Heart Disease in pregnancy

Honorary Prof. Dr Wan Azman Wan Ahmad

MBBS, MRCP, FRCP, FAMM, FNHAM, FAPSC, FAsCC, FAPSIC, FSCAI, FACC, FESC, FASc
Senior Consultant Cardiologist
University Malaya Medical Centre
 Heart Disease in Pregnancy
Incidence in Malaysia was 0.55% in 2013 and 0.45% in 2014.

CVD as a Cause of Maternal Deaths in Malaysia

CVD 2009-2011 2012*** 2013*** 2014***

15.3% 16.1% 13.9% 12.1%

% of total maternal
deaths**
(66/430) (18/112) (15/108) (14/116)

51.2% 50% 50% 53.8%

% of indirect deaths
(66/129) (18/36) (15/30) (14/26)

* Based on data from Confidential Enquiries into Maternal Deaths

**Refers to Indirect and Direct (obstetrics) deaths
*** Unpublished data
Launched 2016
Clinical Questions Addressed:
▪ Issues in a pregnant patient with cardiac disease:
➢ What are the haemodynamic changes and impact of the normal
physiological changes in pregnancy on the cardiovascular system?
➢ What are the effects of the mother’s existing cardiac disease on the
pregnancy?

▪ How do you diagnose patients suspected of cardiac disease in

pregnancy?
▪ How do you risk stratify these patients?
Clinical Questions Addressed:
▪ What are the indications for termination of pregnancy?
▪ What are the safe medications during pregnancy and lactation?
▪ Who and when do you refer to the relevant specialist(s)?
▪ What are the indications for cardiac intervention or surgery in these
pregnant patients?

▪ What are the safe contraceptive methods in patients with cardiac

disease?
 Normal Hemodynamic Changes During Pregnancy

Hemodynamic Change During Change During Change During

Parameter Normal Pregnancy Labor and Delivery Postpartum

Blood volume ↑ 40-50% ↑ ↓

↑ 10-20beats per
Heart rate ↑ ↓
minute
↑ initially with ↑ in
↑ 30-50% above
Cardiac output ↑ additional 50% preload, then ↓
baseline
with diuresis
Returns to
Blood pressure ↓ 10 mm Hg ↑
baseline
↑ 1st and 2nd
↑ (300-500 cc per
Stroke volume trimester; slight ↓ 3rd ↓
contraction)
trimester
Systemic vascular Returns to
↓ ↑
resistance baseline
 Deleterious effects in the pregnant patient
with cardiac disease
• The rise in cardiac output may cause women with limited cardiac
function to develop cardic failure

• The increased preload is a problem for patients with obstructive

lesions (such as severe mitral or aortic stenosis) and/or ventricular
dysfunction.

• Tachycardia causes palpitations and may impair ventricular filling.

 Deleterious effects in the pregnant patient
with cardiac disease
• The hypercoagulable state due partly to an increase in clotting
factors, may predispose to thrombo-embolism

• The changes in renal blood flow may have an impact on drug

excretion thus some drug dosages may need to be modified

• Compression of the inferior vena cava by the uterus can lead to

venous stasis and supine hypotensive syndrome
 Diagnosis
Most forms of cardiac disease can be detected :
• Physical examination
• ECG
• Echocardiography.
• In cases of new HF or if there is diagnostic uncertainty non-contrast
CMR may be considered.
 Commonly encountered cardiac diseases
in pregnancy

▪ Valve disease: Most patients tolerate pregnancy well. Patients with

severe obstructive lesions (mitral and aortic stenosis) should undergo
cardiac intervention prior to pregnancy
▪ Congenital Heart Disease: Most acyanotic and repaired/corrected
patients tolerate pregnancy well.
▪ Patients with pulmonary hypertension and Eisenmenger syndrome
are High Risk and termination of pregnancy should be considered
▪ Patients with Peripartum cardiomyopathy and impaired LV function:
Obstetric and cardiac risk will depend upon the baseline left ventricular
function
 Commonly encountered cardiac issues
▪ Cardiac Failure
▪ Arrhythmias
▪ Anticoagulation especially in patients with mechanical
heart valves
▪ Hypertension – both chronic hypertension (before 20
weeks) and pregnancy induced hypertension (after
20 weeks)
 Peripartum cardiomyopathy(PPCM)
• PPCM presents as HF secondary to LV systolic dysfunction, occurring during third
trimester or in the months following delivery without any other identifiable
cause. The majority of PPCM cases are diagnosed in post-partum.

