Peripartum Cardiomyopathy - Treatment and Prognosis

10/27/2017 Peripartum cardiomyopathy: Treatment and prognosis - UpToDate
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Peripartum cardiomyopathy: Treatment and prognosis
Authors: Wendy Tsang, MD, Roberto M Lang, MD

Section Editor: Candice Silversides, MD, MS, FRCPC
Deputy Editor: Susan B Yeon, MD, JD, FACC
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2017. | This topic last updated: Oct 24, 2017.
INTRODUCTION — Peripartum cardiomyopathy (PPCM, also called pregnancy-associated cardiomyopathy) is a

rare cause of heart failure (HF) that affects women late in pregnancy or in the early puerperium [1]. Although
initially described in 1849 [2], it was not recognized as a distinct clinical entity until the 1930s [3]. Earlier terms for
this condition include toxic postpartum HF, Meadows’ syndrome, Zaria syndrome, and postpartum myocardiosis.
Treatment of PPCM is similar to that employed for other types of HF with left ventricular systolic dysfunction.
However, modifications to standard therapy are often necessary to ensure the safety of the mother and the
unborn or breastfeeding child. (See "Management of heart failure during pregnancy", section on 'Management
goals'.)
Etiology, clinical manifestations, and diagnosis of PPCM, critical illness during pregnancy and the peripartum
period, HF during pregnancy, and issues related to pregnancy in women with acquired or congenital heart
disease are discussed separately. (See "Peripartum cardiomyopathy: Etiology, clinical manifestations, and
diagnosis" and "Critical illness during pregnancy and the peripartum period" and "Management of heart failure
during pregnancy" and "Acquired heart disease and pregnancy" and "Pregnancy in women with congenital heart
disease: General principles".)
MANAGEMENT — Treatment of peripartum cardiomyopathy (PPCM) is largely similar to treatment for other
types of heart failure (HF). Additional therapeutic issues for this population may include arrhythmia management,
anticoagulation therapy, mechanical support, and investigational therapies such as bromocriptine [4].
Heart failure treatment — In women with PPCM and HF, the goals of medical therapy are similar to those in
patients with acute and chronic HF with reduced ejection fraction due to other causes. These include:
● Supplemental oxygen and assisted ventilation as needed

