Myocardial infarction during pregnancy: A rare occurrence.

Sir,

Pregnancy-associated acute myocardial infarction (AMI) is rare, but is associated with high morbidity and mortality. The estimated incidence of AMI during pregnancy is 3-10 cases/100,000 deliveries with a maternal mortality rate of 21% and fetal mortality rate of 13%.[1] Pregnancy-associated changes in the cardiovascular system and coagulation system increases the risk of AMI by approximately 3 to 4-fold.[1] We describe a case of AMI and its management during caesarean delivery in our institute.

A 30-year-old female, gravida 5, para 4, at 36 weeks of gestation got admitted with the complaints of bleeding per vagina and diffuse abdominal pain. Patient was in distress, but alert and oriented. Her pulse was 140/min and blood pressure (BP) was 74/46 mm Hg. After securing two peripheral lines, initial intravenous fluids resuscitation was carried out by administrating 1500 ml crystalloid (lactated ringer solution) and 500 ml colloid (hydroxyethyl starch 130/0.4). As the BP was very low dopamine infusion at 12 mcg/kg/min was started simultaneously. Over a period of time as haemodynamics improved and patient started responding to fluid therapy; dopamine infusion was titrated according to BP. On auscultation of chest normal vesicular breath sounds were heard. The cardiac examination revealed no obvious murmurs, gallops or pericardial rub. The electrocardiogram (ECG) demonstrated normal sinus rhythm with ST segment T wave changes in all leads, which was attributed to tachycardia, hypotension and anaemia. Laboratory results were as follows: Haemoglobin - 5.5 g/dl, haematocrit - 17.6%, total leukocyte count - 14,500/ul, platelet count -.2.44 lac/ul, Random Blood Sugar (RBS) - 79 mg/dl, blood urea nitrogen - 23 mg/dl, S.creatinine - 0.79 mg/dl, S.bilirubin - 0.93 mg/dl, serum glutamic oxaloacetic transaminase/serum glutamic pyruvic transaminase - 36/39 IU/L and S.alkaline phosphatase - 369 IU/L. Ultrasonography revealed single intrauterine live foetus of gestational age 34.5 weeks with placenta previa grade 3. Patient received two units of packed red blood cells. Her BP picked up to 106/54 mm Hg on dopamine infusion (7 mcg/kg/min) and was posted for emergency caesarean section.

General anaesthesia was planned due to haemodynamic instability of the patient. Rapid sequence induction was performed using propofol 1 mg/kg and ketamine 1 mg/kg and concomitant preoxygenation. Endotracheal intubation was done following injection of succinylcholine 1.5 mg/kg. Patient was maintained on isoflurane 0.7% with O2/N2O (40/60) and atracurium 0.5 mg/kg. Just after delivery of baby, patient developed pulseless ventricular tachycardia. Cardiopulmonary resuscitation was started immediately. Meanwhile, defibrillator was prepared and a shock of 150 joule (biphasic waveform) was delivered. Patient reverted to sinus rhythm, but ST segment elevation appeared on continuous ECG monitoring. Injection oxytocin 10 units was added to 1 L of ringer lactate and given at a rate of 10 ml/min. Patient remained stable during the rest of surgery and was shifted to intensive care unit for elective ventilation and further management.

A 12 lead ECG in the immediate post-operative period showed normal sinus rhythm with ST segment elevation and T wave inversion in lead I, aVL and V1 to V4. Laboratory results were as follows: Troponin I positive; creatinine kinase-MB fraction - 39 U/L; triglycerides - 310 mg/dL; total cholesterol - 250 mg/dL; high-density-lipoprotein - 38 mg/dL and low-density-lipoprotein - 163 mg/dL. Cardiologist consultation and bedside echocardiography demonstrated left ventricular wall motion abnormalities at the apex and anterior wall; and ejection fraction of 35 to 40% and mild mitral regurgitation. Patient was treated with aspirin, clopidogrel, unfractionated heparin, metoprolol and morphine. In the next 24 h patient was weaned off from the ventilator and vasopressor support and was shifted to cardiac catheterization laboratory, where angiography revealed 80% block of left anterior descending artery, but no active intervention was done at that time. Patient was transferred to the cardiac intensive care unit (CICU) and started on a regimen of carvedilol, 12.5 mg; aspirin, 150 mg; clopidogrel, 75 mg; atorvastatin, 20 mg and ivabradine, 7.5 mg. Patient remained stable in CICU and on day 3 she was transferred back to the ward and was discharged on the 7th day with the advice of cardiology follow-up.

The most common underlying mechanisms implicated in AMI during pregnancy are atherosclerotic coronary artery disease (CAD), coronary thrombosis with hypercoagulability and coronary artery dissection. Complications of pregnancy that are significantly associated with AMI are severe anaemia, preeclampsia, postpartum haemorrhage, postpartum infection, shock, ergometrine, prostaglandin E1, fluid and electrolyte imbalances.[2345]

All causes of tachycardia, hypertension, hypotension, anaemia and pain should be treated aggressively. The interventions include vasopressors to maintain BP, β-blockers to slow heart rate, managing blood volume, post-operative pain and respiratory function. Emergent coronary intervention, anticoagulants or glycoprotein IIb/IIIa antagonists are rarely indicated in the immediate post-operative course and are hazardous because of the risk of bleeding, unless ST elevation or intractable cardiogenic shock ensues.[6]

With this case report, we highlight the possibility of presence of unknown CAD and occurrence of perioperative AMI, apart from tachycardia and anaemia in pregnant patients having ST-T changes in ECG. Tachycardia, hypotension, hypertension, anaemia, hypoxemia and systolic and diastolic myocardial dysfunction are common causes of prolonged ST-depression and myocardial infarction in patients with stable CAD undergoing major noncardiac surgery. Careful perioperative monitoring for ischemia, a low threshold for treating and preventing tachycardia while avoiding hypotension, decreased cardiac output and/or cardiac decompensation help prevent perioperative myocardial infarction (PMI). Coronary intervention is rarely indicated as the first line of treatment and antithrombotic therapy may exacerbate bleeding. Future studies are needed to determine, which patients with PMI require intensified post-operative surveillance, medical therapy and/or coronary intervention to improve the long-term survival.