Fetal dysrhythmias

Edgar Jaeggi; Nico A. Blom; Tara Bharucha

doi:10.1017/CBO9780511997778.010

Chapter 8.1 - Fetal dysrhythmias

The effects of antiarrhythmic therapy on the immature heart

from Section 2 - Fetal disease

Published online by Cambridge University Press: 05 February 2013

Nico A. Blom and

Edited by

Anthony Johnson and

Mark D. Kilby: Affiliation:
Department of Fetal Medicine, University of Birmingham
Anthony Johnson: Affiliation:
Baylor College of Medicine, Texas
Dick Oepkes: Affiliation:
Department of Obstetrics, Leiden University Medical Center

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Summary

Introduction

Supraventricular tachyarrhythmias (SVT) belong to the common cardiac causes of fetal hydrops and perinatal death [1, 2]. With cross-sectional echocardiography providing the non-invasive means to detect and monitor tachyarrhythmias in utero, the fetus has increasingly become the target of pharmacological treatment to prevent or treat heart failure. Survival in excess of 95% is now possible for fetal SVT when existing recommendations are implemented. These include the principles that the best treatment is one targeted specifically to the disease mechanism, and that the potential benefits of drug administration should outweigh the risks to the fetus and the co-treated mother. Hence, successful antiarrhythmic therapy necessitates a thorough knowledge of fetal-maternal physiology, arrhythmia mechanisms, treatment indications and limitations, pharmacokinetics, and effects of the elected drug. Antiarrhythmic agents affect the generation and/or propagation of the cardiac rhythm by their actions on one or several ion channel currents (channel blocker) and/or the autonomous nervous system (beta-blocker; digoxin; adenosine). The Singh Vaughan Williams (SVW) classification is often used to describe the specific drug actions. Class I agents (e.g. flecainide) block cardiac Na+ channels; class II agents are anti-sympathetic agents (beta-blocker); class III agents (sotalol; amiodarone) affect K+ efflux; and class IV agents (verapamil) inhibit calcium channels. Digoxin and adenosine have actions that were not included in the original SVW classification. The main focus of this chapter will be on five antiarrhythmic agents (digoxin; flecainide; sotalol; amiodarone; adenosine) which, due to their relative safety and efficacy, are considered the foundation of transplacental and/or direct pharmacological therapy of fetal SVT.

Keywords

sotalol fetal supraventricular tachyarrhythmias drug management digoxin fetal dysrhythmias flecainide pharmacological therapy antiarrhythmic therapy adenosine amiodarone

Type: Chapter
Information: Fetal Therapy
Scientific Basis and Critical Appraisal of Clinical Benefits
, pp. 78 - 86

DOI: https://doi.org/10.1017/CBO9780511997778.010 [Opens in a new window]

Publisher: Cambridge University Press

Print publication year: 2012

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References

Naheed, ZJ, Strasburger, JF, Deal, BJ, Benson, DW Jr, Gidding, SS. Fetal tachycardia: mechanisms and predictors of hydrops fetalis. J Am Coll Cardiol 1996;27(7):1736–40.Google Scholar

Simpson, JM, Milburn, A, Yates, RW, Maxwell, DJ, Sharland, GK. Outcome of intermittent tachyarrhythmias in the fetus. Pediatr Cardiol 1997;18(2):78–82.Google Scholar

Artman, M, Coetzee, W. Developmental regulation of cardiac ion channels. In: Zipes, D, Jalife, J, eds. Cardiac Electrophysiology From Cell to Bedside. Philadelphia, PA, Saunders Elsevier. 2009; 157–68.

Creazzo, T. Functional developmental biology of the myocardium. In: Loewy Kirby, M, ed. Cardiac Development. New York, NY, Oxford University Press. 2007; 53–68.

Friedman, WF. The intrinsic physiologic properties of the developing heart. Prog Cardiovasc Dis 1972;15(1):87–111.Google Scholar

Romero, T, Covell, J, Friedman, WF. A comparison of pressure-volume relations of the fetal, newborn, and adult heart. Am J Physiol 1972;222(5):1285–90.Google Scholar

Schmidt, MR, Kristiansen, SB, White, P, et al. Glucose-insulin infusion improves cardiac function during fetal tachycardia. J Am Coll Cardiol 2004;43(3):445–52.Google Scholar

Vanoli, E, Cerati, D, Pedretti, RF. Autonomic control of heart rate: pharmacological and nonpharmacological modulation. Basic Res Cardiol 1998;93 Suppl 1:133–42.Google Scholar

Brace, RA. Effects of outflow pressure on fetal lymph flow. Am J Obstet Gynecol 1989;160(2):494–7.Google Scholar

