European Journal of Heart Failure 2009 11(2):220-222; doi:10.1093/eurjhf/hfn034
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.
Rapid left ventricular recovery after cabergoline treatment in a patient with peripartum cardiomyopathy
Jonas S.S.G. de Jong1,*,
Kirsten Rietveld2,
Laura T. van Lochem1 and
Berto J. Bouma1
1 Departments of Cardiology, Academic Medical Center, Room B2-238, PO Box 22660, 1100 DD Amsterdam, The Netherlands
2 Department of Gynecology, Academic Medical Center, Amsterdam, The Netherlands
* Corresponding author. Tel: +31 205669111 pager 58073, Fax: +31 847550017, Email: j.s.s.g.dejong{at}amc.nl
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Abstract
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The aetiology of peripartum cardiomyopathy (PPCM) is still largely
unknown. Recent evidence suggests that the breakdown products
from prolactin can induce cardiomyopathy. Prolactin secretion
can be reduced with bromocriptine which had beneficial effects
in a small study. We present a case of a patient with PPCM who
received cabergoline, a strong and long lasting antagonist of
prolactin secretion. Following treatment, her prolactin levels
dropped swiftly. N-terminal pro-BNP levels, which had remained
high up to that point, dropped within 1 day (7006 to 4408 pg/mL).
Echocardiographic left ventricular ejection fraction recovered
from 26% on Day 4 postpartum to 32% and later 47% on Days 2
and 5 after cabergoline treatment. To our knowledge, this is
the first description of a case of PPCM in which cabergoline
was administered.
Key Words: Heart failure • Peripartum cardiomyopathy • Cabergoline treatment
Received July 15, 2008; Revised October 2, 2008; Accepted November 19, 2008
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Case report
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A 27-year-old patient from the Dutch Antilles (of Caribbean
descent) underwent her third Caesarean section at a gestational
age of 39 weeks and 2 days. There was a contraindication for
vaginal delivery as she had given birth twice before through
a Caesarean because of disproportionally large neonates. Her
pregnancy until then had been uncomplicated; there was no record
of hypertension, proteinuria, or placental insufficiency. She
had had some exertional dyspnoea in the weeks before. After
standard intravenous fluid administration before spinal anaesthesia,
the patient developed severe dyspnoea and needed prompt intubation.
During intubation, evident acute pulmonary oedema was present.
No severe drop in blood pressure or anaphylactic reaction was
observed. A healthy girl was born. Total blood loss was 800
mL. Postpartum echocardiography showed severely decreased left
ventricular function with an estimated ejection fraction of
26% (
Figure 1A). The patient was diagnosed with peripartum
cardiomyopathy (PPCM).
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Figure 1 Echocardiography on the fourth day postpartum showed severe left ventricular dysfunction (LVEDD 67 mm, LVESD 58 mm, LVEF 26%). On the sixth day, LVEF started to improve (LVEDD 65 mm, LVESD 54 mm, LVEF 32%, A). Left ventricular function on the ninth day postpartum and after cabergoline treatment improved greatly (LVEDD 61 mm, LVESD 41 mm, LVEF 47%, B).
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Treatment was commenced and consisted of furosemide infusion,
dobutamine, and angiotensin converting enzyme inhibition, which
largely relieved the symptoms of dyspnoea. However, at Day 4
after delivery, the N-terminal pro-BNP (NT-proBNP, a serum marker
of heart failure) level remained elevated. The patient complained
of breast tenderness due to milk engorgement as she was not
breastfeeding. The gynaecologist advised a one-off cabergoline
treatment to facilitate ablactation. A single 1 mg dose of cabergoline
was administered on Day 4 postpartum. NT-proBNP and prolactin
levels were measured before and after cabergoline treatment.
As expected, a sharp drop in prolactin levels was observed,
beyond the natural course postpartum.
1 In accordance with previous
findings during bromocriptine treatment,
2 a drop in NT-proBNP
was also observed (
Figure 2). The patient recovered well.
Nine days postpartum, echocardiography showed recovery of left
ventricular function with some remaining left ventricular dilatation
(
Figure 1B). The patient was discharged. NT-proBNP level
was normal (74 pg/mL) 1 month postpartum.
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Discussion
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Peripartum cardiomyopathy is defined as the onset of cardiac
failure with no identifiable cause in the last month of pregnancy
or within 5 months after delivery, in the absence of heart disease
before the last month of pregnancy.
3 The incidence has been
estimated from 1 per 299 live births in Haiti to 1 per 9861
live births in US Hispanics.
4 Long-term survival has been reported
to be between 85% and 94% at 5 years.
5,6 This is probably due
to the high rate of spontaneous recovery of left ventricular
function in PPCM. However, patients who do not show recovery
of normal or near normal function have a prognosis similar to
other forms of non-ischaemic cardiomyopathy. Mortality in these
patients has been reported to be as high as 41%.
5 Women who
develop PPCM are at increased risk of heart failure during subsequent
pregnancies.
7
The pathophysiology of PPCM is largely unknown. On endomyocardial biopsy, histological evidence of myocarditis has been found in 
50% of patients.8 Increased levels of tumour necrosis factor-
have been measured in PPCM patients. In addition, two small studies have shown improvement of PPCM after administration of pentoxifylline or intravenous immune globulin.5,9,10 Recently, Hilfiker-Kleiner et al.11,12 have published two interesting papers that shed new light on the pathogenesis of PPCM. In one report, they observed that signal transducer and activator of transcription 3 (STAT3) knock-out mice readily develop PPCM. STAT3 has several cardioprotective functions in the heart, including protective effects against oxidative stress. Oxidative stress can result in cleavage of prolactin into an anti-angiogenic 16 kDa form. The authors showed that this 16 kDa form induced cardiomyopathy in these mice. Interestingly, this effect could be abolished by treatment with bromocriptine, a prolactin antagonist. In a subsequent study of 12 women with previous PPCM, who presented with another pregnancy and who were therefore at increased risk of developing PPCM, 6 were treated with bromocriptine. In the treated group, all women survived with preserved LV function, whereas all women in the control group had deteriorated LV function and three women died.11 A recent observational study, found three-fold higher serum prolactin levels in PPCM patients compared with age and gravida matched peripartum controls. Prolactin was also associated with worse outcome in PPCM patients.12 Like bromocriptine, cabergoline is a potent dopamine receptor agonist. It has the advantage that its effect is long-lasting (14–21 days) and a single dosage can often suffice. To our knowledge, we present the first case that suggests a beneficial effect of cabergoline on PPCM. This provides additional proof of the role of prolactin in PPCM, which now warrants further clinical studies.
Conflict of interest: none declared.
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References
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Abstract
Case report