● Optimization of preload
● Hemodynamic support with inotropes and vasopressors if required
● Relief of symptoms
● When possible, institute chronic therapies that improve long-term outcomes
Due to the unique issues related to pregnancy and the peripartum period, each therapeutic decision has
additional implications. The treatment of HF in pregnant and breastfeeding patients is discussed in detail
separately. Briefly, women with HF during pregnancy should be treated similarly to other patients with HF.
However, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, angiotensin receptor-
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neprilysin inhibitor, and aldosterone antagonists are to be avoided, as they are contraindicated in pregnancy.
(See "Management of heart failure during pregnancy", section on 'Treatment regimens'.)
For women with peripartum cardiomyopathy who have delivered and are not breastfeeding, acute and chronic
HF are managed using standard therapy. (See "Treatment of acute decompensated heart failure: Components of
therapy" and "Overview of the therapy of heart failure with reduced ejection fraction".)
Arrhythmia management — Arrhythmias are common in patients hospitalized for PPCM [5]. The reported
incidence of ventricular arrhythmias has been variable. A large inpatient database study reported that of 9841
hospitalizations for PPCM, 18.7 percent had an arrhythmia, with ventricular tachycardia occurring in 4.2 percent
and cardiac arrest in 2.2 percent. Much smaller series have reported rates between 20 and 25 percent [6,7].
Atrial fibrillation also occurs commonly and was observed in 3.1 to 11.9 percent of patients with PPCM in various
studies [6,8,9]. Management of arrhythmias during pregnancy is discussed separately. (See "Supraventricular
arrhythmias during pregnancy" and "Ventricular arrhythmias during pregnancy".)
Device therapy — Decisions regarding use of implantable cardioverter defibrillator (ICD) and cardiac
resynchronization therapy in patients with PPCM should include consideration of the natural history of these
diseases, including the potential of recovery of ventricular function [1].
Specific indications for use of ICD therapy have not been established for PPCM [1], since scant evidence on use
of these devices is available in this patient population [10]. Since up to 20 to 60 percent of women with PPCM
have complete recovery of left ventricular ejection fraction (LVEF) to normal by six months to five years (see
'Recovery of left ventricular function' below), ICD placement should generally be deferred at least three months
and possibly even six months following presentation, with the patient receiving optimum medical therapy to
determine whether criteria for placement are present. Whether a wearable defibrillator would prevent sudden
cardiac death in those being monitored for LVEF improvement is untested [7,11]. Furthermore, a wearable
defibrillator is not without its risks and concerns. (See "Primary prevention of sudden cardiac death in heart
failure and cardiomyopathy" and "Secondary prevention of sudden cardiac death in heart failure and
cardiomyopathy" and "Wearable cardioverter-defibrillator", section on 'Newly diagnosed nonischemic
cardiomyopathy'.)
Information on the use of cardiac resynchronization therapy in PPCM is limited, but a limited observational case
series of eight patients suggests that resynchronization in medically optimized patients resulted in improved
systolic function and cardiac remodeling [12]. Cardiac resynchronization therapy should generally be deferred
until at least three months and possibly even six months following presentation, with the patient receiving
optimum medical therapy to determine whether criteria for placement are present. (See "Cardiac
resynchronization therapy in heart failure: Indications".)
Antithrombotic therapy — Patients with PPCM are at high risk for thrombus formation and thromboembolism
due to both the hypercoagulable state of pregnancy and stasis of blood due to severe LV dysfunction [13,14].
However, data are inconclusive on the utility of antithrombotic therapy (antiplatelet therapy or anticoagulation) to
reduce thromboembolic events or mortality in patients with systolic HF who are in sinus rhythm. (See
"Antithrombotic therapy in patients with heart failure", section on 'Role of antithrombotic therapy'.)
For pregnant women who require anticoagulation, anticoagulation decisions and choosing a specific
anticoagulation regimen are challenging due to specific risks during various stages of pregnancy, including the
potential teratogenic effects of warfarin in the first trimester, dosing complexities of the various agents, and
management during labor and delivery. These issues are discussed in detail separately. (See "Use of
anticoagulants during pregnancy and postpartum".)
Our approach to antithrombotic therapy in patients with PPCM is the same as that for other patients with LV
systolic dysfunction (with or without HF). For patients with LV systolic dysfunction (with or without HF) without LV
thrombus or other indications for antithrombotic therapy, we do not recommend antiplatelet or anticoagulant
therapy (see "Antithrombotic therapy in patients with heart failure", section on 'Our approach'). One exception is
for patients with PPCM receiving bromocriptine, as thromboembolic events (including stroke and myocardial
infarction) have been reported as a complication of bromocriptine use [15]. We suggest anticoagulation in
patients with PPCM treated with bromocriptine (which we consider investigational in this setting, as discussed
below), although controlled data are lacking [16]. (See 'Bromocriptine' below.)
Although data are limited, we suggest anticoagulation for patients with PPCM who have acute intracardiac
thrombus or evidence of systemic embolism. This recommendation is consistent with recommendations for
management of acute ventricular thrombus or thromboembolism in patients with HF generally. (See
"Antithrombotic therapy in patients with heart failure", section on 'Role of antithrombotic therapy'.)
Standard guidelines for antithrombotic therapy for atrial fibrillation should be followed in patients with PPCM and
atrial fibrillation, including recommending anticoagulation for patients with PPCM with HF and atrial fibrillation.
(See "Atrial fibrillation: Anticoagulant therapy to prevent embolization".)
Mechanical circulatory support and cardiac transplantation — Mechanical circulatory support (MCS) should
