38-year-old woman in labor with concomitant ST elevation myocardial infarction treated with primary coronary angioplasty: A case report

Introduction

Myocardial infarction (MI) during pregnancy, labor, or the puerperium is an extremely rare condition associated with a high-risk of death for both mother and fetus. ST elevation myocardial infarction (STEMI) in emerging labor represents a major clinical challenge due to the rarity of its occurrence, lack of clear management guidelines in this type of clinical scenario, and the absence of a risk assessment system for appropriate clinical decision-making [1]. The incidence of MI in pregnant women is estimated to be approximately 5 in 100,000 cases [2]. Based on the analysis of pregnancies in the US in the years 2003-2015 (total number of analyzed cases: 11,328,236), only 913 MIs were recorded, with 111 occurring during labor and only 15 ending with primary coronary intervention (PCI) [3]. Apart from the classic risk factors (i.e., hypertension, obesity, hyperlipidemia, and smoking), the main causes of MIs in pregnant women include increased progesterone levels during pregnancy affecting degeneration of the connective tissue of coronary vessels, possibly causing spontaneous coronary artery dissection. It was estimated that the latter factor is responsible for about 43% of pregnancy-related MIs [4]. Furthermore, the growing incidence of MI during pregnancy is influenced by the increasing age of pregnant women [5]. It is important to note that the mortality rate of pregnant women with MI is twice as high when the MI occurs in the perinatal period compared with the antenatal and postnatal periods [6].

Case description

A 38-year-old female (height: 165 cm, weight: 108 kg) in her 9th pregnancy (37 weeks + 2 days) was admitted to the Department of Obstetrics, Gynecology, and Gynecologic Oncology of the Regional Specialist Hospital in Grudziadz due to myometrial activation (Day –1). Up to that date, the patient had been treated for both pregnancy-induced hypertension (treated with methyldopa) and gestational diabetes mellitus (treated with diet), both conditions diagnosed during the current pregnancy. With no family history of cardiovascular diseases, she was not a cigarette smoker (long-term passive smoker). Ultrasound examination confirmed the presence of a live eutrophic fetus in the cephalic position, normal volume of amniotic fluid, and placenta without signs of pathology located on the posterior wall of the uterus. In morning medical examination (Day 0, 10:15 a.m.), the patient reported chest discomfort and increasing pain in the upper abdomen. In subsequent cardiology consultation, the patient was conscious and circulatory and respiratory efficient; an auscultation over the lungs revealed a physiological bilateral vesicular murmur, no heart murmur, a regular heart rate about 100 per min., and blood pressure of 110/70 mmHg. Electrocardiography (ECG) showed a regular sinus rhythm at 100 per min., normal heart axis, ST-T segment elevation in leads I, aVL, V2-V6, QRS of 80 ms, PR about 160 ms, and QTc about 393 ms, without conduction disturbances (Figure 1). The consulting cardiologist diagnosed the patient with STEMI, and qualified her for urgent invasive treatment. Due to high-risk of deterioration of the patient’s condition as well as the ongoing MI and increasing contractility of the uterine muscle, the patient was not transferred to a gynecological referral center; the decision was made to urgently terminate the pregnancy via caesarean section under epidural anesthesia (Day 0, 11:10 a.m.). The procedure was performed using the Misgav–Ladach method, and a live full-term son was delivered (weigh: 3,580 g, length: 55 cm, Apgar score of 7 at 1 minute and 9 at 3 minutes). The patient was transferred to the catheterization laboratory of the local hospital in good general condition. She received 300 mg oral acetylsalicylic acid and 4,000 I.U. intravenous unfractionated heparin prior to the procedure. Coronary angiography was performed via the right radial artery, showing occlusion of the left anterior descending artery (LAD) in the middle segment (TIMI flow 0) [7]. The periphery of the artery was partially filled with collateral circulation from the right coronary artery, while the remaining coronary arteries were free of significant stenoses. Prior to PCI, a second antiplatelet agent, clopidogrel, was administered at a loading dose of 600 mg, and 4,000 I.U. of unfractionated heparin was added intravenously. The coronary guidewire was advanced to the periphery of LAD, and several predilations were performed in the middle segment of LAD with a semi-compliant balloon to achieve LAD recanalization (Day 0, 12:13 p.m.). Time from diagnosis to balloon was 118 minutes. Subsequently, drug eluting stent (3.0 × 19 mm) was implanted at the LAD occlusion site. Finally, TIMI 3 flow was achieved in the LAD.
Laboratory tests results (Day 0) were as follows: high sensitive troponin I (TNIhs) concentration of 17,795 ng/l (normal range, 0-120 ng/l), creatine kinase isoform MB (CK-MB) concentration of 34.75 ng/ml (normal range, 0-5 ng/ml). Other results of an ionogram, renal function parameters, and peripheral blood morphology were within normal ranges. Echocardiography (ECHO) revealed akinesia of the left ventricular apex, apical, mid-anterior, and part of the mid-posterior segment of the interventricular septum (IVS), apical segments of the anterior, inferior, and lateral walls, left ventricular ejection fraction (LVEF) of 48%, left ventricular diastolic diameter (LVDd) of 55 mm, left atrial (LA) diameter of 39 mm, LA area of 27 cm2, IVS (interventricular septum) of 12 mm, and no significant valves abnormalities (Day 0).
The patient was transferred to the intensive care unit (ICU) for further management. On the same day (Day 0), the patient developed severe dyspnea at rest. On physical examination, there were features of exacerbation of heart failure. A bedside ECHO of the heart showed no new contractile abnormalities, with an LVEF of approximately 45%, without echocardiographic signs of high-risk pulmonary embolism. Therefore, a typical pharmacological treatment for acute heart failure, consisting of intravenous infusion of furosemide and nitroglycerine, a 24-hour intravenous infusion of levosimendan, was administered. After stabilization of clinical condition, the patient was transferred from the ICU to the cardiology department (Day +2), where pharmacotherapy was modified with a Beta-blocker and angiotensin-converting enzyme inhibitor, and clopidogrel was exchanged with prasugrel. The patient was discharged on the 6th day after PCI (Day +6), with the recommendation to take acetylsalicylic acid 75 mg once daily, prasugrel 10 mg once daily for the next 12 months, atorvastatin 40 mg once daily, nebivolol 5 mg once daily, zofenopril 15 mg daily, bromocriptine 2.5 mg twice daily for 10 days, and enoxaparin 60 mg once daily for 10 days from the discharge date.

