Abstract：
BACKGROUND: J waves may be augmented by coronary angiography (CAG) or intracoronary drug administration but the underlying mechanism is unknown.
OBJECTIVE: The effect of intracoronary normal saline (NS) on J waves were investigated.
METHODS: After the standard CAG using iopamidol (IopamiroR Inj), NS was injected into the right coronary artery in 10 patients with and eight patients without J waves at the baseline. The 12-lead ECG was monitored, stored on a computer and retrieved later for measurement of the J wave amplitude before or during the coronary interventions.
RESULTS: J waves in leads II, III and aVF at baseline increased significantly in each lead during the right CAG and NS injection into the right coronary artery. The J wave changes were similar between the two interventions and distinct similar alterations were observed in the QRS complex. We postulated that the ischemic myocardium that was induced during CAG or intracoronary NS administration slowed the conduction velocity of depolarization in the perfusion territory and delayed the timing of J waves to appear. Then, the delayed appearance of J waves would be less opposed by electromotive force from other areas resulting in augmentation.
CONCLUSIONS: J wave augmentation was observed during CAG and intracoronary NS administration. As a mechanism of augmentation, we postulated that contrast media and NS induce myocardial ischemia and delay the timing of J waves to a point of less opposition by electromotive force from other areas.
CONCLUSIONS: J wave augmentation has been reported during intracoronary injection of contrast media or drugs. The present study confirmed that normal saline alone was able to augment J waves. Mechanistically, coronary interventions using anoxic solutions can cause regional myocardial ischemia and reduce the conduction velocity of depolarization. Then, delayed J waves are less opposed by the electromotive force from remote areas which leads to augmentation. When a drug is diluted in normal saline and given intracoronarily, changes in J waves can be due to normal saline. The pathophysiological and clinical significance of J waves augmented during coronary interventions need to be established.
OBJECTIVE: The effect of intracoronary normal saline (NS) on J waves were investigated.
METHODS: After the standard CAG using iopamidol (IopamiroR Inj), NS was injected into the right coronary artery in 10 patients with and eight patients without J waves at the baseline. The 12-lead ECG was monitored, stored on a computer and retrieved later for measurement of the J wave amplitude before or during the coronary interventions.
RESULTS: J waves in leads II, III and aVF at baseline increased significantly in each lead during the right CAG and NS injection into the right coronary artery. The J wave changes were similar between the two interventions and distinct similar alterations were observed in the QRS complex. We postulated that the ischemic myocardium that was induced during CAG or intracoronary NS administration slowed the conduction velocity of depolarization in the perfusion territory and delayed the timing of J waves to appear. Then, the delayed appearance of J waves would be less opposed by electromotive force from other areas resulting in augmentation.
CONCLUSIONS: J wave augmentation was observed during CAG and intracoronary NS administration. As a mechanism of augmentation, we postulated that contrast media and NS induce myocardial ischemia and delay the timing of J waves to a point of less opposition by electromotive force from other areas.
CONCLUSIONS: J wave augmentation has been reported during intracoronary injection of contrast media or drugs. The present study confirmed that normal saline alone was able to augment J waves. Mechanistically, coronary interventions using anoxic solutions can cause regional myocardial ischemia and reduce the conduction velocity of depolarization. Then, delayed J waves are less opposed by the electromotive force from remote areas which leads to augmentation. When a drug is diluted in normal saline and given intracoronarily, changes in J waves can be due to normal saline. The pathophysiological and clinical significance of J waves augmented during coronary interventions need to be established.
摘要：
背景：J波可以通过冠状动脉血管造影（CAG）或冠状动脉内给药而增强，但潜在的机制尚不清楚。
目的：研究冠状动脉内生理盐水（NS）对J波的影响。
方法：使用碘帕醇（IopamiroRInj）进行标准CAG后，基线时，10例患者和8例无J波患者的右冠状动脉注射NS。监测12导联心电图,存储在计算机上，然后在冠状动脉介入治疗之前或期间检索J波振幅的测量。
结果：导联II中的J波，在右CAG和NS注射到右冠状动脉期间，基线时的III和aVF在每个导联中均显着增加。两种干预措施之间的J波变化相似，并且在QRS波群中观察到明显相似的变化。我们推测，在CAG或冠状动脉内NS给药过程中诱发的缺血心肌减慢了灌注区域去极化的传导速度，并延迟了J波出现的时间。然后，J波的延迟出现将较少与来自其他区域的电动势相反，从而导致增强。
结论：在CAG和冠状动脉内NS给药期间观察到J波增强。作为一种增强机制，我们假设造影剂和NS会引起心肌缺血，并将J波的时间延迟到其他区域电动势的相反程度。
结论：已经报道了冠状动脉内注射造影剂或药物时的J波增强。本研究证实，单独的生理盐水能够增强J波。机械上,使用缺氧溶液的冠状动脉介入治疗可引起局部心肌缺血并降低去极化的传导速度。然后，延迟的J波较少受到来自偏远地区的电动势的反对，从而导致增强。当药物在生理盐水中稀释并在冠状动脉内给药时，J波的变化可能是由于生理盐水引起的。需要建立在冠状动脉介入治疗过程中增强的J波的病理生理和临床意义。
目的：研究冠状动脉内生理盐水（NS）对J波的影响。
方法：使用碘帕醇（IopamiroRInj）进行标准CAG后，基线时，10例患者和8例无J波患者的右冠状动脉注射NS。监测12导联心电图,存储在计算机上，然后在冠状动脉介入治疗之前或期间检索J波振幅的测量。
结果：导联II中的J波，在右CAG和NS注射到右冠状动脉期间，基线时的III和aVF在每个导联中均显着增加。两种干预措施之间的J波变化相似，并且在QRS波群中观察到明显相似的变化。我们推测，在CAG或冠状动脉内NS给药过程中诱发的缺血心肌减慢了灌注区域去极化的传导速度，并延迟了J波出现的时间。然后，J波的延迟出现将较少与来自其他区域的电动势相反，从而导致增强。
结论：在CAG和冠状动脉内NS给药期间观察到J波增强。作为一种增强机制，我们假设造影剂和NS会引起心肌缺血，并将J波的时间延迟到其他区域电动势的相反程度。
结论：已经报道了冠状动脉内注射造影剂或药物时的J波增强。本研究证实，单独的生理盐水能够增强J波。机械上,使用缺氧溶液的冠状动脉介入治疗可引起局部心肌缺血并降低去极化的传导速度。然后，延迟的J波较少受到来自偏远地区的电动势的反对，从而导致增强。当药物在生理盐水中稀释并在冠状动脉内给药时，J波的变化可能是由于生理盐水引起的。需要建立在冠状动脉介入治疗过程中增强的J波的病理生理和临床意义。
