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PREGNANCY &
HEART DISEASE
John S. Child, M.D., F.A.C.C.
Streisand/AHA Professor of
Medicine/Cardiology
Director, Ahmanson-UCLA Adult
Congenital Heart Disease Center
David Geffen School of Medicine at UCLA
-No conflicts
-No disclosures
Pregnancy in Heart Disease
• Cardiovascular Disease is the most
common cause of maternal death
• Most common cardiac causes of death are
cardiomyopathy or PHTN
• In developed nations, the most common
cardiovasc diseases are congenital HD
• Surgical advances over 50 years allow
most women with CHD to conceive and
bear children
Pregnancy and Heart Disease –
General Considerations
• Preconception evaluation
• Antepartal & peripartal care –team
effort with GYN, nurses, anesthesia,
and cardiology
• Labor and Delivery
• Early Puerperium
• Antibiotic Prophylaxis
• Anticoagulants
CV hemodynamics & Pregnancy
Increased blood volume
alters SV & CO
CO ~30% higher
beginning week 5-6 peaking middle 2nd to
3rd trimester
Early ↑CO due to ↑SV,
later ↑HR
3rd Trimester Body
position: supine IVC
compression by
Gravid Uterus
decreases preload &
Cardiac Output
60
50
40
CO
30
20
SV
10
HR
0
Baseline
1st
2nd
3rd
PP
Cardiorespiratory Signs & Sxs
of normal Pregnancy
• Dyspnea
(hyperventilation)
•
•
•
•
•
•
•
Fatigue
Exercise intolerance
lightheaded
syncope
peripheral edema
basilar rales
small waterhammer
pulse
• prom JV crests &
troughs
• brisk displaced LVI
• Palpable RV
•
•
•
•
•
•
•
•
Increased S1
Persistent split S2
Third heart sound
Pulmonary outflow
MSM
Supra-clavicular
systolic Murmur
Continuous Murmurs
ECG changes:
rhythm, axis,
repolarization
CXR: lat displacement
apex, increased lung
markings
LABOR & DELIVERY
HEMODYNAMICS
• UTERINE CONTRACTIONS INCREASE SV &
CARDIAC OUTPUT ~ 50%
• Increased CO > in lateral than supine position
• ~ 3-fold increase in O2 consumption
• Heart rate response varies
• Increased systolic & diastolic BP, esp stage II
• Rx of anxiety and pain limits but does not
prevent increase in CO
L&D Monitoring -Left
Decubitus Position
Fetal heart rate
Uterine contractions
POSTPARTUM HEMODYNAMICS
• Immediately after delivery: Pressure on IVC
relieved
• Auto-transfusion: Blood shifts from contracting,
emptied uterus into central circulation
• Venous return increases immediately
postpartum - extra preload may cause clinical
deterioration
• Increase in SV and CO (though within first hour
heart rate (HR) drops limiting the CO)
• By 24 hrs, CO usually = 10-20% above prepregnancy levels where it may remain for up to
12-24 wks, particularly if breast feeding
MATERNAL OUTCOME in
Pregnancy & Heart Disease -1
• Functional capacity, **ventricular
function**
• **PA Pressure**
• Nature of primary disease e.g.
obstructive lesions
• ?Presence of satisfactory surgical
repair or palliation
• Degree of **cyanosis**
MATERNAL OUTCOME in
Pregnancy & Heart Disease-2
• CHF and / or arrhythmias often seen with
impaired functional status or cyanosis, or
superimposed HTN
• Risk of coronary/aortic dissection
• Concerns about pulmonary or systemic
embolism
• Endocarditis risks
Predictors of FETAL
OUTCOME in Pregnancy &
Heart Disease
• Maternal functional capacity
• Degree of maternal cyanosis espec
O2 sat <85%
• Note: if maternal congenital heart
disease, estimated transmission rates 215% (average 4-5%)
• Note: if maternal Marfan’s, autosomal
dominant = 50%
General Principles of Management
of Pregnancy & Heart Dz
• Maternal and fetal mortality are each
proportional to functional class : I & II <1%, III
~7% and IV~ 30%
• Consider Therapeutic AB if “High-risk” group
• Minimize the demands on the cardiovascular
system
– control heat/humidity
– restrict Na and calories
– control non-cardiac disease –e.g.- anemia, thyroid dz,
pyelonephritis, respiratory infection, etc.
