Heart Diseases in Pregnancy

8/13/2019 Heart Diseases in Pregnancy

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INTRODUCTION

Prevalence of maternal heart disease -< 1%, itspresence increases the risk of adverse maternal,fetal, and neonatal outcomes

0.24% of all pregnancies in western industrializedcountries. {Am J Obstet Gynecol 1998;179:16431653.}.

In western countries maternal heart disease is nowthe major cause of maternal death duringpregnancy


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RHD dominates in non-westerncountries [5689% ]

Congenital heart disease [just 919%].

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


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STUDY

A Canadian study analyzed the outcomes ofpregnancy in a group of women with congenital oracquired heart disease (562 women and 599pregnancies)

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


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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


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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 riskfactors.

2% among those with none of these risk factors.


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WHO CLASS II

Most arrythmias

WHO CLASS II/III

Mild LV impairmentVHD not included in class IV

WHO CLASS IIIMechanical valve


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CLASS IV

Pulmonary hypertension of anycause

Previous PCM with LV impairmentSevere MS and severe symptomatic

AS

Severe LV dysfunction


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Evaluation

The evaluation- Pre conceptional and entail a full cardiacassessment.

H/o exercise capacity, current or past evidence of heartfailure and associated arrhythmias.

Cardiac hemodynamics -PAP and the severity of valvedysfunction - assessed by echo.

Exercise testing - Assessment of functional capacity.

During pregnancy evaluation of each trimester - Assess anydeterioration in maternal cardiac status.


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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.


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TMT 80% of predicted heart rate

No evidence of spontaneous abortion

Dobutamine stress should be avoidedAssessment of myocardial reserve pre pregnancy in

PPCM & VHD

Nuclear stress tests are avoided.


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Fluoroscopy risks

Majority of procedures are < 1mGy to fetus

RCR -2009 guidelines

During the first 14 days of fertilization -no riskAfter 14 days major risk occurs if doses > 100mGy

Doses


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Valvular Heart DiseaseSeverity

Risk Stenotic lesions > Regurgitant lesion

Left sided diseases> Right sided disease


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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 priorintervention

Fetal risks- prematurity 20-30%; IUGR 5-20% ( El Kayam & Hameed 2001)& Silversides

JACC 2001: 37:893-899


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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 PAPabove 50 mm Hg despite optimal medical therapy.

MVR during pregnancy- high fetal loss (30%) hencereserved till all measures fail and mother`s life is in

danger.Anticoagulation in AF OR in bed rest.


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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/sOMC 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


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PERIPARTUM MANAGEMENTVaginal delivery is the usual approach.

Avoidance of volume overload and tachycardia is themain hemodynamic goal.

In unstable patients, monitoring with arterial line and

PCWP aids in optimum hemodynamic management.


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PERIPARTUM MANAGEMENT Epidural analgesia.

Assisted-delivery devices during the second stageof delivery eliminate hemodynamic effects ofvalsalva maneuver during pushing.

Caesarean section for obstetrical indications.


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Pharmacological management of symptoms

MS with symptoms or PAH, restricted activities and 1-selective blockers are recommended. Diuretics are

recommended when congestive symptoms persist despite -

blockers.

BMVNYHA class III/IV or sys PAP > 50mm Hg, preferably after 20

weeks POG. [CI in asymptomatic women]

AnticoagulationParoxysmal or Permanent AF, LA thrombus, prior embolism

Considered in mod/sev MS with spontaneous echo contrast, LA >

40ml/m2, low CO, CCF


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MITRAL REGURGITATIONWell tolerated due to reduction in SVR.

Women with symptomatic MR may benefit frommitral-valve surgery (preferably repair))beforebecoming pregnant.

Diuretics may be indicated.

Outcome data that would help to guide clinical

decision making in this area are lacking.


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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%and 32% respectively have been reported.

(Pieper et al 2008)


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AORTIC STENOSIS Symptomatic patients - peak outflow gradient > 50 mm

Hg are advised to delay conception until after surgicalcorrection.

Termination of pregnancy- if patient is symptomaticbefore the end of the 1st trimester.

Even severe AS may be asymptomatic

Aortic-valve replacement and palliative aortic balloon

valvuloplasty have been performed during pregnancywith associated maternal and fetal risk.


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CONTD..

