Prognostic Value of Echocardiography in Peripartum

Cardiomyopathy
Jeff B. Chapa, MD, Heather B. Heiberger, MD, Lynn Weinert, RDCM, Jeanne DeCara, MD,
Roberto M. Lang, MD, and Judith U. Hibbard, MD
OBJECTIVE: To estimate whether echocardiography findings at the time of diagnosis of peripartum cardiomyopathy are predictive of persistent cardiac dysfunction.
METHODS: Chart review of patients with peripartum cardiomyopathy between 1988 and 2001 was performed. Data
from echocardiography, including fractional shortening
and left ventricular end diastolic dimension, were recorded
both at the time of diagnosis and at follow-up. Left ventricular dysfunction was defined by echocardiography as fractional shortening less than 30% and left ventricular end
diastolic dimension of 4.8 cm or more.
RESULTS: Of 32 patients meeting our definition for peripartum cardiomyopathy and for whom follow-up data were
available, 13 (41%) had recovery of ventricular function,
while 19 (59%) continued to have persistent left ventricular
dysfunction. Those who did not recover cardiac function
had a higher left ventricular end diastolic dimension and a
lower fractional shortening at diagnosis than those who
recovered. A fractional shortening value less than 20% and
a left ventricular end diastolic dimension 6 cm or greater at
the time of diagnosis was associated with a more than
3-fold higher risk for persistent left ventricular dysfunction.
CONCLUSION: Along with being an important diagnostic
tool in peripartum cardiomyopathy, echocardiography
may provide significant prognostic information with regards to recovery of cardiac function. (Obstet Gynecol
2005;105:1303 8. 2005 by The American College of
Obstetricians and Gynecologists.)
LEVEL OF EVIDENCE: III

Despite its original description in the medical literature

during the nineteenth century by Ritchie and Virchow,
peripartum cardiomyopathy remains a diagnosis associated
with great uncertainty.1 The incidence is estimated to be 1
in 3,000 4,000 deliveries in the United States, with 1,000
1,350 new cases reported annually,2,3 although tertiary
centers such as ours often report much higher incidences.4,5
Although a precise etiology for peripartum cardiomyopathy is unknown, there is much current interest in infectious,
From the Departments of Obstetrics and Gynecology and Internal Medicine,
University of Chicago, Pritzker School of Medicine, Chicago, Illinois.

VOL. 105, NO. 6, JUNE 2005

2005 by The American College of Obstetricians and Gynecologists.
Published by Lippincott Williams & Wilkins.

autoimmune, and genetic factors that may play a role in the

inciting event.6 Epidemiologic risk factors, well known to
the obstetrician, include age greater than 30 years, black
race, multiple gestation, obesity, preeclampsia, and chronic
hypertension.7 Peripartum cardiomyopathy historically
has had a 2550% mortality rate, a rate that may still persist
at some centers, with nearly one-half of all related deaths
occurring within the first 3 months after delivery.8 Despite
advances in medical therapy and the development of cardiac transplantation, the condition remains a significant
cause of maternal mortality, accounting for 6% of all maternal deaths among liveborn gestations in the United States.9
Recently, we described specific echocardiographic criteria to define the disorder,10 providing a more objective
definition than the traditional subjective parameters for
peripartum cardiomyopathy,11 because echocardiography is now the standard noninvasive tool for measuring
cardiac function, quantifying left ventricular performance and providing a definitive diagnosis of left ventricular dysfunction. Similar to idiopathic dilated cardiomyopathy, OConnell et al12 suggested that survivors of
peripartum cardiomyopathy have better echocardiographic ventricular function at the time of diagnosis
compared with those who succumb. Witlin et al,13 in a
series of only 9 patients, suggested that fractional shortening and end diastolic dimension at the time of diagnosis were prognostic. Although most patients with persistent cardiac dysfunction after the index pregnancy are
advised to avoid subsequent pregnancies, those parturients who experience prompt resolution of their symptoms and normalization of cardiac function may be more
problematic to counsel.
After recently reviewing and analyzing existing data,
the National Heart, Lung, and Blood Institute of the
National Institutes of Health concluded that uncertainty
regarding many aspects of peripartum cardiomyopathy
warrants further investigation and reporting of data.14
We have undertaken the current work to review our
own experience with peripartum cardiomyopathy and to
determine whether echocardiographic parameters at the

