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Pregnancy and Heart Disease
Pregnancy and Heart Disease
Pregnancy and Heart Disease
Thrombosis
Valvular heart disease
HTN
Pregnancy related CMP
Thromboses during Pregnancy
Leading cause of maternal mortality.
Levels of AT III, protein C and S fall throughout
pregnancy. F VIII, IX, XI increase in pregnancy
Prior DVT, emergency C section.
AT III deficiency associated with 2-4 fold higher
risk (14%) than PC or PS.
F V Leiden (PC resistance) and F II 20210A
(inhibits fibrinolysis) combo increases risk of DVT.
Heterozygous 4% risk. If Hx DVT and both factors
present, 50% risk.
AT deficiency and FV Leiden worse post-partum.
Risk 41% homozygous,9.2% double homozygous
Risk Stratification
Thrombosis
Valvular heart disease
HTN
Pregnancy related CMP
CV System and Pregnancy
Increase up to 40-50% plasma volume
Relative anemia
Increases in CO (HR increases, SVR and PVR decrease,
therefore wide PP)
IVC obstruction (supine) abrupt decrease CO.
In labor increase in CO 60-80%. Post delivery increases in
preload
CV complications (13%): poor FC, LVOT obstruction (>30
mmHg), EF <40%, cyanosis, prior events or arrhythmias.
Risk 27% with 1 risk factor, 70% with >2.
Neonatal complications (20%): FC, cyanosis, LVOT
obstruction, anticoagulation, smoking, multiple prior
pregnancies.
Physical Exam
Faster HR (10-20 beats), bounding
pulses, widened PP, low N SBP,
warm extremities.
High normal JVP. Thyroid may be
enlarged. S2 widely split. S3 is
common. I-II/VI SEM LUSB. Conti-
nuous murmur. Diastolic M unusual.
MS or AS M increase, AI or MR less.
VHD associated with low Maternal
and Fetal Risk
Asymptomatic AS with low mg (<50)
with normal EF.
NYHA FC I or II AI with N EF.
NYHA FC I or II MR with N EF.
MVP with no MR or mild to mod MR
and N EF
Mild to mod MS (MVA >1.5 cm2, mg
5 mmHg) without pulmonary HTN.
Mild to moderate PV stenosis
VHD lesions associated with high
Maternal and/or Fetal Risk
Severe AS with or without symptoms
AI with NYHA FC III-IV.
MS with NYHA FC II-IV.
MR with NYHA FC III-IV.
AVD or MVD with severe pulm HTN.
AVD or MVD with EF< 40%.
Mechanical prosthesis.
AI in Marfan Syndrome
CV System and Pregnancy
Regurgitant lesions are well tolerated
Stenotic lesions increase morbidity of
mother and fetus. Higher incidence of
CHF, arrhythmias, hospitalizations pre-
term delivery, low birth weight.
Correct, if possible VHD prior to
conception.
In MS: BB, diuretics, anticoagulation, PBV
if severe SXS.
In AS: Rx CHF, if severe PBV or AVR.
Prosthetic Mechanical Valves
Discontinue warfarin as soon as Dx
of pregnancy is established.
Start heparin (or if lawyers do not
scare you, LMWH), S/Q to prolong
PTT to therapeutic range.
Replace heparin with warfarin (INR
2.5-3.5) at week 12 and continue to
middle of 3rd trimester, then restart
heparin.
UNsafe drugs during Pregnancy
Drug Effects
Fetal hemorrhage embryopathy,
Warfarin
CNS abnormalities
IUGR, prematurity,
Amiodarone
hypothyroidism
Nitroprusside Thiocyanate toxicity, fetal loss
Skull ossification defect, IUGR,
ACE-I
PDA, LBW, ATN, anemia, death
Placental hypo-perfusion, low
Diuretics
platelets, jaundice, low Na+ & HR
Outline
Thrombosis
Valvular heart disease
HTN
Pregnancy related CMP
HTN in Pregnancy
2nd leading cause of maternal
mortality (15% deaths).
HTN disorders 6-8% pregnancies.
Contributes to still-births and neo-
natal morbidity and mortality.
Abruptio placenta, DIC, cerebral
hemorrhage, hepatic failure, ATN.
Etiology unknown.
Risk of CHF, encephalopathy PP.
Classification of HTN
Chronic HTN (>140/90 mmHg).
Pre-eclampsia-eclampsia (>20 wks).
Pre-eclampsia superimposed upon
chronic HTN.
Gestational HTN (<20 weeks):
- Transient, if no pre-eclampsia. BP
returns to normal by 12 weeks
- Chronic HTN if it persists.
Pre-eclampsia
Proteinuria: > 0.3 g protein in 24 hr. Correlates 1+ dipstick
or 30 mg/dL.
SBP >160 or DBP >110 mmHg.
Proteinuria >2g/day (1st time).
Increase serum creatinine (>1.2)
Platelet ct <100K and/or micro-angiopathic anemia (high
LDH).
High liver enzymes
Persistent headache or cerebral/visual abnormalities.
Persistent epigastric pain.
Eclampsia= seizures in pre-eclampsia.
Edema no longer a criteria.
Pre-eclampsia
Can progress slowly or very fast (hrs).
Maternal: vasospasm, activation of
coagulation system, perturbation in
volume and BP control (sensitive AII, loss
circadian rhythm). Oxidative stress and
inflammatory-like responses.
Pathologic changes ischemic and affect
placenta, brain, kidney, liver.