Rudolph, A. The fetal circulation and postnatal adaptation. In: Rudolph, A, ed. Congenital Heart Disease of the Heart. Armonk, NY: Future Publishing Company. 2001; 3–44

Schmidt, KG, Ulmer, HE, Silverman, NH, Kleinman, CS, Copel, JA. Perinatal outcome of fetal complete atrioventricular block: a multicenter experience. J Am Coll Cardiol 1991;17(6):1360–6.Google Scholar

Simpson, JM, Sharland, GK. Fetal tachycardias: management and outcome of 127 consecutive cases. Heart 1998;79(6):576–81.Google Scholar

Jaeggi, E, Carvalho, J, De Groot, E, et al. Comparison of transplacental treatment of fetal supraventricular tachyarrhythmias with digoxin, flecainide and sotalol: results of a non-randomized multicenter study. Circulation 2011; 124(16):1747–54.Google Scholar

Jaeggi, E, Fouron, JC, Fournier, A, et al. Ventriculo-atrial time interval measured on M mode echocardiography: a determining element in diagnosis, treatment, and prognosis of fetal supraventricular tachycardia. Heart 1998;79(6):582–7.Google Scholar

Miller, JM, Zipes, DP. Therapy for cardiac arrhythmias. In: Bonow, RO, Mann, DL, Zipes, DP, Libby, P, Braunwald, E, eds. Braunwald;s Heart Disease. A Textbook of Cardiovascular disease, 9th edn. Philadelphia, PA, Elsevier Saunders. 2012; 715.

Parkash, R, Green, MS, Kerr, CR, et al. The association of left atrial size and occurrence of atrial fibrillation: a prospective cohort study from the Canadian Registry of Atrial Fibrillation. Am Heart J 2004;148(4):649–54.Google Scholar

Hansmann, M, Gembruch, U, Bald, R, Manz, M, Redel, DA. Fetal tachyarrhythmias: transplacental and direct treatment of the fetus-a report of 60 cases. Ultrasound Obstet Gynecol 1991;1(3):162–8.Google Scholar

Jaeggi, E, Fouron, JC, Drblik, SP. Fetal atrial flutter: diagnosis, clinical features, treatment, and outcome. J Pediatr 1998;132(2):335–9.Google Scholar

van Engelen, AD, Weijtens, O, Brenner, JI, et al. Management outcome and follow-up of fetal tachycardia. J Am Coll Cardiol 1994;24(5):1371–5.Google Scholar

Newburger, JW, Keane, JF. Intrauterine supraventricular tachycardia. J Pediatr 1979;95(5 Pt 1):780–6.Google Scholar

Ebenroth, ES, Cordes, TM, Darragh, RK. Second-line treatment of fetal supraventricular tachycardia using flecainide acetate. Pediatr Cardiol 2001;22(6):483–7.Google Scholar

Frohn-Mulder, IM, Stewart, PA, Witsenburg, M, et al. The efficacy of flecainide versus digoxin in the management of fetal supraventricular tachycardia. Prenat Diagn 1995;15(13):1297–302.Google Scholar

Kleinman, CS, Copel, JA, Weinstein, EM, Santulli, TV Jr, Hobbins, JC. Treatment of fetal supraventricular tachyarrhythmias. J Clin Ultrasound 1985;13(4):265–73.Google Scholar

Krapp, M, Baschat, AA, Gembruch, U, Geipel, A, Germer, U. Flecainide in the intrauterine treatment of fetal supraventricular tachycardia. Ultrasound Obstet Gynecol 2002;19(2):158–64.Google Scholar

Fouron, JC, Fournier, A, Proulx, F, et al. Management of fetal tachyarrhythmia based on superior vena cava/aorta Doppler flow recordings. Heart 2003;89(10):1211–16.Google Scholar

Jaeggi, E, Tulzer, G. Pharmacological and interventional fetal cardiovascular treatment. In: Anderson, R, Baker, E, Penny, D, et al. eds. Paediatric Cardiology, 3rd edn. Philadelphia, PA, Churchill Livingstone Elsevier. 2010; 199–218.

