- Email: [email protected]
Peripartum cardiac chest pain and troponin rise
K. Tatham et al.
453
with Gitelman’s syndrome, with an expectant approach to hypotension. In conclusion, potassium and magnesium supplementation and monitoring are essential in Gitelman’s syndrome complicating pregnancy although normalisation of levels is not an absolute requirement for good obstetric and neonatal outcomes. The anaesthetic management of these women requires a detailed preoperative assessment with optimisation, serial monitoring of electrolytes, and an awareness of potential complications.
References 1. Gitelman HJ, Graham JB, Welt LG. A new familial disorder characterised by hypokalemia and hypomagnesemia. Trans Assoc Am Physicians 1966;79:221–35. 2. Amirlak I, Dawson KP. Bartter syndrome: an overview. QJM 2000;93:207–15. 3. Knoers NV, Levtchenko EN. Gitelman syndrome. Orphanet J Rare Dis 2008;3:22.
4. Bartter FC, Pronove P, Gill JR, MacCardle RC. Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. A new syndrome. Am J Med 1962;331:811–28. 5. Bettinelli A, Bianchetti MG, Girardin E et al. Use of calcium excretion values to distinguish two forms of primary renal tubular hypokalemic alkalosis: Bartter and Gitelman syndromes. J Pediatr 1992;120:38–43. 6. Ferrandis Capella P, Gargallo Maicas C, Granell Gill M. Anesthesia for cesarean section in Gitelman’s syndrome. Rev Esp Anestesiol Reanim 2002;49:437–8. 7. Bolton J, Mayhew JF. Anesthesia in a patient with Gitelman syndrome. Anesthesiology 2006;105:1064–5. 8. Basu A, Dillon DS, Taylor R, Davison JM, Marshall SM. Is normalisation of serum potassium and magnesium always necessary in Gitelman Syndrome for a successful obstetric outcome? BJOG 2004;111:630–4. 9. Arriba G, Sanchez-Heras M, Basterrrechea MA. Gitelman syndrome during pregnancy: a therapeutic challenge. Arch Gynecol Obstet 2009;280:807–9. 10. de Haan J, Geers T, Berghout A. Gitelman syndrome in pregnancy. Int J Gynaecol Obstet 2008;103:69–71. 11. Scholl UI, Lifton RP. Molecular genetics of Gitelman’s and Bartter’s syndromes and their implications for blood pressure variation. Genetic Diseases of the Kidney 2009;13:227–47.
0959-289X/$ - see front matter c 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.ijoa.2010.04.005
Peripartum cardiac chest pain and troponin rise K. Tatham, Y. Hughes-Roberts, S. Davies, M. Johnson, K. Ashpole, M. Cox Chelsea and Westminster Hospital NHS Foundation Trust, London, UK ABSTRACT The incidence of myocardial ischaemia is increasing in the obstetric population. This has been attributed to several factors including greater maternal age, the increasing incidence of obesity and diabetes, and the growing population of patients with grown-up congenital heart disease who now reach adulthood and become pregnant. A number of cases of myocardial ischaemia in pregnant women have been documented, during and after delivery, for which no cause has been established. We present a case of a nulliparous woman who developed cardiac chest pain, bradycardia, hypertension and a raised troponin I after vaginal delivery of twin boys at 36 weeks of gestation. Ischaemic electrocardiogram changes were noted. Detailed investigations demonstrated a normal coronary circulation. A patent foramen ovale was found on bubble echocardiography. c 2010 Elsevier Ltd. All rights reserved.
Keywords: Chest pain; Cardiac ischaemia; Troponin; Pregnancy; Patent foramen ovale
Introduction Chest pain around the time of delivery may be the presenting complaint of several potentially life-threatening Accepted June 2010 Correspondence to: Dr. Kate C. Tatham, Magill Department of Anaesthetics, Intensive Care and Pain Medicine, Chelsea and Westminster Hospital NHS Foundation Trust, 369 Fulham Road, London SW10 9NH, UK. Tel.: +44 20 8746 8000. E-mail address: [email protected]
conditions including pulmonary embolus, aortic dissection, coronary artery dissection and myocardial infarction (MI). Of these MI is rare in the obstetric population, with a quoted rate of 0.01%.1 Chest pain and electrocardiogram (ECG) changes during labour and delivery are not uncommon, especially during caesarean section.2 Usually this is not associated with other symptoms or signs, and is ultimately dismissed by clinicians once ongoing ischaemia has been excluded. However, the incidence of myocardial ischaemia is
454 increasing in the obstetric population.3 This has been attributed to several factors: greater maternal age, advances in fertility medicine allowing women to delay pregnancy, the increasing incidence of obesity and diabetes, and the increasing number of patients with grown-up congenital heart disease (GUCH) who now reach childbearing age. We present a case of chest pain in the peripartum period associated with ischaemic ECG changes, significantly elevated troponin I but no evidence of coronary artery disease. On follow-up the only abnormality discovered was that of a patent foramen ovale (PFO).
