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INTRODUCTION

Prevalence of maternal heart disease -< 1%, its presence increases the risk of adverse maternal, fetal, and neonatal outcomes
0.24% of all pregnancies in western industrialized countries. {Am J Obstet Gynecol 1998;179:16431653.}.

In western countries maternal heart disease is now the major cause of maternal death during pregnancy

RHD dominates in non-western

countries [5689% ] Congenital heart disease [just 919%].

Eur J Heart Fail 2008;10:855-860, Circulation 2001;104:515-521.

STUDY
A Canadian study analyzed the outcomes of

pregnancy in a group of women with congenital or acquired heart disease (562 women and 599 pregnancies)

CARPREG study (Circulation.2001;104:515-21.)

Maternal outcomes
Incidence of adverse maternal cardiac events 13% of completed pregnancies More likely if:

EF below 40% Left heart obstruction (AS with a valve area of less than 1.5 cm2 or MS with a valve area of less than 2.0 cm2) Previous cardiovascular events or arrhythmia NYHA class > II or cyanosis.

These events occurred in: 4% of the women with none of these risk factors 27 % of those with one risk factor 62 % of those with two or more risk factors The 3 women that died had two or more risk factors Sui et al

Fetal outcomes
NYHA class III or IV and left heart obstruction were

predictors of fetal outcomes also.

Other predictors of adverse fetal outcomes include:


The use of anticoagulant drugs Smoking during pregnancy. Multiple gestation. Mothers age (> 35 yrs or < 20 yrs). ZAHARA study

Fetal mortality :
4 % among pregnancies in women with one or more of these risk

factors. 2% among those with none of these risk factors.

WHO CLASS II Most arrythmias WHO CLASS II/III Mild LV impairment VHD not included in class IV WHO CLASS III Mechanical valve

CLASS IV Pulmonary hypertension of any cause Previous PCM with LV impairment Severe MS and severe symptomatic AS Severe LV dysfunction

Evaluation

The evaluation- Pre conceptional and entail a full cardiac

assessment.

H/o exercise capacity, current or past evidence of heart failure and associated arrhythmias.
Cardiac hemodynamics -PAP and the severity of valve

dysfunction - assessed by echo.

Exercise testing - Assessment of functional capacity. During pregnancy evaluation of each trimester - Assess any

deterioration in maternal cardiac status.

INVESTIGATIONS -ECHO
Gradients in RVOT and LVOT increase
Increased stroke volume cause increase in severity of

regurgitation. LVEDD increased TEE can be performed safely Fetal echo best in 20 weeks gestation.

TMT
80% of predicted heart rate
No evidence of spontaneous abortion Dobutamine stress should be avoided

Assessment of myocardial reserve pre pregnancy in

PPCM & VHD Nuclear stress tests are avoided.

Fluoroscopy risks
Majority of procedures are < 1mGy to fetus RCR -2009 guidelines During the first 14 days of fertilization -no risk After 14 days major risk occurs if doses > 100mGy Doses <50 mGy no risk 50-100 mGy risk not clear

Estimated radiation exposure

Valvular Heart Disease


Severity Risk Stenotic lesions > Regurgitant lesion

Left sided diseases> Right sided disease

MS
Poorly tolerated [ moderate & severe MS]- Tachycardia, increased plasma

volume
PHT, Trans valvular gradients, PAP measurements are less reliable marker

of severity
Maternal Risks- HF symptoms, Pulmonary edema in II & III trimester. AF

[increases risk of T.Emb, pulmonary edema] ( El Kayam etal, 2005 JACC)


Moderate & severe MS counseled against pregnancy without prior

intervention Fetal risks- prematurity 20-30%; IUGR 5-20% ( El Kayam & Hameed 2001) & Silversides JACC 2001: 37:893-899

MS INTERVENTIONS
NYHA III or IV patients or valve area less than 1 cm2 ,

BMV or MVR before pregnancy. BMV - second trimester in NYHA III/ IV or with PAP above 50 mm Hg despite optimal medical therapy. MVR during pregnancy- high fetal loss (30%) hence reserved till all measures fail and mother`s life is in danger. Anticoagulation in AF OR in bed rest.