Maternal riskHF 10%, Arrhythmias 3-25%(Pieper etal 2008)

Fetal risk- Preterm Labour, IUGR, LBW


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PERIPARTUM MANAGEMENTVaginal 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 positiveoutcomes.


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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 15mm)

TMT- symptoms or falling BP

Recent progression of ASAsc. Aorta> 50 MM (27.5mm/m2)

During Pregnancy

Severe symptomatic AS + refractory to medical therapy/

life threatening symptomsNon calcified valve may besubjected to BAV/ emergency AVR

Delivery

Vaginal delivery + regional anesthesia in non-sev AS

LSCS in Sev AS


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Aortic Regurgitation

Root dilatation (Marfan syndrome ),BicuspidAortic 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 leftventricular dysfunction are predicted to have a high riskof abnormal maternal outcomes, but few data

concerning this population are available


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Tricuspid valve lesions Better tolerated

Maternal risk- HF, Arrhytmias, Progressive worsening of regurgitations

Moderate to severe Regurgitant lesions may undergo exercise testing todecide 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


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PS & PRPS 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 inNYHA class III/IV despite medical therapy and bed rest,

in whom percutaneous pulmonary valvotomy cannot beperformed or has failed.

Hameed et al ( JACC 2003 )


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Severe PR with impaired RV function

Pre-pregnancy pulmonary valve replacement (preferablybioprosthesis) should be considered


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Prosthetic valvesMechanical valves

Excellent H.D. Performances

Long term durability

Thrombogenic

Bioprosthetic valves

Good H.D Performances

Much less thrombogenic

High risk of valve

degeneration [~50% women

A,T position

Reoperation mortality risk addl

5%


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Management of valve thrombosis

in pregnancy Presents as embolism or dyspnoea

TTE and then TEE is required. If still not confirmed afluoroscopy is done

Fibrinolysis is recommended

ESC 2010 guidelines - anticoagulation optimisation forsmall clots

Thrombolysis has shown little negative effects on fetus Streptokinase bolus of 250000 IU followed by 100000

iu/hr for 72hrs


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General Management Percutaneous intervention-

After 4thmonth in the second trimester [ organogenesiscomplete, fetal thyroid still inactive, volume of uterus small]

ACT b/w 200-300s

CPBypass-

13th& 28thweek [Fetal malformation - I trim & maternalcomplication - III trim]

3-6% late neurological impairment in children, high fetalmortality hence Sx only when refractory to medical therapy,interventional procedures fail, mothers life threatened


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Peripartum cardiomyopathy

Eur J Heart Fail 2010;12:767

778.


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Etiology

Cathepsin D in response tooxidative stress cleaves

Prolactin into angiostatic &

proapoptotic fragment 16 kDa

Prolactin

Fas/Apo-1, C-reactiveprotein,

IFN-gand IL-6

Viruses

Autoimmune


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Differential diagnosis

Eur J Heart Fail 2010;12:767778.


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Natural history

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

.


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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


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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 gadoliniumenhancement)


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FOLLOW UP Repeat echo after 6weeks, 6months and then annually

MRI at 6months and annually for accurate assessmentof LV volumes and function


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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 transplantationLVAD used as bridge to transplantation or destination

therapy


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Management of stable heart failureACEI 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 6months post presentation

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


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Delivery need not be done in asymptomatics

Encouraged in deteriorating patients

Vaginal delivery encouraged but LSCS in critically illpatients

Left lateral position encouraged


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Prognosis No European studies

Vary geographically


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LV func.returnsto normal in

2341%

SA- 6m &2yrmortalityrates 10% &

28%.Brazil &Haiti 6mrate 1416%Turkey- 4yr

rate 30%

Eur J Heart Fail 2010;12:767778.


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Counselling LVEF


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Hypertensive disordersAccounts 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 deliveryVMA and plasma metanephrine analysis along with USGabdomen

Doppler USG for uteroplacental perfusion.


