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 Table of Contents  
Year : 2021  |  Volume : 11  |  Issue : 2  |  Page : 106-108

Caesarean section in a case of acute coronary syndrome - A case report

Consultants in Private Practice, Namah Healthcare, Kandivali West, Mumbai, Maharashtra, India

Date of Submission27-Jan-2021
Date of Acceptance31-Mar-2021
Date of Web Publication01-Oct-2021

Correspondence Address:
Dr. Neha Mehta
2F/304 N G Suncity Phase 1, Thakur Village, Kandivali East, Mumbai - 400 101, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/joacc.JOACC_94_20

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Acute coronary syndrome (ACS) during pregnancy is a rare event and can be a significant contributor to maternal and foetal mortality. We present here one such case of a 40-year-old primigravida posted for elective caesarean section at 36 weeks of pregnancy with a history of acute myocardial infarction (AMI) and left ventricular failure which was treated conservatively.

Keywords: Acute coronary syndrome, acute myocardial infarction, caesarean section, cardiac failure, epidural, full-term pregnancy

How to cite this article:
Mehta N, Shah K, Bhatt Y. Caesarean section in a case of acute coronary syndrome - A case report. J Obstet Anaesth Crit Care 2021;11:106-8

How to cite this URL:
Mehta N, Shah K, Bhatt Y. Caesarean section in a case of acute coronary syndrome - A case report. J Obstet Anaesth Crit Care [serial online] 2021 [cited 2022 Jan 20];11:106-8. Available from: https://www.joacc.com/text.asp?2021/11/2/106/327418

  Introduction Top

New ischemic heart disease of pregnancy is estimated to occur in 1-6.2 per 100,000 deliveries,[1] a rate three to four times higher than in non-pregnant women of comparable age.[2] Spontaneous coronary artery dissection (SCAD) and atherosclerotic coronary artery disease are the most common causes of AMI in pregnancy.[3],[4]

We describe a case of a 40-year-old primigravida for elective caesarean section at 36 weeks of pregnancy with a history of acute myocardial infarction (AMI) and left ventricular failure at 32 weeks of pregnancy which was treated conservatively.

  Case History Top

A 40-year-old primigravida was posted for elective caesarean section at 36 weeks of pregnancy. She had a history of ICU admission 4 weeks ago (32 weeks of gestation) with orthopnoea, epigastric pain, nausea and vomiting. At that time, she had an acute inferior wall myocardial infarction (MI) and was in left ventricular failure with frank pulmonary oedema, 40% ejection fraction (EF), dilated cardiac chambers and pulmonary hypertension. The emergency treatment that time comprised bilevel positive airway pressure (BiPAP) support, furosemide, metoprolol, low molecular weight heparin, aspirin and clopidogrel. Foetal heart sound (FHS) monitoring and Foetal Doppler Study were within normal limits. After 2 days, her orthopnoea reduced and coronary angiography could be done revealing significant double-vessel disease (80% tubular stenosis of left anterior descending artery) and 100% occlusion of the mid segment of the right coronary artery with good collaterals. FHS monitoring (done 6 hourly) and Foetal Doppler Study (repeated before discharge) remained within normal limits. It was decided to continue conservative cardiac management till foetal maturity. She was discharged from the hospital on Day 5 with a prescription to take metoprolol 25 mg, ecosprin 75, clopidogrel 75, aldactone 25 mg and trimetazidine 35 mg once a day and furosemide 40 mg twice a day with weekly follow-ups with the obstetrician and cardiologist.

At the time of her admission for caesarean section, she was hemodynamically stable; all routine blood investigations were normal, ECG showed features of old inferior wall MI. An Echocardiography (ECHO) done that time revealed 40% EF and normal chamber dimensions, pulmonary pressures and a collapsible Inferior Vena Cava (IVC). She had been asked to withhold clopidogrel for 5 days before elective surgery and continue the rest of her medications. Epidural anaesthesia with invasive monitoring was planned. On the morning of the surgery, she was given oral metoprolol 25 mg, IV ondansetron 8 mg and IV pantoprazole 40 mg. In addition to all the standard monitoring, a 7 French right internal jugular central line, a 20 gauge right radial arterial line and a Foley's catheter for monitoring urine output, were placed. The cardiac tracing showed a sinus rhythm with the rate of 70-75 beats/min. Central Venous Pressure (CVP) was found to be 6-8 cm of water and maternal BP was 120/60 mmHg. Foetal heart rate was 140-150 beats/min.

