ST‐elevation acute myocardial infarction in pregnancy: 2016 update

Abstract

Acute myocardial infarction (AMI) during pregnancy or the early postpartum period is rare, but can be devastating for both the mother and the fetus. There have been major advances in the diagnosis and treatment of acute coronary syndromes in the general population, but there is little consensus on the approach to diagnosis and treatment of pregnant women. This article reviews the literature relating to the pathophysiology of AMI in pregnant patients and the challenges in diagnosis and treatment of ST‐elevation myocardial infarction (STEMI) in this unique population. From a cardiologist, maternal–fetal medicine specialist, and anesthesiologist's perspective, we provide recommendations for the diagnosis and management of STEMI occurring during pregnancy.

1. INTRODUCTION

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 general population are due to coronary thrombosis associated with a disrupted atherosclerotic plaque.2 One of the proposed pathologic processes in pregnancy is the excess progesterone leading to degeneration of the connective tissue in the intima and media of the coronary arteries. Pregnancy‐related hypertension, along with physiologic increase in blood volume and cardiac output in pregnancy, may present additional stress to blood vessels and increase the risk of coronary 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 literature.1 Certain obstetric conditions are additional important risk factors 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 therapy and radiation exposure during cardiac catheterization are of foremost 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. DIAGNOSIS OF ACS IN PREGNANCY

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 during delivery, and oxytocin administration.4 Therefore, these electrocardiogram (ECG) changes must be interpreted within the context of the patient's clinical presentation, and alongside further diagnostic testing. Importantly, ST elevations are never seen in normal pregnancy and should prompt immediate further investigation.

Table 1.

Drugs indicated in STEMI and their level of risk in pregnancy

Drug	Teratogenicity	Recommendation
ASA	Gastrochesis, premature closure of patent ductus arteriosis	Recommended given the benefits outweigh risks
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 magnesium sulfate may induce hypotension (mother) and fetal hypoxia	May be used with caution if benefits outweigh the risks
Isosorbide dinitrate	Bradycardia	Recommended if benefits outweigh the risks
ACE‐I and ARB	Renal Tubular dysplasia, oligohydraminos, growth retardation, ossification disorders of the skull, lung hypoplasia, contractures, large joints, anemia, intrauterine fetal death	Not to be given during pregnancy
Aldosterone antagonists	Sprinolactone specifically is associated with antiandrogenic effects, oral clefts (first trimester)	Not to be given during pregnancy
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 Administration; 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.

2.2. Cardiac biomarkers

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 increase in the serum levels of troponin I in the absence of pregnancy‐associated hypertension is indicative of a primary coronary event.4

Although elevations in troponin are never seen in normal pregnancy, creatine kinase myocardial band (CK MB) is normally present in the uterus and placenta, and rises in the first 24 hours after delivery with a decline thereafter.5 It may be elevated up to 4 times the upper limit of normal, rendering CK MB less specific for diagnosis of AMI during pregnancy.5 However, assessing both CK MB and troponin concentrations forms a sensitive and essential diagnostic tool for the diagnosis of AMI during pregnancy.

2.3. Echocardiography

It is important to recognize several physiological changes in pregnancy that may be reflected on echocardiographic examination.6 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 gestation exhibit additional increase in left ventricular mass.6 Regional wall motion abnormalities (RWMA) are not seen in normal pregnancy, and 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 indicators for further cardiac events.7

2.4. Coronary angiography

Coronary angiography remains the gold standard for diagnosis of coronary artery disease (CAD).8, 9, 10 There is, however, a higher incidence of iatrogenic coronary artery dissection in pregnant women.11 Measures, such as avoiding deep catheter intubation, minimizing the number of low‐pressure contrast injections, and limiting the use of fractional flow reserve pressure guidewires, suction devices, and balloons, should be performed if possible. Imaging techniques, such as intravascular ultrasound (IVUS) or optical coherence tomography (OCT), may be used during angiography to aid in elucidating the extent of CAD or the presence of coronary artery dissection and guiding intervention.11

2.4.1. Arterial access

The site of arterial access is an important consideration in the pregnant 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 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 trimester exposure.14 Nevertheless, measures should be taken to minimize 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 abdominal shielding, employing the radial approach, using simple fluoroscopy, utilizing lower magnification, using low fluoroscopy frame rates, and careful collimation.

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.

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 Radiology 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 angiography. Although it is important to avoid unnecessary maternal and fetal radiation exposure during pregnancy, this should not deter physicians from performing indicated lifesaving procedures.

3. APPROACH TO THE ACUTE MANAGEMENT OF STEMI IN PREGNANCY

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 pharmacokinetic 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 malformations. However, bleeding at the uteroplacental junction is possible, 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 anticoagulation 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 concern 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 inhibitors in pregnancy have not reported maternal or fetal complications.18, 19, 20, 21, 22 In general, we recommend reserving its use during percutaneous coronary intervention (PCI) for patients at high ischemic risk, including those with prior myocardial infarction, high thrombus 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 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 minutes) make this class of medications an attractive option in pregnancy. 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 thromboembolism 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 demonstrated in the SYNERGY (Superior Yield of the New Strategy of Enoxaparin, 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 pregnancy.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 documented 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 attribute any adverse effects to clopidogrel therapy, maternal thrombocytopenia, 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 practice, 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 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 during 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 recommend 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 pregnancy has been reported to be as high as 50% in the peripartum period.35 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 pregnant 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 coronary 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 atherosclerotic 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 pregnancy. 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 have been associated with increased rates of stent thrombosis, and hence longer duration of DAPT is recommended.38 The optimal duration of DAPT with the newer generation of DES is currently an area of active research, but a minimum of 3 months duration is now considered reasonable.39, 40 There is less experience using the newer generation 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 obstetricians, 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 discontinue clopidogrel 5 to 7 days before the scheduled delivery and initiate LMWH or UFH.18, 19, 20, 21, 22, 42 The concern with this management is that studies have failed to show that heparin is effective in preventing acute and subacute stent thrombosis.43 Stent thrombosis is a platelet‐mediated process, and therefore anticoagulants are ineffective 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 thienopyridine 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 metatarsals, abortion, intrauterine losses, and fetal growth retardation in animal studies.