General Principles of Peri-Partum
Management
•prevent thromboembolism
•IV air bubble filters if have shunts
•Leg vein care•Anti-Infective Endocarditis prophylaxis where appropriate
•Controlled vaginal versus C-Section delivery
•Invasive hemodynamic monitoring?
•Balloon flotation pulmonary artery catheter
•Intra-arterial line
•Special issues with specific problems
•Prosthetic Valves
•anticoagulation
“High Risk” L & D Algorithm
• At ~36-38 wks, amniocentesis = fetal maturity
• Elective admit @ ~38 wks:
– If on oral anticoagulants, change to heparin 2-3 wks in
advance, IV heparin at admit or onset of labor
– cervical prostaglandin E1 (Misoprostol) for
softening/ripening of cervix and uterotonic action- labor
results
– Artificial membrane rupture- anti IE Rx started
– oxytocin augments uterine contractions
– Narcotic epidural anesthesia
• Fetal / uterine monitoring
• vaginal delivery (vacuum extraction/forceps
assist as required) when possible
CESAREAN DELIVERY &
HEMODYNAMICS
• Attempting to avoid hemodynamic changes
during vaginal delivery, some advocate Csection for women with cardiovascular disease
• C-section delivery has significant effects:
intubation, anesthesia , blood loss (AVERAGES
1400 ml vs VD 500 ml), abdominal surgery, relief
of IVC compression, extubation, and,
postoperative awakening & discomfort
• Generally, standard vaginal delivery
with careful analgesia is preferable
except for OB reasons or few specific
CV disorders
Cesarean-Section Delivery
rather than Vaginal Delivery?
Some commonly used considerations:
• Obstetrical reasons – CPD, breech, etc.
• Onset of Labor during Anticoagulation
with coumadin (warfarin)
• Symptomatic Severe fixed obstructive
cardiac lesions
• Severe pulmonary HTN
• Marfan’s with dilated aorta or dissection
Pregnancy and underlying VHD
• In U.S., congenital heart disease now most
common issue
• Rheumatic VHD still an issue
• Stenosis worse (increased flow and heart rates
of pregnancy ) than regurgitation (lessened by
decreased SVR)
• Issues of pre-pregnancy counseling and planning
• Management issues include Rx abortions,
anticoagulation, interventional cath or surgery,
mode of delivery, IE prophylaxis
Rheumatic Heart Dz & Pregnancy
• Main problem = MS (90%) {MR (6%), AS/AR (4%)}
• Most with mild-moderate & occasionally severe
lesions can be managed through pregnancy
• MS functionally progressively worse with
Pregnancy
– faster HR, decreased LA emptying time
– increased CO
– increased diastolic gradient
– increased pulmonary venous pressure
• Major risks are pulmonary edema & PHTN
• Other risks: Pulmonary & Systemic Emboli, Atrial
Fibrillation, RV Failure, IE
MS & pregnancy management TEE guided BMV
Cardiac Surgery during Pregnancy
• Relative maternal safety unless significant
hemodynamic compromise &/or emergency
operation
• Fetal mortality ~20% 2nd to reduced placental
blood flow or hypothermia, worse the earlier in
pregnancy
• VHD and aortic dz most common reasons for
cardiovascular surgery during pregnancy
• Maternal morbidity/mortality worse if surgery
performed peripartum or shortly after delivery (c/w
high hemodynamic load of late pregnancy)
Pregnancy and Congenital Heart
Disease
• Maternal mortality 2-11/100,000 cases
– Mainly with PHTN/pulm vasc dz or dissecting aortic
aneurysm (especially Marfan)
– Others include severe AS, heart failure/ventricular
dysfunction, cyanotic or complex ACHD
• Left-to-right shunts- if no PHTN, usually welltolerated- issues of paradoxical embolus or
arrhythmias
• LVOT obstruction -usually BAV/CoA, HOCM
• Cyanotic CHD - incr CO/decr SVR, worse
shunt/cyanosis; note O2 sat<85%
Aortic Stenosis & Pregnancy
• Mild-moderate AS usually tolerated; current era most are bicuspid AS in the U.S.
