Wang P J, Sosa-Suarez G, Friedman P L
Clinical Electrophysiology Laboratory, Brigham and Women's Hospital, Boston, MA 02115.
Circulation. 1990 Sep;82(3):817-29. doi: 10.1161/01.cir.82.3.817.
The hypothesis that human atrioventricular (AV) nodal function can be modulated selectively with a new technique of AV nodal artery catheterization was tested in eight subjects referred for diagnostic cardiac catheterization or electrophysiological studies. Three patients had no history of arrhythmias. Three patients had supraventricular tachycardia (SVT) due to reentry confined to the AV node (AVNRT). One patient had SVT due to reentry over a concealed AV bypass tract (AVRT-CBT), and one patient had nonsustained ventricular tachycardia. In each subject, sinus cycle length, AH interval, HV interval, AV nodal effective refractory period (AVN-ERP), and Wenckebach paced cycle length were measured in a control state. A flexible infusion catheter was then positioned selectively in the AV nodal artery of each subject. Through this catheter, a constant infusion of 0.1 mg/min procainamide at a flow rate of 0.125 ml/min (n = 1) or 50 micrograms/min acetylcholine at a flow rate of 0.25 ml/min (n = 4) was administered. Electrophysiological parameters were determined again during selective AV nodal artery drug infusion and during infusion of saline at identical rates. Two subjects developed transient AV nodal block during selective AV nodal catheterization alone and did not receive an infusion of drug or saline. A stable position of the AV nodal artery catheter could not be achieved in one other subject, who also received no drug or saline. In the other five subjects, drug infusion caused an increase in AVN-ERP from a control value of 312 +/- 52 msec to a value of 543 +/- 228 msec (p less than 0.05) and an increase in Wenckebach paced cycle length from a control value of 360 +/- 47 msec to a value of 572 +/- 217 msec (p less than 0.05). These parameters were unchanged from control during selective saline infusion. In two patients with AVNRT, drug infusion abolished SVT by causing complete blockade of ventriculoatrial conduction as well as lengthening of anterograde AVN-ERP. In the patient with AVRT-CBT, drug infusion abolished SVT by preventing repetitive anterograde AV conduction. Saline had no effect on SVT inducibility. Selective AV nodal artery catheterization enables AV nodal function to be modulated exclusively. Delivery of ablative agents to the AV node by this technique may be useful in patients with refractory SVT.
采用一种新的房室结动脉导管插入技术能否选择性调节人体房室（AV）结功能这一假说，在8例因诊断性心导管检查或电生理研究而就诊的受试者中进行了验证。3例患者无心律失常病史。3例患者因局限于房室结的折返（房室结折返性心动过速，AVNRT）而发生室上性心动过速（SVT）。1例患者因隐匿性房室旁路通道折返（AVRT-CBT）而发生SVT，1例患者有非持续性室性心动过速。在每例受试者的对照状态下，测量窦性周期长度、AH间期、HV间期、房室结有效不应期（AVN-ERP）和文氏起搏周期长度。然后将一根可弯曲的输液导管选择性地置于每例受试者的房室结动脉中。通过该导管，以0.125 ml/min的流速持续输注0.1 mg/min普鲁卡因胺（n = 1）或以0.25 ml/min的流速持续输注50μg/min乙酰胆碱（n = 4）。在选择性房室结动脉药物输注期间以及以相同流速输注生理盐水期间，再次测定电生理参数。2例受试者在单纯选择性房室结导管插入过程中出现短暂性房室结阻滞，未接受药物或生理盐水输注。另一例受试者无法实现房室结动脉导管的稳定定位，该受试者也未接受药物或生理盐水输注。在其他5例受试者中，药物输注使AVN-ERP从对照值312±52毫秒增加至543±228毫秒（p<0.05），文氏起搏周期长度从对照值360±47毫秒增加至572±217毫秒（p<0.05）。在选择性生理盐水输注期间，这些参数与对照相比无变化。在2例AVNRT患者中，药物输注通过导致室房传导完全阻滞以及延长前传AVN-ERP而终止SVT。在AVRT-CBT患者中，药物输注通过阻止反复的前传房室传导而终止SVT。生理盐水对SVT的诱发无影响。选择性房室结动脉导管插入术能够专门调节房室结功能。通过该技术将消融剂输送至房室结可能对难治性SVT患者有用。
