Curr Cardiol Rep (2016) 18:92
DOI 10.1007/s11886-016-0760-7
ECHOCARDIOGRAPHY (JM GARDIN, SECTION EDITOR)
Echocardiography in Pregnancy: Part 1
Shuang Liu 1 & Uri Elkayam 2 & Tasneem Z. Naqvi 1
# Springer Science+Business Media New York 2016
Abstract Cardiovascular disease (CVD) remains the
leading cause of maternal mortality, and clinical diagno-
sis of CVD in women during pregnancy is challenging.
Pregnant women with known heart disease require care-
ful multidisciplinary management by obstetric and medi-
cal teams to assess for maternal and fetal risk.
Echocardiography is a safe and effective diagnostic tool
indicated in pregnant women with cardiac symptoms or
women with known cardiac disease for appropriate selec-
tion of women who require close monitoring of cardiac
condition and valvular function. Echocardiography is the
single most important clinical tool to diagnose and man-
age heart disease during pregnancy. Echocardiography is
able to characterize cardiac structural abnormalities and
corresponding hemodynamic changes, identifies heart
diseases that are poorly tolerated in pregnancy, and helps
select patients who may require a cesarean delivery be-
cause of hemodynamic instability. An understanding of
the physiologic alterations including increased heart rate,
blood volume, and cardiac output as well as the de-
creased vascular resistance is important for early recog-
nition and monitoring of the consequences of cardiac
This article is part of the Topical Collection on Echocardiography
Electronic supplementary material The online version of this article
(doi:10.1007/s11886-016-0760-7) contains supplementary material,
which is available to authorized users.
* Tasneem Z. Naqvi
naqvi.tasneem@mayo.edu
1
Echocardiography Laboratory, Department of Cardiology, Mayo
Clinic, 13400 E Shea Blvd, Scottsdale 85259, AZ, USA
2
Division of Cardiology, LA County-USC Medical Center, University
of Southern California, Los Angeles, CA 90033, USA
disease in pregnancy. This review will focus on common
acquired cardiac lesions encountered during pregnancy
and the role of echocardiography in the diagnosis and
management of these diseases.
Keywords Echocardiography . Pregnancy . Heart disease
Introduction
Maternal cardiac disease complicates approximately 0.2
to 4 % of pregnancies at present, which is a major cause
of non-obstetric morbidity [1•]. The number of pregnant
women who develop cardiac problems is becoming more
prevalent than before as women are increasingly seeking
pregnancy at a later age [2]. Echocardiography is, by far,
the preferred diagnostic test for cardiac disease in preg-
nant women for its safely and general availability with
no risk of radiation to the mother and the fetus.
Echocardiography provides precise information about
structural abnormalities and illuminates the pathophysiol-
ogy of cardiac disease and its hemodynamic conse-
quences. In addition, echocardiography helps in deter-
mining whether intervention should be performed prior
to or during pregnancy or if the severity of cardiac con-
dition deems pregnancy very high risk and, hence,
contraindicated.
Physiologic Alterations During Pregnancy
Significant cardiovascular hemodynamic changes occur dur-
ing pregnancy. These physiologic alterations in the cardiovas-
cular system mimic cardiac disease, making clinical diagnosis
of heart disease challenging. Cardiac output increases by
92 Page 2 of 10 Curr Cardiol Rep (2016) 18:92

approximately 50 % at the early to mid-third trimester and is
maintained until term. While increased preload and stroke
volume contribute to the increased cardiac output during the
first trimester, the increased heart rate accounts for the in-
creased cardiac output in the second trimester [3]. Increases
in hormonally mediated blood volume and red cells also lead
to a major increase in cardiac output in pregnancy [4]. During
labor, pain and uterine contractions also produce increases in
cardiac output and blood pressure during labor and delivery.
Furthermore, relief of caval compression and auto-transfusion
from the emptied and contracted uterus immediately after de-
livery results in a further increase in cardiac output. Peripheral
vascular resistance decreases during pregnancy. The mean ar-
terial pressure decreases about 10–15 mmHg to accommodate
the increased cardiac output and preserve the efficiency of
ventricular-arterial coupling and diastolic perfusion pressure
at the end of the second trimester [5•]. These hemodynamic
changes often resolve by 2 weeks postpartum [6].
Echocardiographic Findings in Normal Pregnancy
The echocardiographic changes during pregnancy summa-
rized in Table 1 are based on the physiologic alterations as
mentioned above. The increased blood volume and cardiac
output during pregnancy lead to dilation of the heart; the left
ventricular (LV) end-diastolic dimension increases slightly but
remains within normal limits in normal pregnancy. A revers-
ible Bphysiologic^ LV hypertrophy also exists during preg-
nancy. The LV mass increases resulting from the increased
LV diameter and increased LV posterior wall and intraventric-
ular septal thickness. Similar to the LV, the right ventricle (RV)
increases in size over the course of pregnancy because of
increased preload [8, 9].
