The incidence of, and the risk factors for, cardiovascular disease in individuals and patient groups - pregnant patients

Cardiac disease in pregnancy

Cardiac disease in pregnancy.

The leading cause of indirect maternal death in Australia and the UK
Two groups, with different problems:
- Pre-existing cardiac disease - congenital (now the majority in high-income settings), rheumatic (over-represented in Aboriginal and Torres Strait Islander women and migrants), cardiomyopathy, aortopathy, ischaemic
- Pregnancy-acquired - peripartum cardiomyopathy, SCAD, pre-eclampsia-associated, gestational hypertension, arrhythmia, PE

Haemodynamics of normal pregnancy - why lesions decompensate

Variable	Change
Blood volume	inc 40-50% (plasma > red cell mass -> dilutional anaemia)
Cardiac output	inc 30-50%, peaks ~24-28 weeks
Heart rate	inc 10-20 bpm
SVR	dec ~30% (nadir mid-trimester)
BP	dec in 2nd trimester, returns by term
Coagulation	Hypercoagulable (inc factors, dec protein S)

Labour: each contraction autotransfuses 300-500 mL; CO rises a further 30-50%
Immediately postpartum: CO rises ~60-80% from relief of caval compression + uterine autotransfusion
- -> *the first 24-72 hours postpartum are the highest-risk period, not delivery itself*

The rule

Fixed-output and pressure-overload lesions tolerate pregnancy badly (cannot increase output; falling SVR worsens gradients or shunt reversal)
Regurgitant lesions and left-to-right shunts tolerate pregnancy well (falling SVR unloads the ventricle)

Epidemiology

Cardiac disease complicates ~1-4% of pregnancies
Highest maternal risk lesions
- *Severe pulmonary arterial hypertension and Eisenmenger syndrome - maternal mortality historically 30-50%*, still ~10-25% in modern series
- Cardiomyopathy with NYHA II symptoms or EF <40%
- Severe obstructive lesions: severe aortic stenosis, severe mitral stenosis, severe pulmonary stenosis
- Marfan syndrome with aortic root >40-45 mm; bicuspid valve with ascending aorta >45-50 mm; vascular EDS
- Prior peripartum cardiomyopathy with any residual LV dysfunction
- Fontan circulation with any complication; severe systemic ventricular dysfunction
- Mechanical prosthetic valve (anticoagulation dilemma)
Aboriginal and Torres Strait Islander women: acute rheumatic fever and RHD rates among the highest in the world -> mitral stenosis in pregnancy

Why specific lesions fail

Mitral stenosis - fixed orifice; inc HR shortens diastole -> inc LA pressure -> pulmonary oedema, often at 20-30 weeks or in labour. Tachycardia is the enemy
Aortic stenosis - fixed output; cannot meet the inc demand -> angina, syncope, HF
Pulmonary arterial hypertension / Eisenmenger - fixed pulmonary vascular resistance; dec SVR -> inc right-to-left shunt -> worsening cyanosis; unable to accommodate the postpartum volume load
- Death typically in the first week postpartum
Aortopathy - inc CO and wall stress + oestrogen/relaxin-mediated medial change -> dissection risk highest in the third trimester and early postpartum
Peripartum cardiomyopathy - a cleaved 16 kDa prolactin fragment with antiangiogenic action (and sFlt-1 from the placenta) -> microvascular damage -> systolic dysfunction
- The rationale for bromocriptine
SCAD - hormonal effect on arterial media + shear stress; third trimester/early postpartum; the commonest cause of pregnancy-associated MI
Mechanical valve thrombosis - hypercoagulable state plus sub-therapeutic anticoagulation

Risk factors for an adverse cardiac event

Prior cardiac event (HF, arrhythmia, stroke) - the single strongest predictor
NYHA class III-IV or cyanosis
Systemic ventricular EF <55%
Left heart obstruction
Mechanical valve
Pulmonary hypertension
Late or no antenatal cardiac care

