CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 4, May 2013
AFRICA
e15
dysfunction, renin release and angiotensin production due
to decreased uterine perfusion in the supine position, ergot
derivatives that are used to control postpartum or post abortion
haemorrhage or to suppress lactation.
Several case reports described coronary embolism as a
cause of MI during pregnancy. Sources of emboli included
prosthetic valves, the left atrium in mitral stenosis or vegetations
in infective endocarditis, intracavitary thrombus in peripartum
cardiomyopathy or paradoxical embolism.
Coronary thrombosis without evidence of atherosclerotic
disease was reported in 8% of cases and was explained by the
hypercoagulable state of pregnancy.
1
The main reason for the
increased risk of thrombosis is hypercoagulability, which has
most likely evolved to protect women against the bleeding
challenges associated with miscarriage and childbirth. The
hypercoagulability of pregnancy is present as early as the first
trimester, as is the increased risk of thrombosis.
Acute coronary syndrome during pregnancy and puerperium
will continue to pose a great challenge for the physician for
many reasons. First, the challenge of initial diagnosis; owing to
the relative rarity of this condition, the misinterpretation of its
signs and symptoms and because of a low level of suspicion, a
rapid and accurate diagnosis of this condition will continue to be
a challenge for physicians.
Second, the different pathophysiology; unlike ACS in
non-pregnant women and in men where acute MI is typically
due to atherosclerosis, most of the coronary events complicating
pregnancy are not due to coronary atheroma. Different aetiologies
of ACS during pregnancy make uniform recommendations very
difficult. AMI in pregnant women is diagnosed in the same
way as in non-pregnant patients, including the constellation of
symptoms, electrocardiographic changes, and cardiac markers.
14
At the same time, however, the diagnostic approach is also
influenced by foetal safety and the normal changes in pregnancy.
The management of AMI during pregnancy should follow the
usual principles of care for AMI; however, selection of diagnostic
and therapeutic approaches may be influenced by foetal safety.
For patients with ischaemic symptoms characteristic of acute MI
of up to two hours’ duration and persistent ST-segment elevation,
prompt and complete restoration of flow in the infarct-related
artery can be achieved with a pharmacological (fibrinolysis),
percutaneous coronary (PCI) or surgical intervention.
PCI has been well documented during pregnancy and
is considered safe for maternal and foetal survival.
1,4,15-18
In
most cases PCI is preferred over thrombolysis because of
the decreased risk of haemorrhage in pregnancy and because
coronary dissection is a significant cause of AMI in pregnancy.
The first reports of angioplasty in a patient with postpartum MI
came in the 1990s.
All patients with STEMI who seek medical care within the
first 12 hours of onset of symptoms should be considered for
urgent reperfusion of the infarct-related artery. Although it is not
uncommon, because the symptoms and signs can be mistaken
for normal manifestations of pregnancy and labour, and because
there is a low index of suspicion, many pregnant women with
STEMI will present beyond the ideal time frame for reperfusion.
The cardiovascular risks of angioplasty in pregnancy are
similar to those in the non-pregnant patient.
19
The bleeding and
radiation risks can be reduced by use of a radial approach,
20
appropriate abdominal shielding, and decreasing fluoroscopy
time. The use of an intra-aortic balloon pump to improve left
ventricular output and coronary perfusion is also considered
safe,
21
although the patient should be positioned in the left lateral
recumbent position to reduce compression of the inferior vena
cava.
All reported stenting during the acute phase of MI during
pregnancy was performed with bare-metal stents;
1,4
the safety of
drug-eluting stents in pregnant women is currently still unknown.
Because drug-eluting stents require prolonged antiplatelet
therapy with clopidogrel and the incidence of cesarean deliveries
in patients with heart disease is relatively high, the use of a drug-
eluting stent during pregnancy may be problematic and should
be avoided if possible.
14
Hundreds of cases of cardiopulmonary bypass have been
reported in the literature since it was first used during pregnancy
in 1959. Over time, there have been significant improvements
in maternal and foetal outcomes. At present, maternal mortality
in CABG is the same as that in the general population, at 1.7
to 3%, with a foetal mortality rate of 9.5 to 19%.
22-25
Surgery
in the first trimester is associated with more foetal congenital
malformations but does not affect foetal mortality.
23,24
The timing
of the CABG does affect foetal mortality, and if the foetus is over
28 weeks of gestation, consideration must be given to deliver the
child immediately before or during the cardiac surgery.
24
CABG surgery is considered the gold-standard treatment
of unprotected left main coronary artery (ULMCA) disease.
Severe LMCA disease will reduce flow to a large portion of the
myocardium, placing the patient at high risk for life-threatening
events of left ventriculrar dysfunction and arrhythmias.
Thrombolytic therapy is considered to be relatively
contraindicated in pregnancy,
26
and because pregnant patients
have been traditionally excluded from clinical trials, the available
information is anecdotal.
27-29
Although maternal and foetal
outcomes were favourable in most cases,
30
some reports have
documented complications, such as maternal haemorrhage,
preterm delivery, foetal loss, and spontaneous abortion.
30-34
The most appropriate medication regimen for pregnant
patients with ischaemic heart disease or AMI is unknown. There
is a significant amount of anecdotal evidence supporting the use
of salicylates,
β
-blockers, nitroglycerin, calcium antagonists and
heparin during pregnancy but little is known about the optimal
combination of these medications.
19
In the present case, multiple factors (such as hypercholes-
terolaemia and hypercoagulability state) may have contributed to
the AMI. To our knowledge, this is the first case reporting severe
atherosclerotic LMCA stenosis as a cause of post-partum AMI.
Conclusion
This case underlines how during pregnancy or puerperium, it is
important to evaluate the cardiovascular risk profile in order not
to underestimate clinical signs of myocardial ischaemia. AMI
in pregnancy is uncommon but not as rare as it used to be. As
pregnancy itself represents a risk factor, clinicians should be
aware of classical risk factors for coronary artery disease and
typical symptoms of myocardial ischaemia. Particularly older
childbearing women should be closely monitored. If coronary
artery disease is suspected or diagnosed, interdisciplinary
teamwork between the general practitioner, cardiologist,
cardiovascular surgeon, obstetrician and anaesthetist is required.
