Pregnancy & Heart Disease

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Pregnancy & Heart Disease Dr Nithin P G

description

Pregnancy & Heart Disease. Dr Nithin P G. Introduction. 0.2–4% of all pregnancies in western industrialized countries Am J Obstet Gynecol 1998;179:1643–1653 . Ht Dis. & Mortality - PowerPoint PPT Presentation

Transcript of Pregnancy & Heart Disease

Page 1: Pregnancy & Heart Disease

Pregnancy & Heart Disease

Dr Nithin P G

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Introduction

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

• Ht Dis. & Mortality– In western countries maternal heart disease is now the major cause of

maternal death during pregnancy [UK 2003-2005].

– In South India, 30% H’ge, 17% sepsis, 13% hypertensive disorders [2001-2003 Special Survey Of Deaths].

• Optimum treatment of both Mother & Fetus must be targeted

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Introduction

• Hypertensive disorders - most frequent CV events during pregnancy [6–8% of all pregnancies] Eur. Heart J. 2011:ehr218v1-ehr218

• Among heart diseases,– Western world Congenital heart disease, most frequent CVD (75–

82%), with shunt lesions predominating (20–65%).– 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.

• Cardiomyopathies are rare. Peripartum cardiomyopathy (PPCM) is the most common.

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Physiological changes in pregnancy

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CO increases after 5wks, 45% by 24 wks, decreases to near normal by 10 days PP SV-increases from 8 to peak at 20wks, decreases to baseline by 2 wks PP

Pl. volume- increases by 6 wks, 1.5-2 times normal by II trimester, plateaus [TBW by 6-8L, Na retension- 500-900 meq]

Increased Aortic compliance, A-V shunting in uterus

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•C.O. at labour 7L/min, increases to 9L/min to 10L/min [500 ml autotransfused/ contraction] [Epidural Anesthesia-8L/min, LSCS- 7-8L/min]

•Immediately after delivery- sudden increase in blood volume by abrupt increase in venous return, autotransfusion, lack of IVC compression autotransfusion continues for 24-72 hrs [risk of Pulm. Edema]

•Complex interactions of gestational hormones, RAA, PG, NO, ANP, BNP pathways produce these changes

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Clinical Findings in Normal PregnancyElevated JVP [increased

plasma vol.]

Tachycardia, low DBP, Pulse Pressure increased [bounding pulses]Pulsatile fingertips, warm hands, occ. Quincke

Apex slight down & out, prominent impulse, active precordium[volume loaded ventricles]

Reduced B.S. at lung bases [diaphragm moves up]

Pedal oedema >60% women [increased plasma vol., increased venous pressures]

S1 Loud [Tachy, increased LV mass], S2 wide split accentuated [P2 delayed], occ S3Flow murm @ aortic, pulm; ESM grade 3 @ LLSB; cervical venous hum; mammary souffle @ LLSB,

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Investigations in normal pregnancy

Investigation Comments

ECG •Tachycardia•LAD [ elev. Diaphragm]•Increased ventricular voltage•Increased Atrial & Ventricular Arrhythmias [increased repolarization changes]

CXR •CE•Horizontal shift of heart•Fullness of Left cardiac border & pulmonary vasc

Echo •LV mass increased, LVED increased, RV & both Atrial enlarges•Increased LVOT & RVOT velocities[ gradients less reliable marker of stenotic severity, 2D valve area best]•Increased regurgitant lesions•Pros. Valve- valve gradients, PHT serial changes to be measured

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Pathological conditions & pregnancy

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Hypertensive disorders

• Hypertension- MC medical problem in pregnancy [15% of pregnancies & 1/4 of all antenatal admissions]

• Hypertensive disorders in pregnancy have been recognized as an important risk factor for CVD in women [ Risk for CAD twice; HTN four times] Circulation 2011;123:1243-1262

• Requires high readings on two separate occasions for diagnosis

Severity • Mild - >140/ 90 mm Hg• Severe- >160/110 mm Hg

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Hypertensive disordersType Criteria Comments

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

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

Gestational HTN >140/ 90 mm Hg, develops >20 weeks POG

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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Pre-eclampsia

• RF- Primi, multiple fetuses, hydatidiform mole or DM

• MC cause for IUGR

Features of Severe Pre-eclampsia• Right upper quadrant/epigastric pain due to liver oedema + hepatic H’ge• Headache + visual disturbance (cerebral oedema)• Occipital lobe blindness• Hyperreflexia + clonus• Convulsions (cerebral oedema)• HELLP syndrome: hemolysis, elevated liver enzymes, low platelet count.

