Received: 17 October 2016 Accepted: 9 November 2016

DOI: 10.1002/clc.22655

REVIEWS

ST-elevation acute myocardial infarction in pregnancy: 2016

update
Sahar Ismail1 | Cynthia Wong2 | Priya Rajan3 | Mladen I. Vidovich4

1
Division of Cardiology, Emory University,
Atlanta, Georgia Acute myocardial infarction (AMI) during pregnancy or the early postpartum period is rare, but
2
Department of Anesthesia, University of can be devastating for both the mother and the fetus. There have been major advances in the
Iowa Carver College of Medicine, Iowa diagnosis and treatment of acute coronary syndromes in the general population, but there is lit-
City, Iowa
tle consensus on the approach to diagnosis and treatment of pregnant women. This article
3
Department of Obstetrics and Gynecology,
reviews the literature relating to the pathophysiology of AMI in pregnant patients and the chal-
Maternal–Fetal Medicine, Northwestern
University Feinberg School of Medicine, lenges in diagnosis and treatment of ST-elevation myocardial infarction (STEMI) in this unique
Chicago, Illinois population. From a cardiologist, maternal–fetal medicine specialist, and anesthesiologist’s per-
4
Division of Cardiology, University of Illinois spective, we provide recommendations for the diagnosis and management of STEMI occurring
at Chicago, Chicago, Illinois during pregnancy.
Correspondence
Mladen I. Vidovich, MD, 840 S Wood Street,
KEYWORDS
MC 715, Suite 935, Chicago, IL 60612
Email: miv@uic.edu PCI, PRENANCY, STEMI

1 | I N T RO D UC T I O N
The incidence of acute myocardial infarction (AMI) in pregnancy
ranges from 3 to 100 per 100 000 deliveries.1 The maternal case
fatality is as high as 11%, with an associated fetal mortality of 9%. It
is reported that coronary artery dissection is found in 16%, thrombus
without atherosclerotic disease in 21%, normal coronary arteries in
29%, and atherosclerosis with or without intracoronary thrombus in
43% of cases.1 In contrast, the majority of cases of AMI in the gen-
eral population are due to coronary thrombosis associated with a dis-
2
rupted atherosclerotic plaque. One of the proposed pathologic
processes in pregnancy is the excess progesterone leading to degen-
eration of the connective tissue in the intima and media of the coro-
nary arteries. Pregnancy-related hypertension, along with physiologic
increase in blood volume and cardiac output in pregnancy, may pres-
ent additional stress to blood vessels and increase the risk of coro-
nary dissection and thrombotic rupture.1 Despite this distinctive
underlying pathophysiology, traditional risk factors for cardiovascular
disease have been linked to pregnancy-related AMI. Age greater than
30 years, African American race, hypertension, diabetes, physical
inactivity, and smoking have been previously reported in the litera-
ture.1 Certain obstetric conditions are additional important risk fac-
tors for AMI, including preeclampsia, thrombophilia, postpartum
hemorrhage, blood product transfusion, and postpartum infection.1
AMI can occur during any trimester, and each trimester carries its
own diagnoses and treatment challenges. Early in pregnancy, at the
height of organogenesis, the teratogenic risk of pharmacologic ther-
apy and radiation exposure during cardiac catheterization are of fore-
most concern. In the later stages of pregnancy, balancing the risk of
bleeding during delivery against the risk of stent thrombosis if dual
antiplatelet therapy (DAPT) is discontinued is the main challenge. This
review will address the challenges of the diagnosis of acute coronary
syndrome (ACS) in pregnancy and propose a standardized approach
to treating pregnant women presenting with specifically ST-elevation
acute myocardial infarction (STEMI).
2 | DI A G N O S I S OF A C S I N P RE G N A N C Y
2.1 | Electrocardiogram in pregnancy
New ST depressions, T wave inversions, and left axis deviation may
be normally seen in pregnancy.3 ST segment depressions are most
commonly reported, and is likely the result of the administration of
anesthesia, anxiety, hyperventilation, changes in autonomic tone dur-
ing delivery, and oxytocin administration.4 Therefore, these electro-
cardiogram (ECG) changes must be interpreted within the context of
the patient’s clinical presentation, and alongside further diagnostic

Clinical Cardiology. 2017;40:399–406. wileyonlinelibrary.com/journal/clc © 2017 Wiley Periodicals, Inc. 399