With all aseptic precautions and in sitting position, an 18G epidural catheter was sited via L2, 3 space up to 9 cm, checked and fixed. The patient was made supine with a small wedge under the right iliac crest. Incremental doses of 2% preservative-free lignocaine (total 13 cc) were injected over 10 min. Sensory block of T6 level (checked with loss of sensitivity to ice) was achieved within 10 min. At this time, her Heart Rate (HR) was 80/min and BP 120/70 mmHg. IV noradrenaline infusion (0.08 mg/mL) started at 2 mL/h as a falling trend in Invasive blood pressure/arterial blood pressure (IBP) was noted and it was titrated to maintain mean arterial pressure (MAP) between 70 and 100 mm Hg. A healthy baby weighing 2.2 kg was delivered uneventfully within 6 min of incision; patient was comfortable and hemodynamically stable. Oxytocin 10 units was started at baby delivery as a slow infusion. After delivery of the placenta, the patient complained of palpitations and developed sinus tachycardia of 140 beats/min accompanied by falling trend in MAP. Noradrenaline infusion rate was titrated up from 4 mL/h to 7 mL/h. As tachycardia was persistent, Inj. esmolol 3 mg was given which reduced the heart rate and the palpitations ceased. Total blood loss during the surgery was about 500 mL, urine output 200 mL and 500 mL lactated Ringer's solution was transfused. Epidural catheter was removed after completion of the surgery and IV paracetamol 1 g was given stat and continued 8 hourly.

The patient was shifted to ICU with IV noradrenaline infusion at 5 mL/h with stable vital parameters. Oxytocin infusion was continued at 10 units/h for 6 h. In the ICU, after 2 h of surgery, intermittent asymptomatic unifocal ventricular ectopics were observed for which she was given 12.5 mg metoprolol orally. After overnight ICU stay and weaning off noradrenaline support (requirement was up to maximum 5 mL/h), she was shifted out the next morning.

Clopidogrel and aspirin were restarted after 24 h of surgery (24 h of removal of epidural catheter). She was discharged with a healthy baby 2 days later. Active coronary intervention was planned for 2 weeks after discharge. However, it was deferred further in view of improvement in 2D ECHO parameters.

  Discussion Top

Our patient presented with acute MI in the third trimester of pregnancy, which accounts as the period for the highest risk of mortality and foetal loss. Stabilising the patient before any diagnostic invasive procedure with intense foetal monitoring is necessary.

Coronary angiography remains the standard diagnostic procedure for conclusive evaluation of the cause of MI as per European Society guidelines.[5],[6] If the patient undergoes a percutaneous coronary intervention, the challenges include radiation exposure to the foetus, and initiation and maintenance of antiplatelet therapy. However, the dose of radiation is not enough to cause any significant damage to the foetus, even long term.[3],[6],[7] Drug eluting stents (DES) are used when delivery is at least 3-6 months away and bare metal stents (BMS) are safer closer to due date given that they afford the option of discontinuing dual antiplatelet therapy after 4 weeks.[8]

It is recommended that clopidogrel be discontinued 5 days prior to the planned delivery and bridging with GP IIb/IIIa inhibitors tirofiban or eptifibatide for cases in which the risk of stent thrombosis is high, continued up to 4-6 h before delivery and clopidogrel can be usually resumed within 24 h after consultation with the obstetricians and the anaesthetists.[8] There is no recommendation for bridging where stents are not in place.

Management of such a patient for delivery requires a multidisciplinary approach involving the attending obstetrician, internist or cardiologist, and anaesthetist with ICU capable of providing maternal and foetal monitoring, comprehensive obstetric service equipped for emergency delivery of a potentially viable foetus in the case of sudden maternal deterioration as well as Cardiac Cath Lab for any coronary intervention should it be needed.

Caesarean section is preferred in the presence of severe cardiac illness including severe aortic stenosis, pulmonary arterial hypertension, and aortic dissection to avoid the prolonged hemodynamic stresses associated with vaginal delivery.[3]

Invasive hemodynamic monitoring (central line, arterial line) is recommended for a minimum of 24 h peripartum.[5] During the first 24-72 h, significant fluid shift occurs, which may lead to congestive cardiac failure. Invasive BP monitoring gave us advantage of being able to pick up the slightest change at the earliest for prompt treatment.

General anaesthesia should be administered in case of emergency in patients receiving anticoagulants and with severely compromised cardiac output using a modified rapid sequence induction (e.g., using etomidate and succinylcholine) over 1-2 min without compromising hemodynamic stability. Opioids should preferably be administered after baby delivery.[9]

Our patient refused general anaesthesia favouring regional anaesthesia and staying awake for baby delivery. There is increased incidence of MI (37-45%) during labour and delivery,[10] so our goal was maintenance of myocardial oxygen demand and supply balance.

Epidural analgesia/anaesthesia is very useful in modifying stress response of labour and delivery.[11] It avoids sudden uncontrolled reduction in systemic vascular resistance (like spinal anaesthesia), which would compromise coronary pressures.[9] We used lignocaine which features quicker onset of blockade as compared with bupivacaine or ropivacaine. Despite contrary evidence, abdominal muscle relaxation with lignocaine was perceived to be better than with bupivacaine in many previous instances by our obstetricians. We avoided use of adrenaline to prevent any sympathomimetic effect leading to cardiac compromise.