There is discrepancy among studies as to whether LV con-
tractility increases in pregnancy. Most studies have found no
significant change in ejection fraction [5•, 6, 10, 11]. Some
have found a decrease in the ratio of wall stress to velocity of
circumferential fiber contraction, implying enhanced intrinsic
myocardial contractility [11], whereas others have concluded
that ejection fraction or contractility as measured by fractional
shortening and velocity of circumferential fiber contraction
decline slightly, especially in the late third trimester [12–14].
We found a slight decrease in LV ejection fraction in the third
trimester using 3D echocardiography [15]. Others have shown
a decrease in longitudinal LV shortening, as measured by lon-
gitudinal tissue Doppler strain, toward the end of pregnancy,
and an increase in LV globularity [16]. However, our own
observations using speckle tracking strain rate indicate an in-
crease in cardiac contractility as demonstrated by an increase
in LV radial and longitudinal rate of deformation, particularly
during first and second trimesters [17]. Savu and colleagues
[9] also observed increased LV and RV longitudinal strain rate
in the first trimester. These discrepancies reported in strain/
strain rate appear related to the load dependency of these mea-
surements along with differences in imaging techniques. The
tethering effect of neighboring segments influences tissue
Doppler imaging measurements [18]. In contrast, speckle
tracking is a 2D technique not subject to the angle dependency
of Doppler and of motion of surrounding segments.
There have been conflicting reports regarding changes in
diastolic function during pregnancy. Because of substantial
alterations in the heart rate and contractility, preload and
afterload, LV mass, and volume in pregnancy, assessment of
LV diastolic function requires a combination of load-
dependent and load-independent parameters. Most studies
show that LV diastolic function is preserved in normal preg-
nancy, although the preload is increased [19, 20]. The peak

Table 1 Echocardiographic
changes during pregnancy Echocardiographic variables Changes during pregnancy

Left ventricular dimension and volume Increases

Left ventricular wall thickness and left ventricular mass Increases
Left ventricular ejection fraction Unchanged
Left ventricular fractional shortening Unchanged
Left ventricular radial and longitudinal strain rate Increases
Aortic root diameter Mildly increases
Right ventricular dimension and volume Increases
Right ventricular ejection fraction Unchanged
Left atrial size and volume Increases
Stroke volume (as measured using pulsed wave Doppler) Increases
Mitral E wave velocity Increases, then decreases
Mitral A wave velocity Increases
Peak pulmonary artery systolic pressure estimated using tricuspid regurgitation jet Unchanged

Cardiac chamber dimensions. This table was adapted from Naqvi and Elkayam [7]; copyright Elsevier
LVOT left ventricular outflow tract, TR tricuspid regurgitation, VTI velocity-time integral
Curr Cardiol Rep (2016) 18:92
early and late diastolic mitral inflow (E wave and A wave)
velocities increase resulting from increased preload and blood
volume. However, the change in the A wave is greater than E
wave; therefore, a decreased E/A ratio is found in normal
pregnancy that may be caused by the enhanced atrial contrac-
tion forced by increased left atrial filling pressures [21].
Similarly, the early and late diastolic myocardial velocity ratio
(E’/A’) also decreases because of increased atrial contractility
[20]. However, the E/E’, which is a validated marker of left
atrial pressure, does not change beyond normal range. The
normalization of mitral flow occurs around 2 months after
childbirth [4].
The left atrium serves as a reservoir, a conduit, and a boost-
er pump during the cardiac cycle [22]. The atrial size increases
gradually in pregnancy, although the measurement still re-
mains within normal limits [23]. Song et al. evaluated left
atrial function using speckle tracking echocardiography in
pregnancy and found that the left atrial reservoir and booster
pump function is increased. The conduit function is decreased,
which may be caused by the physiological myocardial hyper-
trophy during pregnancy. However, the changes are reversible
[24].
Few echocardiographic studies have evaluated RV function
during pregnancy. Savu and associates using tissue Doppler
strain rate imaging of the RV free wall [9] found an increase in
RV longitudinal strain rate in the first and second trimesters
and a decrease in the third trimester indicating an increase in
RV contractility during early and mid pregnancy.
Other normal cardiac structural changes that can be shown
by echocardiography include an increase in aortic root, mitral,
and tricuspid annular size; and an increase in stroke volume
leading to an increase in Doppler flow velocity across the
aortic valve. Mild valvular regurgitation occurs normally in
pregnancy and has been demonstrated in up to 28, 94, and
94 % of mitral, tricuspid, and pulmonic valves [25•].
Asymptomatic pericardial effusions occur in approximate-
ly 40 % of pregnant women, and effusions become more com-
mon in the third trimester and in women who gain more than
12-kg weight, suggesting that increased fluid retention may
play an important role in the development of effusion [26].
Pericardial effusion was reported to be completely resolved in
all patients on repeat echocardiograms done at 6 weeks after
delivery [26].