be considered early in patients who are hemodynamically unstable and unresponsive to medical therapy with
maximal inotropic support. A device can be implanted in the acute phase either as a "bridge-to-recovery" with
subsequent weaning as ventricular function improves or as a "bridge-to-bridge" with implantation of a more
durable device if continued circulatory support is required. A "bridge-to-transplantation" approach is rarely
required as the initial approach because a high proportion of PPCM patients will have some recovery of
ventricular function. Thus, a temporary device should always be initially preferred.
In patients with PPCM, a severely depressed baseline LVEF alone should not be considered an indication for
use of aggressive therapies such as MCS and cardiac transplantation. In PPCM, lower baseline LVEF is
associated with lower likelihood of recovery of LVEF with medical management as discussed below. However,
the baseline LVEF does not adequately predict the probability of recovery in individual patients. (See 'Maternal
outcome' below.)
When MCS is indicated, devices that can be used include intra-aortic balloon counter pulsation (IABP),
venoarterial extracorporeal membrane oxygenation (ECMO), and LV assist device (LVAD) [16]. The choice of
which initial device to implant will depend on patient hemodynamics and local availability and expertise.
Venoarterial ECMO has been associated with an increase in prolactin levels, which may be detrimental in PPCM
patients [17]. Some experts have suggested administration of bromocriptine doses up to 10 mg twice daily to
suppress prolactin levels in patients receiving venoarterial ECMO with significantly elevated prolactin levels [18].
However, we do not use of bromocriptine to suppress prolactin levels in patients receiving venoarterial ECMO as
there is little evidence to support this treatment [18].
Outcomes were reported for 1258 women, which included 99 with PPCM, who had received durable mechanical
circulatory support [19]. Women with PPCM who received durable mechanical circulatory support had better
survival than women without PPCM, with two-year survival of 83 percent for the PPCM cohort. These differences
were likely due to the fact that women with PPCM were younger and had fewer comorbidities. However, rates of
recovery of myocardial function were poor at 6 percent in the PPCM group and 2 percent in those without PPCM.
Indications and use of mechanical circulatory support are discussed separately. (See "Short-term mechanical
circulatory assist devices" and "Intermediate- and long-term mechanical circulatory support" and "Practical
management of long-term mechanical circulatory support devices".)
Older studies found that transplantation was performed in up to one-third of women with PPCM [20-22].
Contemporary reports demonstrate that transplantation rates vary from 4 to 23 percent of patients [23-27]. Thus,
women with PPCM and significant LV systolic dysfunction should be managed at a center with transplant
capabilities. (See "Indications and contraindications for cardiac transplantation in adults".)
In addition to the potential maternal and fetal risks related to pregnancy after heart transplantation for any reason
(see "Pregnancy after cardiac transplantation"), women who have been transplanted for PPCM have worse
outcomes compared with other cardiac transplant recipients. The largest series of cardiac transplantation for
PPCM included 485 patients from the UNOS database and found worse long-term survival in patients
transplanted for PPCM compared with all others undergoing transplantation [27]. Women with PPCM who
received a cardiac transplant had higher mortality, higher incidence of rejection, poorer graft survival, and higher
retransplantation rates. Younger patient age, higher allosensitization, higher pretransplant acuity, and increased
rejection rates are all thought to play a role in these poorer outcomes.
Investigational therapy — The following investigational therapies are not recommended for PPCM since the
efficacy and safety of these approaches have not been established.
Bromocriptine — The role of bromocriptine therapy in PPCM is controversial. While preliminary data have
suggested a benefit from bromocriptine in patients with PPCM, further trials are needed to establish safety and
efficacy. Until additional data are available, we suggest not routinely using bromocriptine for patients with PPCM.
Some other experts advocate using bromocriptine routinely in this setting.
This treatment strategy is based upon an experimental observation of prevention of PPCM in mice via prolactin
blockade with bromocriptine [28]. A small randomized pilot study and several observational reports have
suggested a beneficial response to bromocriptine therapy in patients with PPCM [4,29-32]. However, available
data are insufficient to recommend routine use of bromocriptine treatment for PPCM. Of note, the drug stops the
production of breast milk making breastfeeding impossible.
In a randomized open-label study performed in South Africa, 20 women with newly diagnosed PPCM were
randomly assigned to receive either standard care plus bromocriptine (2.5 mg twice daily for two weeks followed
by 2.5 mg daily for six weeks) or standard care alone [4]. The 10 women receiving bromocriptine demonstrated
significantly greater improvement in LVEF as compared with the 10 women receiving standard care only (27 to
58 percent versus 27 to 36 percent). One patient in the bromocriptine group died as compared with four in the
standard care group. Fewer patients in the bromocriptine group reached the composite end point of death, New
York Heart Association functional class III or IV HF (table 1), or LVEF <35 percent at six months, as compared
with patients in the standard care group (one versus eight). The generalizability of these results is unclear given
the small sample size, the higher than expected mortality rate in the standard care group, and differences in
characteristics of PPCM in patients in Africa as compared with those elsewhere [33].
A subsequent multicenter trial performed in Germany enrolled 63 women with PPCM with LVEF ≤35 percent who
were randomly assigned to short-term bromocriptine (one week of 2.5 mg daily) or long-term bromocriptine (eight
weeks: 5 mg for two weeks followed by 2.5 mg for six weeks) in addition to standard HF therapy [34].
Improvement in LVEF as assessed by cardiac magnetic resonance imaging at six months was similar in the two