400 ISMAIL ET AL.

TABLE 1 Drugs indicated in STEMI and their level of risk in pregnancy

Drug Teratogenicity Recommendation

ASA Gastrochesis, premature closure of patent ductus Recommended given the benefits outweigh risks
arteriosis
Clopidogrel Unknown Recommended given the benefits outweigh risks
Prasugrel and ticagrelor Unknown Given insufficient data to evaluate risks versus
benefits, favor use of clopidogrel
Heparin None known Recommended given the benefits outweigh risks
Glyoprotein IIb/IIIa inhibitors Unknown May be given only if the potential benefit
outweighs the risk
Direct thrombin inhibitors Unknown Recommended to be given for patients with HIT
β-blockers Bradycardia and hypoglycemia Recommended given its benefits outweigh the
risks
Long-acting calcium channel blockers Tocolytic; application and potential synergism with May be used with caution if benefits outweigh
magnesium sulfate may induce hypotension the risks
(mother) and fetal hypoxia
Isosorbide dinitrate Bradycardia Recommended if benefits outweigh the risks
ACE-I and ARB Renal Tubular dysplasia, oligohydraminos, growth Not to be given during pregnancy
retardation, ossification disorders of the skull,
lung hypoplasia, contractures, large joints,
anemia, intrauterine fetal death
Aldosterone antagonists Sprinolactone specifically is associated with Not to be given during pregnancy
antiandrogenic effects, oral clefts (first trimester)
Statins Congenital anomalies Not to be given during pregnancy

Abbreviations: ACE-I, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; ASA, acetylsalicylic acid; FDA, Food and Drug Adminis-
tration; STEMI, ST-elevation myocardial infarction.
On December 13, 2014, the FDA changed the labeling requirements for the pregnancy and lactation sections for prescription drugs and biological agents.
The FDA removed the pregnancy letter categories and created descriptive subsections for pregnancy exposure and fetal risk that is to be included in all
package inserts.

testing. Importantly, ST elevations are never seen in normal preg- motion abnormalities (RWMA) are not seen in normal pregnancy, and
nancy and should prompt immediate further investigation. if observed, indicate myocardial ischemia or injury.7 This finding is
especially helpful in the setting of equivocal ECG changes, when
RWMA not only serves as diagnostic guides, but also as prognostic
2.2 | Cardiac biomarkers
indicators for further cardiac events.7
During pregnancy, troponin elevation is almost invariably suggestive
of underlying myocardial damage. Mild troponin elevations may be
seen in preeclampsia and gestational hypertension.5 However, an 2.4 | Coronary angiography
increase in the serum levels of troponin I in the absence of
Coronary angiography remains the gold standard for diagnosis of cor-
pregnancy-associated hypertension is indicative of a primary coronary
onary artery disease (CAD).8–10 There is, however, a higher incidence
event.4
of iatrogenic coronary artery dissection in pregnant women.11 Mea-
Although elevations in troponin are never seen in normal preg-
sures, such as avoiding deep catheter intubation, minimizing the num-
nancy, creatine kinase myocardial band (CK MB) is normally present
ber of low-pressure contrast injections, and limiting the use of
in the uterus and placenta, and rises in the first 24 hours after deliv-
fractional flow reserve pressure guidewires, suction devices, and bal-
ery with a decline thereafter.5 It may be elevated up to 4 times the
loons, should be performed if possible. Imaging techniques, such as
upper limit of normal, rendering CK MB less specific for diagnosis of
intravascular ultrasound (IVUS) or optical coherence tomography
AMI during pregnancy.5 However, assessing both CK MB and tropo-
(OCT), may be used during angiography to aid in elucidating the
nin concentrations forms a sensitive and essential diagnostic tool for
extent of CAD or the presence of coronary artery dissection and
the diagnosis of AMI during pregnancy.
guiding intervention.11

2.3 | Echocardiography 2.4.1 | Arterial access

It is important to recognize several physiological changes in preg-
6
nancy that may be reflected on echocardiographic examination.
Increased preload, in conjunction with the decreased peripheral
resistance, leads to an increase in cardiac output. These physiologic
changes lead to left ventricular remodeling and mild left ventricular
hypertrophy. Pregnant women with preeclampsia and multiple gesta-
tion exhibit additional increase in left ventricular mass.6 Regional wall
The site of arterial access is an important consideration in the preg-
nant population. In pregnant women, radial access is preferred
because it eliminates the technical challenges that are encountered
using the femoral artery approach because of the presence of the
enlarged uterus and positioning difficulties. Left lateral decubitus
positioning is required in pregnant women from 20 weeks’ gestational
age onward to avoid aortocaval compression and its untoward
ISMAIL ET AL. 401