Case report A 33-year-old, previously healthy nulliparous female with a dichorionic, diamniotic twin pregnancy presented in spontaneous labour at 36 weeks of gestation. Pregnancy had been uneventful. During labour she received patient-controlled epidural analgesia (2 lg ml 1 fentanyl/0.1% bupivacaine). When the cervix was fully dilated she was transferred to the operating theatre for vaginal delivery. An epidural top-up of 5 mL lidocaine 2% with adrenaline and bicarbonate produced a block to cold to T10 on the right and T5 on the left. She delivered twin boys, the first cephalic, the second breech, with minimal surgical assistance. She remained normotensive and stable throughout the delivery. There was an estimated blood loss of 400 mL. She received, at surgical request, 5 IU of oxytocin intravenously and continued on an infusion of 10 IU h 1 for 4 h. Diclofenac 100 mg, was administered rectally. The midwife also inadvertently gave an intramuscular dose of Syntometrine (ergometrine maleate 500 lg, oxytocin 5 IU). One hour after delivery she developed hypertension in the recovery room (158/100 mmHg), and complained of central chest pain that radiated through to the back. She had proteinuria (3+ on catheter urine dipstick). Labetolol 100 mg was administered orally. Although she complained of no associated symptoms, a bradycardia of 42 beats/min was noted and she looked pale. Her arterial oxygen saturation remained at 99% on room air and she described no respiratory symptoms. A diagnosis of preeclampsia was considered but not confirmed as the hypertension resolved quickly and no further symptoms or signs were present. The ECG showed a sinus bradycardia with left axis deviation, features consistent with left anterior fascicular block and T wave inversion in leads V1 and V2. Aspirin (150 mg 12 hourly) and enoxaparin (60 mg 12 hourly) were commenced and intravenous atropine 500 lg was given to treat the bradycardia. She was urgently reviewed by a cardiologist. A spiral computed tomogram pulmonary angiogram (CTPA) scan excluded a major pulmonary thromboembolic event, and a transthoracic echocardiogram was normal,
Cardiac chest pain and raised troponin in labour Table 1
Troponin I levels
Time from chest pain (h) 3 22 46 Troponin I (lgL 1) [normal range 0–0.032] 1.00 2.55 1.54
showing no regional wall motion abnormalities and normal left ventricular function. Magnetic resonance angiography excluded aortic dissection. Her cardiac enzymes were, however, abnormal (Table 1). She was transferred to a quaternary cardiology centre for cardiac catheterisation (including optical coherence tomography), which showed no evidence of coronary atheroma or dissection. She remained well and pain-free throughout this period and, after transfer back to our hospital, was discharged home. She continued to take aspirin. Some weeks later she underwent a gadoliniumenhanced cardiac MR. This was normal. However, a bubble contrast transthoracic echocardiogram showed a patent foramen ovale (PFO) with right to left interatrial communication on Valsalva manoeuvre.