Peripartum Cardiomyopathy
The European Society of Cardiology (ESC) Working Group
defined peripartum cardiomyopathy (PPCM) as a form of di-
lated cardiomyopathy which presents with heart failure signs
in the last month of pregnancy or within 5 months postpartum
[27]. In this classification, the diagnosis is made in the absence
of other abnormal loading conditions such as hypertension,
Page 3 of 10 92
valvular heart diseases, or coronary disease. In 2010, the heart
failure association of ESC Working Group expanded the def-
inition as follows: BPeripartum cardiomyopathy is an idio-
pathic cardiomyopathy presenting with heart failure second-
ary to LV systolic dysfunction towards the end of pregnancy
or in the months following delivery, where no other cause of
heart failure is found. It is a diagnosis of exclusion. The LV
may not be dilated but the LVEF is nearly always reduced
below 45 %^ [28].
PPCM is a disease with high morbidity and mortality, and
the true prevalence and etiology are unknown because of few
population-based studies in PPCM. The pathophysiology is
unclear, and coincidental presence of multiple factors such
as inflammation, impaired vasculature, and oxidative stress
in previously healthy women has been blamed. Many re-
searchers consider pregnancy-induced hypertension as a risk
factor for PPCM [29, 30]; however, hypertensive heart failure
of pregnancy was defined as the occurrence of peripartum
heart failure related to any form of hypertension. A recent
study focused on the differentiation between PPCM and hy-
pertensive heart failure of pregnancy showed that LV diastolic
and systolic dimensions are larger, while the left ventricular
ejection fraction (LVEF) and LV fractional shortening are low-
er, in PPCM patients [31].
The diagnosis of PPCM requires exclusion of other causes
of cardiomyopathy and the confirmation of reduced LV sys-
tolic function and/or LV dilation, usually by echocardiography
[28]. Video 1 shows the decreased wall motion in a patient
with PPCM. LV mural thrombi can sometimes be visualized
[32]. Additionally, echocardiography can predict the progno-
sis in PPCM. The early recovery was 6.4-fold higher in pa-
tients with an LVEF ≥30 % upon presentation than in the
patients with an LVEF of 10–19 % [33]. Figure 1 shows echo-
cardiographic findings of PPCM in a 31-year-old female with
an LVEF of 25 % and peak longitudinal speckle tracking
strain of -9.0 % (normal is more negative than -18 %).
LV contraction involves longitudinal, radial, and circum-
ferential shortening. The longitudinally directed fibers mainly
situated in the subepicardium and subendocardium of the LV
and RV free walls play a dominant role in maintaining normal
ejection fraction and determining atrioventricular interaction
[34]. When ventricular size is increased, the longitudinal fiber
contraction is always reduced in addition to the reduced ejec-
tion fraction. Besides longitudinal strain, this longitudinal
contraction can also be assessed by mitral or tricuspid systolic
annular plane excursion [35], providing a simple method to
evaluate LV and RV function.
A recent study used tricuspid annular plane systolic excur-
sion (TAPSE) to compare RV systolic function in patients
with PPCM and idiopathic dilated cardiomyopathy (DCM)
and found that the mean TAPSE was significantly less in
PPCM (12.58 ± 4.27 vs 14.46 ± 3.21 mm, P < 0.028), sug-
gesting that the RV systolic function in PPCM was worse
92 Page 4 of 10
Fig. 1 Transthoracic echocardiographic images in a 31-year old female
with postpartum cardiomyopathy. a Transthoracic parasternal long-axis
view showing a dilated left ventricle. b Biplane left ventricular ejection
[34]. Ventricular long-axis function can also be assessed using
tissue Doppler that is able to detect LV dysfunction earlier
than conventional 2D and Doppler measures [36]. Speckle
tracking imaging is a two-dimensional method and more ro-
bust than tissue Doppler to assess LV and RV function.
However, it has not been evaluated in PPCM.
Acquired Valvular Heart Disease
Rheumatic heart disease is the most common acquired valve
disease present during pregnancy and accounts for up to 90 %
of valve disease during pregnancy worldwide. Maternal and
fetal risks in patients with valvular disease correlate with the
type and severity of the valve lesion, LV function, pulmonary
artery pressure, and functional capacity (Table 2). A recent
study reported that mitral valve disease including mitral
Curr Cardiol Rep (2016) 18:92
fraction is 25 %. c Peak longitudinal strain in apical four-chamber view is
−9.4 %. d Bull’s eye plots generated by two-dimensional speckle tracking
echocardiography showing a global longitudinal strain of −9.0 %
stenosis and/or regurgitation accounts for 63 % and the aortic
valve disease for another 23 % [37].
Mitral Valve Stenosis
Rheumatic mitral stenosis (MS) is the most common valve
disease during pregnancy. The patient may be asymptomatic
until the hemodynamic changes associated with pregnancy
unmask its presence. The 2014 AHA/ACC guidelines for val-
vular heart disease define severity of mitral valve stenosis as
follows: mitral valve area (MVA) >2.0 cm2 = mild, 1.6–
2.0 cm2 = moderate, and ≤1.5 cm2 = severe, along with dia-
stolic pressure half-time ≥150 ms (diastolic pressure half-time
≥220 ms with very severe MS), severe left atrial enlargement,
and pulmonary artery systolic pressure >30 mmHg [38]. Mild
MS is associated with much less morbidity, while moderate
and severe stenoses are associated with increased rates of ad-
verse events.