groups (28 to 49 percent in the one-week group and 27 to 51 percent in the eight-week group). The frequency of
full recovery (LVEF ≥50 percent) was nominally but not significantly higher in the eight-week group compared
with the one-week group (68 versus 52 percent). None of the patients required heart transplantation, left
ventricular assist devices (LVAD), or died during the study period. Thus, the patients in this trial had better
outcomes than observed in prior series of PPCM, but a placebo control group was not included in the study. (See
'Maternal outcome' below.)
As noted above, we suggest anticoagulation in patients with PPCM treated with bromocriptine (when this
investigational therapy is used) given the risk of thromboembolic complications. (See 'Antithrombotic therapy'
above.)
Immunosuppressive agents — Immunosuppressive therapy is not recommended for PPCM [1]. Although
immunosuppressive therapy has been reported in patients with PPCM and biopsy-proven myocarditis in an
observational study [20], its efficacy is unclear. Empiric immunosuppression, in the absence of evidence of a
responsive form of myocarditis (eg, giant cell myocarditis), is not recommended since most reported cases have
nonspecific biopsy findings [35]. These drugs often have significant side effects, and studies in other forms of
myocarditis have not shown clear benefit from immunosuppressive therapy [36]. (See "Treatment and prognosis
of myocarditis in adults", section on 'Immunosuppressive therapy'.)
Intravenous immune globulin — Intravenous immune globulin (IVIG) has been tried in patients with
myocarditis or recent-onset dilated cardiomyopathy with no clear evidence of clinical benefit. A retrospective
study of six women with PPCM treated with IVIG and 11 historical controls found a greater increase in LVEF at
six months in patients treated with IVIG compared with controls (26 versus 13 percent) [37]. However, the
efficacy of this approach has not been confirmed in this setting or other types of myocarditis. (See "Treatment
and prognosis of myocarditis in adults", section on 'Intravenous immune globulin'.)
DELIVERY — Limited data are available to guide the timing and mode of delivery in peripartum cardiomyopathy
(PPCM). Decisions regarding timing and mode of delivery should be based on combined input from the
cardiology, obstetrics, anesthesiology, and neonatology services [1]. In this regard, multidisciplinary conferences
are often useful.
In women with PPCM with advanced heart failure (HF), we suggest prompt delivery for maternal cardiovascular
indications. Urgent delivery may be required in women with advanced HF with hemodynamic instability [1].
Planned cesarean delivery is preferred for women with advanced HF requiring inotropic therapy or mechanical
circulatory support [1,38].
For other women, the risks and benefits of early delivery should be considered and discussed with the patient.
The 2010 European Society of Cardiology working group statement advised that early delivery is not required if
the maternal and fetal conditions are stable [1]. However, patient-specific issues, including gestational age,
cervical status, fetal status, and the potential cardiovascular impact of continuing pregnancy should be
considered in timing delivery. As for women with other types of cardiac conditions, cesarean delivery in patients
with stable cardiovascular status is generally reserved for obstetrical indications (eg, failure of progression of
labor, placenta previa, fetal intolerance of labor). (See "Acquired heart disease and pregnancy", section on 'Mode
and timing of delivery'.)
BREASTFEEDING — Some experts, including the 2010 European Society of Cardiology working group, suggest
that breastfeeding be avoided because of the potential effects of prolactin subfragments [39] (see "Peripartum
cardiomyopathy: Etiology, clinical manifestations, and diagnosis", section on 'Role of prolactin'). However, one
study designed to examine predictors of ventricular recovery found that in 37 of 55 patients who chose to
breastfeed, none had adverse maternal effects and that rate of recovery of left ventricular function was
significantly higher in lactating women. Overall, given the benefits of breastfeeding and this report, some experts
have recommended that women who are clinically stable should not be discouraged from breastfeeding as long
as it is compatible with their heart failure medications [40].
If a decision is made to proceed with breastfeeding, we suggest avoiding angiotensin II receptor blockers due to
lack of safety data. (See "Management of heart failure during pregnancy", section on 'Avoid angiotensin
inhibition'.)
CONTRACEPTION — Women with peripartum cardiomyopathy (PPCM) or history of PPCM should receive
counseling regarding risk of recurrence and family planning and contraception options.
Direct evidence is lacking on the safety of contraceptives in women with PPCM [41] and limited data are
available on the risk of recurrence, so our approach, which is consistent with the Centers for Disease Control and
Prevention guidelines, is based upon indirect evidence. (See 'Prognosis' below.)
Since women with PPCM with persistent left ventricular (LV) dysfunction or LV ejection fraction (LVEF) ≤25
percent at diagnosis are at high risk of recurrent PPCM, we suggest avoiding future pregnancy in such patients
[1]. We suggest that the patient or her partner undergo a sterilization procedure or the patient use a highly
effective non-estrogen method of contraception, such as the etonogestrel implant, a copper intrauterine device
(IUD), or levonorgestrel-releasing IUD. Depot medroxyprogesterone acetate is not as highly effective, so it is
considered a second line alternative.
Though the risk of recurrence appears to be less in women with PPCM with recovered LV function and LVEF >25
percent at diagnosis, such patients should receive counseling, including the option of avoidance of subsequent
pregnancy due to the risk of relapse of PPCM, heart failure (HF), and death.
Estrogen-progestin contraceptives (eg, pills, patch, vaginal ring) may increase fluid retention, which may worsen
HF. In general, estrogen-progestin contraceptives should be avoided, particularly early after diagnosis and in
women with persistent LV dysfunction because of their potential to increase the risk of thromboembolism [41,42].
THERAPY AFTER RECOVERY OF LEFT VENTRICULAR FUNCTION — Peripartum cardiomyopathy patients