0029-7844/05/$30.00
doi:10.1097/01.AOG.0000161382.30233.ba

1303

time of diagnosis are predictive of outcome in our cohort

of patients. Furthermore, we wished to evaluate outcomes in those women undertaking a subsequent pregnancy after a diagnosis of peripartum cardiomyopathy.
MATERIALS AND METHODS
We performed an analysis of all patients with the diagnosis of peripartum cardiomyopathy who were cared for
at the University of Chicago from May 1988 to March
2001. Institutional review board approval was obtained
before beginning this investigation. Using International
Classification of Diseases, 9th Revision, discharge summary codes from cardiology outpatient clinics, echocardiographic laboratory records, and a computerized obstetric research database, we identified women with the
potential diagnosis of peripartum cardiomyopathy. The
inpatient and outpatient medical records of these patients, including echocardiographic data, were reviewed
to confirm the diagnosis. In each case, other potential
causes of heart failure in late gestation, including severe
preeclampsia, fluid overload, and amniotic fluid embolism, were determined not to be present. We used our
echocardiographic-based precise definition for peripartum cardiomyopathy, which requires a fractional shortening calculation of less than 30% and left ventricular
end diastolic dimension 4.8 cm or greater at the time of
diagnosis.10 Fractional shortening is defined as left ventricular end diastolic dimension minus left ventricular end
systolic dimension divided by left ventricular end diastolic dimension (LVEDD LVESD/LVEDD). Patients who did not meet these criteria were excluded
from our analysis.
Epidemiologic data, including age, race, and parity,
were recorded, as well as information on timing of
presentation in relation to gestation, presenting signs and
symptoms, risk factors, and subsequent pregnancy outcome. Patients were monitored with echocardiography
after delivery. Those who demonstrated either a return
of fractional shortening to more than 30% or left ventricular end diastolic dimension to less than 4.8 cm at the
time of follow-up were classified as recovered. Patients
who did not meet either of these criteria at follow-up
were classified as having persistent dysfunction. If available, data from long-term assessment of patients with left
ventricular dysfunction were collected, with particular
emphasis on outcomes such as need for transplantation
or patient death. For those who undertook a subsequent
pregnancy, the same criteria for follow-up were used.
Statistical analysis included comparison between patients with recovery of left ventricular function and those
with residual dysfunction using t tests for continuous
variables and Fisher exact test for categorical variables.

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Echocardiography in Peripartum Cardiomyopathy

For left ventricular end diastolic dimension and fractional shortening results, the distribution of values for
both the recovered and persistent dysfunction subgroups
were assessed with the Lilliefors test for normality. Values for skewness and kurtosis were determined, and
there was little evidence found against a normal distribution for these results among either of the subgroups.
Relative risk (RR) and 95% confidence intervals for
recovery of left ventricular function were calculated, as
were P values for significance. We selected the values of
left ventricular end diastolic dimension greater than 6.0
cm and fractional shortening less than 20% at the time of
initial diagnosis as risk factors for persistent dysfunction
based on data from a previous study.13
RESULTS
During the study period, 40,200 live births occurred at
the University of Chicago. Of the 56 patients identified
as potentially suffering peripartum cardiomyopathy, 35
met our criteria for diagnosis and were included in this
investigation, corresponding to an incidence of 1 case per
1,149 live births. Three patients with peripartum cardiomyopathy were lost to follow-up. Twenty-one patients
who did not meet the criteria for this study were excluded. Preexisting disease, such as idiopathic dilated
cardiomyopathy or concurrent cardiovascular risk factors, including hypertension and alcoholism, were the
primary reasons for patient exclusion, as well as 6 cases
with insufficient data.
Eighty percent of study patients were African American, while the remainder were white, corresponding to
the overall obstetric population at our institution. The
mean age at the time of diagnosis of peripartum cardiomyopathy was 27 6 years, with a range of 16 38
years. Parity in the index pregnancy ranged from 1 to 6,
with a median value of 2. The diagnosis of peripartum
cardiomyopathy was made in the antepartum period in 7
gravidas and in the postpartum period in 28 women.
Included in our analysis are 2 patients who presented 2
and 3 months before delivery and one who presented at
7 months postpartum. Four women had multifetal gestations (3 twin, 1 triplet). Five gravidas had preeclampsia
and an additional five had been treated with tocolytics
for preterm labor with oral terbutaline for 6 56 days
(mean 24.5 days). The most common presenting symptoms and signs were dyspnea (90%), tachycardia (62%),
or peripheral edema (59%). One patient had a concomitant diagnosis of cerebral vascular accident. Only 2
women underwent endomyocardial biopsy, but neither
procedure was contributory to the diagnosis because one
revealed no abnormality and the other sample was insufficient for diagnostic purposes.