In summary, there is no consensus on the best approach to managing 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/American 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 delivery, prior to the completion of the recommended 12 months.9, 10 Based on the new guidelines, it is also reasonable to discontinue DAPT after 6 months of treatment in those who are deemed at high risk of bleeding (class IIb recommendation).40 We therefore recommend treatment for at least 6 months of uninterrupted DAPT after implantation of DES (or BMS) prior to delivery. In patients presenting with STEMI in the third trimester, BMS, as discussed previously, is preferred to ensure that the patient receives at least 1 month of uninterrupted DAPT. If the patient is receiving DAPT near the time of delivery, we recommend discontinuing clopidogrel 5 days prior to planned delivery and only bridging with tirofiban or eptifibatide in instances in which the risk of stent thrombosis is high, including those with prior MI, complex PCI, or high thrombosis risk.9, 10, 47 Tirofiban and eptifibatide should be continued up to 4 to 6 hours before delivery. We do not recommend reinitiating GP IIb/IIIa inhibitors after delivery, expect in rare cases of complex PCI that are deemed of very high thrombotic burden. If the patient received DAPT for less than 6 months prior to delivery, clopidogrel should be resumed as soon as it is deemed safe after delivery by the obstetrician and anesthesiologist (typically 24 hours after delivery) to complete at least 12 months of DAPT, as indicated for ACS.47 If the patient received at least 6 months of DAPT prior to delivery, it may be reasonable to forgo reinitiating clopidogrel after delivery if the risk of bleeding outweighs the benefits of continued DAPT.

3.3.3. Thrombolytic therapy

Thrombolytic therapy (TT) is not advocated for the management of AMI in pregnancy.8 Reported complications have included maternal hemorrhage, preterm delivery, fetal loss, spontaneous abortion, placenta abruption, uterine bleeding, and postpartum hemorrhage.8, 48, 49 Importantly, given the prevalence of coronary dissection in pregnancy, TT may be harmful, increasing the risk of bleeding and progression of the dissection.48, 49 For these reasons, TT is rarely utilized for AMI treatment in pregnancy. Nonetheless, if PCI access for STEMI during pregnancy is not available, TT may be an alternative management strategy.

4. OBSTETRIC CONSIDERATIONS

Labor induction may be pursued to allow for planned discontinuation of antithrombin therapy before delivery. Labor may be induced with an oxytocin infusion with careful monitoring of fluid status and cardiovascular effects.50 ST‐segment depression, myocardial ischemia, arrhythmias, and even maternal deaths have been reported in association with continuous infusion and bolus dosing of oxytocin.50 Synthetic prostaglandin analogs carry a risk of coronary vasospasm and arrhythmias.8 For these reasons, spontaneous onset of labor is favored.8

In terms of the mode of delivery, vaginal delivery is generally preferred 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 certain situations, it is typically reserved for the usual obstetric indications.8

4.1. Anesthesia considerations

Neuraxial (spinal, epidural, combined spinal–epidural) analgesia for labor and neuroaxial anesthesia for cesarean delivery are generally preferred. If emergency cesarean delivery is required, epidural analgesia may be quickly converted to epidural anesthesia, thus avoiding the need for general anesthesia. Neuraxial anesthesia for cesarean delivery is associated with fewer hyperdynamic hemodynamic changes than general anesthesia, and recovery is faster. Although the risk of hypotension is greater with neuraxial anesthesia, hypotension can be minimized with low‐dose local anesthetic techniques and careful titration of vasoconstrictors and intravenous fluids. The low‐dose spinal component of block provides dense anesthesia, and if it proves inadequate for surgical anesthesia, administration of additional local anesthesia via the epidural catheter can be used to titrate further anesthesia.

A major concern with neuraxial anesthesia is the risk of spinal‐epidural hematoma formation and consequent neurological impairment in patients receiving DAPT. Although several retrospective studies have failed to make this association, the American Society of Regional Anesthesia and Pain Medicine recommends that clopidogrel be discontinued 5 to 7 days prior to performance of neuraxial anesthesia.47 Neuraxial anesthesia can be performed safely in patients receiving aspirin therapy alone. However, UFH and LMWH must be discontinued before the initiation of neuraxial anesthesia procedures (24 hours for therapeutic doses of LMWH).47 Close communication among the members of the multidisciplinary care team is necessary to determine when DAPT should be initiated in the postpartum period. This decision must weigh the risks of postpartum and neuraxial hemorrhage against the risk of coronary thrombosis.

5. CONCLUSION

Pregnancy poses several challenges to both the diagnosis of ACS and management of STEMI. Standardizing the approach to its treatment may minimize maternal and fetal complications. The approach to the diagnosis of ACS in pregnancy is similar to that in nonpregnant patients with the exceptions of a few considerations. Coronary angiography remains the gold standard for diagnosis, and concerns about ionized radiation exposure should not delay this potentially life‐saving intervention. PCI should be performed via the radial approach. DES or BMS may be employed, depending on the stage of pregnancy. DAPT may be interrupted by delivery; however, with the favorable characteristics of new‐generation DES, this may be accomplished with lower risk of stent thrombosis. Most importantly, employing a multidisciplinary team and monitoring patients in the critical care setting is unarguably essential for the care for this special population.

Conflict of interests

The authors declare no potential conflict of interests.

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. 10.1002/clc.22655