with persistent left ventricular (LV) dysfunction should be continued on standard heart failure (HF) treatment
indefinitely. A subset of patients with peripartum cardiomyopathy will achieve full recovery of LV function (ejection
fraction [LVEF] >50 percent). It must be emphasized that LV dysfunction can re-occur despite initial full recovery
and this recurrence risk is not limited to occurring during subsequent pregnancies. For patients with recovery of
LV function, there are limited studies examining the relationship between medication withdrawal and clinical
outcomes and there are no major societal guidelines regarding this management pathway. Clinical markers (ie,
contractile reserve on stress echocardiography) or biomarkers that may predict outcomes in this group are under
study.
In those patients who demonstrate persistent normal LV function (LVEF >50 percent) for a period of at least
six months, we suggest stepwise weaning of the HF regimen with close clinical follow-up (eg, every three to four
months) and with echocardiographic monitoring (eg, every six months) to ensure stability of LV function during
and for at least one to two years after weaning of HF medications to ensure stability.
An example of such a protocol is described in a review, as follows [43]. If LV structure and function have
recovered and remain normal for six months, mineralocorticoid receptor antagonist (eg, spironolactone) is
withdrawn with continuation of beta blockade and angiotensin converting enzyme (ACE) inhibitors/angiotensin II
receptor blockers (ARBs). If, six months after stopping the mineralocorticoid receptor antagonist, LV function
remains normal and the patient remains free of clinical HF symptoms, withdrawal of the ACE inhibitor/ARB is
suggested. The patient then continues on beta blockade alone. If there is no decline in LV function, the patient is
then weaned from beta blocker therapy, preferably over a period of two to four weeks to avoid rebound
phenomena, and again with close clinical monitoring and echocardiographic follow-up. Loop diuretics or thiazides
may be discontinued at any time (even before full recovery of LV function) if the patient is free of congestive
symptoms; recurrence of congestive symptoms would prompt reintroduction of these medications.
A decline in LV systolic function as documented by echocardiographic assessment, or the recurrence of HF