Curr Cardiol Rep (2016) 18:92
Table 2 Classification of valvular heart disease according to risk during pregnancy
Low risk
AR with normal LV function and
NYHA class I or II
MV prolapse (isolated or with mild/moderate
MR and normal LV function)
MR with normal LV function and NYHA class I or II
Asymptomatic AS with low mean gradient and
normal LV function (EF >50 %)
Mild MS (MV area >1.5 cm2, mean gradient <5 mmHg)
without severe pulmonary HTN
Mild/moderate PS
AR aortic valve regurgitation, LV left ventricle, MS mitral valve stenosis, AS aortic valve stenosis, PS pulmonic stenosis, MV mitral valve, MR mitral
valve regurgitation, LVEF left ventricular ejection fraction
The normal cardiovascular changes of pregnancy,
superimposed on the stenotic mitral valve with restricted flow
from the left atrium to the LV, worsen maternal and perinatal
complications. Because the flow across the valve is essentially
fixed, the progressively increased preload with advancing ges-
tation leads to an increase in the pressure gradient from the left
atrium to the LV. The elevated left atrial pressure may lead to
pulmonary edema or pulmonary hypertension in extreme
cases. Arrhythmias such as atrial fibrillation may result from
the chronically elevated left atrial pressure. Women with MS
should be diagnosed and evaluated prior to conception by a
multidisciplinary team; however, oftentimes, both patient and
the physician are unaware of underlying valve disease until
symptoms prompt echocardiography during pregnancy [39].
The physiologic hypervolemia and increased heart rate can
significantly increase the transmitral pressure gradient, which
may lead to an overestimate of MS severity. The Doppler
pressure half-time method (MVA = 220/pressure half-time)
may overestimate valve areas in pregnancy and may lead to
life-threatening consequences. The continuity equation, which
is calculated as stroke volume / transmitral velocity time inte-
gral, appears to be a valid method for estimating MVA during
pregnancy [40]. Planimetry has been shown to have the best
correlation with anatomic MVA as assessed by explanted
valves [41]. However, it tends to overestimate MVA compared
with 3D TEE measurements, especially in patients with a large
left atrium [42]. Mitral valve gradient is a hemodynamic factor
of substantial prognostic value in patients with acquired mitral
valve disease [43]. Figure 2 shows echocardiographic findings
of severe rheumatic MS in a pregnant woman; video 2 and
video 3 demonstrate severe mitral stenosis in the short-axis
view and the turbulent diastolic color Doppler of mitral valve
stenosis in the same patient.
The severity of MS correlates with the incidence of mater-
nal complications. Pulmonary edema occurred in approxi-
mately 60 % of patients with significant MS at the gestational
Page 5 of 10 92
Intermediate risk High risk
Moderate/severe MS Symptomatic obstructive cardiac lesions:
severe AS, PS, uncorrected coarctation of aorta
Mild/moderate AS Systemic ventricular dysfunction
(LVEF <40 %)
Severe PS Prosthetic valves
Severe pulmonary hypertension
age of 30 weeks, when the vascular volume is near its peak,
and in 20 % of these patients occurred in the presence of atrial
tachyarrhythmias [44]. Supraventricular tachycardias and atri-
al fibrillation, especially with a rapid ventricular response, can
lead to reduced ventricular diastolic filling and cardiac output
[25•], as well as left atrial appendage thrombus with a risk of
embolization.
Percutaneous mitral balloon valvuloplasty can be per-
formed without significant maternal or fetal risk during
pregnancy and has been used as a viable option for the
treatment of pregnant women with severe mitral valve
stenosis [45]. An echocardiographic score in MS includ-
ing valvular thickness, mobility, calcification, and
subvalvular disease is relatively important, with a score
of ≤8 predicting a more successful outcome [46]. In ad-
dition, transthoracic echocardiography also can be used
to diagnose concomitant mitral regurgitation, subvalvular
stenosis, and left atrial thrombi. Transesophageal echo-
cardiography also has been established as a diagnostic
and safe option in pregnant women, especially for eval-
uation of mitral valve anatomy and for the detection of
left atrial thrombus prior to consideration for balloon
valvuloplasty during or after pregnancy [47].