Discussion Cardiac disease is now the most common cause of death in the maternal population in the United Kingdom and is increasing in its severity. It poses significant risk to the mother and in the developed world is most commonly due to ischaemic heart disease.4 Anecdotal evidence suggests transient chest pain with accompanying ischaemic ECG changes is often discounted during childbirth. As cardiac ischaemia may be more common than is currently appreciated, ischaemic symptoms may warrant further investigation. Troponin, a sensitive marker of cardiac damage, is routinely used to identify cases of myocardial infarction. It is rarely measured in pregnancy, although small but significant elevations in troponin levels have been reported in asymptomatic patients with preeclampsia but only at levels up to 0.16 lg L 1.5 Its reliability during the peripartum period has been further validated by a group who measured troponin levels in low-risk women during and after term deliveries. They found troponin levels were consistently below the upper limit of normal.6 The high values recorded in our case, peaking at 2.55 lg L 1, are consistent with that of significant myocardial ischaemia with myocardial damage.7 In the absence of demonstrable coronary atheromatous disease, other causes of myocardial ischaemia must be considered. Paradoxical coronary embolism and coronary spasm are two such rare causes. Systemic emboli reaching the coronary and cerebral circulations are rare but associated with potentially catastrophic cardiac and neurological complications. These occur as a result of abnormal right to left cardiac communications, such as a PFO, occurring at rest or with Valsalva manoeuvre (for example pushing during the sec-
K. Tatham et al.
455
ond stage of labour). Coronary air emboli have also been demonstrated during caesarean section.8 The presence of a PFO has also been linked to migraines, with paradoxical cerebral emboli being implicated. Closure of a PFO may improve migraine patterns.9 Asymptomatic PFOs, potentially present in up to one quarter of the population,10 may become clinically relevant during pushing in labour. It seems unlikely that parturients will be screened for PFOs, although patients known to have an abnormal cardiac communication should be discouraged from pushing at delivery or be considered for closure of the defect prior to childbirth. Care must be taken to avoid the introduction of potential emboli, such as air, into the venous circulation. Our patient has subsequently been offered closure of her PFO and is awaiting outpatient follow-up to discuss the procedure in more detail. Coronary vasospasm is another recognised cause of myocardial ischaemia in the absence of coronary artery disease. Although rare it has been documented in pregnancy and can cause significant myocardial infarction.11 In a series of 136 cases of myocardial infarction in pregnancy, half had normal vessels, in which spasm was considered the culprit.12 The cause of vasospasm often remains elusive although reports have implicated drugs such as ergometrine and oxytocin. Ergometrine is a potent coronary vasoconstrictor, historically used to induce coronary spasm when diagnosing atypical chest pain.13 It has also been reported to cause myocardial infarction, secondary to vasospasm, and cardiac arrest postpartum.14,15 Ergometrine is used routinely in many parturients. It may be that a small number of these patients experience significant coronary spasm. Oxytocin has also been shown to cause dose-dependent coronary vasoconstriction16 and ST segment depression, likely to be a consequence of its hypotensive effect.17 This may be relevant in our case due to the inadvertent administration of additional oxytocic agent. It has also been postulated that renin release secondary to a transiently ischaemic chorion while the patient is in the supine position can cause coronary vasospasm and transmural myocardial infarction.18 Our patient showed significant myocardial ischaemia and was found subsequently to have an underlying congenital defect. Chest pain and ischaemia may represent increased risk for future morbidity and mortality, even in this low-risk population. We therefore advocate that chest pain should be more thoroughly investigated rather than being dismissed if the symptoms resolve. Patients with known abnormal cardiac communications should be counselled about the potential risks during childbirth, and offered a cardiology opinion and closure
0959-289X/$ - see front matter c 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.ijoa.2010.06.004
of the defect if appropriate. Uterotonic agents have a range of side effects that require increased vigilance, especially if given in combination.
