Heart Disease in Pregnancy - part 7 doc

should be encouraged and measures set in place to maintain a lifelong healthy lifestyle. Congenital coronary anomalies Congenital coronary anomalies are occasionally encountered in pregnancy and patients with repaired tetralogies and other defects have now lived long enough to be seen with acquired atheromatous coronary disease. Occasional patients with previously unrecognized corrected transposition are referred with angina and ‘mitral’ regurgitation thought to be ischemic in origin. They often have poor function of the systemic right ventricle and atrial fibrillation or atrioven- tricular conduction defects. A continuous murmur caused by a coronary cameral fistula may first be de- tected during antenatal examination. It is usually distinguishable from a patent duct by an unusual location. Echocardiography will usually display the anom- aly but small ones may be hard to spot (Figure 15.2). Even large fistulae may be symptom free and cause no trouble in pregnancy but should be closed after the pregnancy. Small fistulae should be left alone. Connections can be multiple and are best tackled percutaneously. Anomalous origin of a coronary artery (usually the left) from the pulmonary artery, with poor left ventricular function as a result of neonatal infarction or progressive ischaemia caused by increasing fistulous flow from right to left coronary artery, may present with angina, 45 mitral regurgitation or left ventric- ular failure. The patient illustrated in Figure 15.3 had undergone two unevent- ful pregnancies before she was referred with angina, mitral regurgitation and failure. She did well after ligation of the left coronary artery at its ostium and 212 Chapter 15 Figure 15.2 One frame from a left coronary angiogram of a young girl who was found to have a murmur at a routine examination. This was continuous and placed maximally at the third left interspace too low for a patent ductus. Echocardiography showed flow into the main pulmonary artery just distal to the valve. Coronary angiography showed a coronary artery fistula with abnormal branches from the anterior descending coronary artery draining into the main pulmonary artery which is opacified from the left coronary injection. This rare abnormality carries no adverse prognostic significance. internal mammary artery bypass into the left anterior descending artery and mitral valve replacement. Pregnancy after myocardial infarction The occurrence of a heart attack in pregnancy is deeply distressing and likely to be followed by considerable depression and insecurity even if recovery is good. Little is known about the risk of further pregnancies, which depends on the mechanism and the residual left ventricular function. Subsequent successful pregnancies have been reported but both patients and their doctors will usually be fearful because the risk of repetition of dissection is unknown. Conclusion Myocardial infarction is a rare complication of pregnancy with a high mortality. Rapid intervention with coronary stenting or bypass is usually indicated. The most common cause is probably spontaneous dissection but the prevalence of atheroma has increased in association with the older age of many pregnant women. References 1 Wenger NK. Coronary heart disease: the female heart is vulnerable. Prog Cardiovasc Dis 2003;46:199–229. 2 Von der Lohe E. Coronary Heart Disease in Women. Berlin: Springer, 2003. Coronary artery disease 213 Figure 15.3 Aortogram showing the dilated right coronary artery in a patient with anomalous origin of the left coronary artery from the pulmonary artery (described in the text). The left coronary artery is faintly opacified by fistulous flow from the right coronary artery but has no connection with the aorta. 3 Brosius FC, Waller BF, Roberts WC. Radiation heart disease: analysis of 16 young (aged 15–33 years) necropsy patients who received over 3500 rads to the heart. Am J Med 1981;70:519–30. 4 Mallilos-Perez M, Orteger-Carnicer O, Gutierrez-Millet V, Pazmino-Narvaez L. Post partum acute myocardial infarction associated with polyarteritis nodosa. Med Clin 1982;78:32–4. 5 Rallings P, Exner T, Abraham R. Coronary artery vasculitis and myocardial infarction associated with antiphospholipid antibodies in a pregnant woman. Aust NZ J Med 1989;19:347–50. 6 Parry G, Goudevenos J, Williams DO. Coronary thrombosis postpartum in a young woman with Still’s disease. Clin Cardiol 1992;15:305–7. 