Mitral Valve Insufficiency
Mitral valve insufficiency accounts for the second most
frequent valve disease during pregnancy. Mitral valve
prolapse from myxomatous mitral valve disease is the
most common etiology in the developed world. Mitral
valve insufficiency can also result from rheumatic heart
disease, ischemic heart disease, and rupture of chordae
tendineae. Although an increase in the overall blood
volume leads to an increase in mitral valve insufficien-
cy, the reduced systemic resistance and systolic blood
pressure may lead to a decrease in the regurgitation
92 Page 6 of 10
Fig. 2 Transthoracic echocardiographic images showing severe
rheumatic aortic valve stenosis in a 32-year-old Mongolian female grav-
ida 2 para 0 (G2P0). Images were taken at 29-week gestation. a
Transthoracic parasternal long-axis view. b Parasternal short-axis view
during pregnancy [43]. Therefore, patients often tolerate
mitral regurgitation well—although severe mitral regur-
gitation with increased end-diastolic pressure may lead
to heart failure [48]. Echocardiography should be used
to assess the etiology of regurgitation, as well as ven-
tricular function, especially for those who develop acute
regurgitation and decompensation [43].
Aortic Valve Stenosis
The incidence of aortic valve stenosis is 0.5–3 % in pregnancy
with heart valve diseases [47–50]. The most common etiolo-
gies are congenital bicuspid aortic valve and rheumatic heart
disease. Figure 3 shows severe rheumatic aortic valve stenosis
in the same patient as in Fig. 2, who also had severe rheumatic
mitral valve stenosis. Similar to MS, mild-to-moderate aortic
stenosis with normal ventricular function is often well
Curr Cardiol Rep (2016) 18:92
showing a stenotic mitral valve. c Color Doppler across mitral valve in the
apical four-chamber view showing a marked increase in turbulence across
the mitral valve. d Continuous wave Doppler across mitral valve showing
a marked increase in peak and mean mitral valve gradients
tolerated, while severe aortic stenosis is poorly tolerated dur-
ing pregnancy. The severe complications of aortic stenosis
including angina, syncope, and congestive heart failure neces-
sitate prompt evaluation. A significant increase in pressure
gradient can be found due to hypervolemia, increased heart
rate, and increased cardiac output during pregnancy. There
may be associated LV hypertrophy. Despite increased demand
in pregnancy, the cardiac output is fixed in severe aortic ste-
nosis. Similar to mitral valve stenosis, an increased preload
can lead to elevation in left atrial and pulmonary artery pres-
sures. However, decreased preload can cause life-threatening
underperfusion to the coronary arteries and the brain in pa-
tients with severe aortic stenosis. Echocardiography can mea-
sure the aortic valve area and pressure gradient, in addition to
determining the severity of LV hypertrophy and systolic dys-
function; video 4 is transesophageal short-axis view at the
mid-esophageal level showing stenotic aortic valve. A
Curr Cardiol Rep (2016) 18:92
Fig. 3 Transthoracic (a, b) and transesophageal (c, d) echocardiographic
images showing severe rheumatic aortic valve stenosis in a 32-year-old
Mongolian female gravida 2 para 0 (G2P0). Images were taken at 29-
week gestation. a Transthoracic parasternal long-axis view. b Continuous
maximum pressure gradient increase of 20 to 35 mmHg may
result from the increased blood volume and flow in the third
trimester in normal pregnancy. Hence, aortic valve planimetry
and the ratio of velocity-time integrals estimated for aortic
valve and LV outflow tract are better markers of severity with
a good correlation with the actual aortic valve area in preg-
nancy [40].
Aortic Valve Insufficiency
Similar to mitral valve insufficiency, aortic valve regurgitation
is well tolerated in pregnancy, except in severe cases. As aortic
valve regurgitation results in a fraction of stroke volume being
directed back to the LV in diastole, long-standing aortic valve
regurgitation may cause LV dilation and dysfunction.
Echocardiography can assess the severity of aortic regurgita-
tion, LV size, and ejection fraction.
Page 7 of 10 92
Doppler in apical five-chamber view. c Mid-esophageal view showing a
stenotic aortic valve in short axis. d Stenotic aortic valve with doming of
leaflets in the long-axis view
Pulmonic and Tricuspid Stenosis and Regurgitation
Since pulmonary vascular resistance is low at baseline, pul-
monic and tricuspid stenosis and regurgitation are generally
well tolerated in pregnancy. As severe lesions are usually
corrected in childhood, the presence of severe pulmonary
and tricuspid valve disease in adulthood is rare. Besides con-
genital lesions, the etiology of pulmonary and tricuspid le-
sions also includes endocarditis from intravenous drug use.
Echocardiography can determine the tricuspid valve function,
size, severity of pulmonary stenosis, and regurgitation, as well
as right ventricular enlargement/hypertrophy.
Pulmonary Hypertension
Primary and secondary pulmonary hypertensions have been
often associated with approximately 30 and 50 % maternal
92 Page 8 of 10
mortality, respectively, despite improvement in medical ther-
apy over the past decade [49, 50, 51•, 52]. Since most mater-
nal deaths take place in the first month after delivery, recog-
nition of pulmonary hypertension is essential in pregnant
women. Echocardiography plays an important role in defining
the etiology and the degree of pulmonary hypertension.
Although the blood volume increases, the pulmonary vascular
resistance decreases simultaneously and the mean pulmonary
artery pressure should be <25 mmHg at rest in pregnancy. A
pulmonary arterial systolic pressure of 50 mmHg or greater
than two thirds the systemic pressure is considered high risk
during pregnancy.