References 1. Nabatian S, Quinn P, Brookfield L, Lakier J. Acute coronary syndrome and preeclampsia. Obstet Gynecol 2005;106:1204–6. 2. Moran C, Ni Bhuinneain M, Geary M, Cunningham S, McKenna P, Gardiner J. Myocardial ischaemia in normal patients undergoing elective caesarean section: a peripartum assessment. Anaesthesia 2001;56:1051–8. 3. Karamermer Y, Roos-Hesselink JW. Coronary heart disease and pregnancy. Future Cardiology 2007;3:559–67. 4. Gelson E, Gatzoulis MA, Steer P, Johnson MR. Heart disease – why is maternal mortality increasing? BJOG 2009;116:609–11. 5. Fleming SM, O’Gorman T, Finn J, Grimes H, Daly K, Morrison JJ. Cardiac troponin I in pre-eclampsia and gestational hypertension. BJOG 2000;107:1417–20. 6. Shivvers SA, Wians Jr FH, Keffer JH, Ramin SM. Maternal cardiac troponin I levels during normal labor and delivery. Am J Obstet Gynecol 1999;180:122–7. 7. Antmann EM, Tanasijevic MJ, Thompson B et al. Cardiacspecific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med 1996;31: 1342–9. 8. Nims M, Hallonquist H, Camann W. Coronary arterial air embolus occurring during cesarean delivery. Int J Obstet Anesth 2006;15:166–9. 9. Schwedt TJ, Demaerschalk BM, Dodick DW. Patent foramen ovale and migraine: a quantitative systematic review. Cephalalgia 2008;28:531–40. 10. Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17–20. 11. Iadanza A, Del Pasqua A, Barbati R, et al. Acute ST elevation myocardial infarction in pregnancy due to coronary vasospasm: a case report and review of literature. Int J Cardiol 2007;115:81–5. 12. Kulka PJ, Scheu C, Tryba M, Gru¨newald R, Wiebalck A, Oberheiden R. Myocardial infarction during pregnancy. Anaesthetist 2001;50:280–4. 13. Dalal JJ, Dart AM, Davies HA, Sheridan DJ, Ruttley MS, Henderson AH. Coronary and peripheral arterial responses to ergometrine in patients susceptible to coronary and oesophageal spasm. Br Heart J 1981;45:181–5. 14. de Labriolle A, Gene´e O, Heggs LM, Fauchier L. Acute myocardial infarction following oral methyl-ergometrine intake. Cardiovasc Toxicol 2009;9:46–8. 15. Tsui BC, Stewart B, Fitzmaurice A, Williams R. Cardiac arrest and myocardial infarction induced by postpartum intravenous ergonovine administration. Anesthesiology 2001;94:363–4. 16. Fortner CL. Effects of synthetic oxytocin with and without preservatives upon coronary blood flow in the dog. J Pharmacol Exp Ther 1969;165:258–66. 17. Jonsson M, Hanson U, Lidell C, Norde´n-Lindeberg S. ST depression at caesarean section and the relation to oxytocin dose. A randomised controlled trial. BJOG 2010;117:76–83. 18. Sasse L, Wagner R, Murray FE. Transmural myocardial infarction during pregnancy. Am J Cardiol 1975;35:448–52.
453
with Gitelman’s syndrome, with an expectant approach to hypotension. In conclusion, potassium and magnesium supplementation and monitoring are essential in Gitelman’s syndrome complicating pregnancy although normalisation of levels is not an absolute requirement for good obstetric and neonatal outcomes. The anaesthetic management of these women requires a detailed preoperative assessment with optimisation, serial monitoring of electrolytes, and an awareness of potential complications.
References 1. Gitelman HJ, Graham JB, Welt LG. A new familial disorder characterised by hypokalemia and hypomagnesemia. Trans Assoc Am Physicians 1966;79:221–35. 2. Amirlak I, Dawson KP. Bartter syndrome: an overview. QJM 2000;93:207–15. 3. Knoers NV, Levtchenko EN. Gitelman syndrome. Orphanet J Rare Dis 2008;3:22.
4. Bartter FC, Pronove P, Gill JR, MacCardle RC. Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. A new syndrome. Am J Med 1962;331:811–28. 5. Bettinelli A, Bianchetti MG, Girardin E et al. Use of calcium excretion values to distinguish two forms of primary renal tubular hypokalemic alkalosis: Bartter and Gitelman syndromes. J Pediatr 1992;120:38–43. 6. Ferrandis Capella P, Gargallo Maicas C, Granell Gill M. Anesthesia for cesarean section in Gitelman’s syndrome. Rev Esp Anestesiol Reanim 2002;49:437–8. 7. Bolton J, Mayhew JF. Anesthesia in a patient with Gitelman syndrome. Anesthesiology 2006;105:1064–5. 8. Basu A, Dillon DS, Taylor R, Davison JM, Marshall SM. Is normalisation of serum potassium and magnesium always necessary in Gitelman Syndrome for a successful obstetric outcome? BJOG 2004;111:630–4. 9. Arriba G, Sanchez-Heras M, Basterrrechea MA. Gitelman syndrome during pregnancy: a therapeutic challenge. Arch Gynecol Obstet 2009;280:807–9. 10. de Haan J, Geers T, Berghout A. Gitelman syndrome in pregnancy. Int J Gynaecol Obstet 2008;103:69–71. 11. Scholl UI, Lifton RP. Molecular genetics of Gitelman’s and Bartter’s syndromes and their implications for blood pressure variation. Genetic Diseases of the Kidney 2009;13:227–47.