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Classification Pre existing hypertension

Gestational hypertension

Pre existing hypertension with superimposedgestational hypertension with proteinuria

Antenatally unclassifiable hypertension

Hypertension defined as SBP> or = 140 & DBP > or = 90

Mild- 140-159/90-109 , Severe ->or = 160/110mmHg


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Hypertensive disordersType Criteria Comments

Pre-existing HTN >140/ 90 mm Hg, eitherprecedes pregnancy or develops

140/ 90 mm Hg, develops >20weeks gestation

Usu resolves within 42 days

PP; 6-7% pregnancy

Pre-eclampsia Gest HTN +proteinuria[>0.3g/day or

>30mg/mmol U. creatinine]

Upto 25% of prev HTN

Eclampsia Pre-eclampsia + seizures Immediate termination ofpregnancy required

Pre-existing HTN +

superimposedgestational HTN with

proteinuria

Pre-existing HTN+ further

worsening of BP+ proteinuria[>0.3g/day] after 20 wks

Antenatally unclassifiable

hypertension

BP first recorded after 20 wks Re- assessment after 42 days

PP


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Management Non pharmacological- salt restriction, calcium

supplementation

Low dose aspirin(75-150mg) at early onset


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Contd

Management of crisis iv Nitroprusside- caution oncyanide toxicity.

Patient with pulmonary edema can be managed withiv Nitroglycerin

Methyldopa should be avoided postpartum because itcauses depression.

Earlier the onset of HT in pregnancy the more thechance of recurrence in next pregnancy


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Recommendations in hypertension


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CAD 3-6 /100000 deliveries.

Coronary artery dissection is a common cause.(LAD is thecommon culprit artery).

Aortic dissection, pulmonary embolism and pre eclampsiaalso 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


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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 ofclopidogrel is not known

Vaginal delivery is most appropriate


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Tachyarrhythmia

Premature extra beats / sustained tachyarrhythmias become morefrequent 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


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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 andmonomorphic VT.

Oral metoprolol, propranolol or verapamil - idiopathicsustained VT (Long-term management). Ifunsuccessful oral sotalol, flecainide, propafenone

ICD implantation, recommended prior to pregnancyand during pregnancy also. Implantation of PPI orICDs -considered with echo guidance, especially if thefetus > 8 weeks gestation.


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Bradyarrythmia Rare

Favourable outcome

30% of congenital AV blocks present during pregnancy

Vaginal delivery carries no extra risks

Temporary pacing in patients with CHB withsymptoms

Permanent pacing can be done once fetus is > 8weeksof age.

Echo guidance is used.


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Anticoagulation

No results of RCT to guide the choice of anticoagulanttherapy 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 volumeand body weight.

In a series of 976 women with a total of 1234 pregnanciesthe use of any anticoagulant therapy resulted in majorbleeding in 2.5 % of the pregnancies, with bleeding

usually occurring at the time of delivery.Arch Intern Med

2000;160:191-196

Anticoagulation Strategies


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OAC

UFH

LMWH

OAC

UFH


Maternal outcomes- Chan et al(2000)

OACLMWH

3.9 %

9.2

35

9

3.6

2 %

4

15

Valve thrombosis Maternal mort.


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OAC In women with mechanical valves the use of OAC -Greatest maternal protection.(Risk of thromboembolism-3.9%, 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 twicethat 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.


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Heparin

If heparin rather than warfarin was used during the 1st

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

The use of heparin throughout pregnancy was associatedwith the highest risks of maternal thromboembolism andmaternal death (25% and 7 % respectively).

Long-term use of heparin - HIT and osteopenia.

Arch Intern Med 2000;160:191-6.


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LMWH Lower risks of thrombocytopenia and osteopenia than

UFH

There are insufficient data from studies of women withprosthetic heart valves to support the efficacy of thistherapy.

No data regarding the use in AF with valvular disease.

To be monitored with anti X a levels. Target 6 hr post dose0.8 to 1.2 U/ mL.

J CardioPharmacol Ther 2004;9:107-15.


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OAC throughout pregnancy best strategy [esp. if warf


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Differences In strategy


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BOOK REFERENCES BRAUNWALD`S HEART DISEASE

HURST`S THE HEART

VALVULAR HEART DISEASE WANG VALVULARHEART DISEASE IN PREGNANCY

TOPOL TEXTBOOK OF CARDIOVASCULARMEDICINE


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ARTICLES AND REVIEWSCARPREG study (Circulation.2001;104:515-21.)

Am J Obstet Gynecol 1998;179:16431653Am J Cardiol 2006;97(8):1206-1212Am J Obstet Gynecol 2008;199:415

Circulation 2001;104:515-521

Eur J Heart Fail 2008;10:855-860Eur J Heart Fail 2010;12:767778

N Engl J Med 2001;344:1567-71Arch Intern Med 2000;160:191-196


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Heart Diseases in Pregnancy

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