Pre-eclampsia
Renal lesion: glomeruli are swollen due to
hypertrophy of endothelial and mesangial
cells which encroach the capillaries
(“glomerular endotheliosis”). Decrease
25% GFR and RBF, however since renal
function increases 35-50% in pregnancy, a
normal creatinine does not exclude pre-
eclampsia. ATN. Hyperuricemia. Low
calciuria. Low intra-vascular volume.
Pre-eclampsia
Thrombocytopenia (<100K) rarely
severe. Cause unknown (deposit at
sites of endothelial damage and/or
immunologic process). Fetuses born
show no problems.
Liver: range from mild necrosis to
ominous HELLP syndrome (hemolysis
elevated enzymes, hepatic bleeding
or rupture.
Pre-eclampsia
CNS: Headache, visual disturbance
(blurred vision, scotomata, cortical
blindness), focal signs. Seizures
(eclampsia) due to coagulopathy and/or
HTN encephalopathy.
High risk for it: in pts with Hx HTN,
previous gestation, multiparous, DM CVD,
renal vascular or parenchymal disease,
multi-fetal pregnancy.
Sonogram to evaluate fetal growth 25-28
weeks.
Pre-eclampsia superimposed on
Chronic HTN
Much worse prognosis.
HTN without proteinuria <20 weeks.
Sudden increase in proteinuria.
Sudden increase in BP, previously
under control.
Thrombocytopenia (<100K).
Increase in LFT’s.
Gestational HTN
Thrombosis
Valvular heart disease
HTN
Pregnancy related CMP
As a Cardiologist, I worry when:
90% of the reports of PPCMP are
published in non-cardiology journals.
Tremendous variability in definitions,
response to treatment and outcomes
in various reports.
No controlled randomized studies.
The NIH decides to hold a “panel of
experts” to shed light on a “rare and
catastrophic disease”
NIH Expert Panels
Meetings in Bethesda.
Attempts to reach “consensus”. After
all, they are supporting the meeting:
Reimbursement for:
• meals/day: $25. Marriot’s breakfast:
19.90+7= $26.90
• Hotel: $100. Actual cost: $187
• Airfare: $495. Actual cost: $980
ABILITY TO IMPRESS YOUR GRANDMA:..PRICELESS
Perspective
4.6 million people Rx for CHF.
550,000 new annual cases.
1 and 5 year survival rates 76/35%.
Numerous clinical (older age, NYHA,
LVEF, RVEF), biochemical (NE, BNP),
EPS (VT, AF) and hemodynamic
variables (MVO2) influence survival.
Underlying ischemia (59 Vs 69%) 5
yr survival.
Perspective (cont.)
Auto immunity
Ventricular dysfunction
50
Percent of women
40
All women
30
Group 1
20 Group 2
10
0
Index Postpartum Subsequent Last F/U
1.2
1 Dobutamine
0.8 Ba
se
lin
ec
0.6 on
tr a
cti
lity
0.4 lin
e
0.2
0
0 20 30 40 50 60 70
Hemodynamics in PPCMP
40
30
20
% Change
10
Recovered
0 Control
-10
-20
-30
HR CO PVR
Prognosis
28 women; 8 SXS ante-partum; 20 post-
partum. 19 with pre-eclampsia or HTN Hx.
13 premature deliveries. Perinatal
mortality: 36/1000 births.
ECG: LVH (14), NSSTT (7).
1 recovered completely; 2 died early, 3 in
follow up, 3 required transplant and 18
had stabilization of symptoms.
6 had subsequent pregnancies, and 4 had
relapses of their PPCMP.
Other reports, 50% have good prognosis.
Witlin A. AJOBGYN 1997;176:182.
War Time Joke
During a French-British war, a
French officer asked a British one:
How come you guys wear red coats?
It makes it so easy to identify you!!!
The British answered, we do it so
that if we get injured, our soldiers
will not see us bleed and panic.
Since then, the French were brown
pants.
Effect of New Pregnancies
44 pts with Hx PPCMP. Nine pregnant
again. Two lost F/U.
All 7 tolerated pregnancy relatively
well and delivered healthy babies.
4 pts with FC II, and 2 with III, no
change. One from III to II.
EDD was same (61 to 58 mm), ESD
(50 to 47 mm, p=.008), FS (19 to
23%).
De Souza JL J Card Fail 2001;7:30
Course of Subsequent Pregnancy
34 pts (mean 26 yrs).
5 in FC II, 1 in FC III, 28 in FC IV.
All advised against new pregnancies.
12 (35.3%) became pregnant. 6 (Gp 1)
had normal heart size, 6 had persistent
cardiomegaly (Gp 2).
5/6 in Gp 1 did well pre- post- pregnancy.
All Gp 2 tolerated pregnancy well,
however 2/6 deteriorated and died 8 & 13
years after.
3 year interval post recovery LVEF safe.
Filho A. Arq Bras Cardiol 1999;73:47
Summary
Outcome highly variable. Regardless of
initial severity, some pts clinical and echo
status improve rapidly, and others
deteriorate rapidly and need
transplantation or die. Others have
persistent dysfunction and over years
improve.
Hemodynamic stress of pregnancy can
unmask impaired reserve.
Anticoagulants, ACE. IABP in severe cases
Reimold SC. NEJM 2001; 344:1629
If worse comes to worse….would
transplant work?
Case reports.
22 yo with multi-organ failure post
partum. CI 1.9 L/min, IABP, Novacor
LVAD. Bx severe non-inflammatory
lesions c/w DCMP. TIA’s, acute
abdomen: thrombosis SMA, bowel
resection ileostomy. 158 days later!!
Orthotopic heart transplant.
Tandler R. EJCT Surg 1997;11:394