0959-289X/$ - see front matter c 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.ijoa.2010.04.005
Peripartum cardiac chest pain and troponin rise K. Tatham, Y. Hughes-Roberts, S. Davies, M. Johnson, K. Ashpole, M. Cox Chelsea and Westminster Hospital NHS Foundation Trust, London, UK ABSTRACT The incidence of myocardial ischaemia is increasing in the obstetric population. This has been attributed to several factors including greater maternal age, the increasing incidence of obesity and diabetes, and the growing population of patients with grown-up congenital heart disease who now reach adulthood and become pregnant. A number of cases of myocardial ischaemia in pregnant women have been documented, during and after delivery, for which no cause has been established. We present a case of a nulliparous woman who developed cardiac chest pain, bradycardia, hypertension and a raised troponin I after vaginal delivery of twin boys at 36 weeks of gestation. Ischaemic electrocardiogram changes were noted. Detailed investigations demonstrated a normal coronary circulation. A patent foramen ovale was found on bubble echocardiography. c 2010 Elsevier Ltd. All rights reserved.
Keywords: Chest pain; Cardiac ischaemia; Troponin; Pregnancy; Patent foramen ovale
Introduction Chest pain around the time of delivery may be the presenting complaint of several potentially life-threatening Accepted June 2010 Correspondence to: Dr. Kate C. Tatham, Magill Department of Anaesthetics, Intensive Care and Pain Medicine, Chelsea and Westminster Hospital NHS Foundation Trust, 369 Fulham Road, London SW10 9NH, UK. Tel.: +44 20 8746 8000. E-mail address: [email protected]
conditions including pulmonary embolus, aortic dissection, coronary artery dissection and myocardial infarction (MI). Of these MI is rare in the obstetric population, with a quoted rate of 0.01%.1 Chest pain and electrocardiogram (ECG) changes during labour and delivery are not uncommon, especially during caesarean section.2 Usually this is not associated with other symptoms or signs, and is ultimately dismissed by clinicians once ongoing ischaemia has been excluded. However, the incidence of myocardial ischaemia is
454 increasing in the obstetric population.3 This has been attributed to several factors: greater maternal age, advances in fertility medicine allowing women to delay pregnancy, the increasing incidence of obesity and diabetes, and the increasing number of patients with grown-up congenital heart disease (GUCH) who now reach childbearing age. We present a case of chest pain in the peripartum period associated with ischaemic ECG changes, significantly elevated troponin I but no evidence of coronary artery disease. On follow-up the only abnormality discovered was that of a patent foramen ovale (PFO).
Case report A 33-year-old, previously healthy nulliparous female with a dichorionic, diamniotic twin pregnancy presented in spontaneous labour at 36 weeks of gestation. Pregnancy had been uneventful. During labour she received patient-controlled epidural analgesia (2 lg ml 1 fentanyl/0.1% bupivacaine). When the cervix was fully dilated she was transferred to the operating theatre for vaginal delivery. An epidural top-up of 5 mL lidocaine 2% with adrenaline and bicarbonate produced a block to cold to T10 on the right and T5 on the left. She delivered twin boys, the first cephalic, the second breech, with minimal surgical assistance. She remained normotensive and stable throughout the delivery. There was an estimated blood loss of 400 mL. She received, at surgical request, 5 IU of oxytocin intravenously and continued on an infusion of 10 IU h 1 for 4 h. Diclofenac 100 mg, was administered rectally. The midwife also inadvertently gave an intramuscular dose of Syntometrine (ergometrine maleate 500 lg, oxytocin 5 IU). One hour after delivery she developed hypertension in the recovery room (158/100 mmHg), and complained of central chest pain that radiated through to the back. She had proteinuria (3+ on catheter urine dipstick). Labetolol 100 mg was administered orally. Although she complained of no associated symptoms, a bradycardia of 42 beats/min was noted and she looked pale. Her arterial oxygen saturation remained at 99% on room air and she described no respiratory symptoms. A diagnosis of preeclampsia was considered but not confirmed as the hypertension resolved quickly and no further symptoms or signs were present. The ECG showed a sinus bradycardia with left axis deviation, features consistent with left anterior fascicular block and T wave inversion in leads V1 and V2. Aspirin (150 mg 12 hourly) and enoxaparin (60 mg 12 hourly) were commenced and intravenous atropine 500 lg was given to treat the bradycardia. She was urgently reviewed by a cardiologist. A spiral computed tomogram pulmonary angiogram (CTPA) scan excluded a major pulmonary thromboembolic event, and a transthoracic echocardiogram was normal,
Cardiac chest pain and raised troponin in labour Table 1
Troponin I levels
Time from chest pain (h) 3 22 46 Troponin I (lgL 1) [normal range 0–0.032] 1.00 2.55 1.54
