Myocardial Infarction in Pregnancy

This blog post is based on an old yet very important TOG “Myocardial Infarction and Pregnancy” published in 2013. As cardiac disease is the leading cause of maternal death in UK, so this article is a must to cover before the exam. 

I hope this summary is helpful.

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Outline of Maternal Medicine Module: Click Here

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Introduction

• Heart disease 
• complicates → 0.2-4% of all pregnancies
• In UK the leading cause of maternal death since 2000
• 1/5th of All maternal deaths
• Majority due to acquired heart disease
• Acute Myocardial Infarction (AMI) → rare but in pregnancy RR is 3-4x higher
• Be aware of pregnancy specific physiological changes in CVS & keep low threshold for dx & mx

Physiological changes in pregnancy

Cardiovascular changes

• ↑ plasma volume & ↓ peripheral resistance as early as 6 wks
• ↑ in blood volume until plateaus at 140-150% @32 wks
• ↑ Cardiac output until 25wk first d/t ↑ in stroke volume & then d/t ↑ in maternal HR
• Further haemodynamic changes during labour & delivery

• Cardiac output→ ↑ by 50% with each contraction
• 300-400ml blood transferred from uterus with each contraction
• Valselva manoeuvre→ large variations in CVP
• After 3rd stage completed→ approx.500 ml uterine blood returns to circulation→ ↑ ventricular preload, cardiac output & CVP
• After 48 hrs→ diuresis & natriuresis starts. 
• Return of cardiac output , blood volume & peripheral resistance → pre-pregnancy state 4-12wks

Haematological changes

• Pregnancy a hypercoagulabale state 
• ↑ procoagulant: fibrinogen, factor VII, VIII & X & von Willebrand's factor
• ↓ anticoagulants: lower levels of functional protein S
• Changes do not return to normal until more than 8 wks after delivery
• Risk of thrombosis even higher post-delivery

Pathophysiology of Acute Myocardial Infarction (AMI)

• AMI characterised by: presence of myocardial necrosis in a clinical setting consistent with myocardial ischaemia
• Classified into NSTEMI and STEMI on basis of ECG
• Both share common pathophysiology
• Most common underlying cause → ATHEROSCLEROSIS
• Partial occlusion of vessel with thrombi → NSTEMI
• Total occlusion →STEMI
• Peripartum period is most vulnerable time d/t ↑ cardiac output
• Up to 50% MI occur peripartum

Risk factors for Acute Myocardial Infarction (AMI)

• Main risk factors same as non pregnant

• Advancing maternal age >30yrs Smoking Obesity Chronic HTN Pre-existing DM Hyperlipidemia Strong family history

• Risk of AMI 30 times higher if aged >40 vs at age 20
• 64% who died of MI were obese or overweight (last report)
• Lipid Profile in pregnancy
• HDL ↓
• No change in triglycerides & LDL. 
• Dyslipidemia may worsen
• Causes of AMI in pregnancy: two broad categories 
• Atherosclerotic (often with CV risks)
• Non-atherosclerotic (consider in women with no known risk factors) which includes 
• Coronary artery dissection (22%) Highest risk in 3rd tri & up to 3 months postpartum
• Coronary atheroma (50%)
• Coronary artery thrombosis (14%)
• Left anterior descending coronary artery involved in 80% with associated mortality 30-40%
• Pregnant women can also have AMI even when the coronary vessels are normal  on angiogram
• Proposed mechanisms→ transient coronary spasm, drugs like terbutaline, ergotamine, bromocriptine
• Other causes→ cocaine use, vasculitis such as Kawasaki disease, collagen vascular disease, AFI & pheochromocytoma

Risk factors for Myocardial Infarction

Ref: TOG

Main causes of AMI in Pregnancy

Ref: TOG

Diagnosis

• May be difficult
• Diagnostic criteria → same as for non-pregnant
• In addition to chest pain, typical features of pregnancy such as epigastric pain, vomiting or dizziness, particularly if known AMI risk factors should be investigated further
• Low index of suspicion is important

