ACQUIRED HEART DISEASES IN PREGNANCY ANTICOAGULATION IN PREGNANCY.

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ACQUIRED HEART DISEASES IN PREGNANCY ANTICOAGULATION IN PREGNANCY

Transcript of ACQUIRED HEART DISEASES IN PREGNANCY ANTICOAGULATION IN PREGNANCY.

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ACQUIRED HEART DISEASES IN PREGNANCY

ANTICOAGULATION IN PREGNANCY

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INTRODUCTION

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

• 0.2–4% of all pregnancies in western industrialized countries. {Am J Obstet Gynecol 1998;179:1643–1653.}.

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

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• RHD dominates in non-western countries [56–89% ] Congenital heart disease [just 9–19%].

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

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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.)

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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.• Mother’s 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.

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WHO CLASS IIMost arrythmiasWHO CLASS II/III

Mild LV impairment VHD not included in class IV

WHO CLASS IIIMechanical valve

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CLASS IV Pulmonary hypertension of any cause

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 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.

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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 avoided• Assessment 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 fetusRCR -2009 guidelinesDuring the first 14 days of fertilization -no riskAfter 14 days major risk occurs if doses >

100mGyDoses <50 mGy –no risk50-100 mGy –risk not clear

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Estimated radiation exposure

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Valvular Heart Disease

Severity • 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 prior intervention

• 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 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.

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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/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

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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.

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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.

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Pharmacological management of symptomsMS with symptoms or PAH, restricted activities and β1-selective blockers are recommended. Diuretics are recommended when congestive symptoms persist despite β-blockers.

BMVNYHA 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

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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.

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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 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.

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CONTD…..

• Maternal risk HF 10%, Arrhythmias 3-25%(Pieper et al 2008)

• Fetal risk- Preterm Labour, IUGR, LBW

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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.

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Pharmacological management of symptomsHF- treat with diureticsAF- 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 PregnancySevere 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

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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

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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 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

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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 )

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Severe PR with impaired RV function– Pre-pregnancy pulmonary valve replacement

(preferably bioprosthesis) should be considered

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Prosthetic valves

Mechanical 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 <30yrs at 10 yr post implant] – M> 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 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

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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, mother’s 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 to oxidative stress cleaves Prolactin into angiostatic & proapoptotic fragment 16 kDa Prolactin

Fas/Apo-1, C-reactiveprotein,IFN-g and IL-6

Viruses

Autoimmune

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Differential diagnosis

Eur J Heart Fail 2010;12:767–778.

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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 gadolinium enhancement)

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FOLLOW UP

• Repeat echo after 6weeks, 6months and then annually

• MRI at 6months and annually for accurate assessment of 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 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)

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• Delivery need not be done in asymptomatics• Encouraged in deteriorating patients• Vaginal delivery encouraged but LSCS in

critically ill patients• Left lateral position encouraged

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Prognosis

• No European studies• Vary geographically

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LV func. returnsto normal in 23–41%

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

Eur J Heart Fail 2010;12:767–778.

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Counselling

• LVEF <25% subsequent pregnancies discouraged

• High risk of relapse in subsequent pregnancies Elkayam et al and Habli et al ( 2

studies)

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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

abdomenDoppler USG for uteroplacental perfusion.

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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

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Hypertensive disordersType Criteria Comments

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

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

Gestational HTN >140/ 90 mm Hg, develops >20 weeks 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 of pregnancy 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<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.

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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

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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 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

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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

of clopidogrel is not known• Vaginal delivery is most appropriate

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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

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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 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.

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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 with

symptoms • Permanent pacing can be done once fetus is >

8weeks of age.• Echo guidance is used.

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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

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OAC

UFH

LMWH

OAC

UFH

Anticoagulation StrategiesMaternal 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 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.

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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.

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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.

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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 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

OAC UFH/L OAC UFH/L UFH

36 wks12 wks6 wks 6 hrs

H

6 hrs

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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 –

VALVULAR HEART DISEASE IN PREGNANCY • TOPOL TEXTBOOK OF CARDIOVASCULAR

MEDICINE

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

Am J Obstet Gynecol 1998;179:1643–1653 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;12:767–778

N Engl J Med 2001;344:1567-71

Arch Intern Med 2000;160:191-196

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THANK YOU