BMV OUTCOMES
BMV in pregnancy KEM study (Gupta et al) successful

outcomes of 40 pregnancies. Ribeiro et al (1992)study on maternal outcomes in 78 patients-8 patients developed mod MR, No evidence of PE De Souza et al(2001) compared the outcomes of PBMV v/s OMC in 21 pts with severe MS -38% fetal death in OMC Current consensus PBMV to symptomatic patients with severe MS with OMT/ MVA 0.75-1.2cm2 Complications- CT , AF ,MR ,emboli, uterine contractions & labor

PERIPARTUM MANAGEMENT
Vaginal delivery is the usual approach.
Avoidance of volume overload and tachycardia is the

main hemodynamic goal.


In unstable patients, monitoring with arterial line and

PCWP aids in optimum hemodynamic management.

PERIPARTUM MANAGEMENT
Epidural analgesia.
Assisted-delivery devices during the second stage

of delivery eliminate hemodynamic effects of valsalva maneuver during pushing.


Caesarean section for obstetrical indications.

Pharmacological management of symptoms MS with symptoms or PAH, restricted activities and 1selective blockers are recommended. Diuretics are recommended when congestive symptoms persist despite blockers.

BMV NYHA class III/IV or sys PAP > 50mm Hg, preferably after 20 weeks POG. [CI in asymptomatic women]

Anticoagulation Paroxysmal or Permanent AF, LA thrombus, prior embolism Considered in mod/sev MS with spontaneous echo contrast, LA > 40ml/m2, low CO, CCF

MITRAL REGURGITATION
Well tolerated due to reduction in SVR.
Women with symptomatic MR may benefit from

mitral-valve surgery (preferably repair))before becoming pregnant. Diuretics may be indicated. Outcome data that would help to guide clinical decision making in this area are lacking.

AORTIC STENOSIS
Congenital valvular abnormalities are usually the cause

of AS in young women in the US.

Severe AS is poorly tolerated during pregnancy.

Maternal and perinatal mortality of 17%


(Pieper et al 2008)

and 32% respectively have been reported.

AORTIC STENOSIS
Symptomatic patients - peak outflow gradient > 50 mm

Hg are advised to delay conception until after surgical correction. Termination of pregnancy- if patient is symptomatic before the end of the 1st trimester. Even severe AS may be asymptomatic Aortic-valve replacement and palliative aortic balloon valvuloplasty have been performed during pregnancy with associated maternal and fetal risk.

CONTD..
Maternal risk HF 10%, Arrhythmias 3-25%(Pieper et

al 2008) Fetal risk- Preterm Labour, IUGR, LBW

PERIPARTUM MANAGEMENT
Vaginal delivery is the usual approach.
Oxytocin may decrease the SVR and increase PAP. Epidural analgesia may be given. Avoid sudden decrease in SVR.

Cesarean section GA has traditionally being advocated to avoid sudden decreases of SVR. Case reports of regional anesthesia with positive outcomes.

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 falling 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/ emergency AVR
Delivery Vaginal delivery + regional anesthesia in non-sev AS LSCS in Sev AS

Aortic Regurgitation
Root dilatation (Marfan syndrome ),Bicuspid

Aortic valve, and RHD are the commonest causes.