7 Nolan TE, Savage RW. Peripartum myocardial infarction from presumed Kawasaki’s disease. Southern Med J 1990;83:1360–1. 8 Hankins GDV, Wendel GD, Leveno KL, Stoeham J. Myocardial infarction during pregnancy: a review. Obstet Gynecol 1985;65:139–46. 9 Jaffe BD, Broderick TM, Leier CV. Cocaine induced coronary artery dissection. N Eng J Med 1994;330:510–11. 10 Liu SS, Forrester RM, Murphy GS, Chen K, Glassenberg R. Anaesthetic management of a parturient with myocardial infarction related to cocaine use. Can J Anaesth 1992;39:858–61. 11 Livingston JC, Mabie BC, Ramanathan J. Crack cocaine, myocardial infarction and troponin I levels at the time of caesarean delivery. Anesth Analg 2000;91:913–15. 12 Bonnet J, Aumailley M, Thomnas D, Grosgogeat Y, Broustet JP, Bricaud H. Sponta- neous coronary artery dissection; case report and evidence for a defect in collagen metabolism. Eur Heart J 1986;7:904–9. 13 Anderson RA, Fineron FW: Aortic dissection in pregnancy: importance of pregnancy induced changes in the vessel wall and bicuspid aortic valve in pathogenesis. Br J Obstet Gynaecol 1994;101:1085–18. 14 Basso C, Morgagni GL, Thiene G. Spontaneous coronary artery dissection: a neglected cause of acute myocardial ischaemia and sudden death. Heart 1996;75: 451–4. 15 Dhawan R, Singh G, Fesniack H. Spontaneous coronary artery dissection: the clinical spectrum. Angiology 2002;53:5383–93. 16 Maeder M, Ammann P, Angehrn W, Rickli H. Idiopathic spontaneous coronary artery dissection: incidence, diagnosis and treatment. Int J Cardiol 2005;101:363–9. 17 Sheikh AU, Harper MA. Myocardial infarction during pregnancy: management and outcome of two pregnancies. Am J Obstet Gynecol 1993;163:279–83. 18 Antoniucci D, Magdidilgenti I. Spontaneous dissection of the three major coronary arteries. Eur Heart J 1990;11:1130–4. 19 Black MD, Catzavelos C, Boyd D, Walley VM. Simultaneous spontaneous dissections in three coronary arteries. Can J Cardiol 1991;7:34–6. 20 Emori T, Goto, Y, Maeda T, Chiba Y, Haze K. Multiple coronary artery dissections diagnosed in vivo in a pregnant woman. Chest 1993;104:289–90. 21 Togni M, Ammann FW, Follath F. Spontaneous multivessel coronary artery dissec- tion in a pregnant woman treated successfully with stent implantation. Am J Med 1999;107:407–8. 22 Greenblatt JM, Kochar GS, Albornoz MA. Multivessel spontaneous coronary artery dissection in a patient with severe systolic hypertension: a possible association. A case report. Angiology 1999;50:509–13. 214 Chapter 15 23 Choi JW, Davidson CJ. Spontaneous multivessel coronary artery dissection in a long distance runner successfully treated with oral antiplatelet therapy. J Invasive Cardiol 2002;14:675–8. 24 De Maio JJ Jr, Kinsella SH, Silverman ME. Clinical course and long term prognosis of spontaneous coronary artery dissection. Am J Cardiol 1989;64:471–4. 25 Jorgensen MB, Aharonian V, Mansukhani V, Mahrer PR. Spontaneous coronary dis- section; a cluster of cases with this rare finding. Am Heart J 1994;127:1382–7. 26 Dowling GP, Buja LM. Spontaneous coronary artery dissection occurs with and with- out periadventitial inflammation. Arch Pathol Lab Med 1987;111:470–2. 27 Chanler Smith J. Dissecting aneurysms of coronary arteries. Arch Pathol 1975;99: 1127–31. 28 Robinowitz M, Virmani R, McAllister H. Spontaneous coronary dissection and eosinophilic inflammation: a cause and effect relationship? Am J Med 1982;72: 923–8. 29 Curiel P, Petrella A et al. Postpartum coronary artery dissection followed by heart transplantation. Am J Obstet Gynecol 1990;163:538–9. 30 Movsesiam MA, Wray RB. Postpartum myocardial infarction. Br Heart J 1989;62: 154–6. 31 Thayer JO, Healy RW, Maggs PR. Spontaneous coronary artery dissection. Ann Thorac Surg 1987;44:97–102. 32 Engelman DT, Thayer J, Derossi J, Scheinerman J, Brown N. Pregnancy related coronary artery dissection: a case report and collective review. Conn Med 1993;57: 135–9. 33 Koller PT, Cliffe CM, Ridley DJ. Immunosuppressive therapy for peripartum-type spontaneous coronary artery dissection: case report and review. Clin Cardiol 1998;21:40–6. 34 Ferrari E, Tozzi P, von Segesser LK. Spontaneous coronary artery dissection in a young woman: from emergency coronary artery bypass grafting to heart transplanta- tion. Eur J Cardiothorac Surg 2005;28:349–51. 35 Liao JK, Cockrill BA, Yurchak PM. Acute myocardial infarction after ergonovine administration. Am J Cardiol 1991;68:623–4. 36 Fujiwara Y, Yamanaka O, Nakamura T, Yokoi H, Yamaguchi H. Acute myocardial infarction induced by ergonovine administration for artificially induced abortion. Jpn Heart J 1993;34:803–8. 