Risk stratification - mWHO 2.0 (2025 ESC)

Risk stratification - mWHO 2.0 (2025 ESC)

Class	Risk	Examples
I	No detectable increase	Small/repaired ASD, VSD, PDA; mild PS; isolated ectopy
II	Small increase in mortality, moderate in morbidity	Unoperated ASD/VSD, repaired tetralogy, most arrhythmias
II-III	Intermediate	Mild LV impairment, HCM, native or tissue valve disease not in I/IV, Marfan without aortic dilatation, repaired coarctation
III	Significantly increased - expert counselling, monthly cardiac + obstetric review	Mechanical valve, systemic RV, Fontan, unrepaired cyanotic CHD, moderate MS, severe AS, Marfan aorta 40-45 mm
IV	*Pregnancy contraindicated* - if pregnant, discuss termination	Pulmonary arterial hypertension of any cause, severe systemic ventricular dysfunction (EF <30% or NYHA III-IV), previous PPCM with residual impairment, severe MS, symptomatic severe AS, Marfan aorta >45 mm, bicuspid aorta >50 mm, vascular EDS, native severe coarctation

Maternal cardiac event rates rise from ~3-10% (class I) to ~40-50% (class IV)
Pregnancy Heart Team involvement from preconception through postpartum for mWHO II-III and above

Distinguishing normal pregnancy from disease

Normal in pregnancy	Always abnormal
Soft ejection systolic murmur, loud S1, S3	Any diastolic murmur
Mild dyspnoea, fatigue, ankle oedema	Orthopnoea, PND, resting dyspnoea
Displaced apex, venous hum, mammary souffle	Raised JVP, loud P2, clubbing/cyanosis
Sinus tachycardia, ectopy	Sustained arrhythmia, syncope on exertion
Mild dilatation of chambers, physiological regurgitation on echo	Chest pain, haemoptysis

ECG in pregnancy: left axis shift, small Q and inverted T in III, sinus tachycardia, ectopy
NT-proBNP - useful; a normal level makes cardiac decompensation unlikely
Echocardiography is safe and first-line; MRI without gadolinium is safe (avoid gadolinium)
CTPA and V/Q both acceptable for suspected PE - fetal dose is low with either; V/Q gives lower maternal breast dose
Do not withhold necessary imaging for fear of radiation - fetal dose from a CTPA is well below the 50 mGy threshold for harm

Preconception - the single most valuable intervention

A. Preconception - the single most valuable intervention

Risk stratify with mWHO 2.0, counsel about maternal mortality and fetal risk, and discuss contraception and alternatives to pregnancy
Optimise or repair the lesion first - valve intervention, aortic root replacement, ablation
Switch teratogenic drugs: stop ACEi, ARB, ARNI, MRA, statins, amiodarone, warfarin (dose-dependent embryopathy)
Genetic counselling - recurrence risk ~3-5% for most CHD, 50% for autosomal dominant conditions (Marfan, HCM, LQTS)
Folate, vaccination, dental review

Antenatal

B. Antenatal

Pregnancy Heart Team: cardiologist, obstetric physician, obstetrician, anaesthetist, midwife, neonatologist
Frequency of review by class (monthly or more in mWHO III)
Fetal echocardiography at 18-22 weeks where there is maternal CHD
Serial growth scans (cardiac disease -> placental insufficiency, IUGR, prematurity)
Drugs generally safe: beta blockers (metoprolol, labetalol - atenolol associated with IUGR, avoid), methyldopa, nifedipine, hydralazine, digoxin, adenosine, frusemide (with care), heparins, aspirin
Aspirin 100-150 mg from 12 weeks for pre-eclampsia prophylaxis in at-risk women