Diagnosis of AMI in Pregnancy

Troponin elevation (>1 ng/ml CKMB elevation (>4x normal ECG with ST changes (ST
elevations highly suggestive of MI) TTE with RWMA
highly suggestive of MI) highly suggestive of MI)

Anti-Thrombin Therapy

Peri-procedural GP IIb/IIIa
Low dose ASA (continue UFH (Argatroban for inhibitors in patients with
Clopidogrel TT relatively contraindicated
throughout delivery) patients with history of HIT) prior MI, high thrombus
burden, complex PCI

Coronary angiography via radial access for all pregnant patients presenting with STEMI .

Revascularization per standard clinical practice in those found to have atherosclerotic disease or
coronary artery dissection in select cases*

POBA with provisional stent placement

DES or BMS in the first two trimesters BMS in the final trimester
(less preferable)

FIGURE 1 Approach to STEMI in pregnancy. Care of patients with ACS during labor, delivery, and postpartum is ideally provided by a
multidisciplinary team of cardiologists, obstetricians, and anesthesiologists working in experienced maternal–fetal medicine units. Vaginal
spontaneous delivery is preferred; however, the timing and mode of delivery is ultimately determined on a case basis dictated by maternal
cardiac and hemodynamic status and obstetric factors. *In most cases of coronary dissection, conservative treatment is preferred for stable
patients without ongoing pain. Patients with ongoing chest pain, ischemia, ST elevation, hemodynamic instability, dissected left main, or
dissection affecting leading to sizable myocardial jeopardy and amenable to PCI, should undergo percutaneous revascularization. Abbreviations:
AMI, acute myocardial infarction; ASA, acetylsalicylic acid; BMS, bare-metal stent; CKMB, creatine kinase myocardial band; DES, drug-eluting
stent; ECG, electrocardiogram; GP IIb/IIIa, glycoprotein IIb/IIIa; HIT, heparin-induced thrombocytopenia; MI, myocardial infarction; PCI,
percutaneous coronary intervention; POBA, plain old balloon angioplasty; RWMA, regional wall motion abnormalities; STEMI, ST-elevation
myocardial infarction; TT, thrombolytic therapy; TTE, transthoracic echocardiography; UFH, unfractionated heparin.