symptoms at any point in the process of weaning HF medications, would dictate a reinstitution of standard HF
therapy.
These recommendations are based on expert opinion only; there is a paucity of data in this area to guide
clinicians. Therefore, it is imperative that if HF therapies are withdrawn, the patient should be followed clinically
and by echocardiography to ensure stability, as described above.
PROGNOSIS — The prognosis of peripartum cardiomyopathy (PPCM) includes maternal, obstetric, and
neonatal outcomes, and the effect of subsequent pregnancy.
Maternal outcome — Several studies have evaluated the outcome of women with PPCM [10,23-25,44-48].
Whether women with PPCM have a different prognosis than pregnant women with other forms of
cardiomyopathy is not clear. (See "Acquired heart disease and pregnancy", section on 'Cardiomyopathy'.)
Mortality and morbidity — The mortality rate for PPCM has been reported as approximately 10 percent in
two years [23], with rates ranging from 6 percent in five years (figure 1) [45] and 11 percent in three years [10] to
as high as 28 percent in a report of 29 black patients [44]. Cardiac transplantation rates of less than 1 to 2
percent per year have been reported [10,23,24].
Death due to PPCM is usually caused by progressive pump failure, sudden death, or thromboembolic events.
The following adverse prognostic factors have been identified in various studies:
● Worse New York Heart Association functional class (table 1) [49]
● Left ventricular ejection fraction (LVEF) ≤25 percent [31]
● Black race [38,44]
● Indigent status [50]
● Multiparity [38]
● Age greater than 30 to 35 years [51,52]
PPCM is associated with significant extracardiac morbidity including brain injury. In a study of 182 women with
PPCM, 46 had major adverse events (MAE) including death, cardiac transplantation, mechanical circulatory
support, cardiopulmonary arrest, fulminant pulmonary edema, thromboembolic complications, and defibrillator or
pacemaker implantation [53]. In half of the patients with an MAE, the MAE preceded diagnosis of PPCM. One-
third of patients who had an MAE other than death or cardiac transplantation had residual brain damage as a
result of cerebrovascular accident or cardiopulmonary arrest.
Recovery of left ventricular function — Partial or complete recovery of LV function is common among
patients with PPCM and appears to be more frequent than with other types of dilated cardiomyopathy [54].
Complete recovery of LV function (defined as recovery to an LVEF >50 percent) has been reported in 20 to 60
percent of patients in various series [10,23,44,54-56]. Although nearly all recovery of LV function occurred within
six months of diagnosis in some series [23,44,57], delayed recovery of LV function has been observed in other
studies [9,10,50,58]. In one series of 100 patients, 42 women showed partial or complete improvement in LVEF
occurring over months to five years [10]. In this series, only 4 of 23 women who eventually had complete
recovery achieved this within six months.
Various studies have identified the following predictors of persistent LV dysfunction at follow-up:
● LVEF ≤30 percent [23]
● Fractional shortening less than 20 percent and an LV end-diastolic dimension ≥6 cm [59]
● Elevated cardiac troponin T [60]
● Black race [10,54]
● Diagnosis during pregnancy [10]
● Reduced right ventricular function measured using fractional area change on echocardiography [61] or
volumes on cardiac magnetic resonance imaging [62]
While recovery of LV function in patients with PPCM is related to the degree of dysfunction at the time of
diagnosis, baseline LVEF has limited sensitivity for prediction of improvement in individual patients [55]. Small
preliminary studies of the value of dobutamine stress echocardiography to predict recovery of LV function have
yielded mixed results [63,64].
The impact of preeclampsia or hypertension on prognosis of PPCM is unclear. Some studies have suggested
that PPCM associated with preeclampsia or hypertension may have better outcomes [31,56,65]; it has been
postulated that PPCM may have developed because of these conditions, and therefore resolution of these
conditions would facilitate recovery from PPCM. In contrast, the Investigations of Pregnancy-Associated
Cardiomyopathy (IPAC) study found that hypertension and preeclampsia were not associated with improved
outcomes among patients with PPCM [66].
Obstetric and neonatal outcomes — Data are more limited on obstetric and fetal outcomes. In the above
report of 123 patients, cesarean delivery was performed in 40 percent of patients, largely for obstetric indications
[23]. Preterm birth (<37 weeks) occurred in 25 percent, the mean birth weight was 3.1 kg (range 1.4 to 5.0 kg),
and 5.9 percent of infants were small for date. There were two stillbirths, one neonatal death, and four newborns
had congenital anomalies.
Subsequent pregnancy — Women with PPCM or history of PPCM should receive counseling regarding the risk
of recurrence with subsequent pregnancies [1]. The available data on risk of recurrence of PPCM come from
several small studies, which suggest that the risk of complications is high, particularly among women who do not
have full recovery of LV function. Termination of pregnancy may not prevent relapse. Although limited data are
available, we suggest that patients with PPCM with persistent LV dysfunction (LVEF <50 percent) or LVEF ≤25
percent at diagnosis should be advised to avoid a subsequent pregnancy due to the risk of HF progression and
death [1]. Other patients with PPCM should also be advised of the risk of recurrence. (See 'Contraception'
above.)
Recovered LV function — Among women in whom LV function returns to normal, the risk of subsequent
pregnancy appears lower than for those with persistent LV dysfunction, but elevated compared with the general
population [67,68]. In a series of 28 women who recovered to an LVEF ≥50 percent after the initial episode, the
following results in subsequent pregnancies were noted [67]:
● There were no deaths
● There was a reduction in the mean LVEF (56 to 49 percent), and the LVEF fell by more than 20 percent in
six women (21 percent)
● Six patients developed HF symptoms
The persistent risk in such women may be related to subtle residual dysfunction that is not detected on resting
evaluations. Support for this hypothesis comes from a report of seven women with a history of PPCM who
regained normal resting LV size and performance [48]. Contractile reserve, assessed by dobutamine challenge,
was significantly impaired compared with matched controls.
In summary, some women who recover LV function after an initial episode of PPCM will have significant decline
in LV function during a subsequent pregnancy. Women with PPCM with normalized LV function should be
counseled about the potential risks of recurrence and carefully monitored for signs of ventricular dysfunction if
they choose to become pregnant again.
Persistent LV dysfunction — The potential risks of subsequent pregnancy in women who have persistent LV
systolic dysfunction appear to be substantial, as illustrated by the following observations:
● In a series of 16 women with PPCM with persistent LV dysfunction who had subsequent pregnancies, three
died (19 percent) [67]. In addition, there was a further reduction in the mean LVEF (36 to 32 percent), HF
symptoms developed in seven patients, premature delivery in six, and therapeutic abortion in four.
● In a report of six women who had subsequent pregnancies after PPCM, two who had persistent LV
dysfunction died three months postpartum due to HF [69].
● A more complex pattern was illustrated in a review of 15 women with PPCM, 14 of whom had incomplete LV
recovery [70]. Subsequent pregnancy resulted in worsening HF in eight women (53 percent) and one death
from worsening HF 10 months postpartum. Seven women did not develop worsening HF during the second
pregnancy; these women all had continued improvement and normalization of LV function (LVEF ≥50
percent) within 30 months of the subsequent pregnancy.
Therapy to improve LV function — A study of 34 patients with PPCM with a subsequent pregnancy found
that patients who treated immediately after delivery with at least four weeks of bromocriptine therapy in addition
to standard therapy for heart failure (HF) had higher rates of recovery and higher LVEFs compared with those
who were treated with standard HF therapy alone [71]. However, further studies are needed in order to determine
the efficacy and safety of this approach.
SUMMARY AND RECOMMENDATIONS
● The management of heart failure (HF) due to peripartum cardiomyopathy (PPCM) is similar to that of HF due
to other causes that occur during pregnancy with special attention to particular risks during pregnancy,
including fetal risks. (See 'Heart failure treatment' above and "Management of heart failure during
pregnancy", section on 'Management goals'.)
● Decisions regarding use of implantable cardioverter defibrillator and cardiac resynchronization therapy in
patients with PPCM should include consideration of the natural history of the disease, including the potential
of recovery of ventricular function. (See 'Device therapy' above.)
● The role of bromocriptine therapy in PPCM is controversial. While preliminary data have suggested a benefit
from bromocriptine in patients with PPCM, further trials are needed to establish safety and efficacy. Until
additional data are available, we suggest not routinely using bromocriptine for patients with PPCM (Grade
2C). Some other experts advocate using bromocriptine routinely in this setting. (See 'Bromocriptine' above.)
● Decisions regarding the timing and mode of delivery in PPCM should be made based upon combined input
from cardiology, obstetrics, anesthesiology, and neonatology services. Prompt delivery is suggested in
women with PPCM with advanced HF. (See 'Delivery' above.)
● The limited available data suggest that the risk of recurrence with subsequent pregnancy is highest among
women with persistent left ventricular (LV) systolic dysfunction, although women with recovered LV systolic
function are also at risk for recurrence. (See 'Subsequent pregnancy' above.)
● All women with PPCM should receive counseling on the potential risk of recurrence with future pregnancies.
We suggest that women with a history of PPCM who have persistent LV dysfunction (LV ejection fraction
<50 percent) or LV ejection fraction ≤25 percent at diagnosis be advised to avoid pregnancy due to the risk
of HF progression and death. (Grade 2C). (See 'Subsequent pregnancy' above and 'Contraception' above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Amy Bales, MD, who
contributed to earlier versions of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 95071 Version 8.0
GRAPHICS
NYHA and other classifications of cardiovascular disability
New York Heart Canadian

