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CLINICAL STUDIES

Atrial flutter in the perinatal age group: diagnosis, management and outcome

Lukas A. Lisowski, MD^*, Paul M. Verheijen, MD^*, Avraham A. Benatar, MD, AFACC, Daniel J. G. Soyeur, MD, Phillip Stoutenbeek, MD^*, Joel I. Brenner, MD, FACC, Charles S. Kleinman, MD, FACC and Erik J. Meijboom, MD, FACC^*

^* Department of Obstetrics and Pediatric Cardiology, University Medical Center, Utrecht, The Netherlands
Department of Pediatric Cardiology, University Hospital, Liege, Belgium
Department of Pediatric Cardiology, University of Maryland Medical Systems, Baltimore, Maryland, USA
Department of Obstetrics/Gynecology and Pediatric Cardiology, Yale University Hospital, New Haven, Connecticut, USA

Manuscript received May 21, 1999; revised manuscript received September 23, 1999, accepted November 10, 1999.

Reprint requests and correspondence: Erik Jan Meijboom, MD, PhD, Division of Pediatric Cardiology, University Medical Center (UMC), KG 01.3190/PO Box 85090, 3508 AB Utrecht, The Netherlands

OBJECTIVES

The aim of this retrospective study was to evaluate perinatal atrial flutter (AF) and the efficacy of maternally administered antiarrhythmic agents, postpartum management and outcome.

BACKGROUND

Perinatal AF is a potentially lethal arrhythmia, and management of this disorder is difficult and controversial.

METHODS

Forty-five patients with documented AF were studied retrospectively.

RESULTS

Atrial flutter was diagnosed prenatally in 44 fetuses and immediately postnatally in 1 neonate. Fetal hydrops was seen in 20 patients; 17 received maternal therapy, 2 were delivered and 1 was not treated because it had a severe nontreatable cardiac malformation. In the nonhydropic group of 24 patients, 18 were treated and the remaining 6 were delivered immediately. In the hydropic group, 10 received single-drug therapy (digoxin or sotalol) and 7 received multidrug therapy. In the nonhydropic group, 13 received a single drug (digoxin or sotalol) and 5 received multiple drugs. One patient with rapid 1:1 atrioventricular conduction (heart rate 480 beats/min) died in utero and another died due to a combination of severe hydrops because of the AF, sotalol medication, stenosis of the venous duct and hypoplastic placenta. Of the 43 live-born infants, 12 were in AF at birth. Electrical cardioversion was successful in eight of nine patients. No recurrences in AF have occurred beyond the neonatal period. Four patients with fetal flutter and hydrops showed significant neurological pathology immediately after birth.

CONCLUSIONS

Fetal AF is a serious and threatening rhythm disorder; particularly when it causes hydrops, it may be associated with fetal death or neurological damage. Treatment is required and primarily aimed at reaching an adequate ventricular rate and preferably conversion to sinus rhythm. Digoxin failed in prevention of recurrence at time of delivery in a quarter of our patients, whereas with sotalol no recurrence of AF has been reported, suggesting that class III agents may be the future therapy. Once fetuses with AF survive without neurological pathology, their future is good and prophylaxis beyond the neonatal period is unnecessary.

Abbreviations and Acronyms   AF = atrial flutter   AV = atrioventricular   CTG = cardiotonography   DCC = direct current cardioversion   HLHS = hypoplastic left heart syndrome   TVAOP = transvenous atrial overdrive pacing

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