The reduced SVR of pregnancy reduces the volume of

regurgitated blood

Women with an abnormal functional capacity or left

ventricular dysfunction are predicted to have a high risk of abnormal maternal outcomes, but few data concerning this population are available

Tricuspid valve lesions


Better tolerated
Maternal risk- HF, Arrhytmias, Progressive worsening of regurgitations Moderate to severe Regurgitant lesions may undergo exercise testing to

decide pre pregnancy intervention


Severe lesions + symptoms/ impaired LV function/ Ventricular

dilatation treated surgically, if possible repair


TV repair if moderate Secondary TR with annular dilatation >40mm,

usually during left sided valve surgeries

PS & PR
PS is generally well tolerated
Complications of sev PS- RV failure & Arrhythmias Pre pregnancy balloon valvuloplasty in severe stenosis

(peak Doppler gradient > 64 mmHg) LSCS is considered in patients with severe PS and in NYHA class III/IV despite medical therapy and bed rest, in whom percutaneous pulmonary valvotomy cannot be performed or has failed. Hameed et al ( JACC 2003 )

Severe PR with impaired RV function


Pre-pregnancy pulmonary valve replacement (preferably

bioprosthesis) should be considered

Prosthetic valves
Mechanical valves
Excellent H.D. Performances

Bioprosthetic valves
Good H.D Performances

Long term durability


Thrombogenic

Much less thrombogenic


High risk of valve

degeneration [~50% women <30yrs at 10 yr post implant]


M> A,T position Reoperation mortality risk addl

5%

Management of valve thrombosis in pregnancy


Presents as embolism or dyspnoea TTE and then TEE is required. If still not confirmed a

fluoroscopy is done Fibrinolysis is recommended ESC 2010 guidelines - anticoagulation optimisation for small clots Thrombolysis has shown little negative effects on fetus Streptokinase bolus of 250000 IU followed by 100000 iu/hr for 72hrs

General Management
Percutaneous intervention After 4th month in the second trimester [ organogenesis complete, fetal thyroid still inactive, volume of uterus small] ACT b/w 200-300s CPBypass 13th & 28th week [Fetal malformation - I trim & maternal complication - III trim] 3-6% late neurological impairment in children, high fetal mortality hence Sx only when refractory to medical therapy, interventional procedures fail, mothers life threatened

Peripartum cardiomyopathy

Eur J Heart Fail 2010;12:767778.

Etiology
Cathepsin D in response to oxidative stress cleaves Prolactin into angiostatic & proapoptotic fragment 16 kDa Prolactin Fas/Apo-1, C-reactiveprotein, IFN-g and IL-6 Viruses Autoimmune

Differential diagnosis

Eur J Heart Fail 2010;12:767778.

Natural history
.

Am J Obstet Gynecol 2008;199:415.e1-415.e5.

PRESENTATION
First 4 months after delivery- most of them(78%)
Last month of pregnancy- 9% > than 4months after delivery or before 1month of pregnancy 13%

CLINICAL FEATURES Features of right heart or left heart failure or both Can present as ventricular arrythmia 92% heard a third heart sound (2005 South African study) LV thrombosis is seen

INVESTIGATIONS
Diagnosis of exclusion
ECG 66% LVH, 96% ST-T changes Elevated BNP and NT pro BNP

Echo Not all have LV dilatation and LVEDD>60

predicts poor recovery MRI is a better predictor of LV functions and assesses the chamber volumes better.( Late gadolinium enhancement)

FOLLOW UP
Repeat echo after 6weeks, 6months and then annually
MRI at 6months and annually for accurate assessment

of LV volumes and function

MANAGEMENT
Similar to HF management
O2 administration to reach saturation of>95% NIV and PEEP 5-7.5 cm H2O

Loop diuretics and NTG


Inotropics when required Pts after OMT and IABP ,the pt may require assist

device or cardiac transplantation LVAD used as bridge to transplantation or destination therapy

Management of stable heart failure


ACEI and ARB avoided
Hydralazine and nitrates combination used safely Beta 1 selective agents are preferred

LMWH and UFH used in pregnancy


Role of CRT AND ICD- pt with LV dysfunction for 6

months post presentation Bromocriptine- used in acute stage- 2.5mg bd (Denise etal 2007)

Delivery need not be done in asymptomatics


Encouraged in deteriorating patients Vaginal delivery encouraged but LSCS in critically ill

patients Left lateral position encouraged

Prognosis
No European studies
Vary geographically

SA- 6m & 2yr mortality rates 10% & 28%. Brazil & Haiti 6m rate 14 16% Turkey- 4yr rate 30%

LV func. returns to normal in 2341%

Eur J Heart Fail 2010;12:767778.

