Key content
Myocardial infarction is a rare but life-threatening medical
condition during pregnancy.
If unrecognised and not managed appropriately, the associated
mortality and morbidity are high.
A high index of suspicion, early diagnosis and treatment are
essential.
Multidisciplinary management involving the obstetric physician,
cardiologist, anaesthetists and obstetrician is key to improving
outcomes.
Learning objectives
To revise the physiological cardiovascular changes in pregnancy.
To recognise the pathophysiology of myocardial infarction during
pregnancy.
Identify risks factors for myocardial infarction.
Recognise symptoms and signs of myocardial infarction.
To learn the general management principles of myocardial
infarction in pregnancy.
Ethical issues
Should asymptomatic pregnant women with multiple risk factors
be screened for coronary heart disease?
Keywords: chest pain / ischaemic heart disease / myocardial
infarction / pregnancy
Physiological changes in pregnancy
Cardiovascular changes
There are significant physiological changes in pregnancy that
affect the cardiovascular system and increase myocardial
oxygen demand.12,13 As early as 6 weeks of gestation, an
increase in plasma volume and reduction in peripheral
vascular resistance occurs because of activation of the
renin–angiotensin system and a mild reduction of the plasma
atrial natriuretic peptide levels.13 The increase in blood volume
continues until it plateaus at a level of 140–150% at around 32
weeks of gestation compared with the nonpregnant state.14
Cardiac output increases steadily until 25 weeks of gestation,
initially secondary to the increase in stroke volume and later
because of an increase in maternal heart rate.15,16
During labour and delivery, further haemodynamic
changes occur. The heart rate and blood pressure increase
significantly as a result of pain, anxiety and uterine
contractions. The increase in heart rate is similar to that
observed during moderate-to-heavy physical exercise.17–19
Cardiac output increases by 50% with each contraction.
About 300–400 ml blood is transferred from the uterus into
the circulation with each contraction. In the active phase of
the second stage of labour, the Valsalva manoeuvre results in
larger variations in the central venous pressures. The
completion of the third stage of labour results in
approximately 500 ml uterine blood being returned to the
maternal circulation, with associated increases in ventricular
preload, cardiac output and central venous pressures.17
Approximately 48 hours after delivery, diuresis and
natriuresis start, with return of cardiac output, blood
volume and peripheral resistance to the pre-pregnancy state
occurring over the course of 4 to 12 weeks.20
Haematological changes
Increased levels of procoagulants and reduced levels of
natural anticoagulants during pregnancy induce a
hypercoagulable state. While these changes aim to reduce
intrapartum blood loss, they increase the risk of
thromboembolism. Levels of fibrinogen, factors VII, VIII
and X and von Willebrand’s factor increase in pregnancy
and contribute to the procoagulant state. In addition,
during pregnancy the natural anticoagulants decrease as a
result of lower levels of functional protein S secondary to
increased levels of its binding protein, the complement
component C4b and increased levels of plasminogen
activator inhibitor type 1.13,21–24 These changes in the
coagulation system do not return to prepregnancy levels
until more than 8 weeks postpartum.22 Compared with the
risk during pregnancy, the risk of thrombosis is even higher
after delivery.22
Pathophysiology of acute myocardial
infarction
Acute myocardial infarction (AMI) is characterised by the
presence of myocardial necrosis in a clinical setting consistent
with myocardial ischaemia. It is classified on the basis of
electrocardiogram (ECG) findings as non-ST elevation
myocardial infarction (NSTEMI) and ST elevation
myocardial infarction (STEMI). Both types share a common
pathophysiology. The most common underlying cause is
atherosclerosis, a process of plaque formation in arteries,
which continues throughout life. A number of factors interact
before an atherosclerotic plaque causes an acute ischaemic
event. Risk factors for coronary disease such as diabetes and
smoking can cause damage to the endothelium covering the
atherosclerotic plaque. Dysfunction of injured endothelium
leads to inflammation of the underlying plaque, which can
fissure or rupture. The ruptured plaque is prothrombotic,
causing platelet activation and aggregation as well as
activation of the coagulation cascade. This progresses to
thrombus formation and causes myocardial ischaemia. The
severity of plaque rupture, degree of inflammation and the
coagulability status of the patient all influence the progression
of thrombus formation. Partial occlusion of a vessel with
thrombus causes findings consistent with NSTEMI while
total occlusion of the vessel presents as STEMI.
Impact of physiological changes on risk of
myocardial infarction
Cardiovascular changes in pregnancy lead to significantly
increased myocardial oxygen demand. At the same time, the physiological anaemia of pregnancy, hypercoagulability and
decrease in diastolic blood pressure may reduce the
myocardial oxygen supply and contribute to the aggravation
of myocardial ischaemia where the coronary arterial blood
supply is already compromised. Increased cardiac output in
the immediate postpartum period, resulting from
decompression of the inferior vena cava and transfer of
blood from the contracted uterus, makes peripartum a period
of particularly high risk.
