PREGNANCY & HEART DISEASE

• 0.2–4% of all pregnancies are complicated by

cardiovascular diseases (CVD)
• and the number of the patients who develop
cardiac problems during pregnancy is
increasing
 RISK FACTORS
• diabetes,
• hypertension,
• obesity
• treatment of congenital heart disease has
improved, resulting in an increased number of
women with heart disease reaching
childbearing age.
 Poor prognostic indicators
• h/o heart failure, ischemic attack, stroke
• Arrhythmias,
• Base line NYHA class 3 and 4
• MV area below 2cm sq., AV area below 1.5
• Ejection fraction less than 40%
• Hypertensive disorders 6–8% of all pregnancies
• congenital heart disease is the most frequent (75–
82%),
• shunt lesions predominating (20–65%).
• Congenital heart disease represents just 9–19% outside
Europe and North America.
• Rheumatic valvular disease dominates in non-western
countries, comprising 56–89% of all cardiovascular
diseases in pregnancy
• Cardiomyopathies are rare, but represent severe
causes of cardiovascular complications in pregnancy.
• Peripartum cardiomyopathy (PPCM) is the most
common cause of severe complications
• The hemodynamic changes are profound and
begin early in the first trimester.
• The plasma volume begins to increase in the sixth
week of pregnancy and, by the second trimester
approaches 50% above baseline. The plasma
volume then tends to plateau until delivery.
• This increased plasma volume is followed by a
slightly lesser rise in red cell mass, which results
in the relative anemia of pregnancy.
• In early pregnancy increased CO is primarily
related to the rise in stroke volume; however, in
late pregnancy, heart rate is the major factor.
• Heart rate starts to rise at 20 weeks and increases
until 32 weeks.
• It remains high 2–5 days after delivery.
• Systemic BP falls early in gestation and diastolic
BP is usually 10 mmHg below baseline in the
second trimester.
 CO In labor
• Beginning of labor : > 7 L/min
• Uterine contraction : > 9 L/Min
• Anesthesia : < 8 L/min
• Post partum CO continues to increase up to 72
hours due to auto transfusion from uterus and
reabsorption of edema fluid

• CO falls to non pregnant values in a few wks after

delivery
• The heart can increase its size by up to 30%,
which is partially due to dilatation.
• Data regarding systolic and diastolic function
in pregnancy are scarce.
• Systolic function increases first but may
decrease in the last trimester.
• Reports on diastolic function are conflicting.
 HEMOSTATIC CHANGES
• increase in concentration of coagulation
factors, fibrinogen, and platelet adhesiveness,
as well as diminished fibrinolysis, which lead
to hypercoagulability and an increased risk of
thrombo-embolic events.
• In addition, obstruction to venous return by
the enlarging uterus causes stasis and a
further rise in risk of thrombo-embolism.
• SBP and DBP increase 15–25% and 10–15%,
respectively, during uterine contractions.
• Such increases are associated with a rise in pressure in
the amniotic fluid, and in the intrathoracic venous,
cerebrospinal, and extradural fluids.
• CO increases by 15% in early labour,
• by 25% during stage 1,
• and by 50% during expulsive efforts.
• It reaches an increase of 80% early post-partum due to
auto transfusion associated with uterine involution and
resorption of leg oedema.
Clinical Findings in Normal Pregnancy
Elevated JVP [increased
plasma vol.]

S1 Loud [Tachy, increased LV mass], S2 wide split

Reduced B.S. at lung accentuated [P2 delayed], occ S3
bases [diaphragm Flow murmur @ aortic, pulm; ESM grade 3 @
moves up] LLSB; cervical venous hum; mammary soufflé @
LLSB,

Apex slight down & out, prominent impulse,

active precordium[volume loaded ventricles]