• Bicuspid disease associated with aortic dz &
dissection
• Severe AS may have poor outcome due to
– fixed SV; CO increases mainly by increased HR
– Preload dependent
• Concerns: CHF, syncope, death
• Avoid
– volume depletion or afterload reduction
– negative inotropic agents
• Balloon valvuloplasty vs. open heart surgery?
Bicuspid Aortic Stenosis
• 26 y/o F-BAV & AS
• CHF @ 32 wks gestation; AVA = 0.9 cm2
– Balloon valvuloplasty- AVA = 1.1 cm2 & 1+AR
• At 38 wks, amniocentesis = fetal maturity
• Elective admit:
– cervical prostaglandin E2 (misoprostol) for
softening of cervix- labor results
– Artificial membrane rupture- anti IE Rx started
– oxytocin augments uterine contractions
– Narcotic epidural anesthesia
• vaginal delivery & vacuum extraction assist
Coarctation of the Aorta
• pregnancy = important potential
cardiovascular morbidity with
hormonally mediated tissue changes and
increased CO/ stroke volume
–
–
–
–
Hypertension ( low incidence of toxemia)
Coronary arterial or aortic dissection
Rupture of aneurysm of circle of Willis
LV failure possible but uncommon
• Infective endarteritis or IE on bicuspid AV
Coarctation & Pregnancy
• Despite repair or Balloon dilatation,
residual para-coarctation tissue defect
risks aneurysm or dissection
– Procedure of choice for women = resection
of coarctation site & para-coarct area with
end-to-end anastomosis
– Balloon angioplasty undesirable; outcomes
with stents uncertain to date for women and
pregnancy
Coarct Balloon Dilatation
Coarct
balloon
waist
Coarct
Dissection Flap
Pregnancy & Complex CHD
• Complex CHD- risk depends on adequacy of repair and
the residua / sequelae of specific lesion and type of repair
• TOF and ICR –main issues vent fn, PS/PR, arrhythmias
• TGA –main issues vent function, degree of TV regurg,
SSS, arrhythmias
– Cardiac complications in 14% pregnancies, 1 death per 44 live
births (Genonin Jr et al Heart 1999;81:276)
– TGA-Mustard usually well-tolerated but carries risk of deterioration
of RV fn (25%) and incr TR (50%) of which some were irreversible
(Guédès et al JACC 2004;44:433)
– CCTGA- successful preg in most but may have CHF/progressive
TR or fetal loss/low birth weight (Connolly et al JACC
1999;33:1692)
• “SV” physiology and Fontan-33 preg/ 21 women, 15
term pregnancies with no maternal deaths, 2 card events,
39% 1st trimester misscarriage rate. Context of Fontan 10yr
survival 60-80%. (Mair et al JACC 1996;28:763)
Primary Pulmonary
Hypertension
• more common in women (F:M = 5:1)
• Sudden death can occur with minor stress
• Effort syncope (bad prognosis!), chest pain,
fatigue may appear first during pregnancy
• Increased CO with decreased SVR not
tolerated because of fixed elevated PVR due to
obliterative pulmonary vascular disease
• MATERNAL MORTALITY~ 50%- may
occur even more than 1 week after delivery!!!
Developmental Connective
Tissue Defects & Pregnancy
• Spontaneous Aortic or
Arterial Dissection
– ~50% of Aortic
Dissection in women
<40 yrs occur with
pregnancy
• spontaneous
coronary arterial
dissection
*highest incidence from
3rd trimester
to labor and 1st 48 hrs
postpartum*
MARFAN’S & Pregnancy
• Preferable to Avoid pregnancy!