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Non-pharmacological management [normal diet without salt restriction, Calcium supplementation of at least 1 g daily, Low dose acetylsalicylic acid (75–100 mg/day) H.S. is used prophylactically in women with a h/o of early-onset (<28 weeks) pre-eclampsia]

140-149/ 90-99

140-149/ 90-99 +•Gestational HTN•Pre-existing HTN superimposed by gestational HTN •Subclinical organ damage or symptoms at any time during pregnancyOr, ≥150/95

≥170/110

Pharmacological management a-Methyldopa [SE- PP depression], Labetalol, MetoprololNifedipine, isradipine

Pharmacological management Nitroprusside [fetal cyanide toxicity], Nitroglycerine, I.V. Labetalol, oral methyl dopa

Severe Pre-eclampsia

Termination of pregnancyParenteral Magnesium sulphate to prevent eclampsia

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Valvular Heart Disease

• Risk Stenotic lesions > Regurgitant lesion

[ increased C.O. increased transvalvular gradient increased upstream

pressures] vs. [ reduced SVR reduces Regurgitant volume]

• 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]

• Fetal risks- prematurity 20-30%; IUGR 5-20%

• Moderate & severe MS counseled against pregnancy without prior intervention

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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

Delivery•Vaginal delivery in mild MS, NYHA I/II, no PAH•LSCS in Mod/Sev MS, NYHA III/IV, PAH despite medical therapy & BMV cannot be performed or failed.

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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

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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 fallin 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/o.w. emergency AVR

Delivery•Vaginal delivery + regional anesthesia in non-sev AS•LSCS in Sev AS

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Regurgitant 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, usu during left sided valve surgeries

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PS & PR

PS is generally well tolerated – Complic of sev PS-RV failure & Arrhythmias. – Prepregnancy 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.

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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OAC

UFH

LMWH

OAC

UFH

Anticoagulation Strategies

OACLMWH

3.9 %

9.2

35

9

3.6

2 %

4

15

Arch Intern Med 2000;160:191-196

Valve thrombosis Maternal mort.

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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 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

36 wks12 wks6 wks 6 hrs

H

6 hrs

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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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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.Dr Nithin P G

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Natural history

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

•Group 1 (28) EF after index pregnancy > 50% Group 2 (16) EF <50 %•More HF symptoms in group 2 [44 vs. 21%]•Group 2- 3 deaths during subsequent pregnancy

N Engl J Med 2001;344:1567-71.

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Other cardiomyopathies

DCM• Typical symptoms of HF, LV dilation, and LV systolic dysfunction of

unknown origin. • Differentiation from PPCM is supported by the ‘time of manifestation’

– If not known before conception, the condition is unmasked during the I or II trimester when hemodynamic load is increasing.

– Family history of DCM

• Secondary cardiomyopathies, such as infiltrative , toxic CM & storage diseases manifest themselves in pregnancy.

• Maternal risk- Risk of deterioration of DCM during gestation and PP. LVEF < 40% is a predictor of high risk. LVEF is <20% MTP may be considered.

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Other cardiomyopathies

HCM

• Frequently diagnosed for the first time in pregnancy by echocardiography.

• Characterized by diastolic dysfunction due to hypertrophied non-compliant myocardium[ HF, Pulmonary congestion] , severe LVOTO [syncope] and arrhythmias [SVT & VT].

• Maternal risk -usually tolerate pregnancy well. Risk is increased in those

symptomatic before pregnancy and in those with a high outflow gradient.

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Management

• Managed as in non pregnant states• Hydralazine & nitrates instead of ACEI, b1- selective blockers should be used

[n/b- hypoglycemia, bradycardia, resp. depression]. Diuretics used judiciously [ Aldosterone antagonists avoided]. Anticoagulation- I/C thrombus, AF

HCM• b-Blockers - >mild LVOTO and/or wall thickness >15 mm to prevent sudden

pulmonary congestion. Delivery under b-blockers recommended• b-Blockers- rate control in AF & to suppress ventricular arrhythmias. Verapamil

second choice (AV block in the fetus). Cardioversion for persistent arrhythmia because AF poorly tolerated. Therapeutic anticoagulation as indicated

• Severe LVOTO- Epidural anaesthesia must be used with caution • I.V. fluids given judiciously [in view of diastolic dysfunction]• Syntocinon slow infusion [hypotension, arrhythmias, and tachycardia]

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Congenital Heart diseases and PAH

(Elective)

(>20 weeks)

• Miscarriage rate higher in more complex diseases• Maternal cardiac complications in 12% of completed pregnancies & pts are at higher

risk of late cardiac events after pregnancy• Offspring mortality (4%) more frequent than general population

Eur. Heart J. 2011:ehr218v1-ehr218

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Shunt lesions

• Hemodynamically significant shunt best repaired pre pregnancy• Insignificant lesions, good LV function no indication for closure

during pregnancy• Severe PAH/ eisenmenger syndrome – high risk• Pre-pregnancy evaluation of the severity of a shunt, residual

defect in case of repair, estimation of pulmonary pressures, cardiac dimensions & function