Risk factors for myocardial infarction7,11,26–28
Risk factors identified from CEMACH/CMACE reports:
Higher parity (>3)
Increasing maternal age (>35 years)
Pre-existing hypertension
Pre-existing diabetes
Pre-existing ischaemic heart disease
Smoking
Obesity
Strong family history
Other risk factors mentioned in the literature:
Hyperlipidaemia
Pre-eclampsia
Eclampsia
Thrombophilia
Migraine headaches
Postpartum infections
Blood transfusions
Main causes of AMI in pregnancy 6,13,17,21,31–33
Coronary atherosclerosis
Non-atherosclerotic causes:
Coronary artery dissection
Coronary artery thrombosis
Coronary artery spasm:
-Spontaneous
-Drug-induced e.g. terbutaline, ergotamine, bromocriptine
ECG changes in pregnancy4–8,18,20
Diagnosis ECG changes
Acute myocardial
infarction
ST elevation
ST depression
Symmetrical T wave inversion
Newly developed Q waves
Normal variations
in pregnancy
15–20 degrees left axis shift
ST segment depression
T-wave inversion in inferior and lateral leads
Small Q wave and inverted T wave in lead III
Q wave in lead AVF
Inverted T waves in V1, V2 and occasionally V3
Investigations
Electrocardiography
Electrocardiograms (ECGs) are classically the first-line test in
making a diagnosis of AMI in any patient presenting with
chest pain. The most sensitive and specific ECG marker is ST
elevation, which normally appears within a few minutes of
onset of symptoms.1,43,44 Table 2 shows the ECG changes
seen. Serial ECGs are fundamental as the initial ECG can be
normal with changes evolving over time.8 It must be noted
that the sensitivity of 12-lead ECGs has been reported to be as
low as 50% to identify ischaemia.1,44 Therefore, other
markers of cardiac damage must be used in conjunction
with ECGs.
Blood cardiac markers
Cardiac-specific troponin I and troponin T are the biomarkers
of choice for diagnosing myocardial infarction.13,45 Different
hospitals will use either troponin I or troponin T and
recommended sampling times vary depending on the assay,
so clinicians should check their local hospital guidelines. A
negative troponin at presentation does not exclude cardiac
damage as it can take 12 hours for the level to peak.13
Troponin is never increased above the upper limit of
normal in healthy pregnant women and is not affected by
anaesthesia, a prolonged labour or caesarean section, and
therefore is the investigation of choice.45,46 In contrast, other
cardiac markers – myoglobin, creatinine kinase, creatinine
kinase isoenzyme MB – can be increased significantly in
labour.45 The troponin levels can be raised in pre-eclampsia,
gestational hypertension and pulmonary embolism in the
absence of significant coronary disease.13,47,48 It is important
to note that in pre-eclampsia the troponin level is never
above standard threshold set for MI.
Echocardiogram
Transthoracic echocardiogram is a useful method of
excluding other conditions, which may produce symptoms
similar to AMI such as aortic dissection. The use of
echocardiogram to diagnose AMI is limited but can be an
adjunctive technique to examine left ventricular function
and wall motion abnormalities.26 It can be undertaken safely
in pregnancy.13
Coronary angiography
Coronary angiography aids in the diagnosis and potential
treatment in AMI. It is reassuring to note that there is no
evidence to suggest an increased risk of congenital
malformations, intellectual disability, growth restriction or
pregnancy loss at doses of radiation of less than 50 mGy to the pregnant woman.
Estimated fetal and maternal effective doses for diagnostic
and interventional radiology procedures in AMI1
Procedure Fetal exposure Maternal exposure
Chest radiograph (PA
and lateral)
<0.01 mGy 0.1 mGy
CT chest 0.3 mGy 7 mGy
Coronary angiographya 1.5 mGy 7 mGy
Percutaneous coronary
intervention (PCI) or
radiofrequency catheter
ablation
Medical management of AMI in pregnancy20,44,55–57,59
Profiles for use in
pregnancy Drugs
Can be used safely Low-dose aspirin
Nifedipine
Labetalol
Heparin (LMWH and UFH)
Limited use, if no other
alternative
Clopidogrel
Contraindicated in
pregnancy
Statins
Angiotensin-converting enzyme inhibitors
Angiotensin receptor blockers
Timing and mode of delivery and AMI
There are no standardised guidelines for obstetric
management because of the lack of prospective data and
the impact of the variation of individual patient
characteristics in this setting. Collaborative management
involving cardiologist, obstetric physician, obstetrician,
obstetric anaesthetist and neonatologist will guide further
management. Interventions need to be individualised based
on maternal cardiac status and gestational age. If there is a
risk of preterm delivery, maternal steroid injections must be
administered at the earliest opportunity. If possible, delivery
should be delayed by 2–3 weeks following AMI because of the
increased risk of maternal mortality during this time.
Conclusion
Although rare, the incidence of myocardial infarction is
increasing in the UK in pregnant women. This can
probably be explained by the changing demographics of
the obstetric population, women delaying pregnancies,
increasing incidence of obesity, diabetes, pre-existing
hypertension, smoking and a family history of coronary
artery disease.
There is no evidence to support the screening of all
asymptomatic pregnant women with risk factors for AMI.
However, explicit identification of risk factors and
recommendations to reduce modifiable risk factors such as
smoking and excessive weight gain while achieving good
control of hypertension must be supported.
The majority of women with cardiovascular risk factors
have an uneventful pregnancy. In the absence of population
screening, clinicians can improve outcomes by having a low
index of suspicion of AMI in pregnant women. Appropriate
investigations and treatment must not be delayed because of
fetal concerns regarding radiation exposure or the use of
thrombolytic treatment. Treatment outcome is dependent on
the time to treatment and early involvement of the
cardiologist. Multidisciplinary team management is vital for
a good outcome although this may not always be possible in
an acute emergency setting.