showing no regional wall motion abnormalities and normal left ventricular function. Magnetic resonance angiography excluded aortic dissection. Her cardiac enzymes were, however, abnormal (Table 1). She was transferred to a quaternary cardiology centre for cardiac catheterisation (including optical coherence tomography), which showed no evidence of coronary atheroma or dissection. She remained well and pain-free throughout this period and, after transfer back to our hospital, was discharged home. She continued to take aspirin. Some weeks later she underwent a gadoliniumenhanced cardiac MR. This was normal. However, a bubble contrast transthoracic echocardiogram showed a patent foramen ovale (PFO) with right to left interatrial communication on Valsalva manoeuvre.
Discussion Cardiac disease is now the most common cause of death in the maternal population in the United Kingdom and is increasing in its severity. It poses significant risk to the mother and in the developed world is most commonly due to ischaemic heart disease.4 Anecdotal evidence suggests transient chest pain with accompanying ischaemic ECG changes is often discounted during childbirth. As cardiac ischaemia may be more common than is currently appreciated, ischaemic symptoms may warrant further investigation. Troponin, a sensitive marker of cardiac damage, is routinely used to identify cases of myocardial infarction. It is rarely measured in pregnancy, although small but significant elevations in troponin levels have been reported in asymptomatic patients with preeclampsia but only at levels up to 0.16 lg L 1.5 Its reliability during the peripartum period has been further validated by a group who measured troponin levels in low-risk women during and after term deliveries. They found troponin levels were consistently below the upper limit of normal.6 The high values recorded in our case, peaking at 2.55 lg L 1, are consistent with that of significant myocardial ischaemia with myocardial damage.7 In the absence of demonstrable coronary atheromatous disease, other causes of myocardial ischaemia must be considered. Paradoxical coronary embolism and coronary spasm are two such rare causes. Systemic emboli reaching the coronary and cerebral circulations are rare but associated with potentially catastrophic cardiac and neurological complications. These occur as a result of abnormal right to left cardiac communications, such as a PFO, occurring at rest or with Valsalva manoeuvre (for example pushing during the sec-
K. Tatham et al.
455
ond stage of labour). Coronary air emboli have also been demonstrated during caesarean section.8 The presence of a PFO has also been linked to migraines, with paradoxical cerebral emboli being implicated. Closure of a PFO may improve migraine patterns.9 Asymptomatic PFOs, potentially present in up to one quarter of the population,10 may become clinically relevant during pushing in labour. It seems unlikely that parturients will be screened for PFOs, although patients known to have an abnormal cardiac communication should be discouraged from pushing at delivery or be considered for closure of the defect prior to childbirth. Care must be taken to avoid the introduction of potential emboli, such as air, into the venous circulation. Our patient has subsequently been offered closure of her PFO and is awaiting outpatient follow-up to discuss the procedure in more detail. Coronary vasospasm is another recognised cause of myocardial ischaemia in the absence of coronary artery disease. Although rare it has been documented in pregnancy and can cause significant myocardial infarction.11 In a series of 136 cases of myocardial infarction in pregnancy, half had normal vessels, in which spasm was considered the culprit.12 The cause of vasospasm often remains elusive although reports have implicated drugs such as ergometrine and oxytocin. Ergometrine is a potent coronary vasoconstrictor, historically used to induce coronary spasm when diagnosing atypical chest pain.13 It has also been reported to cause myocardial infarction, secondary to vasospasm, and cardiac arrest postpartum.14,15 Ergometrine is used routinely in many parturients. It may be that a small number of these patients experience significant coronary spasm. Oxytocin has also been shown to cause dose-dependent coronary vasoconstriction16 and ST segment depression, likely to be a consequence of its hypotensive effect.17 This may be relevant in our case due to the inadvertent administration of additional oxytocic agent. It has also been postulated that renin release secondary to a transiently ischaemic chorion while the patient is in the supine position can cause coronary vasospasm and transmural myocardial infarction.18 Our patient showed significant myocardial ischaemia and was found subsequently to have an underlying congenital defect. Chest pain and ischaemia may represent increased risk for future morbidity and mortality, even in this low-risk population. We therefore advocate that chest pain should be more thoroughly investigated rather than being dismissed if the symptoms resolve. Patients with known abnormal cardiac communications should be counselled about the potential risks during childbirth, and offered a cardiology opinion and closure
0959-289X/$ - see front matter c 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.ijoa.2010.06.004
of the defect if appropriate. Uterotonic agents have a range of side effects that require increased vigilance, especially if given in combination.