Association Cardiovascular Specific activity
Class
functional Society functional scale [3]
classification [1] classification [2]
I Patients with cardiac Ordinary physical activity, Patients can perform to

disease but without such as walking and completion any activity
resulting limitations of climbing stairs, does not requiring ≥7 metabolic
physical activity. Ordinary cause angina. Angina with equivalents, eg, can carry
physical activity does not strenuous or rapid 24 lb up eight steps; do
cause undue fatigue, prolonged exertion at work outdoor work (shovel snow,
palpitation, dyspnea, or or recreation. spade soil); do recreational
anginal pain. activities (skiing, basketball,
squash, handball, jog/walk
5 mph).
II Patients with cardiac Slight limitation of ordinary Patients can perform to

disease resulting in slight activity. Walking or climbing completion any activity
limitation of physical stairs rapidly, walking uphill, requiring ≥5 metabolic
activity. They are walking or stair climbing equivalents, eg, have sexual
comfortable at rest. after meals, in cold, in intercourse without
Ordinary physical activity wind, or when under stopping, garden, rake,
results in fatigue, emotional stress, or only weed, roller skate, dance
palpitation, dyspnea, or during the few hours after fox trot, walk at 4 mph on
anginal pain. awakening. Walking more level ground, but cannot
than two blocks on the level and do not perform to
and climbing more than one completion activities
flight of ordinary stairs at a requiring ≥7 metabolic
normal pace and in normal equivalents.
conditions.
III Patients with cardiac Marked limitation of Patients can perform to

