients with positive dipyridamole stress test findings, 88% of such patients had an increase in QT dispersion. Analysis of the receiver-operating characteristic curve showed that a QT dispersion increase of > or =20 ms identified positive findings for dipyridamole stress echocardiography with 68% sensitivity and 91% specificity. Thus, QT dispersion is acutely affected by myocardial ischemia induced by the administration of dipyridamole. Measurement of QT dispersion may improve detection of stress-induced ischemia on surface electrocardiograms.
在冠状动脉疾病（CAD）患者进行起搏或运动负荷试验期间，已观察到QT间期离散度增加。目前尚未确定这种现象是否是缺血的结果。因此，我们试图评估通过超声心动图监测局部收缩功能直接检测到的双嘧达莫诱导的心肌缺血是否会影响QT离散度。24例非显著性CAD患者和34例显著性CAD但既往无心肌梗死的患者在未服用药物的情况下接受了双嘧达莫负荷超声心动图检查。在基线以及双嘧达莫输注后的不同时间，通过12导联心电图测量QT离散度。双嘧达莫输注对无CAD患者的QT离散度无影响。在双嘧达莫未诱发室壁运动异常的CAD患者中，QT离散度同样未受影响。相反，在双嘧达莫负荷试验结果阳性的患者中，QT离散度从基线时的60±17毫秒增加至输注高峰时的94±25毫秒（p<0.0001），其时程与收缩异常的发展过程相似。通过给予氨茶碱缓解缺血后，QT离散度恢复至63±25毫秒。QT离散度的增加与双嘧达莫诱导的收缩功能障碍程度显著相关。虽然在双嘧达莫负荷试验结果阳性的患者中只有40%出现ST段压低，但此类患者中有88%的QT离散度增加。对受试者工作特征曲线的分析表明，QT离散度增加≥20毫秒可识别双嘧达莫负荷超声心动图的阳性结果，敏感性为68%，特异性为91%。因此，QT离散度会受到双嘧达莫诱导的心肌缺血的急性影响。测量QT离散度可能会改善体表心电图上应激性缺血的检测。