OBSTETRICS & GYNECOLOGY

Table 1. Predisposing Factors and Echocardiographic Parameters at Diagnosis and Follow-up

Race
African-American
White
Parity
1
1
Age
30
30
Tocolytic use
Preeclampsia
Multiple gestation
At diagnosis
Fractional
shortening (%)
Left ventricular
end diastolic
diameter (cm)
At follow-up*
Fractional
shortening (%)
Left ventricular
end diastolic
dysfunction
(cm)

Recovered
(n 13)

Persistent
Dysfunction
(n 19)

11
2

14
5

.67

8
5

8
11

.47

7
6
2
1
2

7
12
2
4
2

.56

1.00
.62
1.00

22.48 4.82

13.96 6.24

.001

5.90 0.45

6.70 0.83

.003

32.9 2.6

18.8 6.0

5.64 0.82

6.33 0.79

Data presented as n or mean standard deviation.

* Median follow-up time 3 months.

At diagnosis, the mean fractional shortening of the

entire study group was 17.3 7.0%, with a mean left
ventricular end diastolic dimension of 6.4 0.8 cm. Of
the remaining 32 patients, 13 (41%) had recovered left
ventricular function at a median follow-up period of 3
months, while 19 (59%) had persistent ventricular dysfunction at a median of 46 months follow-up. Mean
fractional shortening and left ventricular end diastolic
dimension values, at the time of diagnosis and at followup, are presented for both of these groups in Table 1.
Fractional shortening and left ventricular end diastolic
dimension are significantly different between the group
that recovered left ventricular function and the group
with persistent ventricular dysfunction. An initial fractional shortening below a threshold value of 20% at the
time of diagnosis was associated with a 3-fold increased
risk of persistent left ventricular dysfunction at follow-up
(Table 2). Further, a left ventricular end diastolic dimension of 6.0 cm or greater at the time of the initial
diagnosis was associated with more than a 3.5 times
increased risk for persistent ventricular dysfunction compared with those who recovered (Table 2). With regard
to demographic characteristics and risk factors, there
were no significant differences between women whose

VOL. 105, NO. 6, JUNE 2005

Table 2. Risk for Persistent Left Ventricular Dysfunction

Based on Echocardiographic Parameters at Time
of Initial Diagnosis

Fractional shortening
20%
Left ventricular end
diastolic dimension
6.0 cm

Relative
Risk

95%
Confidence
Interval

3.06

1.317.16

.004

3.55

1.0212.33

.01

cardiac function improved and returned to normal and

those who remained with significant impairment (Table
1). Outcomes following the index pregnancy are presented in Figure 1. Two patients underwent cardiac
transplantation (6.5%), and 3 died from heart failure
(9.6%), including one of the transplant recipients.
Regarding outcomes with subsequent pregnancy after
the index pregnancy, 6 of 35 patients had 8 documented
subsequent gestations (Figure 2). Four of the patients
with recovered left ventricular function had one additional pregnancy each, while the 2 patients with persistent left ventricular dysfunction had 1 and 3 subsequent
pregnancies, respectively. All 4 patients with recovered
left ventricular function became symptomatic and demonstrated echocardiographic evidence of recurrent left
ventricular dysfunction in the third trimester. Three of
these gravidas with recurrence of peripartum cardiomyopathy then had persistent left ventricular dysfunction
after the subsequent pregnancy, while one again demonstrated full cardiac recovery. The 2 patients with persistent left ventricular dysfunction after the index pregnancy had no recurrence of symptoms in their
subsequent gestations, but continued to have stable left
ventricular dysfunction, both during and after the pregnancies (Figure 2).
DISCUSSION
Peripartum cardiomyopathy remains a significant cause
of maternal morbidity and mortality in the United States.
The increased incidence of peripartum cardiomyopathy at
our center is likely due in part to our role as a tertiary care
referral center for a large perinatal network, which serves
an urban, primarily African-American population.
Echocardiography is an important tool in properly
diagnosing peripartum cardiomyopathy and assessing
the degree of cardiac dysfunction. In this work we have
confirmed that the specific parameters of fractional shortening and left ventricular end diastolic dimension at the
time of diagnosis are predictive of the degree of recovery