• Cardiac recovery may occur in the first 3-6 months though it may be delayed up
to 2 years. Recovery rates vary, from 75% to less than 50%.

• Subsequent pregnancies for women with previous peripartum cardiomyopathy

have been associated with further decreases in LV function, maternal death, and
adverse fetal outcomes.

• The strongest prognostic determinant is LVEF <50% before a subsequent

pregnancy
 Risk stratification :Maternal risk
• Pregnant women with heart disease are at risk of adverse
maternal and foetal outcomes.

• Their risk should be assessed before conception or early in the

pregnancy to optimize the outcome of the pregnancy 1C
• Maternal cardiovascular risk can be assessed using the
modified World Health Organisation (WHO) or NYHA
classification
 World Health Organisation (WHO) classification
• WHO Class I: No detectable increased risk of maternal mortality and no/mild
increase in morbidity
• WHO Class II – Small increased risk of maternal mortality or moderate
increase in morbidity
• WHO Class III - Significantly increased risk of maternal mortality or severe
morbidity. Expert counselling is required. If pregnancy is decided upon,
intensive specialist cardiac and obstetric monitoring needed throughout
pregnancy, childbirth, and the puerperium.
• WHO Class IV - Extremely high risk of maternal mortality or severe morbidity;
pregnancy is contraindicated. If pregnancy occurs, termination should be
discussed. If pregnancy continues, care as for class III.
Modified World Health Organization Maternal
Cardiovascular Risk Assessment
Modified World Health Organization Maternal
Cardiovascular Risk Assessment
Modified World Health Organization Maternal
Cardiovascular Risk Assessment
Modified World Health Organization Maternal
Cardiovascular Risk Assessment
Modified World Health Organization Maternal
Cardiovascular Risk Assessment
The functional capacity of the patient can be
classified using the NYHA functional class
New York Heart Association Functional Classification
Risk stratification using the modified WHO
and NYHA classification

NYHA functional
Maternal CV Risk WHO class
class

Low Risk I & II I & II

Moderate Risk II-III & III -

High Risk IV III & IV

 Factors to be considered during maternal
cardiovascular risk assessment
• Lesion specific outcome, e.g. Ventricular septal defect (VSD)
• Complexity of the disease, e.g. VSD with aortic regurgitation (AR)
• Additional or combination of risk factors, e.g. VSD with AR and poor left
ventricle (LV) function
• Pre conception clinical status (NYHA Functional Class) and
investigations (elevated BNP)
• Non cardiac/obstetric factors e.g. hypertension, obesity, Diabetes
Mellitus
• Foetal outcomes, e.g. foeto toxic drugs, genetic transmission17,18
• Individual variations
 Foetal outcomes and risk
▪ Foetal outcome should also be considered when planning the
pregnancy. The following complication is increased in pregnant
patients with cardiac disease.
➢Prematurity,
➢intrauterine growth restriction (IUGR),
➢small for gestational age
➢foetal loss
▪ Foetal complications range between 20–27.8%
▪ Neonatal mortality is 4 times higher compared to a normal
pregnancy
 Genetic transmission
▪ Some maternal cardiac conditions have an increased risk of
genetic transmission to the foetus (e.g. Marfan syndrome)
▪ There is also an increased risk of congenital heart disease
(CHD) in the foetus if either parent has CHD
▪ If neither parent is affected, the risk of recurrence of CHD in a
sibling of an affected individual is between 1-6% and if more
than one sibling is affected the recurrence risk can be up to
10%.
Risk of recurrent congenital heart lesions in the
foetus of parents with CHD
Mother affected Father affected Siblings in unaffected parents
Lesion Risk of Risk of 1 ≥2 siblings
transmission (%) transmission (%) sibling (%) (%)
Atrioventricular
7-11.6 4.3 -7 3-4 NA
septal defect
Aortic stenosis 8.0 3.8 2 6
Coarctation 6.3 3.0 2 6

Atrial septal defect 6.1 3.5 2-3 8

Ventricular septal
6.0 3.6 3 10
defect
Pulmonary stenosis 5.3 3.5 2 6
Persistent ductus
4.1 2.0 NA NA
arteriosus
Tetralogy of Fallot 2-5 1-6 2-3 8
All heart defects 5-7 2.2 NA NA
The maternal predictors of poor neonatal/foetal
outcome in women with heart disease

▪ NYHA Functional Class III & IV

▪ Cyanosis (oxygen saturation <85%)
▪ Mechanical prosthetic valves
▪ Use of heparin or warfarin during pregnancy
▪ Left heart obstructive lesions
▪ Smoking during pregnancy
▪ Twin/multiple pregnancy
 Level of Care will depend on the maternal
CV risk
Low risk: can be managed at their local centre after review by a
family medicine specialist/physician or cardiologist
Moderate risk: should be managed at a tertiary centre by a
multidisciplinary team with cardiac expertise
High risk: should be referred early to the tertiary centre for
assessment. If termination of pregnancy is considered, it can
be performed up to 22 weeks
 HF may develop in pregnancy
• for the first time in a patient with pre-existing heart disease
(congenital and/or valvular) due to decompensation from the stress.