37 Hayashi Y, Ibe T, Kawato H, Futamura N et al. Post partum acute myocardial infarc- tion induced by ergonovine administration. Intern Med 2003;42:983–6. 38 Ruch A, Duhring JL. Postpartum myocardial infarction in a patient receiving bromocriptine. Obstet Gynecol 1989;74:448–9. 39 Ottman EH, Gall SA. Myocardial infarction in the third trimester of pregnancy sec- ondary to an aortic valve thrombus. Obstet Gynecol 1993; 81:804–5. 40 Janion M, Kurzawski J, Konstantinowicz H et al. Myocardial infarction in pregnancy. Kardiologia Polska 1993;38:351–3. 41 Box LC, Hanak V, Arciniegas JG. Dual coronary emboli in peripartum cardiomyopa- thy. Tex Heart Inst J 2004;31:442–4. 42 Butters L, Kennedy S, Rubin PC. Atenolol in essential hypertension during preg- nancy. BMJ 1990;301:587–9. 43 Hameed AB, Tummala PP, Goodwin TM et al. Unstable angina during pregnancy in two patients with premature atherosclerosis and aortic stenosis in association with familial hypercholesterolaemia. Am J Obstet Gynecol 2000;182:1152–5. Coronary artery disease 215 44 Leiserowitz GS, Evans AT, Samuels SJ, Omand K, Kost GJ. J Reprod Med 1992;37:910–16. 45 Zavalloni D, Belli G, Caratti A, Presbitero P. Anomalous origin of the left coronary ar- tery from the pulmonary artery in an adult pregnant patient: surgical and percuta- neous myocardial revascularisation. Ital Heart J 2005;6:348–52. 216 Chapter 15 CHAPTER 16 Heart rhythm disorders David Lefroy, Dawn Adamson Cardiac arrhythmias occur commonly during pregnancy and are a frequent cause for concern for the well-being of both the mother and the fetus. For some mothers the arrhythmias may simply be a recurrence of a previously diagnosed arrhythmia or a manifestation of known heart disease. However, in most cases, there is no previous history of heart disease, and the new occurrence of a cardiac problem generates considerable alarm. Fortunately, most arrhythmias that occur during pregnancy are benign, and simply troublesome, rather than inca- pacitating or life threatening. Advice about appropriate actions during sympto- matic episodes, together with reassurance, is usually all that is needed. In the remaining minority of cases, judicious use of anti-arrhythmic drugs will lead to a safe and successful outcome for both mother and baby. Maternal death from arrhythmia is extremely rare. The aims of investigating a suspected cardiac arrhythmia apply irrespective of whether or not the patient is pregnant. The first aim is accurate diagnosis of the arrhythmia by clinical assessment and appropriate ECG investigation. This en- ables the clinician to give a reliable opinion about the prognosis and appropriate treatment. The temptation to treat symptoms empirically should be resisted be- cause it will frequently lead to the use of ineffective, inappropriate and possibly harmful therapy. 1,2 The second aim is to determine whether or not there is additional heart disease associated with the arrhythmia. For this the echocardiogram is an invaluable ad- junct to the clinical examination, e.g. a patient with atrial fibrillation may be found to have previously undiagnosed mitral stenosis, and this in turn will have an important implication for the use of anticoagulation during pregnancy. The third aim is that systemic disorders may present with arrhythmias and should be actively sought and excluded by appropriate clinical investigation, e.g. abnormalities of thyroid function should always be excluded, and hemor- rhage, pulmonary embolism, infections and inflammatory states must be con- sidered in cases of unexplained sinus tachycardia. 217 Practice points Essential investigations for suspected arrhythmia during pregnancy include: • Resting 12-lead ECG • ECG recorded during tachycardia, 12-lead if at all possible • Echocardiogram • Thyroid function tests. Heart Disease in Pregnancy, Second Edition Edited by Celia Oakley, Carole A Warnes Copyright © 2007 by Blackwell Publishing It is in the realm of treatment that the management of arrhythmias during preg- nancy varies significantly from the approach used in the non-pregnant patient. There are a number of reasons for this. First, the potential for harm to the fetus mandates against the use of procedures that require X-ray fluoroscopy, includ- ing radiofrequency catheter ablation or pacemaker implantation, which are standard treatments for arrhythmias in non-pregnant patients. Second, con- cern about adverse effects on the fetus may preclude the use of several anti- arrhythmic drugs. Third, the altered physiological state of pregnancy may have profound effects on the pharmacokinetics of anti-arrhythmic drugs, leading to unpredictable plasma levels that may limit the safety and efficacy of drug treat- ment. Finally, compared with a non-pregnant patient, a pregnant woman may better accept arrhythmia symptoms without recourse to drug treatment simply because her symptoms are likely to improve spontaneously after delivery. 