Anticoagulation with a mechanical valve - the classic dilemma

C. Anticoagulation with a mechanical valve - the classic dilemma

Warfarin - lowest maternal valve thrombosis risk, but embryopathy (weeks 6-12, dose-dependent; risk lower if <5 mg/day) and fetal intracranial haemorrhage
LMWH - fetally safe but higher valve thrombosis risk; requires weekly anti-Xa monitoring with peak AND trough levels
Typical approach: LMWH weeks 6-12, warfarin to ~36 weeks, then switch to LMWH/UFH before delivery (warfarin crosses the placenta - the fetus is anticoagulated)
DOACs are contraindicated in pregnancy

Delivery planning

D. Delivery planning

Vaginal delivery is preferred in most - less blood loss, less infection, fewer thrombotic events
Caesarean for: aortopathy with dilated aorta, severe AS/PAH in some protocols, warfarin within 2 weeks of delivery, severe decompensated HF, obstetric indications
Assisted second stage to avoid prolonged Valsalva
Regional anaesthesia with careful incremental epidural - avoid rapid sympathetic blockade in fixed-output lesions (severe AS, PAH)
Avoid ergometrine (vasoconstriction, hypertension); oxytocin by slow infusion rather than bolus (bolus causes vasodilation and tachycardia)
Antibiotic prophylaxis only if a prosthetic valve/material and an infected delivery
Consider invasive monitoring and HDU/ICU for high-risk cases

Postpartum - the danger window

E. Postpartum - the danger window

Monitor for at least 24-72 h; longer in mWHO III-IV
Re-establish HF therapy: ACEi (enalapril, captopril) and beta blockers are compatible with breastfeeding; avoid ARNI, MRA, ivabradine while breastfeeding
Thromboprophylaxis
Contraception advice before discharge - avoid combined oral contraceptives in PAH, Fontan, cyanotic disease, prior thrombosis; LARC preferred

Specific conditions

F. Specific conditions

Peripartum cardiomyopathy - standard HF therapy (pregnancy-adapted), consider bromocriptine with prophylactic anticoagulation, wean therapy only after EF normalises and remains stable; counsel against further pregnancy if EF has not recovered
Mitral stenosis - beta blocker to slow HR, diuretic; percutaneous balloon mitral valvuloplasty if refractory (best done after 20 weeks with abdominal shielding)
Aortopathy - continue beta blocker, strict BP control, echo every 4-8 weeks, caesarean if root >45 mm
Arrhythmia - adenosine, metoprolol, flecainide, and DC cardioversion is safe at any gestation (fetal monitoring during)
ACS/SCAD - conservative management favoured in SCAD; PCI if ongoing ischaemia; do not thrombolyse

Associations

Pre-eclampsia and gestational hypertension - now recognised as long-term cardiovascular risk factors (inc lifetime risk of HTN, IHD, stroke, HF)
Gestational diabetes - future type 2 diabetes and cardiovascular risk
Preterm birth and IUGR - both associated with maternal cardiac disease and with future maternal CVD
Venous thromboembolism - leading direct cause of maternal death; risk highest postpartum
Rheumatic heart disease - Aboriginal and Torres Strait Islander women, Pacific Islander and migrant populations
Adult congenital heart disease - the fastest-growing group of pregnant cardiac patients
Anaemia, thyroid disease, obesity - all worsen cardiac tolerance

Natural history

Most women with mWHO I-II have an uncomplicated pregnancy with planned care
Risk concentrates at three points: mid-trimester peak CO (~24-28 weeks), labour, and the first 72 hours postpartum
Heart failure and arrhythmia are the commonest maternal cardiac events; death is rare but disproportionately occurs in unplanned pregnancies in women who were never risk-stratified
Fetal/neonatal events (prematurity, IUGR, fetal loss) rise with maternal mWHO class
Adverse pregnancy outcomes are a long-term cardiovascular risk marker - the 2025 ESC guideline adds a dedicated chapter
- -> pre-eclampsia, preterm delivery, gestational diabetes and PPCM all warrant long-term cardiovascular follow-up
Peripartum cardiomyopathy: ~50% recover EF, mostly within 6 months; recurrence in subsequent pregnancy ~20-30% (higher and more dangerous if EF did not normalise)

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