References 1. Nabatian S, Quinn P, Brookfield L, Lakier J. Acute coronary syndrome and preeclampsia. Obstet Gynecol 2005;106:1204–6. 2. Moran C, Ni Bhuinneain M, Geary M, Cunningham S, McKenna P, Gardiner J. Myocardial ischaemia in normal patients undergoing elective caesarean section: a peripartum assessment. Anaesthesia 2001;56:1051–8. 3. Karamermer Y, Roos-Hesselink JW. Coronary heart disease and pregnancy. Future Cardiology 2007;3:559–67. 4. Gelson E, Gatzoulis MA, Steer P, Johnson MR. Heart disease – why is maternal mortality increasing? BJOG 2009;116:609–11. 5. Fleming SM, O’Gorman T, Finn J, Grimes H, Daly K, Morrison JJ. Cardiac troponin I in pre-eclampsia and gestational hypertension. BJOG 2000;107:1417–20. 6. Shivvers SA, Wians Jr FH, Keffer JH, Ramin SM. Maternal cardiac troponin I levels during normal labor and delivery. Am J Obstet Gynecol 1999;180:122–7. 7. Antmann EM, Tanasijevic MJ, Thompson B et al. Cardiacspecific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med 1996;31: 1342–9. 8. Nims M, Hallonquist H, Camann W. Coronary arterial air embolus occurring during cesarean delivery. Int J Obstet Anesth 2006;15:166–9. 9. Schwedt TJ, Demaerschalk BM, Dodick DW. Patent foramen ovale and migraine: a quantitative systematic review. Cephalalgia 2008;28:531–40. 10. Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17–20. 11. Iadanza A, Del Pasqua A, Barbati R, et al. Acute ST elevation myocardial infarction in pregnancy due to coronary vasospasm: a case report and review of literature. Int J Cardiol 2007;115:81–5. 12. Kulka PJ, Scheu C, Tryba M, Gru¨newald R, Wiebalck A, Oberheiden R. Myocardial infarction during pregnancy. Anaesthetist 2001;50:280–4. 13. Dalal JJ, Dart AM, Davies HA, Sheridan DJ, Ruttley MS, Henderson AH. Coronary and peripheral arterial responses to ergometrine in patients susceptible to coronary and oesophageal spasm. Br Heart J 1981;45:181–5. 14. de Labriolle A, Gene´e O, Heggs LM, Fauchier L. Acute myocardial infarction following oral methyl-ergometrine intake. Cardiovasc Toxicol 2009;9:46–8. 15. Tsui BC, Stewart B, Fitzmaurice A, Williams R. Cardiac arrest and myocardial infarction induced by postpartum intravenous ergonovine administration. Anesthesiology 2001;94:363–4. 16. Fortner CL. Effects of synthetic oxytocin with and without preservatives upon coronary blood flow in the dog. J Pharmacol Exp Ther 1969;165:258–66. 17. Jonsson M, Hanson U, Lidell C, Norde´n-Lindeberg S. ST depression at caesarean section and the relation to oxytocin dose. A randomised controlled trial. BJOG 2010;117:76–83. 18. Sasse L, Wagner R, Murray FE. Transmural myocardial infarction during pregnancy. Am J Cardiol 1975;35:448–52.