hemodynamic consequences. Radial access is also associated with
decreased bleeding complications, reduced length of hospital stay,
and improved patient comfort.12 These advantages, however, may
occur at the expense of slightly increased radiation exposure times.13
2.4.2 | Fetal risks of ionizing radiation
The mean fetal radiation exposure during coronary angiography is
approximately 3 mSv, far less than the doses that have been reported
to be associated with fetal malformations (50–100 Sv) with first tri-
mester exposure.14 Nevertheless, measures should be taken to mini-
mize the amount of radiation exposure. Most fetal exposure occurs
through indirect, scatter radiation; thus, all possible measures should
be taken to reduce exposure. This includes utilizing external abdomi-
nal shielding, employing the radial approach, using simple fluoros-
copy, utilizing lower magnification, using low fluoroscopy frame rates,
and careful collimation.
2.4.3 | Fetal risks of iodinated contrast administration
Another concern with coronary angiography is the use of iodinated
contrast agents and the associated clinical risk of fetal congenital
hypothyroidism.15 There are no studies assessing the amount of free
iodine entering fetal circulation during coronary angiography or the
length of exposure needed to cause fetal harm, but there are no
reports to date to suggest contrast dye is teratogenic.15 Evaluating
fetal thyroid function within the first week of delivery is routinely
performed in the United States regardless of fetal exposure to
iodine.15 The Contrast Media Safety Committee of the European
Society of Urogenital Radiology and the American College of Radiol-
ogy do not recommend any additional testing or intervention beyond
routine thyroid testing at time of birth.15
In summary, the morbidity and mortality associated with AMI in
pregnancy outweigh the potential teratogenic risks of coronary angi-
ography. Although it is important to avoid unnecessary maternal and
402
fetal radiation exposure during pregnancy, this should not deter phy-
sicians from performing indicated lifesaving procedures.
3 | APPROAC H TO THE A CU TE
M A N A G E M E N T O F S T E M I I N P R E G NA N C Y
3.1 | Anticoagulation in STEMI during pregnancy
3.1.1 | Unfractionated heparin
Given its relative safety in pregnancy, fast onset, short half-life, and
ease of dose adjustment, unfractionated heparin (UFH) is commonly
used in pregnancy. Pregnancy leads to alterations in heparin’s phar-
macokinetic parameters because of increased levels of heparin-
binding proteins, factor VIII, and fibrinogen.16 Similar to standard
practice outside of pregnancy, we recommend monitoring its effect
and adjusting the dose of heparin by measurement of the activated
clotting time.9,10 As for its safety in pregnancy, UFH does not cross
the placenta; therefore, it does not cause fetal bleeding and fetal mal-
formations. However, bleeding at the uteroplacental junction is possi-
ble, as with the use of any anticoagulant.16 The use of heparin is also
associated with the development of immunoglobulin G–mediated
heparin-induced thrombocytopenia (HIT) in approximately 3% of
patients.9,10
3.1.2 | Low-molecular-weight heparin
Similar to UFH, physiological changes associated with pregnancy
affect the pharmacokinetics of low-molecular-weight heparin
(LMWH). Increases in maternal weight, renal clearance, and volume
of distribution of LMWH during pregnancy lead to significant dose–
response variability.16 Dosing may be monitored and adjusted
accordingly to the anti-Xa activity target level. However, this practice
is controversial because the optimal target anti-Xa level for anticoa-
gulation for ACS is not well defined, and bedside testing assays are
not readably available at many centers. Finally, its safety in pregnancy
is less well studied than UFH.
3.1.3 | Glycoprotein IIb/IIIa inhibitors
The administration of glycoprotein (GP) IIb/IIIa inhibitors in ACS is
associated with a significant reduction in ischemic events at the cost
of increased risk of bleeding complications, which is a significant con-
cern during delivery.17 Additionally, there are very limited data
regarding potential fetal effects (pregnancy category B). Thus far, a
small number of case reports describing the use of GP IIb/IIIa inhibi-
tors in pregnancy have not reported maternal or fetal complica-
tions.18–22 In general, we recommend reserving its use during
percutaneous coronary intervention (PCI) for patients at high ische-
mic risk, including those with prior myocardial infarction, high throm-
bus burden, and complex PCI.
3.1.4 | Direct thrombin inhibitors
Several trials showed that direct thrombin inhibitors (DTI) are as or
more effective than UFH at reducing the incidence of the composite
outcome of death, myocardial infarction, and repeat vascularization,
as well as bleeding complications in patients with ACS undergoing