Coronary Heart Disease
Coronary heart disease is relatively uncommon in premeno-
pausal women. However, it is one of the most common cardi-
ac causes of maternal death, as cardiac disease is a leading
cause of maternal mortality over the past two decades [51•,
52–54]. While symptoms such as epigastric pain and vomiting
or dizziness related to coronary heart disease are atypical in
pregnancy, the diagnosis can be delayed—especially in those
without known heart disease. The diagnosis of coronary heart
disease in pregnancy is based on ischemic symptoms, electro-
cardiographic findings, and elevations in cardiac biomarkers,
with many of the same criteria as outside of pregnancy [55]. A
normal echocardiogram does not exclude myocardial infarc-
tion, especially non-ST elevation myocardial infarction, dur-
ing pregnancy.
Stress echocardiography has been recognized as a relative-
ly accurate noninvasive test for diagnosing coronary heart
disease. Exercise echocardiography has been shown to be safe
in late gestation [54–57]. If stress testing is required in preg-
nancy, exercise echocardiography is preferred because of no
exposure to radiation or radiopharmaceutical agents [58].
Although there is no evidence that dobutamine stress echocar-
diography is unsafe in pregnant women who are unable to
exercise, the European guidelines on the management of car-
diovascular diseases in pregnancy state that dobutamine stress
echocardiography should be avoided whenever possible [1•].
Conclusions
The cardiovascular hemodynamic and physiologic changes of
pregnancy are reversible. While the normal cardiovascular
system is able to adapt to the increased requirements of preg-
n a n c y, t h e d i s e a s e d h e a r t m a y d e c o m p e n s a t e .
Echocardiography can define the extent and severity of cardi-
ac lesions and evaluate ventricular function as well as valvular
abnormalities. Patients with established heart pathology
should be thoroughly assessed prior to becoming pregnant.
Curr Cardiol Rep (2016) 18:92
Serial echocardiography and follow-up with a team of special-
ists throughout gestation are strongly recommended.
Compliance with Ethical Standards
Conflict of Interest Shuang Liu, Uri Elkayam, and Tasneem Z. Naqvi
declare that they have no conflict of interest.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
References
Papers of particular interest, published recently, have been
highlighted as:
• Of importance
1.• Regitz-Zagrosek V, Blomstrom Lundqvist C, Borghi C, et al. ESC
Guidelines on the management of cardiovascular diseases during
pregnancy: the Task Force on the Management of Cardiovascular
Diseases during Pregnancy of the European Society of Cardiology
(ESC). Eur Heart J. 2011;32:3147–397. The guideline provides a
thorough description of how to manage cardiovascular disease
in pregnancy.
2. Matthews TJ, Hamilton BE. Delayed childbearing: more
women are having their first child later in life. NCHS Data
Brief. 2009;21:1–8.
3. Desai DK, Moodley J, Naidoo DP. Echocardiographic assessment
of cardiovascular hemodynamics in normal pregnancy. Obstet
Gynecol. 2004;104:20–9.
4. Keser N. Echocardiography in pregnant women. Anadolu Kardiyol
Derg. 2006;6:169–73.
5.• Poppas A, Shroff SG, Korcarz CE, et al. Serial assessment of the
cardiovascular system in normal pregnancy. Role of arterial com-
pliance and pulsatile arterial load. Circulation. 1997;95:2407–15.
The study provides a systemic assessment of cardiovascular
system in normal pregnancy.
6. Siu SC, Colman JM. Heart disease and pregnancy. Heart.
2001;85:710–5.
7. Naqvi TZ, Sum LM, Elkayam U. Pregnancy and the heart. In: Lang
RM et al., editors. ASE’s comprehensive echocardiography. 2nd ed.
Philadelphia: Elsevier-Saunder; 2015. p. 797–800.
8. Sadaniantz A, Kocheril AG, Emaus SP, et al. Cardiovascular chang-
es in pregnancy evaluated by two-dimensional and Doppler echo-
cardiography. J Am Soc Echocardiogr. 1992;5:253–8.
9. Savu O, Jurcut R, Giusca S, et al. Morphological and functional
adaptation of the maternal heart during pregnancy. Circ Cardiovasc
Imaging. 2012;5:289–97.
10. Geva T, Mauer MB, Striker L, et al. Effects of physiologic load of
pregnancy on left ventricular contractility and remodeling. Am
Heart J. 1997;133:53–9.
11. Gilson GJ, Samaan S, Crawford MH, et al. Changes in hemodynamics,
ventricular remodeling, and ventricular contractility during normal
pregnancy: a longitudinal study. Obstet Gynecol. 1997;89:957–62.
12. Robson SC, Hunter S, Boys RJ, Dunlop W. Serial changes
in pulmonary haemodynamics during human pregnancy: a
non-invasive study using Doppler echocardiography. Clin
Sci (Lond). 1991;80:113–7.