Chapa et al

Echocardiography in Peripartum Cardiomyopathy

1305

Fig. 1. Left ventricular function

and outcome following index
pregnancy.
Chapa. Echocardiography in Peripartum
Cardiomyopathy. Obstet Gynecol 2005.

of cardiac function at follow-up. Those women with a

fractional shortening less than 20% or left ventricular
end diastolic diameter of 6.0 cm or greater on initial
echocardiogram incurred more than a 3 times increased
risk of not fully recovering their left ventricular function,
and in fact, 3 patients in this group suffered mortality. No

demographic risk factors differed between those women

who recovered and those who continued with ventricular impairment. The prognostic value of fractional shortening and left ventricular end diastolic dimension may
be beneficial in guiding treatment for and counseling
these patients.

Fig. 2. Outcomes in subsequent pregnancy based on left

ventricular function after index
gestation.
Chapa. Echocardiography in Peripartum
Cardiomyopathy. Obstet Gynecol 2005.

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Echocardiography in Peripartum Cardiomyopathy

OBSTETRICS & GYNECOLOGY

Our findings are in accord with the observations of

OConnell et al12 who initially suggested that echocardiographic parameters, such as markedly reduced ejection fraction and increased left ventricular cavity size at
the time of diagnosis, are associated with increased maternal mortality. More recently, Witlin et al13 studied a
cohort of 9 peripartum cardiomyopathy patients and
noted that left ventricular end diastolic dimension of 6.0
cm or greater and fractional shortening of 21% or less
were risk factors for persistent left ventricular dysfunction. The results of this study confirm these findings in a
significantly larger cohort of peripartum cardiomyopathy patients. The morbidity in our patients, measured in
terms of persistent left ventricular dysfunction, is similar
to previous reports, but the mortality rate was lower than
that documented by other investigators.8,15,16 Advances
in cardiac critical care, the increasing availability of cardiac transplantation, and the exclusion of other cardiac
disease with echocardiography are likely causes of the
improvement in overall mortality figures.
Women with a history of peripartum cardiomyopathy
remain at high risk for recurrence of cardiac dysfunction
in subsequent pregnancies, despite seemingly full recovery. Our data, although limited by the small number of
patients embarking on a new conception, suggest that
recovery of left ventricular function after the index gestation, as documented by echocardiography, is not predictive of recurrence or outcome in subsequent pregnancies in our population. We were surprised that all 4 of the
completely recovered women had recurrent left ventricular dysfunction during pregnancy. Sutton et al17 and
DeSouza et al18 describe much better success with subsequent pregnancy in their recovered peripartum cardiomyopathy patients compared with our cohort, although
each report includes only 4 and 7 patients, respectively.
In contrast, Elkayam et al,19 in the largest series to date,
have documented significant deleterious effects of subsequent pregnancies in women with a history of peripartum cardiomyopathy who have echocardiographic evidence of residual dysfunction.
Perhaps additional factors are better indicative of the
hearts ability to compensate for the increased hemodynamic demands of a subsequent pregnancy. Lampert et
al20 demonstrated that patients diagnosed with peripartum cardiomyopathy and completely recovered left ventricular function actually had evidence of decreased left
ventricular contractile reserve, as demonstrated by a
dobutamine challenge test, suggesting that these women
may indeed be at risk for recurrence of disease in future
pregnancies. Because peripartum cardiomyopathy is associated with multiparity, it may be that each subsequent
pregnancy in susceptible individuals further compromises contractile reserve and is more likely to lead to

