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

• Published in: Journal of the American College of Cardiology 2000-03, Vol.35 (3), p.771-777
• Main Authors: Lisowski, Lukas A, Verheijen, Paul M, Benatar, Avraham A, Soyeur, Daniel J.G, Stoutenbeek, Phillip, Brenner, Joel I, Kleinman, Charles S, Meijboom, Erik J
• Format: Article
• Language: English
• Subjects: Anti-Arrhythmia Agents - therapeutic use; Atrial Flutter - complications; Atrial Flutter - diagnostic imaging; Atrial Flutter - drug therapy; Biological and medical sciences; Cardiac dysrhythmias; Cardiology. Vascular system; Digoxin - therapeutic use; Echocardiography, Doppler; Electric Countershock; Electrocardiography; Female; Fetal Diseases - diagnostic imaging; Fetal Diseases - drug therapy; Gestational Age; Heart; Heart Rate; Humans; Hydrops Fetalis - etiology; Infant, Newborn; Medical sciences; Pregnancy; Pregnancy Outcome; Retrospective Studies; Sotalol - therapeutic use; Treatment Outcome; Ultrasonography, Prenatal
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(99)00589-6

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.