Curr Cardiol Rep (2016) 18:92
13. Estensen ME, Beitnes JO, Grindheim G, et al. Altered maternal left
ventricular contractility and function during normal pregnancy.
Ultrasound Obstet Gynecol. 2013;41:659–66.
14. Mone SM, Sanders SP, Colan SD. Control mechanisms for physi-
ological hypertrophy of pregnancy. Circulation. 1996;94:667–72.
15. Lee MS NM, Qamruddin S. et al. Assessment of cardiac structure
and function by three-dimensional echocardiography in healthy
pregnant women. J Am Soc Echocardiogr. 2013; 26.
16. Grindheim G, Estensen ME, Langesaeter E, et al. Changes in blood
pressure during healthy pregnancy: a longitudinal cohort study. J
Hypertens. 2012;30:342–50.
17. Naqvi T.Z. LMS, Aldridge M, et al. Normal cardiac adaptation
during pregnancy—assessment by velocity vector imaging and
three dimensional echocardiography in healthy pregnant women.
Circulation. 2013; 128:A16377
18. Nagueh SF, Sun H, Kopelen HA, et al. Hemodynamic determinants
of the mitral annulus diastolic velocities by tissue Doppler. J Am
Coll Cardiol. 2001;37:278–85.
19. Moran AM, Colan SD, Mauer MB, Geva T. Adaptive mechanisms
of left ventricular diastolic function to the physiologic load of preg-
nancy. Clin Cardiol. 2002;25:124–31.
20. Fok WY, Chan LY, Wong JT, et al. Left ventricular diastolic func-
tion during normal pregnancy: assessment by spectral tissue
Doppler imaging. Ultrasound Obstet Gynecol. 2006;28:789–93.
21. Mesa A, Jessurun C, Hernandez A, et al. Left ventricular diastolic
function in normal human pregnancy. Circulation. 1999;99:511–7.
22. Liu S, Ma C, Ren W, et al. Left atrial systolic and diastolic dysfunc-
tion in patients with chronic constrictive pericarditis: a study using
speckle tracking and conventional echocardiography. PLoS One.
2013;8, e68718.
23. Katz R, Karliner JS, Resnik R. Effects of a natural volume overload
state (pregnancy) on left ventricular performance in normal human
subjects. Circulation. 1978;58:434–41.
24. Song G, Liu J, Ren W, et al. Reversible changes of left atrial func-
tion during pregnancy assessed by two-dimensional speckle track-
ing echocardiography. PLoS One. 2015;10, e0125347.
25.• Roeder HA, Kuller JA, Barker PC, James AH. Maternal valvular
heart disease in pregnancy. Obstet Gynecol Surv. 2011;66:561–71.
The study provides a thorough description of the epidemiology
of valvular heart disease in pregnancy, classify the pathophys-
iology of valvular disease and evaluate the general principles of
maternal and fetal management for cardiac disease.
26. Abduljabbar HS, Marzouki KM, Zawawi TH, Khan AS. Pericardial
effusion in normal pregnant women. Acta Obstet Gynecol Scand.
1991;70:291–4.
27. Elliott P, Andersson B, Arbustini E, et al. Classification of the car-
diomyopathies: a position statement from the European Society Of
Cardiology Working Group on Myocardial and Pericardial
Diseases. Eur Heart J. 2008;29:270–6.
28. Sliwa K, Hilfiker-Kleiner D, Petrie MC, et al. Current state of
knowledge on aetiology, diagnosis, management, and therapy of
peripartum cardiomyopathy: a position statement from the Heart
Failure Association of the European Society of Cardiology
Working Group on peripartum cardiomyopathy. Eur J Heart Fail.
2010;12:767–78.
29. Sliwa K, Fett J, Elkayam U. Peripartum cardiomyopathy. Lancet.
2006;368:687–93.
30. Elkayam U, Akhter MW, Singh H, et al. Pregnancy-associated car-
diomyopathy: clinical characteristics and a comparison between
early and late presentation. Circulation. 2005;111:2050–5.
31. Ntusi NB, Badri M, Gumedze F, et al. Pregnancy-associated heart
failure: a comparison of clinical presentation and outcome between
hypertensive heart failure of pregnancy and idiopathic peripartum
cardiomyopathy. PLoS One. 2015;10, e0133466.
32. Kharwar RB, Chandra S, Dwivedi SK, Saran RK. A pedunculated
left ventricular thrombus in a women with peripartum
Page 9 of 10 92
cardiomyopathy: evaluation by three dimensional echocardiogra-
phy. J Cardiovasc Ultrasound. 2014;22:139–43.
33. Goland S, Bitar F, Modi K, et al. Evaluation of the clinical relevance
of baseline left ventricular ejection fraction as a predictor of recov-
ery or persistence of severe dysfunction in women in the United
States with peripartum cardiomyopathy. J Card Fail. 2011;17:426–
30.
34. Karaye KM, Henein MY. Peripartum cardiomyopathy: a review
article. Int J Cardiol. 2013;164:33–8.
