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Table 2

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Comparison of perinatal outcome

Perinatal outcome

Apgar score < 7 at 1 min


Apgar score < 7 at 5 min
Hyperbilirubinemia
NICU admission
IVH#
Septicemia
RDS##
Neonatal death

Nifedipine

Ritodrine

2
0
4
2
1
1
0
1

5.7

11.4
5.6
2.8
2.8

2.8

12
3
8
6
1
5
1
2

34.2
8.5
22.9
17.1
2.8
14.2
2.8
5.6

Neonatal Intensive Care Unit.


Intraventricular Hemorrhage.
##
Respiratory Distress Syndrome.
#

Eight neonates in ritodrine group and 4 in nifedipine group had


hyperbilirubinemia. These observations were not statistically
significant.

Thirty (85.7%) subjects on ritodrine completed therapy, 3


(8.6%) had intolerable side-effects and 5 (14.3%) had failure to
arrest progress of labor. No nifedipine-treated woman had side
effects of such severity as to warrant discontinuation of
treatment. Thus, nifedipine was found to have better tocolytic
efficacy and tolerability compared to ritodrine. The limitation
of this study is that this was a randomized non-controlled trial
and therefore the possibility of a selection bias cannot be ruled
out.

References
[1] Sirohiwal D, Sachan A, Bano A, Gulati N. Evaluation of ritodrine
for tocolysis in preterm labor. J Obstet Gynaecol India 2001;51:
667.
[2] King JF. Tocolysis for preterm labor using Nifedipine. Aust N Z J
Obstet Gynaecol 2003;43:1928.
[3] Arias F, editor. Practical Guide to High Risk Pregnancy and
Delivery. 2nd edition. New Delhi: Elsevier India Private Ltd;
2004. p. 7195.

Nifedipine-associated pulmonary complications


in pregnancy
A.H. Nassar , G. Ghazeeri, I.M. Usta
Department of Obstetrics and Gynecology, American University of Beirut Medical Center, Beirut, Lebanon
Received 21 December 2006; received in revised form 29 January 2007; accepted 31 January 2007

KEYWORDS
Nifedipine;
Tocolysis;
Rupture of membranes;
Pulmonary edema

Pulmonary edema (PE) is a known side effect of tocolytic agents


[1]. Recently, the first case of PE associated with oral nifedipine
(Adalat, Bayer, Germany) was reported [2]. Two cases are added;
one is a twin gestation who presented at 316/7 weeks in labor with
ruptured membranes (ROM). Forty hours after starting betamethasone, antibiotics and 40-mg nifedipine every 6 h, she developed
dyspnea. Arterial blood gases (ABG) revealed PaO2 = 52 mm Hg and
saturation= 88%. Bilateral crackles were detected. Chest X-ray
revealed mild haziness over the left lower lobe; nifedipine was
Corresponding author. Department of Obstetrics and Gynecology,
American University of Beirut Medical Center, PO Box: 113-6044/B36,
Beirut, Lebanon. Tel.: +961 1 350000; fax: +961 1 370829.
E-mail address: an21@aub.edu.lb (A.H. Nassar).
doi:10.1016/j.ijgo.2007.01.011

discontinued. Oxygen facemask and 3 doses of 20-mg furosemide


(Lasix; Sanofi-Aventis, U.S.A.) resulted in mild improvement. One
episode of 38.3 C temperature was recorded 8 h after
discontinuing nifedipine, so a cesarean delivery was performed.
The second patient presented at 275/7 weeks in labor. She received
betamethasone, penicillin, and 40-mg nifedipine every 6 h. Twenty
hours later, she had ROM and a temperature of 38 C. On day 3,
contractions intensified; nifedipine was discontinued and MgSO4
was given for 3 h. Three hours later, she developed cough and
dyspnea. Bilateral fine crackles were noted. Mg level was 5.7 mg/
dl. ABG revealed PaO2 = 45 mm Hg and saturation = 81%. Chest X-ray
revealed congestion. Duplex scan of the lower extremities was
negative. She received 5 doses of 40-mg furosemide but saturation
remained between 77 and 84% despite oxygen nasal-cannula and
therapeutic heparin. A cesarean delivery was done. Postoperative
chest X-ray suggested hilar pneumonia. Saturation improved on day
2 postoperatively.
Similar to the previously reported case [2], both patients
received steroids, hydration and had ROM. In a study conducted
at the Department of Obstetrics and Gynecology of the American
University of Beirut Medical Center to compare the efficacy of 2
dose-regimens of tocolytic nifedipine, none of the 76 patients