Counselling
LVEF <25% subsequent pregnancies discouraged
High risk of relapse in subsequent pregnancies

Elkayam et al and Habli et al ( 2 studies)

Hypertensive disorders
Accounts for 15% of all pregnancies BP recordings in lateral recumbent posture Ambulatory BP monitoring is superior
Investigations LFT, RFT, urine r/e, Uric acid , Hct Proteinuria >2g/d close monitoring

>3g/d delivery VMA and plasma metanephrine analysis along with USG abdomen Doppler USG for uteroplacental perfusion.

Classification
Pre existing hypertension
Gestational hypertension Pre existing hypertension with superimposed

gestational hypertension with proteinuria Antenatally unclassifiable hypertension

Hypertension defined as SBP> or = 140 & DBP > or = 90 Mild- 140-159/90-109 , Severe ->or = 160/110mmHg

Hypertensive disorders
Type Criteria Pre-existing HTN
>140/ 90 mm Hg, either precedes pregnancy or develops <20 weeks gestation

Comments

Usu. Persists after 42 days PP; 1-5% of pregnancy

Gestational HTN
Pre-eclampsia

>140/ 90 mm Hg, develops >20 weeks gestation


Gest HTN + proteinuria[>0.3g/day or >30mg/mmol U. creatinine] Pre-eclampsia + seizures Pre-existing HTN+ further worsening of BP+ proteinuria [>0.3g/day] after 20 wks

Usu resolves within 42 days PP; 6-7% pregnancy


Upto 25% of prev HTN

Eclampsia Pre-existing HTN + superimposed gestational HTN with proteinuria

Immediate termination of pregnancy required

Antenatally unclassifiable BP first recorded after 20 wks hypertension

Re- assessment after 42 days PP

Management
Non pharmacological- salt restriction, calcium

supplementation Low dose aspirin(75-150mg) at early onset<28 weeks Weight gain- in normal 11.2-15.9kg Pharmacological management- all drugs can be continued except Renin inhibitors , ACEI and ARBs. Severe hypertension iv Labetalol or metaprolol can be used. CCBs are drugs of second choice. Diuretics are not recommended.

Contd
Management of crisis iv Nitroprusside- caution on

cyanide toxicity. Patient with pulmonary edema can be managed with iv Nitroglycerin Methyldopa should be avoided postpartum because it causes depression. Earlier the onset of HT in pregnancy the more the chance of recurrence in next pregnancy

Recommendations in hypertension

CAD
3-6 /100000 deliveries. Coronary artery dissection is a common cause.(LAD is the

common culprit artery).


Aortic dissection, pulmonary embolism and pre eclampsia

also to be ruled out in pregnant women with chest pain Trop I is a useful investigation.
PCI treatment of choice in STEMI.
PCI in high risk NSTEMI only

Contd
PCI preferred to thrombolysis as it will cover up

dissections as well BMS Stents are used CABG carries an extremely high mortality DRUGS- ASA , beta blockers are safe but safety of clopidogrel is not known Vaginal delivery is most appropriate

Tachyarrhythmia
Premature extra beats / sustained tachyarrhythmias become more

frequent and may even manifest for the first time during pregnancy
PSVT in 20-44% of pregnancy. (Am J Cardiol 2006;97(8):1206-1212) Immediate electrical cardioversion - a/c Rx of any tachycardia with

haemodynamic instability
For acute conversion of PSVT- vagal manoeuvre followed by I.V.

adenosine is recommended. I.V. metoprolol or propranolol can also be considered


For long-term management of SVT -oral digoxin or

metoprolol/propranolol is recommended. If not successful oral sotalol or flecainide may be used

