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胎儿心动过速:胎儿水肿的机制及预测因素

Fetal tachycardia: mechanisms and predictors of hydrops fetalis.

作者信息

Naheed Z J, Strasburger J F, Deal B J, Benson D W, Gidding S S

机构信息

Department of Pediatrics, Children's Memorial Hospital, Chicago, Illinois 60614, USA.

出版信息

J Am Coll Cardiol. 1996 Jun;27(7):1736-40. doi: 10.1016/0735-1097(96)00054-x.

Abstract

OBJECTIVES

This study had three objectives: 1) to determine the electrophysiologic mechanisms of fetal supraventricular tachycardia at presentation and postnatally; 2) to identify the clinical and electrophysiologic predictors of hydrops fetalis; and 3) to describe the medium-term follow-up (1 to 7 years) of patients with fetal supraventricular tachycardia.

BACKGROUND

Fetal supraventricular tachycardia causes significant fetal and neonatal morbidity and mortality. Prenatal analysis and postnatal confirmation of fetal supraventricular tachycardia mechanisms have been limited.

METHODS

Supraventricular tachycardia mechanisms were evaluated by prenatal Doppler/M-mode echocardiography, immediate neonatal surface electrocardiography and postnatal transesophageal electrophysiologic procedures in 30 consecutive patients presenting with fetal supraventricular tachycardia (17 managed prenatally, 13 first managed postnatally).

RESULTS

The fetal supraventricular tachycardia mechanism was 1:1 atrioventricular conduction in 22 patients and supraventricular tachycardia with atrioventricular block (atrial flutter) in 8. At the postnatal transesophageal electrophysiologic procedure, tachycardia was induced in 27 of 30 patients; atrioventricular reentrant tachycardia in 25 (93%) of 27 and intraatrial reentrant tachycardia in only 2 (7%) of 27. Hydrops was present in 12 of 30 fetuses. Sustained supraventricular tachycardia (> 12 h) and lower gestation at presentation correlated with hydrops (p < 0.02, p < 0.05), but mechanism of tachycardia and heart rate did not. Gestational age at delivery was significantly greater in those who received intrauterine management (39 +/- 1.3 vs. 37 +/- 2.9 weeks, p = 0.04) despite earlier presentation (32.6 vs. 37.1 weeks). Cesarean section deliveries were reduced in the same group (3 of 17 vs. 11 of 13, p = 0.0006).

CONCLUSIONS

Atrioventricular reentrant tachycardia was the predominant mechanism of supraventricular tachycardia in the fetus. There was a high association of supraventricular tachycardia with atrioventricular block in utero and accessory atrioventricular connections. Outcome at 1 to 7 years was excellent regardless of severity of illness at clinical presentation.

摘要

目的

本研究有三个目的:1)确定胎儿室上性心动过速在产前及产后的电生理机制;2)识别胎儿水肿的临床及电生理预测因素;3)描述胎儿室上性心动过速患者的中期随访情况(1至7年)。

背景

胎儿室上性心动过速可导致显著的胎儿及新生儿发病和死亡。胎儿室上性心动过速机制的产前分析及产后确认一直有限。

方法

对30例连续的胎儿室上性心动过速患者(17例产前处理,13例首次产后处理),通过产前多普勒/M型超声心动图、即刻新生儿体表心电图及产后经食管电生理检查评估室上性心动过速机制。

结果

22例患者胎儿室上性心动过速机制为1:1房室传导,8例为伴有房室阻滞的室上性心动过速(心房扑动)。在产后经食管电生理检查中,30例患者中有27例诱发出心动过速;27例中的25例(93%)为房室折返性心动过速,仅2例(7%)为房内折返性心动过速。30例胎儿中有12例出现水肿。持续性室上性心动过速(>12小时)及就诊时孕周较小与水肿相关(p<0.02,p<0.05),但心动过速机制及心率与水肿无关。尽管就诊时孕周较早(32.6周对37.1周),接受宫内处理的患者分娩时孕周显著更大(39±1.3周对37±2.9周,p=0.04)。同一组剖宫产分娩率降低(17例中的3例对13例中的11例,p=0.0006)。

结论

房室折返性心动过速是胎儿室上性心动过速的主要机制。胎儿期室上性心动过速与宫内房室阻滞及房室旁道高度相关。无论临床表现时疾病的严重程度如何,1至7年的预后均良好。

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