Possibility of AoD/rupture potentiated
by pregnancy-induced tissue change,
SV & CO, especially if aortic root
dimension > 40 mm
• If ECHO aortic root size < 40 mm, most
likely small risk – but – dissection
(usually type I or A) can occur even if
“normal aortic root size” (CXR
inaccurate- need echo or MRI)
• If pregnant, or, proceeds anyway:
– B-Blockade
– planned controlled delivery –consider
CS delivery if significant aortic
aneurysm or dissection
– IE prophylaxis (AR, MVP)
Peri-Partum Cardiomyopathy
• Rare “Dilated CMY” - 1:1,300-1:4,000 live births
(Homans NEJM 1985; 312:1432)
• Cause unknown- ?Immunologic-use of immune
globulin has reported improvement > usual med Rx
(Bozkurt et al JACC 1999; 34: 177)
• Peak incidence 1-2 months postpartum -range
from last month of pregnancy -6 mo postpartum
(DeMakis & Rahimtoola Circulation 1971; 44:964)
• Majority are black women (highest incidence in
Africa)
• Associated factors: increased maternal age > 30 years,
multiparity or twins, malnutrition, HTN or Toxemia
Peri-Partum Cardiomyopathy
• Prognosis worse if late onset sx’s after delivery,
severe LVE or decreased EF, increased PCW, or
IVCD
• Prognosis good if LV size & EF normal in 6
months; improvement or recovery rate ~50-60%
• Recurrence rate ~50%!
• ONE EPISODE SHOULD DISCOURAGE FUTURE
PREGNANCIES! Subsequent pregnancies often
assoc with significant LVEF decrease & can result
in clinical deterioration & death (Elkayam et al:
NEJM 2001; 344:1567)
Use of ACEI and ARB
contraindicated
• Previously shown in 2nd and 3rd trimester to
cause
–
–
–
–
–
–
Renal dysplasia
fetal anuria
Oligohydramnios
limb abnormalities
lung hypoplasia
craniofacial deformities
• Now known to also cause cardiovascular and
CNS malformations if used in 1st trimester (Cooper
et al N Engl J Med 354;23 2443, (June 8) 2006)
Women & Prosthetic Valves
• Selection
– Appropriate size & Hemodynamics for patient
– Durability- accelerated degeneration of tissue
valves with pregnancy?
– ?anticoagulation- risks to mother & fetus
• Risks of Valvular Dysfunction
– Thrombosis with obstruction/regurgitation
– Embolism
• Anticoagulation Management
– Mechanical MV riskier than Mechanical AV
– Early generation mech valves worse risk than
2nd generation
– note changing hypercoagulable state of
pregnancy
• Infective endocarditis- Risk and
prevention
calcification
Ross Procedure
Anticoagulation & Pregnancy
• Anticoagulants do not completely eliminate
thrombo-embolic complications in Mech
Prosthetic Valves –incidence of prosthetic
thrombosis ~ 10% (earlier generations>current,
MV>AV)
• pregnancy has hypercoagulable state
with increased II, VII, VIII, IX plus inhibition
of fibrinolysis worsens the issue
• Coumadin ~ 30% fetal mortality rate
• Reported relation between coumadin dose
>5mg and fetal complications (Vitale et al
JACC 1999; 33: 1637)
Anticoagulation & Pregnancy
• COUMADIN crosses placental barrier
– FETAL WASTAGE (SPONTANEOUS AB &
STILLBIRTHS), FETAL CEREBRAL
HEMORRHAGE
– CNS: optic atrophy, mental
retardation, microcephaly, spasticity2nd trimester
– **Coumadin Embryopathy** (~10%)
nasal bone hypoplasia,
chondrodysplasia punctata
**Greatest Risk period is conception to
13th week**
• If on coumadin at labor, need C-S
delivery to avoid fetal cerebral
hemorrhage
Pregnancy Anticoagulation
GLs 2006
JACC Vol. 48, No. 3, 2006 Bonow et
al.