Parilla, BV, Strasburger, JF, Socol, ML. Fetal supraventricular tachycardia complicated by hydrops fetalis: a role for direct fetal intramuscular therapy. Am J Perinatol 1996;13(8):483–6.Google Scholar

Weiner, CP, Thompson, MI. Direct treatment of fetal supraventricular tachycardia after failed transplacental therapy. Am J Obstet Gynecol 1988;158(3 Pt 1):570–3.Google Scholar

Bourget, P, Pons, JC, Delouis, C, Fermont, L, Frydman, R. Flecainide distribution, transplacental passage, and accumulation in the amniotic fluid during the third trimester of pregnancy. Ann Pharmacother 1994;28(9):1031–4.Google Scholar

Allan, LD, Chita, SK, Sharland, GK, Maxwell, D, Priestley, K. Flecainide in the treatment of fetal tachycardias. Br Heart J 1991;65(1):46–8.Google Scholar

Jouannic, JM, Delahaye, S, Fermont, L, et al. Fetal supraventricular tachycardia: a role for amiodarone as second-line therapy? Prenat Diagn 2003;23(2):152–6.Google Scholar

Hopson, JR, Buxton, AE, Rinkenberger, RL, et al. Safety and utility of flecainide acetate in the routine care of patients with supraventricular tachyarrhythmias: results of a multicenter trial. The Flecainide Supraventricular Tachycardia Study Group. Am J Cardiol 1996;77(3):72A–82A.Google Scholar

Hohnloser, SH, Woosley, RL. Sotalol. N Engl J Med 1994;331(1):31–8.Google Scholar

Peralta, AO, John, RM, Gaasch, WH, et al. The class III antiarrhythmic effect of sotalol exerts a reverse use-dependent positive inotropic effect in the intact canine heart. J Am Coll Cardiol 2000;36(4):1404–10.Google Scholar

Oudijk, MA, Ruskamp, JM, Ververs, FF, et al. Treatment of fetal tachycardia with sotalol: transplacental pharmacokinetics and pharmacodynamics. J Am Coll Cardiol 2003;42(4):765–70.Google Scholar

Oudijk, MA, Michon, MM, Kleinman, CS, et al. Sotalol in the treatment of fetal dysrhythmias. Circulation 2000;101(23):2721–6.Google Scholar

Oudijk, MA, Ruskamp, JM, Ververs, FF, et al. Treatment of fetal tachycardia with sotalol: transplacental pharmacokinetics and pharmacodynamics. J Am Coll Cardiol 2003;42(4):765–70.Google Scholar

Sonesson, SE, Fouron, JC, Wesslen-Eriksson, E, Jaeggi, E, Winberg, P. Foetal supraventricular tachycardia treated with sotalol. Acta Paediatr 1998;87(5):584–7.Google Scholar

Strasburger, JF, Cuneo, BF, Michon, MM, et al. Amiodarone therapy for drug-refractory fetal tachycardia. Circulation 2004;109(3):375–9.Google Scholar

Arnoux, P, Seyral, P, Llurens, M, et al. Amiodarone and digoxin for refractory fetal tachycardia. Am J Cardiol 1987;59(1):166–7.Google Scholar

Gembruch, U, Manz, M, Bald, R, et al. Repeated intravascular treatment with amiodarone in a fetus with refractory supraventricular tachycardia and hydrops fetalis. Am Heart J 1989;118(6):1335–8.Google Scholar

Pezard, PG, Boussion, F, Sentilhes, L, et al. Fetal tachycardia: a role for amiodarone as first- or second-line therapy? Arch Cardiovasc Dis 2008;101(10):619–27.Google Scholar

Bartalena, L, Bogazzi, F, Braverman, LE, Martino, E. Effects of amiodarone administration during pregnancy on neonatal thyroid function and subsequent neurodevelopment. J Endocrinol Invest 2001;24(2):116–30.Google Scholar

Magee, LA, Nulman, I, Rovet, JF, Koren, G. Neurodevelopment after in utero amiodarone exposure. Neurotoxicol Teratol 1999;21(3):261–5.Google Scholar

Vanbesien, J, Casteels, A, Bougatef, A, et al. Transient fetal hypothyroidism due to direct fetal administration of amiodarone for drug resistant fetal tachycardia. Am J Perinatol 2001;18(2):113–16.Google Scholar

Kohl, T, Tercanli, S, Kececioglu, D, Holzgreve, W. Direct fetal administration of adenosine for the termination of incessant supraventricular tachycardia. Obstet Gynecol 1995;85(5 Pt 2):873–4.Google Scholar

Dangel, JH, Roszkowski, T, Bieganowska, K, Kubicka, K, Ganowicz, J. Adenosine triphosphate for cardioversion of supraventricular tachycardia in two hydropic fetuses. Fetal Diagn Ther 2000;15(6):326–30.Google Scholar

Blanch, G, Walkinshaw, SA, Walsh, K. Cardioversion of fetal tachyarrhythmia with adenosine. Lancet 1994;344(8937):1646.Google Scholar

Book contents

Chapter 8.1 - Fetal dysrhythmias

Summary

Keywords

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