disease resulting in marked ordinary physical activity. completion any activity
limitation of physical Walking one to two blocks requiring ≥2 metabolic
activity. They are on the level and climbing equivalents, eg, shower
comfortable at rest. Less one flight in normal without stopping, strip and
than ordinary physical conditions. make bed, clean windows,
activity causes fatigue, walk 2.5 mph, bowl, play
palpitation, dyspnea, or golf, dress without stopping,
anginal pain. but cannot and do not
perform to completion any
activities requiring >5
metabolic equivalents.
IV Patients with cardiac Inability to carry on any Patients cannot or do not

disease resulting in inability physical activity without perform to completion
to carry on any physical discomfort. Anginal activities requiring >2
activity without discomfort. syndrome may be present metabolic equivalents.
Symptoms of cardiac at rest. Cannot carry out activities
insufficiency or of the listed above (specific
anginal syndrome may be activity scale III).
present even at rest. If any
physical activity is
undertaken, discomfort is
increased.
NYHA: New York Heart Association.
References:
1. The Criteria Committee of the New York Heart Association. Nomenclature and Criteria for Diagnosis of Diseases of the
Heart and Great Vessels, 9th ed, Little, Brown & Co, Boston, 1994. p.253.
2. Campeau L. Grading of angina pectoris. Circulation 1976; 54:522.
3. Goldman L, Hashimoto B, Cook EF, Loscalzo A. Comparative reproducibility and validity of systems for assessing
cardiovascular functional class: Advantages of a new specific activity scale. Circulation 1981; 64:1227.
Graphic 52683 Version 13.0
Outcome with a cardiomyopathy is related to the etiology
In a study of 1230 patients with a cardiomyopathy of various etiologies, the adjusted

Kaplan-Meier estimates of survival are related to the underlying cause of cardiomyopathy;
only idiopathic cardiomyopathy and cardiomyopathy due to causes for which survival was
significantly different from that in patients with idiopathic cardiomyopathy are shown. The
best outcome is in those with a peripartum cardiomyopathy, and the worst outcome is in
those with an infiltrative cardiomyopathy or that due to HIV infection.
Data from Felker CM, Thompson RE, Hare JM, et al. N Engl J Med 2000; 342:1077.
Graphic 75646 Version 2.0
Contributor Disclosures
Wendy Tsang, MD Nothing to disclose Roberto M Lang, MD Grant/Research/Clinical Trial Support: Philips
Medical Systems [Tomtec]. Speaker’s Bureau: Philips medical systems. Candice Silversides, MD, MS,
FRCPC Nothing to disclose Susan B Yeon, MD, JD, FACC Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
Conflict of interest policy

Peripartum Cardiomyopathy - Treatment and Prognosis

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10/27/2017 Peripartum cardiomyopathy: Treatment and prognosis - UpToDate

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Peripartum cardiomyopathy: Treatment and prognosis

Authors: Wendy Tsang, MD, Roberto M Lang, MD

INTRODUCTION — Peripartum cardiomyopathy (PPCM, also called pregnancy-associated cardiomyopathy) is a

● Supplemental oxygen and assisted ventilation as needed

THERAPY AFTER RECOVERY OF LEFT VENTRICULAR FUNCTION — Peripartum cardiomyopathy patients

A decline in LV systolic function as documented by echocardiographic assessment, or the recurrence of HF

● Worse New York Heart Association functional class (table 1) [49]

● Left ventricular ejection fraction (LVEF) ≤25 percent [31]

● Black race [38,44]

● Indigent status [50]

● Age greater than 30 to 35 years [51,52]

● LVEF ≤30 percent [23]

● Fractional shortening less than 20 percent and an LV end-diastolic dimension ≥6 cm [59]

● Elevated cardiac troponin T [60]

● Black race [10,54]

● Diagnosis during pregnancy [10]

● There were no deaths

● Six patients developed HF symptoms

SUMMARY AND RECOMMENDATIONS

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 95071 Version 8.0

NYHA and other classifications of cardiovascular disability

New York Heart Canadian

I Patients with cardiac Ordinary physical activity, Patients can perform to

II Patients with cardiac Slight limitation of ordinary Patients can perform to

III Patients with cardiac Marked limitation of Patients can perform to

IV Patients with cardiac Inability to carry on any Patients cannot or do not

NYHA: New York Heart Association.

Graphic 52683 Version 13.0

Outcome with a cardiomyopathy is related to the etiology

In a study of 1230 patients with a cardiomyopathy of various etiologies, the adjusted

Graphic 75646 Version 2.0

Conflict of interest policy

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