BJOG P 380
BJOG P 380
BJOG P 380
DOI: 1 0 . 1 1 1 1 / j . 1 4 7 1 - 0 5 2 8 . 2 0 0 4 . 0 0 0 9 2 . x
CASE REPORT
CASE REPORT
Discussion
Nifedipine, a calcium channel blocker, has recently been
advocated, with atosiban (an oxytocin antagonist) as a
tocolytic of choice by the RCOG.2 It is an attractive alternative to beta-adrenergic agonists and non-selective cyclooxygenase inhibitors because of comparable effectiveness
and fewer maternal or fetal adverse effects.3 The incidence
of significant pulmonary oedema with beta-adrenergic agonists is estimated at 1:350 1:400 treated patients, with more
than 25 maternal deaths in the literature.4
A meta-analysis has reported that, compared with betaadrenergic agonists, there are fewer interruptions of treatment with nifedipine due to maternal adverse effects and
therapy is more effective in prolonging pregnancy, results
in fewer cases of neonatal respiratory distress syndrome
and fewer transfers to NICU.4 Nifedipine is also advantageous due to a relative lack of influence on A V conduction and maternal cardiac output.5
This case report highlights that nifedipine is nevertheless
not without risk, particularly in a woman with an underlying, albeit asymptomatic and stable, cardiac anomaly. The
increased cardiac demands of pregnancy are well appreciated: hormonally mediated increases in blood volume, red
cell mass and heart rate result in a major increase in cardiac
output6 coupled with increased myocardial oxygen demand. Pre-existing cardiac anomalies may compromise
the ability to meet this demand and may be associated with
cardiac decompensation, particularly in later pregnancy, as
the major increase in cardiac output peaks during the
second trimester and remains constant until term.6
We believe that in this case, the native vulnerability of
her ventricular septal defect with the additional cardiovascular stress of pregnancy potentially compromised her cardiac status. The uninvestigated dyspnea following the first
pregnancy may have indicated borderline decompensation
at that time. In this current pregnancy, the further demands
of corticosteroids of increased extracellular volume, increased systemic vascular resistance and increased cardiac
contractility,7 coupled with the negative inotropic effects of
nifedipine, led to more significant cardiac embarrassment.
The cause of her hypoxia is not clear. Pulmonary embolism, pneumonia, cardiomyopathy, obstructive or restrictive
airways disease and ischaemic heart disease were unlikely
on the basis of history, examination and investigations. The
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close-time relationship between corticosteroids and nifedipine and the development of respiratory distress and the
spontaneous recovery all point towards a drug effect. One
small study suggested that nifedipine raised pulmonary
artery pressures in non-pregnant patients with underlying
lung disease and pulmonary hypertension.8 It is unlikely
that corticosteroid therapy would have contributed, as this
has been associated with a reduction in pulmonary arterial
pressure and pulmonary vascular resistance.9
We alert the reader to the fact that women with cardiovascular disease or any medical condition contraindicating
tocolysis were excluded from the trials evaluating the efficacy and safety of nifedipine use for preterm labour.5,10 12
This case poses an interesting dilemma of assessing the
suitability of a patient for nifedipine with known cardiac
disease even when entirely asymptomatic and stable; we
believe this is a setting for caution. It articulates well the
significant impact of pregnancy itself on the cardiovascular
system, and how sensitive its workings are to the added
insult of a little hole and a few red pills.
References
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10. Glock JL, Morales WJ. Efficacy and safety of nifedipine versus magnesium sulfate in the management of preterm labor: a randomised
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Accepted 12 December 2003