Tachycardia, low DBP, Pulse Pressure

Pedal oedema increased [bounding pulses]
>80% women Pulsatile fingertips, warm hands, occ.
[increased plasma Quincke
vol., increased
venous pressures]
GENETIC TESTING AND COUNSELLING
• The recurrence risk varies between 3% and
50%
• an autosomal dominant manner (e.g. Marfan
syndrome, hypertrophic cardiomyopathy, or
long QT syndrome) have an inheritance risk of
50%, regardless of gender of the affected
parent.
• Autosomal recessive and X-chromosomal
recessive inheritance are rare.
• Genetic testing may be useful:
– In cardiomyopathies and channelopathies, such as
long QT syndromes
– when other family members are affected
– when the patient has dysmorphic features,
developmental delay/mental retardation, or when
other non-cardiac congenital abnormalities are
present,
– in syndromes such as in Marfan, 22q11 deletion,
Williams–Beuren, Alagille, Noonan, and Holt–Oram
syndrome
• by chorionic villous biopsy can be offered in the 12th week
of pregnancy.
• All women with congenital heart disease should be offered
fetal echocardiography in the 19th to 22nd week of
pregnancy.
• Measurement of nuchal fold thickness in the 12th to 13th
week of pregnancy is an early screening test for women
over 35 years of age.
• The sensitivity for the presence of a significant heart defect
is 40%, while the specificity of the method is 99%.
• The incidence of congenital heart disease with normal
nuchal fold thickness is 1/1000.
Cardiovascular diagnosis in pregnancy
• There is a 15–20 left axis deviation.
• Common findings include
• transient ST segment and T wave changes,
• the presence of a Q wave and inverted T waves in lead
III, an attenuated Q wave in lead AVF, and
• inverted T waves in leads V1, V2, V3.
• Holter monitoring should be performed in patients
with known paroxysmal or persistent documented
arrhythmia [VT, atrial fibrillation (AF), or atrial flutter]
or those reporting symptoms of palpitations.
Echocardiography
• can be repeated as often as needed
• is the preferred screening method to assess cardiac
function.
Trans esophageal echocardiography
• in the assessment of complex congenital heart disease.
• Is relatively safe during pregnancy.
• The presence of stomach contents, risk of vomiting and
aspiration, and sudden increases in intra-abdominal
pressure should be taken into account, and fetal
monitoring performed if sedation is used.
 EXERCISE TESTING
• submaximal exercise tests to reach 80% of
predicted maximal heart rate in asymptomatic
pregnant patients with suspected CVD.
• There is no evidence that it increases the risk
of spontaneous abortion
• Dobutamine stress should be avoided
 RADIATION EXPOSURE
• Should be delayed till 12 weeks
• No evidence if radiation is < 50 mGy
• Increased incidence of childhood cancer
 MRI
• Useful to image complex CHD
• Avoid gadolinium
• Should be used in all patient s suspected of
ascending Ao Enlargement
•CT
• Not recommended
• Only in APE if other diagnostic tools are not
helpful
 Percutaneous therapy
• After 4th month in 2nd trimester
• By this time
– Organogenesis is complete
– The fetal thyroid is inactive
– Uterus size small
Cardiac surgery with cardiopulmonary
bypass
• Only if Medical therapy and PCI fail & life is threatened
• b/w 20th & 28th weeks
• 1st trimester : high risk of fetal malformations
• 3rd trimester : high incidence of preterm delivery &
maternal complications
• If >26 weeks , LSCS before CABG
• Pump flow >2.5 l /min/m2
• Perfusion pressure >70 mm hg