VOL. 105, NO. 6, JUNE 2005

persistent cardiac dysfunction. Still, a number of other

factors, as yet undefined, including genetic and autoimmune, may underlie and contribute to outcomes in these
women. Surprisingly, in our experience the gestations
that occurred in women with residual cardiac dysfunction after the index pregnancy were uncomplicated and
not marked by a significant worsening of symptoms or
cardiac function. These cases, however, are only 2 in
number, and both patients were receiving ongoing care
and maintained on appropriate medications. Thus, we
caution strongly against the extrapolation of this limited
data to other similar cases.
Improved outcomes in index cases of peripartum cardiomyopathy and in subsequent pregnancies are primarily due to advances in cardiac care, both medical and
surgical. Pharmacologic therapy for heart failure has
evolved tremendously and is now based on sound therapeutic principles that include afterload reduction and
increasing myocardial contractility. The former can be
attained effectively during gestation with careful use of a
potent vasodilator, such as hydralazine, whereas the
latter aim may be achieved with digoxin and other
pressor agents. Angiotensin-converting enzyme inhibitors are also an excellent choice in the postpartum setting
for afterload reduction, but these drugs can lead to
embryopathy when used during pregnancy. Fluid restriction and judicious use of diuretics may also alleviate
some of the symptoms associated with congestive heart
failure in the gravida. Finally, improvements in cardiac
critical care and the emergence of cardiac transplantation
have provided hope to patients who previously would
not have survived.
We have chosen to include 3 patients in our cohort
whose timing of disease is outside the previously suggested time period for diagnosis.11 These women met all
the stringent echocardiographic criteria, as well as all
subjective criteria, with the exception of timing. We
believe the time element is no longer relevant, and in
view of current diagnostic tools, medications, and cardiac intensive care, a diagnosis of peripartum cardiomyopathy antenatally does not automatically imply immediate delivery, particularly if the fetus is quite premature.
Thus, a gravida diagnosed with peripartum cardiomyopathy in the second or third trimester, more than 1
month before delivery, may indeed carry the gestation
much closer to term, allowing for improved fetal maturity. Similarly, the patient diagnosed with cardiomyopathy 7 months after delivery may have had echocardiographic evidence of cardiac dysfunction long before her
presentation. Thus, we believe that timing relative to
gestation may be a somewhat arbitrary consideration,
and inclusion of gravidas who otherwise meet all diagnostic criteria is warranted.

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Echocardiography in Peripartum Cardiomyopathy

1307

We acknowledge that because of the small sample

sizes in this study, which is due to the rarity of this
disease, some of our observations may have limited
statistical power. Additionally, the cases occurred over a
13-year time period, during which significant advances
in cardiac care have been made. Thus, the prognosis and
outcome for patients who presented in the more recent
past would be expected to be improved over those
patients presenting earlier. However, further subanalysis
of the data, according to year of diagnosis during the
study period, was not able to be performed because of
the small sample sizes. These limitations emphasize the
need for larger, prospective multicenter studies.
Echocardiography appears to be extremely valuable
in diagnosing peripartum cardiomyopathy, formulating
prognosis for recovery, and following the course of the
disease. Specific echocardiographic parameters, including fractional shortening and left ventricular end diastolic dimension at the time of diagnosis, may be predictive of long-term cardiac dysfunction. Subsequent
pregnancy in women who have been diagnosed with
peripartum cardiomyopathy should be approached with
extreme caution. Because our understanding of the underlying etiology and natural history of peripartum cardiomyopathy is currently incomplete, management of
these patients can prove to be difficult. We believe an
international registry of cases would greatly aid progress
in unraveling the complexities of this disease.
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Address reprint requests to: Jeff B. Chapa, MD, Department of

Obstetrics and Gynecology, Section of MaternalFetal Medicine, University Hospitals of Cleveland, MacDonald Womens Hospital, 11100 Euclid Avenue, Cleveland, OH 44106;
e-mail: jeff.chapa@uhhs.com.

Received September 14, 2004. Received in revised form February 1,

2005. Accepted February 10, 2005.

OBSTETRICS & GYNECOLOGY