3–5 This chapter is intended to serve as a guide to understanding and managing arrhythmias in pregnant women by covering the underlying principles and dis- cussing individual arrhythmias that may be encountered. Incidence and prevalence of arrhythmia during pregnancy The sinus rate increases by about 10 beats/minute during pregnancy, and sinus tachycardia greater than 100 beats/min is common. 1,2 Ectopic beats, intermit- tent sinus tachycardia and non-sustained arrhythmia are very commonly en- countered in more than 50% of pregnant women who are investigated for symptoms of arrhythmia. 6.7 Sustained tachycardias are less common, and the prevalence in women of child-bearing age has been estimated at around 2–3/1000. 1,5 Some arrhythmias that occur during pregnancy represent a recur- rence of a pre-existing problem, but a substantial number of cases present for the first time in pregnancy. 8,9 Bradyarrhythmias presenting during pregnancy are rare with a prevalence of about 1–20 000, and are usually caused by sinoa- trial disease or congenital complete heart block. Death as a result of maternal tachyarrhythmia is extremely rare, with none recorded in the UK during a 12-year period in women with no evidence of underlying structural heart disease. 1 Tachycardia mechanisms and arrhythmogenic effects of pregnancy The cardiovascular adaptations to pregnancy include increased resting heart rate, raised intravascular volume, increased cardiac output, reduced systemic vascular resistance, dilatation of the cardiac chambers, augmented stroke vol- ume and enhanced catecholaminergic tone. Atrial and ventricular myocardial wall stress is probably increased, and stretch-dependent ionic currents in car- diac myocytes may be activated. In addition to these changes, a state of height- ened visceral awareness in pregnancy may lead a patient to pay attention to 218 Chapter 16 symptoms of sinus tachycardia or occasional ectopic activity which are within normal limits and which otherwise would have been ignored. 3,4 Tachycardias are initiated and perpetuated by one or more of three mecha- nisms — focal, re-entrant or ion channelopathy — all of which may be initiated or modified by the physiological changes of pregnancy. Focal tachycardia A focal tachycardia can arise from a small cluster of abnormal cells called an ‘ec- topic focus’. An ectopic focus may occur anywhere within atrial or ventricular myocardium, but some locations are more common, such as right ventricular outflow tract and the regions adjacent to the atrial connections of the pul- monary and caval veins. An ectopic focus is able to generate depolarizations that pre-empt the next sinus beat, thus generating atrial or ventricular ectopic beats. These may occur singly or in runs of tachycardia. An individual ectopic focus has a unique ECG signature in the form of an abnormal P wave (in the case of an atrial focus) or abnormal QRS complex (in the case of a ventricular focus). The cardiovascular adaptations to pregnancy promote the activity of ectopic foci, and ectopic beats are particularly common during pregnancy. Sustained focal atrial or ventricular tachycardia may present for the first time during preg- nancy. A focal mechanism for tachycardia is suspected clinically when there are frequent ectopic beats and recurrent self-terminating episodes of tachycardia. Focal tachycardias may be triggered by physical exertion and terminate spon- taneously when exercise ceases. They often respond to anti-arrhythmic drugs that act on nodal tissue such as beta blockers, verapamil or digoxin. Re-entrant tachycardia An abnormal electrical circuit (‘re-entry circuit’) may be present within the heart and consists of one or more of the following components: atrial myocar- dium, ventricular myocardium, atrioventicular (AV) node, accessory AV pathway (Figure 16.1). The common feature of re-entrant arrhythmias is that a depolarizing impulse can travel repeatedly around the re-entry circuit, generat- ing one heart beat for each cycle. The greater