• Maternal complications are comparable to non-

pregnant
 Antenatal Follow up
• Ranging from routine follow up to continuous
hospital admission
• Preferably in Tertiary care centre with cardiac
and cardiac surgical facilities
• Clinical examination and follow up echo
• Saturation
 Induction of Labour
• Oxytocin and artificial rupture of the membranes
are indicated when the Bishop score is
favourable.
• A long induction time should be avoided if the
cervix is unfavourable.
• Misoprostol or dinoprostone- there is a
theoretical risk of coronary vasospasm and a low
risk of arrhythmias.
• Dinoprostone also has more profound effects on
BP than prostaglandin E1 and is therefore
contraindicated in active CVD.
 Vaginal or caesarean delivery
• The preferred mode of delivery is vaginal
• Caesarean delivery should be considered for
obstetric indications
• Cardiac Indications-
– Dilatation of the ascending aorta >45 mm,
– Severe aortic stenosis,
– Pre-term labour while on oral anticoagulants
– Eisenmenger syndrome,
– Severe OR worsening heart failure
– Mechanical prosthesis
 Labour
• Once in labour, the woman should be placed in a
lateral decubitus position to attenuate the
haemodynamic impact of uterine contractions.
• Avoid maternal pushing, to avoid the unwanted
effects of the Valsalva
• Delivery may be assisted by low forceps or
vacuum extraction.
• Continuous electronic fetal heart rate monitoring
is recommended.
 Anaesthesia
• Lumbar epidural analgesia is recommendable
to reduce pain related sympathetic activity,
• Reduces the urge to push
• Regional anaesthesia can cause systemic
hypotension and must be used with caution in
patients with obstructive valve lesions.
Delivery in ant coagulated women with
prosthetic valves
• OACs should be switched to LMWH or unfractionated
heparin (UFH) from the 36th week.
• Women treated with LMWH should be switched to i.v. UFH,
at least 36 h before the induction of labour or caesarean
delivery.
• UFH should be discontinued 4–6 h before planned delivery,
and restarted 4–6 h after delivery if there are no bleeding
complications
• Urgent delivery in a patient with a mechanical valve taking
therapeutic anticoagulation may be necessary, and there is
a high risk of severe maternal hemorrhage.
• If emergent delivery is necessary while the patient is still on
UFH or LMWH, protamine should be considered
• In the event of urgent delivery in a patient on
therapeutic OACs, caesarean delivery is preferred to
reduce the risk of intracranial hemorrhage in the fully
ant coagulated fetus.
• If emergent delivery is necessary, fresh frozen plasma
should be given prior to caesarean delivery to achieve
a target international
• normalized ratio (INR) of ≤2.4 Oral vitamin K (0.5–1
mg) may also be given, but it takes 4–6 h to influence
the INR.
• If the mother was on OACs at the time of delivery, the
anticoagulated newborn may be given fresh frozen
plasma and should receive vitamin K.
• The fetus may remain anticoagulated for 8–10 days
after discontinuation of maternal OACs
 Post-partum care
• Slow i.v. infusion of oxytocin
• Prostaglandin F analogues to treat post-
partum haemorrhage
• Meticulous leg care, elastic support stockings,
and early ambulation are important to reduce
the risk of thrombo-embolism
 IE prophylaxis
• Not recommended
• Regular antihypertensive medications not effective in
preventing preeclampsia.
• When preeclampsia develops,
– bed rest usually is initiated,
– with salt restriction and close monitoring,
– and magnesium sulfate prevent eclamptic seizures and to
prolong the pregnancy.
• Urgent delivery usually is necessary,
• after which the blood pressure usually normalizes rapidly.
• Beta blockers, particularly labetalol have been used with
good effect, although a long safety record has been accrued
with methyldopa, which has no adverse effect on mother
or baby.
 Cyanosis
• Fetal and maternal hypoxia
• Increased thromboembolism
• Increased right to left shunt
• Worsening desaturation
• Paradoxical embolism
 Cyanosis management
• Restriction of physical activity
• Monitoring oxygen saturation
• Supplemental oxygen
• Prevention of venous stasis
– Use of compression stockings
– Avoiding the supine position
– For prolonged bed rest, prophylactic heparin
administration
 ASD
• Common L to R shunt complicating pregnancy
• Prognosis
– Pulm hypertension
– Functional status