Follow-up and outcomes

The patient reported to the outpatient cardiology clinic at 5, 13, and 18 months after the occurrence of MI. Throughout the observation period, she had no recurrence of angina symptoms nor complications from antiplatelet treatment, and no evidence of worsening circulatory failure. First follow-up ECHO was performed at 5 months follow-up revealing akinesia of the left ventricular apex, apical segment of the interior and lateral walls, part of the apical segment of the IVS, LVEF of 50%, LVDd of 50 mm, LA diameter of 37 mm, IVS of 12 mm, and no significant valves abnormalities. Final follow-up ECHO at 18 months follow-up showed LVDd of 50 mm, LA diameter of 37 mm, LA area of 18 cm2, IVS of 12 mm, akinesia and partial dyskinesia of the apex and all apical segments, hypokinesia of the middle anterior and inferior lower segment of IVS and the middle segment of the anterior wall, and LVEF of 45-50%, with no significant valves abnormalities. In the first follow-up ECG (5 months post-MI), there was a sinus rhythm, which was regular with a rate of about 72 per min., normal heart axis, QS complex in V1-V3 with persistent 1 mm ST segment elevation, QRS of 110 ms, PR about 160 ms, and QTc about 401 ms (Figure 2).

Discussion

The management of MI in women during labor and the puerperium is controversial due to no clear guidelines. Standard treatments based on recommendations for the management of MI in general population may be difficult to implement because of numerous limitations associated with pregnancy and the puerperium. Based on the ESC guidelines for the management of women with MI during pregnancy, PCI is the preferred method of treatment, but there are no guidelines for the MI management during labor [8]. The most beneficial management would be to delay labor for at least 2 weeks after MI occurrence. However, in the presented case, delaying of labor was not possible, since the labor was already in progress. In the absence of clear guidelines for the management of such a clinical situation, an urgent consultation was held involving a gynecologist, a cardiologist, and (online) provincial consultants in gynecology, obstetrics, and cardiology. In addition to the patient’s multiparity, the choice of caesarean section over natural birth was dictated by the need to expedite labor, shorten its duration, and avoid extreme myocardial stress during natural delivery. Caesarean section as a method of labor shortens the time to PCI, significantly reducing the risk of fetal death or hypoxia. Several scenarios for solving the problem were considered after a multidisciplinary analysis of this clinical case.
Preceding primary coronary intervention with a caesarean section allowed the fetus to be protected from exposure to antiplatelet and anticoagulant drugs, ionizing radiation, and contrast agents. Currently, there are no clear reports describing the effect of contrast and assessing the amount of contrast in maternal-fetal circulation, but its use carries a risk for congenital hypothyroidism. Disadvantages of this approach include high-risk of potentially fatal ventricular arrhythmias (including cardiac arrest) during caesarean section as a result of the ongoing process of acute cardiac ischemia, a potential drop in blood pressure following the administration of epidural anesthetics, which could be fatal in a MI setting, and high-risk of obstetric hemorrhage following a recent caesarean section (related to the administration of anticoagulants and antiplatelet agents).