August 1, 2006:e1–148 ACC/AHA
Practice Guidelines
Anticoagulation in Pregnancy With
Mechanical Prosthetic Valves- Class I
•
•
All pregnant patients with mechanical
prosthetic valves must receive continuous
therapeutic anticoagulation with frequent
monitoring.(Level of Evidence: B)
For women requiring long-term warfarin
therapy who are attempting pregnancy,
pregnancy tests should be monitored with
discussions about subsequent
anticoagulation therapy, so that
anticoagulation can be continued
uninterrupted when pregnancy is achieved.
(Level of Evidence: C)
Anticoagulation in Pregnancy With
Mechanical Prosthetic Valves- Class I
•
Pregnant patients with mechanical prosthetic valves
who elect to stop warfarin between weeks 6-12
gestation should receive continuous intravenous
UFH, dose-adjusted UFH, or dose-adjusted
subcutaneous LMWH. (Level of Evidence: C)
•
For pregnancy & mechanical prosthetic valves, up to
36 weeks of gestation, the therapeutic choice of
continuous intravenous or dose-adjusted
subcutaneous UFH, dose-adjusted LMWH, or
warfarin should be discussed fully. If continuous
intravenous UFH is used, the fetal risk is lower, but
the maternal risks of prosthetic valve thrombosis,
systemic embolization, infection, osteoporosis, and
heparin-induced thrombocytopenia are relatively
higher. (Level of Evidence: C)
Anticoagulation in Pregnancy With
Mechanical Prosthetic Valves- Class I
•In pregnant pts with mechanical prosthetic valves
who receive dose-adjusted UFH, the aPTT should be
at least twice control. (Level of Evidence: C)
•In pregnant pts with mechanical prosthetic valves
who receive warfarin, the INR goal should be 3.0
(range 2.5 to 3.5). (Level of Evidence: C)
•In pregnant patients with mechanical prosthetic
valves, warfarin should be discontinued and
continuous intravenous UFH given starting 2 to 3
weeks before planned delivery. (Level of Evidence: C)
Anticoagulation in Pregnant Patients With
Mechanical Prosthetic Valves- Class I
• In pregnant patients with mechanical
prosthetic valves who receive doseadjusted LMWH, the LMWH should be
administered twice daily
subcutaneously to maintain the anti-Xa
level between 0.7 and 1.2 U per ml 4 h
after administration. (Level of
Evidence: C)
IE prophylaxis & pregnancy
Arrhythmias in pregnancy
• R/O usual suspects: alcohol, caffeine, thyroid
disease; echo useful to look for structural disease
• Must make correct diagnosis and document
rhythm disorder
• Need for treatment must be clear- significant
symptoms or life threatening disorder
• Use as few drugs at lowest effective doses
possible
• UNSAFE= AMIODARONE (IUGR, hypothyroidism,
fetal distress)
• If need to cardiovert, no significant fetal adverse
effects, remove uterine and fetal monitoring leads
first
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HIGH RISK CONDITIONS IN
PREGNANCY
Marfan’s syndrome with dilated aorta (>40mm)
Severe aortic stenosis or Aortic Coarctation
Severe mitral stenosis
Prosthetic valves- espec earlier variants,
MV>AV
Pulmonary HTN (PAP >3/4 systemic) (e.g.
Primary PHTN, Eisenmenger’s syndrome)
Decreased LVEF (<35%) (e.g PPCMY)
Uncorrected cyanotic congenital heart disease
- or - inadequately corrected severe CHD
Onset of labor while on oral anticoagulants
(i.e. warfarin / Coumadin®)
“Key points”
• Pregnancy imposes a significant
hemodynamic burden
• Obstructive lesions are more poorly
tolerated than are regurgitant lesions
• Pulmonary HTN is BAD!
• CYANOSIS risks fetal IUGR or demise
• Need for anticoagulation worsens outcome
• Careful management and hemodynamic
monitoring of the “high risk” cardiac patient
can get many successfully though Labor &
Vaginal Delivery