• Increase in Arrhythmias, T. Emb. and worsening of NYHA class, higher incidence of preeclampsia

• Hemodynamically significant shunt – SGA baby, fetal mortality

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Coarctation of Aorta

• Unrepaired native CoA and those repaired with residual HTN, residual CoA, or aortic aneurysms have an increased risk of aortic rupture and rupture of a cerebral aneurysm during pregnancy and delivery

• Risk Factors to be screened for- aortic dilatation and bicuspid aortic valve

• HTN should be treated[ aggressive treatment avoided to prevent placental hypoperfusion]

• Percutaneous intervention for re-CoA associated with a higher risk of aortic dissection than outside pregnancy [indic- severe HTN despite max medical Rx and there is maternal or fetal compromise] [covered stents may lower the riskof dissection].

• Vaginal delivery with epidural analgesia preferred

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Cyanotic congenital heart disease

• Maternal complications (HF, pulmonary or systemic thrombosis, SVT, IE) occur in 30% of cyanotic pregnant patients.

• If resting O2 sat. <85%- substantial maternal and fetal mortality risk expected and pregnancy is contraindicated. If 85–90%, measure it during exercise Significant and early decrease pregnancy has poor prognosis.

• With resting maternal blood saturation >90%, fetal outcome is good (<10% fetal loss).

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Cyanotic congenital heart disease

Tetralogy of Fallot• In unrepaired patients, surgical repair is indicated before pregnancy [ Repaired TOF

usually tolerate pregnancy well] • Cardiac complications during pregnancy upto 12% of patients. [Arrhythmias & HF-

MC; Thr. Emb., progressive aortic root dilatation, & IE]. • Risk Factors RV Dysfunction &/or mod to sev. PR [Pregnancy associated with

persisting increase in RV size]• In repaired symptomatic TOF, RV dilatation due to severe PR, pre-pregnancy PVR

(homograft)

Ebstein’s anomaly• Ebstein’s anomaly without cyanosis & HF, pregnancy is often tolerated well. • Symptomatic + Cyanosis and/or HF should be treated before pregnancy or

counselled against pregnancy. In severe symptomatic TR pre-pregnancy repair . [haemodynamic status depends on TR severity & RV function]

• Associated ASD & WPW syndrome. (Incidence of arrhythmias increased) • Other complications- shunt reversal and cyanosis; paradoxical emboli

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Cyanotic congenital heart disease

TGA• Atrial switch operation (Senning or Mustard repair)

– Increased risk of arrhythmias & HF – Underlying bradycardia or junctional rhythmB-blockers with caution. – Irreversible decline in RV function in 10% cases. Pts with > moderate impairment of

RV function or severe TR should be advised against pregnancy.

• Arterial switch surgeries – usually normal pregnancy

CCTGA• Risk depends on functional status, ventricular function, presence of

arrhythmias, and associated lesions. • Complications- arrhythmias& HF

– Pre-disposed to developing AV block B-blockers with caution.– Irreversible decline in RV function in 10% cases. – Patients with NYHA functional class III or IV, EF < 40% or severe TR should be

counseled against pregnancy

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Cyanotic congenital heart disease

Fontan patient

• Moderate to high risk pregnancies [Esp. if the Fontan circuit is not optimal]

• Atrial arrhythmias & NYHA class deterioration

• Pregnancy C.I. - O2 saturation < 85% at rest, depressed ventricular function, mod to sev AV regurgitation or with protein-losing enteropathy

• Premature birth, small for gestational age, and fetal death in up to 50%.

• Therapeutic anticoagulation should be considered.

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Pulmonary Hypertension& Eisenmenger

• Low pregnancy-independent exercise capacity, superimposed on the gestational CV demands, Insufficient adaptation of the right heart and Poorly compliant pulmonary vasculature. J Am Coll Cardiol 1998;31:1650 –7

• Even moderate PAH can worsen during pregnancy - decrease in SVR and overload of RV& “no safe cut-off value”

• High maternal mortality risk is reported (30–50% in older series & 17–33% in more recent papers) in pts with severe PAH and Eisenmenger syndrome. Eur Heart J 2009;30:256–265. Eur Heart J 2009;30:256–265.

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Pulmonary Hypertension& Eisenmenger

• Maternal death occurs in “the last trimester of pregnancy & in the first months after delivery”– pulmonary hypertensive crises– pulmonary thrombosis– refractory right heart failure.

• This occurs even in patients with little or no disability before or during pregnancy.

• Risk factors for maternal death are: late hospitalization, severity of PAH, and GA.

• Neonatal survival rates are reported to be 87–89%. Eur Heart J 2009;30:256–265.