• may occur in a patient who had HF previously and still has a

depressed myocardial function. (LVEF < 40%).

• in a patient with a previously unrecognised genetic cardiomyopathy

or a latent cardiac viral infection which has been unmasked or
activated by the stress of pregnancy.
 HF may develop in pregnancy
In a patient with a previously normal heart due to:

• hypertensive complications of pregnancy

➢gestational hypertension and the more severe forms preeclampsia,
➢the HELLP syndrome (H: haemolysis, EL: elevated liver enzymes, LP:
low platelet count).

• peripartum cardiomyopathy.

• Takotsubo syndrome.
 Management
• The management of HF in pregnancy is more difficult than in the non-
pregnant state and should be managed by a multidisciplinary team
consisting of physicians, obstetricians and paediatricians.

• In the management of HF in pregnancy, the following issues need to

be considered:
➢gestational age at presentation.
➢clinical presentation, either as Acute HF or Chronic HF.
➢response to medical therapy.
➢potential maternal and foetal risks.
➢review and replace all fetotoxic drugs
➢timing and mode of delivery
 Antenatal care

• The principles of management of HF in pregnancy are similar to that

in the non-pregnant state.
• If the patient is in decompensated HF requiring inotropes, she should
be transferred to a cardiac centre.
 Non-pharmacological measures

The management of patients with mild symptoms consists mainly of

non-pharmacological measures such as:
• limiting strenuous exercise.
• adequate rest – maintaining a low salt diet.
• treating anaemia and infections early.
• frequent antenatal examinations.
 Pharmacological measures
The following drugs may be used in the pregnant patient with HF:

• Diuretics are the first line therapy in patients who are fluid
overloaded.
• Nitrates and/or hydralazine are used for preload and afterload
reduction.
• β-blockers can be used cautiously most commonly metoprolol,
• Digoxin is safe in pregnancy and during breast feeding.
• ACE-I, ARB, ARNI, MRA, SGLT2i, ivabradine, and vericiguat are
contraindicated in pregnancy.
• ACE-I (enalapril and captopril) can be used in the post partum period
 Other treatment consideration
• Patients with AF who are haemodynamically unstable should be
promptly electrically cardioverted. This is safe in pregnancy.
• Anticoagulation is indicated in the presence of AF, dilated left atrium
or mechanical prosthetic heart valve.
• Patients with valvular lesions who remain symptomatic despite
optimal medical treatment may be considered for percutaneous valve
intervention or surgery.
• Commonly recommended antihypertensive drugs include
methyldopa, labetalol, calcium channel blockers and hydralazine.
 Other treatment consideration
• In patients with peripartum cardiomyopathy and severe AHF,
bromocriptine may be considered.
• In women with acute HF caused by peripartum cardiomyopathy and
LVEF < 30% anticoagulation may be consider at diagnosis, until 6 to 8
weeks postpartum
• Echocardiographic may be considered in the third trimester for
reassessment of myocardial structure and function before labor;
when there is significant changes in HF symptoms or signs during
pregnancy, or if HF medications are reduced or discontinued.
• BNP or NT-proBNP monitoring during pregnancy may have some
value for prediction of cardiovascular events.
 Labour and delivery
• Timing and mode of delivery should be carefully planned by the
multidisciplinary team.
• In the majority of patients, vaginal delivery with epidural anaesthesia
is the preferred mode of delivery

Caesarean section is indicated:

➢ for obstetric reasons.
➢ in patients on warfarin or who have discontinued their warfarin for <
2 weeks and who now are in imminent labour.
➢ in patients with severe pulmonary hypertension.
 Second stage of labour
• It is beneficial to shorten the second stage of labour by forceps or vacuum
assisted delivery.

• Left lateral decubitus position is preferred to attenuate the haemodynamic

effects in the supine position.