– Size of shunt
• Elective closure of an atrial septal defect by
device or operative repair is preferable before
pregnancy
 Ventricular septal defect
• Patients with small VSD tolerate pregnancy
without difficulty
• If large VSD with severe PAH , counselling
regarding the termination.
 PDA
• small ducts with normal or near-normal
pressures usually cause no hemodynamic
perturbations during pregnancy.
• With a large shunt, the added volume load of
pregnancy may precipitate left ventricular
failure.
• Patients with pulmonary hypertension should
be counseled that pregnancy is
contraindicated.
 Pulmonary hypertension
• When the pulmonary hypertension exceeds
approximately 60% of systemic levels, more likely
to be associated with complications.
• The volume load may compromise the poorly
functioning right ventricle
• fall in peripheral resistance augments R-L
shunting =cyanosis
• Labor and delivery are particularly dangerous,
• the highest incidence of maternal death is during
parturition and the puerperium.
 Pulmonary hypertension
• Termination of pregnancy safer option, this is
more complex procedure, and cardiac anesthesia
• successful maternal outcome with the use of
pulmonary vasomodulator drugs.
• Nitric oxide can be administered through nasal
cannula or facemask, and successful pregnancy
also has been reported with intravenous
epoprostenol.
• Sildenafil also has been used, but with all of these
agents, maternal death may still occur days or
weeks after delivery
• In summary, the mortality for pregnant
patients with severe pulmonary hypertension
is high.
• Appropriate advice about contraception
• Estrogen-containing contraceptives are
contraindicated
 Pulmonary valve stenosis
• Relatively well tolerated if the right ventricular
pressure is less than 70% of systemic pressure
• Right ventricular failure
• Arrhythmias.
• Balloon valvuloplasty if PG>64
• CS- severe PS and in NYHA class III/IV despite
OMT
 Cyanosis
• Fetal and maternal hypoxia
• Increased thromboembolism
• Increased right to left shunt
• Worsening desaturation
• Paradoxical embolism
 Cyanosis management
• Restriction of physical activity
• Monitoring oxygen saturation
• Supplemental oxygen
• Prevention of venous stasis
– Use of compression stockings
– Avoiding the supine position
– For prolonged bed rest, prophylactic heparin
administration
 Eisenmenger
• The risks and benefits of anticoagulation
considered on an individual patient basis.
• Diuretics
– The lowest effective dose
– Avoid haemoconcentration
– Intravascular volume depletion.
• Microcytosis and iron deficiency
– Supplemental iron.
 Tetralogy of Fallot
• Pre repair
– Arrhythmias , heart failure , thrombo-embolism
– Progressive aortic root dilatation,
– Endocarditis
• Post repair
– Palliation – depends on the degree of cyanosis
– Dysfunction of the right ventricle
– Moderate to severe pulmonary regurgitation
– Screening for 22q11 deletion - %
 Pulmonary regurgitation
• Severe pulmonary regurgitation
– An independent predictor of maternal
complication
– Bad outcome with impaired ventricular function
• Pulmonary valve replacement
– Pre -pregnancy
– Preferably bioprosthesis
– TPVI – for refractory heart failure
 Ebstein’s anomaly
• Outcome depend on
– The severity of the TR
– right ventricular function
– Cyanosis
– Previous cardiac event
• Usually be managed medically during pregnancy.
• Echocardiographic surveillance of RV function
• Early caesarean delivery If RV function
deteriorates
• After T valve replacement pregnancy is well
tolerated
 Transposition of the great arteries
• Post operative- WHO risk class III.
• Atrial repair
– Atrial arrhythmia
– Severe impairment of RV function
• Great arterial repair
– Obstruction
– Regurgitation
• Bradycardia or junctional rhythm - b-blockers
cautious
• An irreversible decline in RV function in 10%
Congenitally corrected transposition of
the great arteries
• WHO risk class III .
• Pre -disposed to developing AV block
• B-blockers must be used with extreme caution.
• An irreversible decline in RV function has been
described in 10%
• Class 4
– NYHA III or IV,
– EF < 40%
– severe TR
 Fontan circulation
• Successful pregnancy is possible in selected
patients with intensive monitoring - class III
• Class 4
– Patients with oxygen saturation ,85% at rest,
– Depressed ventricular function, and/or moderate
to severe AV regurgitation
 AS