Investigations

Electrocardiography

Ref: TOG

• First-line test
• Most sensitive & specific ECG marker → ST elevation (typically appear within a few minutes on onset of symptoms)
• Serial ECG important
• ECG misses 50% of cases, use other markers in conjunction 

Blood cardiac markers

• Biomarkers of choice →Cardiac specific troponin I & troponin T
• Negative troponin at presentation does not exclude the dx as it takes 12 hr to peak
• Troponin investigation of choice: 
• never ↑ above upper limit in healthy pregnancy
• not affected by anaesthesia
• prolonged labor or c/s
• Troponin can be ↑ in PET, PIH & PE → but never reached the above standard threshold set for MI
• Other cardiac markers — myoglobin, creatinine kinase, creatinine kinase isoenzymes MB — can be ↑ significantly in labour

Echocardiogram

• Tranthoracic echo→ useful method 
• Use is limited but its safe in pregnancy

Coronary angiography

• Aids in dx & potential t/m
• Radial access is recommended with abdominal shield & minimised fluoroscopic time

Treatment

• Same principles as non pregnant
• Aim→ re-establish normal coronary blood flow
• Prompt restoration of blood flow limits myocardial damage &↓ mortality

Reperfusion therapy

ST elevation myocardial infarction (STEMI)

• Mode decided in consultation with cardiologist
• Treatment of choice: Coronary angiography & primary percutaneous coronary intervention (PPCI)
• Bare metal stents preferable over drug-eluting stents
• Thrombolysis is indicated even in pregnancy 
• Agent of choice: I/V t-PA 
• doesn't cross the placenta
• no evidence of teratogenesis
• associated risk of maternal haemorrhage (8%)

Non-ST elevation myocardial infarction (NSTEMI)

• First line of management: Anti-platelet drugs
• Coronary angiography considered if symptoms continue despite medical t/m +/- haemodynamic instability
• Also consider if medical t/m successful but high-risk features

Medications used in AMI (Table4.)

Ref: TOG

Aspirin: 1st line for non pregnant

• In pregnancy use low-dose. (60-150mg)

LMWH & un-fractioned heparin: Safe & Do not cross placenta

• Stop anticoagulant 24 hrs before induction of labour

Nitrates, labetalol & nefidipine: safe

• Avoid nefidipine after acute coronary event as it ↑ mortality
• Labetalol→ ß blocker of choice

Clopidogrel: can be used

• Antithrombogenic 
• Not easily reversed
• Not much evidence for safety

ACE inhibitors/ ARBs/ Statins: contraindicated in pregnancy

Pregnancy with MI: care to be provided in ICU HDU with fetal monitoring & comprehensive obstetrical care. 

• Consider delivery in case maternal condition worsens in potentially viable foetus

Timing and mode of delivery and AMI

• No standard guideline
• Collaborative Mx involving cardiologist, obstetric physician, obstetrician, obstetric anaesthetist & neonatologist— MDT vital
• Intervention individualised: maternal cardiac status & gestational age
• If pre-term → must administer steroids
• Delay delivery until 2-3 wks after MI
• Delivery: in high-risk Obstetric unit with intensive care expertise
• Mode of delivery: depends on maternal & obstetrical factors
• Vaginal delivery: 
• Decide timing on bishop
• Epidural is recommended
• Left lateral position, supplementary O2, continuous EFM, continuous maternal cardiovascular monitoring including pulse oximetry & ECG
• If left ventricular function impaired with recent cardiac event→ invasive monitoring with arterial catheter appropriate
• Shortening of second stage
• Slow I/V infusion of oxytocin (<2 u/mil) after placenta delivery
• After delivery maternal monitoring in ICU / HDU for 24-48 hrs
• For prevention or t/m of myocardial ischaemia during delivery: I/V nitroglycerin, ß blockers & calcium antagonists can be used
• Keep GP updated at all stages
• Arrange for postnatal follow-up with cardiologist
• Contraception & recommendations about future pregnancy

Conclusion

• Identify risk factors and manage
• Majority of women with CVS risk factors have uneventful pregnancy
• Keep low index of suspicion 
• Do not delay appropriate investigations and treatment
• Outcome dependent on time to treatment & early involvement of cardiologist/MDT