35. Kaul S, Tei C, Hopkins JM, Shah PM. Assessment of right ventric-
ular function using two-dimensional echocardiography. Am Heart
J. 1984;107:526–31.
36. Attalla W, Gaber R, Bayomy S. Detection of early left ventricular
dysfunction in patients with maternal placental syndrome using
tissue Doppler and strain rate imaging. Hypertens Pregnancy.
2015;34:80–9.
37. Roos-Hesselink JW, Ruys TP, Stein JI, et al. Outcome of pregnancy
in patients with structural or ischaemic heart disease: results of a
registry of the European Society of Cardiology. Eur Heart J.
2013;34:657–65.
38. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC
Guideline for the management of patients with valvular heart dis-
ease: executive summary: a report of the American College of
Cardiology/American Heart Association Task Force on Practice
Guidelines. Circulation. 2014;129:2440–92.
39. Arafeh JM, Baird SM. Cardiac disease in pregnancy. Crit Care Nurs
Q. 2006;29:32–52.
40. Rokey R, Hsu HW, Moise KJ, et al. Inaccurate noninvasive mitral
valve area calculation during pregnancy. Obstet Gynecol. 1994;84:
950–5.
41. Faletra F, Pezzano Jr A, Fusco R, et al. Measurement of mitral valve
area in mitral stenosis: four echocardiographic methods compared
with direct measurement of anatomic orifices. J Am Coll Cardiol.
1996;28:1190–7.
42. Min SY, Song JM, Kim YJ, et al. Discrepancy between mitral valve
areas measured by two-dimensional planimetry and three-
dimensional transoesophageal echocardiography in patients with
mitral stenosis. Heart. 2013;99:253–8.
43. Lesniak-Sobelga A, Tracz W, KostKiewicz M, et al. Clinical and
echocardiographic assessment of pregnant women with valvular
heart diseases—maternal and fetal outcome. Int J Cardiol.
2004;94:15–23.
44. Elkayam U, Bitar F. Valvular heart disease and pregnancy part I:
native valves. J Am Coll Cardiol. 2005;46:223–30.
45. Esteves CA, Munoz JS, Braga S, et al. Immediate and long-term
follow-up of percutaneous balloon mitral valvuloplasty in pregnant
patients with rheumatic mitral stenosis. Am J Cardiol. 2006;98:
812–6.
46. Abascal VM, Wilkins GT, O’Shea JP, et al. Prediction of successful
outcome in 130 patients undergoing percutaneous balloon mitral
valvotomy. Circulation. 1990;82:448–56.
47. Stoddard MF, Longaker RA, Vuocolo LM, Dawkins PR.
Transesophageal echocardiography in the pregnant patient. Am
Heart J. 1992;124:785–7.
48. Sugishita Y, Ito I, Kubo T. Pregnancy in cardiac patients: possible
influence of volume overload by pregnancy on pulmonary circula-
tion. Jpn Circ J. 1986;50:376–83.
49. Banning AP, Pearson JF, Hall RJ. Role of balloon dilatation of the
aortic valve in pregnant patients with severe aortic stenosis. Br
Heart J. 1993;70:544–5.
50. Arias F, Pineda J. Aortic stenosis and pregnancy. J Reprod Med.
1978;20:229–32.
51.• Weiss BM, Zemp L, Seifert B, Hess OM. Outcome of pulmonary
vascular disease in pregnancy: a systematic overview from 1978
through 1996. J Am Coll Cardiol. 1998;31:1650–7. The study
provides the evidence of maternal prognosis depends on the
92 Page 10 of 10
early diagnosis of pulmonary vascular disease, early hospital
admission, individually tailored treatment during pregnancy
and medical therapy and care focused on the postpartal period.
52. Weiss BM, Hess OM. Pulmonary vascular disease and pregnancy:
current controversies, management strategies, and perspectives. Eur
Heart J. 2000;21:104–15.
53. Callaghan WM. Overview of maternal mortality in the United
States. Semin Perinatol. 2012;36:2–6.
54. Cantwell R, Clutton-Brock T, Cooper G, et al. Saving mothers’ lives:
reviewing maternal deaths to make motherhood safer: 2006–2008.
The Eighth Report of the Confidential Enquiries into Maternal Deaths
in the United Kingdom. Bjog. 2011; 118 Suppl 1:1–203.
Curr Cardiol Rep (2016) 18:92
55. Turitz AL, Friedman AM. Ischemic heart disease in pregnancy.
Semin Perinatol. 2014;38:304–8.
56. MacPhail A, Davies GA, Victory R, Wolfe LA. Maximal exercise
testing in late gestation: fetal responses. Obstet Gynecol. 2000;96:
565–70.
57. Szymanski LM, Satin AJ. Exercise during pregnancy: fetal re-
sponses to current public health guidelines. Obstet Gynecol.
2012;119:603–10.
58. Colletti PM, Lee KH, Elkayam U. Cardiovascular imaging
of the pregnant patient. AJR Am J Roentgenol. 2013;200:
515–21.