We used a slow infusion of oxytocin to enhance uterine involution and prostaglandin F analogues should be reserved for Post partum hemorrhage (PPH) and methyl ergonovine analogues are contraindicated.[12] Oxytocin-related hypotension and tachycardia are known, so we employed noradrenaline and esmolol to reduce cardiac workload by controlling the heart rate which also ensures adequate diastolic coronary filling. Beta blockers like esmolol, atenolol and metoprolol do not interfere with uterine contractions.[13] Noradrenaline has the dual advantage of being vasopressor without intrinsic chronotropic effect.

Adequate postoperative analgesia should be provided via IV and/or epidural route as per hemodynamic stability.[9] We avoided the use of epidural in this patient in view of the risk of hypotension and to reinitiate antiplatelet drug early, or if required, anticoagulant therapy. Bilateral transversus abdominis plane (TAP) block is a safe alternative.[14] We did not give it as it is not a routine practice in our unit. We chose to maintain analgesia via IV route using paracetamol round the clock for 48 h. IV nalbuphine was our drug of choice as rescue analgesic (which was not required), followed by oral paracetamol 650 mg thrice a day for 5 days. Compared with IV paracetamol, IV diclofenac use has a 20% increased rate of major adverse cardiovascular events,[15] so we avoided using it.

After 3 days of hospital stay, the patient went home with a healthy baby and made an uneventful recovery. Cardiac follow-up showed an improvement in EF to 55%.

To conclude, successful management of a parturient with a history of acute myocardial ischemia posted for caesarean section is presented.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Ginz B. Myocardial infarction in pregnancy. J Obstet Gynaecol Br Commonw 1970;77:610-5.  Back to cited text no. 1
Petitti DB, Sidney S, Quesenberry CP Jr., Bernstein A. Incidence of stroke and myocardial infarction in women of reproductive age. Stroke 1997;28:280-3.  Back to cited text no. 2
Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. J Am Coll Cardiol 2008;52:171-80.  Back to cited text no. 3
Elkayam U, Jalnapurkar S, Barakkat MN, Khatri N, Kealey AJ, Mehra A, et al. Pregnancy-associated acute myocardial infarction: A review of contemporary experience in 150 cases between 2006 and 2011. Circulation 2014;129:1695-702.  Back to cited text no. 4
European Society of Gynecology (ESG), Association for European Paediatric Cardiology (AEPC), German Society for Gender Medicine (DGesGM), Regitz-Zagrosek V, Blomstrom Lundqvist C, et al. ESC Guidelines on the management of cardiovascular diseases during pregnancy. Eur Heart J 2011;32:3147-97.  Back to cited text no. 5
Leber AW, Knez A, von Ziegler F, Becker A, Nikolaou K, Paul S, et al. Quantification of obstructive and non-obstructive coronary lesions by 64-slice computed tomography: A comparative study with quantitative coronary angiography and intravascular ultrasound. J Am Coll Cardiol 2005;46:147.  Back to cited text no. 6
James AH, Jamison MG, Biswas MS, Brancazio LR, Swamy GK, Myers ER. Acute myocardial infarction in pregnancy: A United States population-based study. Circulation 2006;113:1564-71.  Back to cited text no. 7
Ismail Sahar, Wong Cynthia, Priya Rajan, Mladen I. Vidovich. ST-elevation acute myocardial infarction in pregnancy: 2016 update. Clin Cardiol 2017;40:399-406.  Back to cited text no. 8
Miriam H, Lawrence CT. Cardiovascular disease. In: Chestnut DH, editor. Obstetric Anesthesia. 4th ed. Principles and Practice. Philadelphia, Pennsylvania: Elsevier Mosby; 2009. p. 881-912.  Back to cited text no. 9
Hands ME, Johnson MD, Saltzman DH, Rutherford JD. The cardiac, obstetric, and anesthetic management of pregnancy complicated by acute myocardial infarction. J Clin Anesth 1990;2:258-68.  Back to cited text no. 10
Rosenlund RC, Marx GF. Anaesthetic management of a parturient with prior myocardial infarction and coronary artery bypass graft. Can J Anaesth 1988;35:515-7.  Back to cited text no. 11
Lin YH, Seow KM, Hwang JL, Chen HH. Myocardial infarction and mortality caused by methylergonovine. Acta Obstet Gynecol Scand 2005;84:1022.  Back to cited text no. 12
Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death executive summary: a report of the American College of Cardiology/American Heart Association task Force and the European Society of cardiology committee for practice guidelines (writing committee to develop guidelines for management of patients with ventricular arrhythmias and the prevention of Sudden cardiac death) developed in collaboration with the European Heart rhythm Association and the Heart rhythm Society. Eur Heart J 2006;27:2099-140.  Back to cited text no. 13
Belavy D, Cowlishaw PJ, Howes M, Phillips F. Ultrasound-guided transversus abdominis plane block for analgesia after Caesarean delivery. Br J Anaesth 2009;103:726-30.  Back to cited text no. 14
Schmidt M, Sørensen HT, Pedersen L. Diclofenac use and cardiovascular risks: Series of nationwide cohort studies. BMJ 2018;362:k3426.  Back to cited text no. 15


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