• A slow i.v infusion of oxytocin immediately after birth, (2 U of oxytocin given

over 10 min followed by 12 mU/min for 4 h) reduces the risk of post partum
haemorrhage and has a minimal impact on cardiovascular parameters.

• Routine antibiotic prophylaxis is not recommended in patients with valvular

heart disease undergoing uncomplicated vaginal delivery or Caesarean
section.
 Post partum care
• After delivery, careful monitoring of haemodynamic status should be
done for at least 24 hours, or longer in high risk patients. In patients with
severe cardiac lesions, haemodynamics may be abnormal up to 10 days
after delivery.

• These patients should be evaluated post partum to assess the need for
corrective surgery.

• The risk of recurrence of HF in subsequent pregnancies should also be

made known to the patient.
 Post partum care
• Follow-up visit at 6 weeks post partum should be attended by the
multidisciplinary team, a full cardiac assessment should be done, and
appropriate contraception should be advised.

• Postpartum women who breastfeed can start ACEi (enalapril or captopril

preferred), and metoprolol remains the preferred beta blocker.
 CASE STUDY-1
▪ 25 year old female
▪ G1P0, 24 weeks gestation
▪ Referred to medical clinic for shortness of breath on exertion(NYHA II)
▪ Not known to have any medical illness
▪ O/E: pulse 90/min regular
BP 110/70 mmHg
JVP – 5cm
CVS – Loud S1
Lung - clear
What is your Diagnosis?
 Severe Mitral Stenosis
MVA 1.0 cm2, Mean gradient 20mmHg
 Issues in Management
▪ Risk assessment
▪ Would you allow her to continue her pregnancy
or consider termination of pregnancy?
▪ How do you manage her symptom?
▪ If she decides to continue her pregnancy, how do you plan her
delivery?
At what gestation age to deliver her?
Allow vaginal delivery or LSCS?
 Case Study 2

▪ 27 years old Sabahan G1P0, 27 weeks gestation

▪ Progressive dyspnoea NYHA class IV.
▪ Prior to pregnancy NYHA class II.
▪ Previously thought to have asthma.
▪ Not known to have heart disease or h/o rheumatic fever
▪ No risk factors for CTEPH
Right axis Dominant R
deviation Wave in V1

ST depression
and T wave inversion
What is your Diagnosis?
 Diagnosis
▪ Echo revealed
• mitral valve area 0.65cm2
• dilated right atrium and ventricle
• Pulmonary artery systolic pressure was 135mmHg
• no atrial thrombus
• Enlarged Left atrium
• Ejection fraction was 65%
▪ Diagnosis: Severe Mitral Stenosis with Severe Pulmonary Hypertension,
Management Issue

Option 1
Patient is 27 weeks gestation
▪ Termination of pregnancy
▪ Survival chance of baby 60-70 % due to
prematurity
▪ Reduces cardiovascular risks to mother
but the risk is still high
Option 2 ✓
▪ To continue with pregnancy
▪ Without intervention, the risk of maternal mortality in this patient is up
to 50%
▪ Intervention options
• Percutaneous Transluminar Mitral Commisuratomy (PTMC)-
challenging MVA 0.6cm2, severe PHT, pregnancy
• Surgical Commissurotomy if PTMC not successful, but with higher
risks of maternal mortality and fetal loss
Cardiac Catheterisation pre and post PTMC

PASP 119/55 mmHg

→ PASP 88/55 mmPHg
 Progress Post PTMC
▪ Post PTMC : Mitral valve area was 1.5cm2 with PASP further reduced to
46mmHg prior to delivery
▪ Within 2 weeks NYHA improved to class II.
▪ She was started on T. Digoxin 0.125 mg OD and s/c clexane 60 mg OD
▪ Pregnancy was successfully prolonged until 35 weeks when LSCS was
done for breech
▪ Post natal follow up, she remained asymptomatic and Im Implanon was
inserted 2 months postnatally
 Summary
• Diagnosis
• Risk assessment
• Multidisciplinary team
• Tertiary centre for high risk patient
• Diuretics for failure symptoms.
• Heart rate control with beta blockers and digoxin
• ACE-I, ARB, MRA, SGLT2I, Ivabradine and Vericiguat are contraindicated in
Pregnancy
• Arrhythmias can be catastrophic. DC cardioversion is safe
• Anticoagulation is indicated in the presence of AF, dilated left atrium or
mechanical prosthetic heart valve.
• Patients with valvular lesions who remain symptomatic percutaneous valve
intervention or surgery may be considered
•