• Usually congenital bicuspid aortic valve [ always

assess aortic diameters]

• Even severe AS may be asymptomatic

• Maternal risk HF 10%, Arrhythmias 3-25%

• Fetal risk- Preterm Labour, IUGR, LBW

Pharmacological management of symptoms
HF- treat with diuretics
AF- b-blockers, CCB to control HR, Digoxin also may be
used

Pre- pregnancy intervention

•Symptomatic severe AS
•LVEF<50%, severe LVH (PW> 15mm)
•TMT- symptoms or fallin BP
•Recent progression of AS
•Asc. Aorta> 50 MM (27.5mm/m2)
During Pregnancy
Severe symptomatic AS + refractory to medical therapy/
life threatening symptoms Non calcified valve may be
subjected to BAV/o.w. emergency AVR

Delivery
•Vaginal delivery + regional anesthesia in non-sev AS
•LSCS in Sev AS
 Coarctation of the aorta
• Repaired
– Restenosis
– Site rupture
• Unrepaired
– Hypertension
– Risk of aortic rupture
– Rupture of a cerebral aneurysm
– PIH
– Associated bicuspid aortic valve- aortic dilation
 Coarctation of the aorta
• Close surveillance of BP
• Avoid aggressive treatment to prevent placental
hypoperfusion.
• PCI is associated with a higher risk of aortic
dissection
• Should only be performed if severe hypertension
persists despite maximal medical therapy and
there is maternal or fetal compromise.
• The use of covered stents may lower the risk of
dissection.
 Hypertrophic cardiomyopathy
• Frequently diagnosed for the first time in pregnancy by
echocardiography.
• Intermittent high catecholamine state of pregnancy ↑ LVOT
obstruction
• Epidural anaesthesia causes systemic vasodilation and
hypotension in severe LVOTO
• Fluids must be given judiciously and volume overload must
be avoided
• The implantation of an ICD should be considered in patients
with high risk factors for sudden cardiac death
• All other management is the same, except for amiodarone
for rhythm control
• Atenolol - class d
 Peripartum Cardiomyopathy
• A form of dilated CMP with LV systolic dysfunction that results in
the signs and symptoms of heart failure
• Criteria
■ Development in last month of pregnancy or the first 5 months after
delivery
■ Absence of heart disease prior to last month of pregnancy
■ Absence of identifiable cause of heart failure
■ LV systolic dysfunction

 Etiology is unknown
 Theories
■ Genetic predisposition
■ Autoimmunity
■ Viral infection
 Peripartum Cardiomyopathy
• Associated risk factors:
■ Age - over 35
■ twin pregnancy
■ gestational hypertension
■ Multiparity
■ use of tocolytic therapy

• Motality rate 25-50%

 Peripartum Cardiomyopathy
• clinical course varies
■ 50-60% of patients demonstrate complete recovery within the
first 6 months
■ The rest of the patients demonstrate either further clinical
deterioration, or premature death, or persistent LV
dysfunction and chronic heart failure
■ Pregnancy contraindicated
• Persistent cardiomegaly
• Cardiac dysfunction
 Peripartum Cardiomyopathy
• Management
■ Acute heart failure treatment with O2, diuretics,
digoxin and vasodilators (hydralazine is safe)
■ Because of the increased incidence of
thromboembolic events, anticoagulation therapy
is recommended
 Anticoagulation Strategies
• OAC throughout pregnancy best strategy [esp. if warf <5 mg, Acitrom
(acenocoumarol) <2 mg]
• Discontinuation of OAC b/w 6 &12 wks and replacement by UFH (a PTT ≥2×
control; infusion in high risk pts) or LMWH twice daily (according to weight and
target anti-Xa level 4-6 hours post-dose 0.8-1.2 U/mL in patients with a warfarin
dose required of >5 mg/day
• OAC discontinued and UFH (a PTT ≥2× control) or adjusted-dose LMWH (anti-Xa
level 4-6 hours post-dose 0.8-1.2 U/mL) started at the 36th week
• LMWH replaced by i.v. UFH at least 36 hours before planned delivery. UFH should
be continued until 4-6 hours before planned delivery and restarted 4-6 hours after
delivery if there are no bleeding complications
• If delivery starts while on OACs, caesarean delivery is indicated to prevent fetal
bleed

OAC UFH/L OAC UFH/L UFH H

6 wks 12 wks 36 wks 6 hrs 6 hrs