J Am Coll Cardiol 1998;31:1650 –7

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Management

• Avoid Pregnancy & MTP• Maintain circulating Volume, and to avoid systemic Hypotension, Hypoxia, and

Acidosis which may precipitate refractory HF• Supplemental O2 therapy if hypoxaemia; Haemodynamic monitoring by Swan–Ganz

catheter not indicated now [PA rupture]• Diuretics must be used judiciously and at the lowest E.D. to avoid

haemoconcentration and intravascular volume depletion. Microcytosis and iron deficiency should be treated with supplemental oral or i.v. iron

• Anticoagulation- Continued in patients were there is indication for use outside pregnancy. Used with caution in Eisenmenger syndrome [prone to haemoptysis and thrombocytopenia]- used in PE or HF

• I.V. Prostacyclin or aerosolized Iloprost [to improve haemodynamics during delivery]

• Continue drugs for PAH [Bosentan-teratogenic, Sildenafil-category B]• Planned LSCS and vaginal delivery with incremental regional anaesthesia are

favoured over emergency LSCS delivery.

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Management of cyanotic mothers

• Medical – Restriction of physical activity and supplemental oxygen are recommended.– Because of the increased risk of paradoxical embolism, prevention of venous

stasis (use of compression stockings & avoiding the supine position) is important. For prolonged bed rest, prophylactic heparin administration should be considered.

– Haematocrit and Hb levels are not reliable indicators of hypoxaemia. – Diuretics and iron therapy are indicated in patients with Eisenmenger

syndrome.

• Vaginal delivery is advised in most cases [timely hospital admission, planned elective delivery, and incremental regional anaesthesia] If the maternal or fetal condition deteriorates, an early caesarean delivery should be planned. [risks of anesthesia]

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Aortic Diseases

• Pregnancy is a high risk period for all patients with aortic pathology, and aortic pathology is reported as one of the leading causes of maternal mortality

• Causes- – Heritable Aortic diseases- pre-disposing patients to both aneurysm

formation and aortic dissection. [ Marfan syndrome, bicuspid aortic valve, Ehlers–Danlos syndrome, Turner syndrome, and familial forms of aortic dissection, aneurysm, or annuloaortic ectasia]

– Congenital heart disease (TOF, aortic coarctation) may be accompanied by aortic dilatation or aneurysm formation.

– non-heritable aortic pathology

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Aortic Diseases

• Susceptibility to dissection- hormonal changes during pregnancy [most often in the last trimester of pregnancy (50%) or the early postpartum period (33%)]– an enlarged aortic root diameter [Marfan > 45mm ;Bicuspid

AoV>50mm (>27mm/m2)]– previous aortic dissection

• Imaging of entire aorta performed before pregnancy

• Vaginal delivery in < 40 mm, Vaginal delivery with epidural anesthesia in 40-45mm, LSCS in >45mm [ In non-marfan, >40mm]

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Arrhythmia

• Premature extra beats and 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 is recommended for 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 ecainide 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 may be considered for a/c conversion of sustained, haemodynamically stable, and monomorphic VT. Not responding Amiodarone

• Oral metoprolol, propranolol or verapamil is recommended in idiopathic sustained VT (Long-term management). If unsuccessful oral sotalol, ecainide, propafenone

• β-blockers recommended during pregnancy and also postpartum in congenital long QT syndrome.

• ICD implantation, if clinically indicated, is recommended prior to pregnancy but if required, during pregnancy also. Implantation of PPI or ICDs (preferably one chamber) should be considered with echo guidance, especially if the fetus is beyond 8 weeks gestation.

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CAD

• Coronary dissection [LAD] as a cause for MI

• ECG & Troponin measurements in all patients with chest pain

• Aortic dissecction also to be ruled out in pregnant women with chest pain

• PCI treatment of choice in STEMI. STK do not cross placenta but can lead to increased H’ge

• PCI in high risk NSTEMI only

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General Management

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Circulation 2001;104:515-521

Risk stratification

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General Management

• Best time for percutaneous intervention in pregnancy-– After 4th month in the second trimester [ organogenesis complete, fetal

thyroid still inactive, volume of uterus small]– ACT b/w 200-300s

• Best time for CPBypass-– 13th & 28th week POG [Fetal malformation in I trim & Preterm delivery

& maternal complication in 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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General Management

• Vaginal delivery in most cases [lumbar epidural anesthesia]• LSCS in preterm labour on anticoagulants, Marfan >45 mm

aorta, a/c or c/c dissection, intractable HF [also considered in severe AS ,severe PAH including Eisenmenger syndrome & a/c HF]

Post Partum-– slow i.v. infusion of oxytocin (<2 U/min), PG F analogues

[Methylergonovine C.I. [vasoconstriction & HTN]– Elastic support stockings, and early ambulation [reduce the risk of T.

Emb]– First 12–24 h [HF] hence, hemodynamic monitoring continued for at

least 24 h after delivery.

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Thank you

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