Reversible Atrioventricular Block and Junctional Ectopic Tachycardia in Coxsackievirus B3-Induced Fetal–Neonatal Myocarditis without Left Ventricular Dysfunction

Takahashi, Hironori; Tsukamoto, Keiko; Takahashi, Satoshi; Nakamura, Tomoo; Ito, Yushi; Kaneko, Masahide; Sago, Haruhiko

doi:10.1055/s-0031-1277102

Cited by 7 publications

(4 citation statements)

References 15 publications

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“…The distribution of the fetal arrhythmia types and the average time for diagnosing (30.4 ± 3.8 weeks) in this study was consistent with the data available: PAC was presented in 29.2% and SVT and AFL in 70.2% of FAs [3,5,9,[52][53][54][55][56][57]. A case series of viral disease during pregnancy and subsequent fetal heart rhythm disturbance described by Hoi-Shan Chan et al, 2001, Savarese et al, 2008, Takahashi et al, 2011, and Dejog et al, 2015 attracted attention to the infectious status of a pregnant woman [58][59][60][61][62][63]. More frequent acute respiratory viral infections (p = 0.025), asymptomatic bacteriuria (p = 0.053), and impaired vaginal microflora (p = 0.002) at the II trimester of pregnancy was found in the FA group compared to the control.…”

Section: Discussionsupporting

confidence: 89%

Transplacental Therapeutic Drug Monitoring in Pregnant Women with Fetal Tachyarrhythmia Using HPLC-MS/MS

Стародубцева

Kindysheva

Potapova

et al. 2023

IJMS

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Fetal arrhythmia develops in 0.1–5% of pregnancies and may cause fetal heart failure and fetal hydrops, thus increasing fetal, neonatal, and infant mortality. The timely initiation of transplacental antiarrhythmic therapy (ART) promotes the conversion of fetal tachycardia to sinus rhythm and the regression of the concomitant non-immune fetal hydrops. The optimal treatment regimen search for the fetus with tachyarrhythmia is still of high value. Polymorphisms of these genes determines the individual features of the drug pharmacokinetics. The aim of this study was to study the pharmacokinetics of transplacental anti-arrhythmic drugs in the fetal therapy of arrhythmias using HPLC-MS/MS, as well as to assess the effect of the multidrug-resistance gene ABCB1 3435C > T polymorphism on the efficacy and maternal/fetal complications of digoxin treatment. The predisposition to a decrease in the bioavailability of the digoxin in patients with a homozygous variant of the CC polymorphism showed a probable association with the development of ART side effects. A pronounced decrease in heart rate in women with the 3435TT allele of the ABCB1 gene was found. The homozygous TT variant in the fetus showed a probable association with an earlier response to ART and rhythm disruptions on the digoxin dosage reduction. high-performance liquid chromatography with tandem mass spectrometry (HPLC-MS/MS) methods for digoxin and sotalol therapeutic drug monitoring in blood plasma, amniotic fluid, and urine were developed. The digoxin and sotalol concentrations were determined in the plasma blood, urine, and amniotic fluid of 30 pregnant women at four time points (from the beginning of the transplacental antiarrhythmic therapy to delivery) and the plasma cord blood of 30 newborns. A high degree of correlation between the level of digoxin and sotalol in maternal and cord blood was found. The ratio of digoxin and sotalol in cord blood to maternal blood was 0.35 (0.27 and 0.46) and 1.0 (0.97 and 1.07), accordingly. The digoxin concentration in the blood of the fetus at the moment of the first rhythm recovery episode, 0.58 (0.46, 0.8) ng/mL, was below the therapeutic interval. This confirms the almost complete transplacental transfer of sotalol and the significant limitation in the case of digoxin. Previously, ABCB1/P-glycoprotein had been shown to limit fetal exposure to drugs. Further studies (including multicenter ones) to clarify the genetic features of the transplacental pharmacokinetics of antiarrhythmic drugs are needed.

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Section: Discussionsupporting

confidence: 89%

Transplacental Therapeutic Drug Monitoring in Pregnant Women with Fetal Tachyarrhythmia Using HPLC-MS/MS

Стародубцева

Kindysheva

Potapova

et al. 2023

IJMS

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“…[11][12][13] In some cases where the etiology was not certain, there are reports that it could be related to viral myocarditis. 14,15 There is an association with other congenital heart defects like ventricular and atrial septal defects. Histologic abnormalities like inflammation, fibrosis, focal degeneration, and fibroelastosis involving the AV node region and BH, division of AV node, left-sided AV node, entrapment, and distortion have been reported.…”

Section: Etiopathophysiology and Mechanismmentioning

confidence: 99%

Junctional ectopic tachycardia in infants and children

Kylat

Samson

2019

Journal of Arrhythmia

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Tachyarrhythmias originating in the atrioventricular (AV) node and AV junction including the bundle of His complex (BH) are called junctional tachycardia (JT) or junctional ectopic tachycardia (JET). Congenital JET (CJET) is a rare arrhythmia that occurs in patients without a preceding cardiac surgery and can be refractory to medical therapy and associated with high morbidity and mortality. CJET has a high rate of morbidity and mortality with death occurring in 35% of cases. JET occurring within 72 hours after cardiac surgery is referred to as postoperative JET (POJET) and caused by direct trauma, ischemic, or stretch injury to the AV conduction tissues during surgical repair of congenital heart defects. Focal junctional tachycardia (FJT) is also known as automatic junctional tachycardia and includes paroxysmal or non‐paroxysmal forms. We discuss a staged approach to therapy with improved pharmacological therapies and the use of catheter‐based therapies.

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“…The congenital form of JET, occurring in the first six months of life, is frequently refractory to antiarrhythmic therapy and historically has relatively high morbidity and mortality. 101 JET has been associated with congenital cardiac tumors, 102 myocarditis, 103 and congenital heart block. 104 In rare cases, infants have been diagnosed with a familial form of JET, and although some family ancestries suggest an autosomaldominant inheritance, the genetic basis for this condition is currently unknown.…”

Section: Junctional Ectopic Tachycardiamentioning

confidence: 99%

PACES/HRS expert consensus statement on the use of catheter ablation in children and patients with congenital heart disease

et al. 2016

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Smaller patients in general weigh less than approximately 15 kg, and larger patients weigh more than approximately 15 kg. þ The precise definition of "medical therapy that is either not effective or associated with intolerable adverse effects" is left up to the practitioner and family to decide. In general, however, the threshold for ineffectiveness and intolerability should be higher in smaller patients. For example, failure or

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Reversible Atrioventricular Block and Junctional Ectopic Tachycardia in Coxsackievirus B3-Induced Fetal–Neonatal Myocarditis without Left Ventricular Dysfunction

Cited by 7 publications

References 15 publications

Transplacental Therapeutic Drug Monitoring in Pregnant Women with Fetal Tachyarrhythmia Using HPLC-MS/MS

Transplacental Therapeutic Drug Monitoring in Pregnant Women with Fetal Tachyarrhythmia Using HPLC-MS/MS

Junctional ectopic tachycardia in infants and children

PACES/HRS expert consensus statement on the use of catheter ablation in children and patients with congenital heart disease

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