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recruited so far developed PE knowing that ROM and multiple
gestations are exclusion criteria.
The observed clinical symptoms were out of proportion with the
chest X-ray findings. These symptoms might be secondary to some
form of chemical irritation to the lungs which makes them prone to
develop PE particularly after excessive hydration. The second case
had possible pneumonia which might have rendered the lungs
vulnerable to the possible nifedipine-inflicted injury. The
contribution of MgSO4 to the clinical picture cannot be quantified
but is probably marginal in view of the therapeutic Mg level.
In conclusion, nifedipine should be used with caution in the
context of preterm labor and rupture of membranes, considering

149
that most of these patients are candidates for corticosteroids and
generous hydration.

References
[1] King JF, Flenady VJ, Papatsonis DN, Dekker GA, Carbonne B.
Calcium channel blockers for inhibiting preterm labour. Cochrane
Database Syst Rev 2003(1):CD002255.
[2] Abbas OM, Nassar AH, Kanj NA, Usta IM. Acute pulmonary edema
during tocolytic therapy with nifedipine. Am J Obstet Gynecol
2006;195:e34.

Viral infection as a possible trigger for the


development of peripartum cardiomyopathy
J.D. Fett
Department of Adult Medicine, Hital Albert Schweitzer, Deschapelles, Haiti, USA
Received 20 December 2006; received in revised form 27 January 2007; accepted 31 January 2007

KEYWORDS
Heart failure;
Peripartum
cardiomyopathy;
Virus;
Pregnancy

The etiology of peripartum cardiomyopathy (PPCM) is unknown.


One hypothesis suggests that viral antigens trigger a process that
includes immune system dysfunction and eventually leads to a
dilated cardiomyopathy and heart failure [1]. It is unknown if
PPCM represents an entirely distinct entity or is a variant of
idiopathic dilated cardiomyopathy, with the unique feature
being the peripartum association.
Although myocarditis and inflammatory cardiomyopathy
have often been found in PPCM patients, only the study of
Bultmann et al. [2] has identified viral genomes in cardiac tissue
of PPCM patients by polymerase chain reaction (PCR) testing.
PPCM patients who were viral-positive had histological evidence
of a cardiac interstitial inflammatory process while control
patients who were viral positive did not. Viruses identified in 8
out of 26 PPCM patients (30.8%) included Epstein-Barr virus,
human cytomegalovirus, human herpes virus 6, and parvovirus
B19.
c/o 611 Sumner Ave., Aberdeen, WA 98520-3343, USA.
E-mail address: fett.sprunger@comcast.net.
doi:10.1016/j.ijgo.2007.01.012

By contrast, Lamparter et al. [3] reported finding no evidence


of viral infection in snap-frozen tissue from 7 PPCM patients
undergoing left ventricular endomyocardial biopsy within 48 h of
diagnosis. Their patients had PCR testing for adenovirus,
coxsackievirus B, influenza virus A, cytomegalovirus, EpsteinBarr virus, herpes simplex virus 1 + 2, human herpes virus 6, and
parvovirus B19.
All other published reports linking the possibility of a viral
etiology of PPCM present indirect evidence only since they
involve findings in non-PPCM patients with myocarditis or
inflammatory cardiomyopathy and/or dilated cardiomyopathy.
Kuhl et al. [4] in a study of 172 consecutive viral-positive patients
with myocarditis and/or dilated cardiomyopathy identified
viruses by PCR testing that included adenovirus (8.1%), enterovirus (32.6%), human herpesvirus 6 (10.5%), parvovirus B19
(36.6%), and dual infection with human herpesvirus 6 + parvovirus
B19 (12.2%). Importantly, that study also confirmed that viral
clearance as assessed by repeat biopsy was associated with
improvement regardless of the type of virus, while viral
persistence was associated with progressive impairment of left
ventricular systolic function.
These studies leave little doubt that viral infection plays an
important role in the pathophysiology of some forms of dilated
cardiomyopathy. However, definitive answers about the role of
viral infection in PPCM will require more endomyocardial
biopsies with PCR testing. The importance and justification for
doing such testing exist particularly for those PPCM patients who
are not experiencing improvement in the early weeks and months
following diagnosis, since emerging new antiviral and

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