ISMAIL ET AL.
PCI.23,24 DTI do not bind plasma proteins, and therefore have a more
predictable dose response than UFH.23 The lower rate of bleeding
complications, fast onset of activity, and short half-life (25 to 45 min-
utes) make this class of medications an attractive option in preg-
nancy. However, there are limited data on its safety during
pregnancy (pregnancy category B). There are no published reports to
date utilizing bivalirudin during pregnancy, but several case reports
document the use of argatroban for the treatment of venous throm-
boembolism in those with HIT.25,26 No adverse effects have been
described in case reports.25,26 Given the relatively limited data on the
fetal effects of DTI, we recommend using argatroban only in those
with HIT.
3.1.5 | Switching between antithrombins
Switching between LMWH and UFH results in an increase in both
catheter-related bleeding and adverse ischemic outcomes as demon-
strated in the SYNERGY (Superior Yield of the New Strategy of Enox-
aparin, Revascularization and Glycoprotein IIb/IIIa Inhibitors) trial.27
Several studies have shown that switching to bivalirudin during PCI
from either UFH or enoxaparin is associated with similar rates of
ischemic events and significantly lower rates of bleeding; however,
there are no data pertaining to the safety of bivalirudin in preg-
nancy.28 Therefore, we recommend anticoagulation with UFH from
time to presentation until conclusion of PCI, while avoiding switching
antithrombin therapy.
3.2 | Antiplatelet therapy in STEMI during
pregnancy
3.2.1 | Aspirin
Numerous studies have reported the use of low-dose aspirin, 80 to
150 mg/day, for the treatment of various disorders in pregnancy.29
Nonsteroidal anti-inflammatory drugs (NSAIDs) may inhibit blastocyst
implantation and lead to subsequent miscarriage.30 NSAIDs can also
lead to premature closure of the ductus arteriosus, particularly if
administered after 32 weeks’ gestation.30 Of the numerous case
reports and case series of AMI in pregnant women, none have docu-
mented adverse effects thought to be secondary to aspirin use.1,4
The benefits of low-dose aspirin largely outweigh the potential risks
of treatment in the setting of STEMI.
3.2.2 | P2Y12 receptor antagonists
All pivotal clopidogrel trials excluded pregnant patients, but there are
numerous case reports of various loading and maintenance doses of
clopidogrel in pregnancy.16,31,32 Although most reports did not attrib-
ute any adverse effects to clopidogrel therapy, maternal thrombocy-
topenia, intrauterine fetal demise, and maternal hemorrhage requiring
blood transfusion were reported.16,31,32 Clopidogrel remains a widely
used thienopyridine in pregnancy (pregnancy category B).
Prasugrel, like clopidogrel, is a thienopyridine that irreversibly
inhibits the P2Y12 adenosine diphosphate receptor, but is thought to
have a faster and more potent antiplatelet response.33 In clinical prac-
tice, these advantageous pharmacological properties translated into
decreased ischemic events but increased bleeding risk compared with
clopidogrel, rendering it a less appealing option in pregnancy.33
ISMAIL ET AL.
Prasugrel is classified as a pregnancy category B. Toxicology studies
performed in animal models did not show any adverse fetal effects;
however, there are no studies evaluating the use of prasugrel in
human pregnancy. Hence, at the present time, its use in STEMI dur-
ing pregnancy is not recommended in favor of clopidogrel.8
Ticagrelor is a reversible nonthienopyridine P2Y12 antagonist that
has minimal interpatient variability. Ticagrelor was associated with
lower adverse cardiac outcomes and cardiac mortality compared with
standard dose clopidogrel in ACS patients managed with and without
PCI.34 Ticagrelor is classified as a pregnancy category C. In animal
studies, ticagrelor caused structural abnormalities, and there are no
data on its safety in human pregnancy. We therefore do not recom-
mend the use of ticagrelor for the management of pregnant patients
with STEMI.
3.3 | PCI in pregnancy
The maternal mortality related to myocardial infarction (MI) in preg-
nancy has been reported to be as high as 50% in the peripartum
35
period. In the last decade, there has been a reduction in the
reported maternal mortality rate to as low as 11% to 5.1%, likely
related to early detection and performance of invasive interventions,
as well as the advances in care in intensive care units, anesthesia,
and high-risk obstetric practice.21 Given the high mortality of MI in
pregnancy, we recommend early coronary angiography in all preg-
nant patients presenting with STEMI. Further investigation with
intracoronary imaging, such as OCT and IVUS, is recommended if
there is suspicion for coronary artery dissection. Spontaneous coro-
nary artery dissection may be managed medically in patients without
any of the following: ongoing chest pain or ischemic changes on