Arrhythmia
Immediate electrical cardioversion of VT is

recommended for sustained, unstable & stable VT . I.V. Sotalol or Procainamide - a/c conversion of sustained, haemodynamically stable and monomorphic VT. Oral metoprolol, propranolol or verapamil - idiopathic sustained VT (Long-term management). If unsuccessful oral sotalol, flecainide, propafenone ICD implantation, recommended prior to pregnancy and during pregnancy also. Implantation of PPI or ICDs -considered with echo guidance, especially if the fetus > 8 weeks gestation.

Bradyarrythmia
Rare
Favourable outcome 30% of congenital AV blocks present during pregnancy

Vaginal delivery carries no extra risks


Temporary pacing in patients with CHB with

symptoms Permanent pacing can be done once fetus is > 8weeks of age. Echo guidance is used.

Anticoagulation
No results of RCT to guide the choice of anticoagulant therapy during pregnancy.
Monitoring to assess whether the antithrombotic effect

is adequate. The effective doses of these drugs change during pregnancy because of changes in intravascular volume and body weight. In a series of 976 women with a total of 1234 pregnancies the use of any anticoagulant therapy resulted in major bleeding in 2.5 % of the pregnancies, with bleeding usually occurring at the time of delivery. Arch Intern Med
2000;160:191-196

Anticoagulation Strategies Maternal outcomes- Chan et al(2000)


Valve thrombosis 3.9 % 9.2 35 UFH UFH OAC OAC Maternal mort. 2% 4 15

LMWH

3.6

LMWH

OAC

OAC
In women with mechanical valves the use of OAC -

Greatest maternal protection.(Risk of thromboembolism3.9%, risk of death-1.8%). High rate of fetal loss including spontaneous abortions, stillbirths, and neonatal deaths (30%). Exposure to warfarin between 6 -12 wks -fetal loss twice that associated with the use of UFH Fetopathic effects - (nasal hypoplasia and bone stippling) occurred in approximately 6 % of cases in doses > 5mg
Vitale et al - J Am Coll Cardio 1999;33:1637-41.

Heparin
If heparin rather than warfarin was used during the 1st

trimester, the risks of maternal thromboembolism and maternal death more than doubled (9.2% and 4.2% respectively).

The use of heparin throughout pregnancy was associated

with the highest risks of maternal thromboembolism and maternal death (25% and 7 % respectively).

Long-term use of heparin - HIT and osteopenia.

Arch Intern Med 2000;160:191-6.

LMWH
Lower risks of thrombocytopenia and osteopenia than

UFH There are insufficient data from studies of women with prosthetic heart valves to support the efficacy of this therapy. No data regarding the use in AF with valvular disease. To be monitored with anti X a levels. Target 6 hr post dose 0.8 to 1.2 U/ mL.
J CardioPharmacol Ther 2004;9:107-15.

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 0.81.2 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 to 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 on OACs, LSCS indicated to prevent fetal bleed
UFH/L
12 wks

OAC

OAC

UFH/L
36 wks

UFH

H
6 hrs

6 wks

6 hrs

Differences In strategy

BOOK REFERENCES
BRAUNWALD`S HEART DISEASE
HURST`S THE HEART VALVULAR HEART DISEASE WANG VALVULAR

HEART DISEASE IN PREGNANCY TOPOL TEXTBOOK OF CARDIOVASCULAR MEDICINE

ARTICLES AND REVIEWS

CARPREG study (Circulation.2001;104:515-21.)

Am J Obstet Gynecol 1998;179:16431653 Am J Cardiol 2006;97(8):1206-1212 Am J Obstet Gynecol 2008;199:415 Circulation 2001;104:515-521 Eur J Heart Fail 2008;10:855-860 Eur J Heart Fail 2010;12:767778 N Engl J Med 2001;344:1567-71 Arch Intern Med 2000;160:191-196

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