In analyzing the reverse sequence of events (caesarean section preceded by PCI), the main issue is the need to use anticoagulants and dual antiplatelet therapy before labor and epidural anesthesia. According to the recommendations of the Anesthesiologic Society, epidural anesthesia require an interval between the administration of antiplatelet drugs: clopidogrel and ticagrelor (5-7 days), prasugrel (7-10 days), and ticlopidine (10 days) [9]. In addition, there are no clear data on the safety and effects of P2Y12 receptor inhibitors or glycoprotein IIb/ IIIa inhibitors on the fetus. Unfractionated heparin is the preferred anticoagulant because it does not cross the maternal placenta. A loading dose of 300 mg of acetylsalicylic acid is considered safe in pregnancies up to 32 weeks’ gestation, while in more advanced pregnancies, a maximum dose of 81 mg is recommended until delivery. The recommended second antiplatelet drug is clopidogrel; stronger antiplatelet drugs, such as prasugrel or ticagrelor, should be used with great caution [10]. The use of both antiplatelet and anticoagulant medications can increase the risk of major bleeding in the mother during labor, increase the risk of spinal-epidural hematoma, and potentially adversely affect the fetus. One of the solutions to avoid the above problem is to recanalize the infarct-related artery (IRA) by balloon predilatation (without subsequent stent implantation), thus avoiding the need for post-procedural dual antiplatelet therapy. In such a post-PCI scenario, the patient would receive an intravenous infusion of protamine sulphate to reverse the anticoagulant effect of unfractionated heparin, followed by caesarean section. Stent implantation would be performed in the second stage of coronary angioplasty procedure, after the period necessary to reduce the risk of obstetric hemorrhage.
Unfortunately, this is not a perfect solution and has its drawbacks. In fact, we can only consider avoiding long-term administration of dual antiplatelet therapy. The omission of a loading dose of dual antiplatelet therapy before PCI is controversial and necessary in complications after balloon angioplasty in the form of slow/ no reflow phenomenon. In addition, stent implantation in the IRA is often unavoidable after balloon predilatation (e.g., significant residual stenosis of the IRA, dissection or perforation of the IRA). It should also be noted that ionizing radiation used during invasive cardiology procedures in the third trimester of pregnancy is not currently thought to pose a significant risk to both the mother and fetus, and only standard procedures should be used to minimize the risk [10, 11]. Ultimately, in our case, it was decided to terminate the pregnancy by caesarean section, followed by coronary angiography and possible PCI.

Conclusions

In the absence of clear guidelines for the management of MI in a patient during pregnancy (and particularly during labor), each case requires an individualized approach and collaboration of a multidisciplinary team. Given the clear tendency in women to postpone decision about having children, and the increasing average age of women giving birth, it is expected that cases of co-occurring conditions, such as MI with pregnancy/labor, will become more common in clinical practice. The above-described method produced expected results in terms of an uncomplicated labor and effective recanalization of the LAD. There were no immediate complications of PCI, no life-threatening bleeding, no post-operative arrhythmias, and no other early post-MI complications. Labor was uneventful and the fetus outcome during hospitalization was good. At 18 months follow-up, there was no recurrence of stenocardia nor evidence of worsening left ventricular failure. ECHO showed mild left ventricular dysfunction (LVEF of 45-50%), no left ventricular dilatation, and no aneurysmal zone in the infarcted area.
In addition, it should be noted that the above clinical scenario and its success were only possible in conditions, which allowed the patient to be transferred directly to the catheterization laboratory after the procedure. In clinical practice, this means the availability of the PCI method in the same center where the caesarean section is performed.

Disclosures

This research received no external funding.
The study was conducted as per the Declaration of Helsinki. According to the Regulations of the Bioethics Committee of Poland, this study did not require the consent of the bioethics committee, as this case was not an experimental procedure.
The authors declare no conflicts of interest.

References