ECG, cardiogenic shock requiring inotropes or mechanical support,
sustained ventricular tachycardia or ventricular fibrillation, or left
main dissection.36 In patients with coronary dissection amenable to
PCI, coronary artery dissection with any of the previously mentioned
clinical criteria, or angiographic findings consistent with atheroscle-
rotic disease, percutaneous revascularization with a stent should be
pursued.
Of note, the use of an intra-aortic balloon pump to improve left
ventricular output and coronary perfusion is also considered safe,
although the patient should be positioned in the left lateral decubitus
position to reduce compression of the inferior vena cava.
3.3.1 | Stent selection
Bare-metal stents (BMS) are commonly employed for STEMI in preg-
nancy. Although plain old balloon angioplasty may be used in STEMI
in pregnancy, repeat revascularization rates are high; restenosis
occurs in over 50% of patients, and recurrent MI in 3% to 5% of
patients.37 BMS have been found to be safe in pregnancy and require
a short duration of DAPT (minimum of 4 weeks).9,10 Therefore, during
the third trimester of pregnancy, a BMS is most appropriate. This
allows for interruption of DAPT (after at least 4 weeks of therapy) at
the time of delivery, reducing potential bleeding complications in the
peripartum period.
Drug-eluting stents (DES) are associated with further reductions
in revascularization compared with BMS, but first-generation devices
403
have been associated with increased rates of stent thrombosis, and
hence longer duration of DAPT is recommended.38 The optimal dura-
tion of DAPT with the newer generation of DES is currently an area
of active research, but a minimum of 3 months duration is now con-
sidered reasonable.39,40 There is less experience using the newer gen-
eration DES in pregnancy; nevertheless, contemporary DES may be
used in the first 2 trimesters with a anticipated interruption of DAPT
near time of delivery.
3.3.2 | DAPT interruption during delivery
Balancing the risk of ST during interruption of DAPT and recurrent
ischemic events in this unique prothrombotic environment against
the risk of perioperative bleeding associated with DAPT is critical.
Most data suggest that taking low-dose aspirin perioperatively in
those undergoing surgery is associated with a low risk of excessive
bleeding. The addition of a thienopyridine to low-dose aspirin results
in a significant increase in bleeding and length of hospital stay after a
surgical procedural.41 Although this risk varies considerably based on
the type of the surgical procedure, the consensus among most obste-
tricians, anesthesiologists, and cardiologists is that the risk of bleeding
during delivery is high on DAPT, and aspirin alone may be continued
through out the peripartum period.
In some of the published case reports of delivery occurring
within 1 month of BMS placement, the physicians decided to discon-
tinue clopidogrel 5 to 7 days before the scheduled delivery and initi-
ate LMWH or UFH.18–22,42 The concern with this management is
that studies have failed to show that heparin is effective in prevent-
ing acute and subacute stent thrombosis.43 Stent thrombosis is a
platelet-mediated process, and therefore anticoagulants are ineffec-
tive at preventing arterial thrombosis.
Several trials have evaluated the use of GP IIb/IIIa inhibitors in
patients with prior coronary stenting in whom interruption of thieno-
pyridine administration was necessary prior to surgery.44,45 However,
none of these studies show that preoperative GP IIb/IIIa inhibitors
provide sufficient antithrombotic protection resulting in a reduction
in the risk of stent thrombosis. This practice may, in fact, carry an
increased risk of perioperative bleeding.44,45
Cangrelor, a new intravenous short-acting P2Y12 inhibitor, has
shown promise in pilot studies as a bridge during coronary artery
bypass grafting surgery.46 In these studies, cangrelor resulted in
greater, sustained platelet inhibition compared to placebo.46 This
drug is currently approved for clinical use; however, it is classified as
a pregnancy category C. Although there are no data on the safety of
cangrelor in human pregnancy, there have been reports of increased
incidence of incomplete ossification and unossified hind limb metatar-
sals, abortion, intrauterine losses, and fetal growth retardation in ani-
mal studies.
In summary, there is no consensus on the best approach to man-
aging DAPT during delivery. A minimum of 12 months of DAPT for
the treatment of STEMI after BMS or DES implantation remains a
class I indication in the 2016 American College of Cardiology/Ameri-
can Heart Association guideline update on the duration of DAPT in
patients with CAD.40 Patients who suffer a STEMI during pregnancy
typically require at least temporary cessation of DAPT proximate to
404 ISMAIL ET AL.

delivery, prior to the completion of the recommended 12 months.9,10 4.1 | Anesthesia considerations
Based on the new guidelines, it is also reasonable to discontinue
Neuraxial (spinal, epidural, combined spinal–epidural) analgesia for
DAPT after 6 months of treatment in those who are deemed at high
labor and neuroaxial anesthesia for cesarean delivery are generally
risk of bleeding (class IIb recommendation).40 We therefore recom-
preferred. If emergency cesarean delivery is required, epidural analge-
mend treatment for at least 6 months of uninterrupted DAPT after
sia may be quickly converted to epidural anesthesia, thus avoiding
implantation of DES (or BMS) prior to delivery. In patients presenting
the need for general anesthesia. Neuraxial anesthesia for cesarean
with STEMI in the third trimester, BMS, as discussed previously, is
delivery is associated with fewer hyperdynamic hemodynamic
preferred to ensure that the patient receives at least 1 month of
changes than general anesthesia, and recovery is faster. Although the
uninterrupted DAPT. If the patient is receiving DAPT near the time
risk of hypotension is greater with neuraxial anesthesia, hypotension
of delivery, we recommend discontinuing clopidogrel 5 days prior to
can be minimized with low-dose local anesthetic techniques and care-
planned delivery and only bridging with tirofiban or eptifibatide in
ful titration of vasoconstrictors and intravenous fluids. The low-dose
instances in which the risk of stent thrombosis is high, including those
spinal component of block provides dense anesthesia, and if it proves
with prior MI, complex PCI, or high thrombosis risk.9,10,47 Tirofiban
inadequate for surgical anesthesia, administration of additional local
and eptifibatide should be continued up to 4 to 6 hours before deliv-
anesthesia via the epidural catheter can be used to titrate further
ery. We do not recommend reinitiating GP IIb/IIIa inhibitors after
anesthesia.
delivery, expect in rare cases of complex PCI that are deemed of very
A major concern with neuraxial anesthesia is the risk of spinal-
high thrombotic burden. If the patient received DAPT for less than
epidural hematoma formation and consequent neurological impair-
6 months prior to delivery, clopidogrel should be resumed as soon as
ment in patients receiving DAPT. Although several retrospective
it is deemed safe after delivery by the obstetrician and anesthesiolo-
studies have failed to make this association, the American Society
gist (typically 24 hours after delivery) to complete at least 12 months
of Regional Anesthesia and Pain Medicine recommends that clopi-
of DAPT, as indicated for ACS.47 If the patient received at least
dogrel be discontinued 5 to 7 days prior to performance of neurax-
6 months of DAPT prior to delivery, it may be reasonable to forgo
ial anesthesia.47 Neuraxial anesthesia can be performed safely in
reinitiating clopidogrel after delivery if the risk of bleeding outweighs
patients receiving aspirin therapy alone. However, UFH and LMWH
the benefits of continued DAPT.
must be discontinued before the initiation of neuraxial anesthesia
procedures (24 hours for therapeutic doses of LMWH).47 Close
3.3.3 | Thrombolytic therapy
communication among the members of the multidisciplinary care
Thrombolytic therapy (TT) is not advocated for the management of
team is necessary to determine when DAPT should be initiated in
AMI in pregnancy.8 Reported complications have included maternal
the postpartum period. This decision must weigh the risks of post-
hemorrhage, preterm delivery, fetal loss, spontaneous abortion, pla-
partum and neuraxial hemorrhage against the risk of coronary
centa abruption, uterine bleeding, and postpartum hemorrhage.8,48,49
thrombosis.
Importantly, given the prevalence of coronary dissection in preg-
nancy, TT may be harmful, increasing the risk of bleeding and pro-
gression of the dissection.48,49 For these reasons, TT is rarely utilized
for AMI treatment in pregnancy. Nonetheless, if PCI access for 5 | CONC LU SION
STEMI during pregnancy is not available, TT may be an alternative
management strategy. Pregnancy poses several challenges to both the diagnosis of ACS
and management of STEMI. Standardizing the approach to its treat-
ment may minimize maternal and fetal complications. The approach
4 | OBSTETRIC CONSIDERATIONS to the diagnosis of ACS in pregnancy is similar to that in nonpreg-
nant patients with the exceptions of a few considerations. Coronary
Labor induction may be pursued to allow for planned discontinuation angiography remains the gold standard for diagnosis, and concerns
of antithrombin therapy before delivery. Labor may be induced with about ionized radiation exposure should not delay this potentially
an oxytocin infusion with careful monitoring of fluid status and cardi- life-saving intervention. PCI should be performed via the radial
ovascular effects.50 ST-segment depression, myocardial ischemia, approach. DES or BMS may be employed, depending on the stage of
arrhythmias, and even maternal deaths have been reported in associ- pregnancy. DAPT may be interrupted by delivery; however, with the
ation with continuous infusion and bolus dosing of oxytocin.50 Syn- favorable characteristics of new-generation DES, this may be accom-
thetic prostaglandin analogs carry a risk of coronary vasospasm and plished with lower risk of stent thrombosis. Most importantly,
arrhythmias.8 For these reasons, spontaneous onset of labor is employing a multidisciplinary team and monitoring patients in the
favored.8 critical care setting is unarguably essential for the care for this spe-
In terms of the mode of delivery, vaginal delivery is generally pre- cial population.
ferred for several reasons, including lower rates of hemorrhagic,
thromboembolic, and infectious complications as well as potential
fetal benefits.8 Although cesarean delivery may be appropriate in cer-
Conflict of interests
tain situations, it is typically reserved for the usual obstetric
indications.8 The authors declare no potential conflict of interests.
ISMAIL ET AL.
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How to cite this article: Ismail S, Wong C, Rajan P and
Vidovich M I. ST-elevation acute myocardial infarction in
pregnancy: 2016 update. Clin Cardiol. 2017;40:399–406.
https://doi.org/10.1002/clc.22655