the distance that the impulse has to travel around the re-entry circuit, the more likely it is that each part of the circuit will have recovered electrical excitability by the time the impulse returns for the next cycle. This condition for sustained re-entry can be expressed as follows: Length of re-entry circuit (mm) > Impulse propagation speed (mm/ms) × Refractory period (ms) The physiological changes of pregnancy make it more likely that this condition will be fulfilled. Dilatation of the cardiac chambers increases the length of a re-entrant circuit, and the increased catecholaminergic tone reduces the refractory period. Re-entrant tachycardias are more common than focal tachycardias and tend to have a more stable heart rate. Class I and III anti-arrhythmic drugs, which act Heart rhythm disorders 219 on atrial and/or ventricular myocardium, tend to be more effective. They work by prolonging the myocardial refractory period and thus preventing the condi- tion for sustained re-entry described above. Ion channelopathy Mutations of the genes coding for cardiac K + and Na + channel proteins result in impaired and delayed cardiac repolarization and cause various forms of congenital long QT syndrome. Genetic polymorphisms may also underlie the susceptibility of individuals to drug-induced and other forms of the acquired long QT syndrome. Other ion channel mutations have been implicat- ed as the cause of some cases of familial atrial fibrillation and Brugada syndrome, in which affected individuals have a characteristic ECG with partial right bundle-branch block and ST segment elevation in leads V1–3, and are prone to syncope and sudden death as a result of ventricular tachycardia. 220 Chapter 16 A FED CB r atrium ivc svc tricuspid valve sa node r ventricle aorta l ventricle cs ostium av node l atrium pa mitral valve pv ostia accessory pathway infarct scar surgical atriotomy scar Figure 16.1 Diagram of re-entrant circuits. Panel A: anatomy of diagram. av, atrioventricular; cs, coronary sinus; ivc, inferior vena cava; l, left; pa, pulmonary artery; pv, pulmonary vein; r, right; svc, superior vena cava. Panel B: AVNRT re-entrant circuit in the region of the AV node. Panel C: Reentrant circuit for the common form of atrial flutter which is anticlockwise around the tricuspid annulus in the right atrium. Panel D: Atrioventricular re-entrant circuit using an accessory pathway to complete the retrograde limb of the circuit in a patient with Wolff–Parkinson–White syndrome. Panel E: Reentrant ventricular tachycardia around a region of infarct scar in the left ventricle. Panel F: Reentrant tachycardia around an old healed surgical incision in the right atrium. The effect of pregnancy on cardiac ion channels, long QT syndrome and poly- morphic ventricular tachycardia has not been studied in detail. The preponder- ance of long QT syndrome in women, despite most cases being autosomal dominant, strongly suggests that expression of the condition is dependent on sex hormones, which in turn suggests that expression of the relevant cardiac ion channels may be affected by the changing hormonal milieu of pregnancy. Heart rhythm disorders 221 Tachycardia mechanisms: practice points Focal tachycardias • Frequent ectopic beats of same QRS morphology as tachycardia • Tendency for frequent ‘stop–starts’ • May be exacerbated by exercise and increased catecholaminergic tone • Usually the heart is structurally normal • Typically respond to beta blockers and verapamil • Cardioversion is often unhelpful; early re-initiations are common. Re-entrant tachycardias • Re-entry is the most common tachycardia mechanism • The echocardiogram and resting ECG may be normal or show evidence of underlying disease • Ectopic beats occur occasionally, may initiate and terminate tachycardias, and are usually different from the morphology of tachycardia • Class I and III anti-arrhythmic drugs are useful, particularly when the AV node is not part of the re-entrant circuit • Cardioversion is an option. Ion channelopathies and long QT syndrome • There are abnormalities of the ST segment and/or T wave on the resting ECG • Syncope and cardiac arrest may occur • Polymorphic ventricular tachycardia and pause-dependent initiation • Acquired forms are related to certain drug classes or electrolyte depletion • Familial tendency • Beta blockers are effective, but other anti-arrhythmic drugs should be avoided because they make the problem worse. Clinical presentation and investigation History Palpitations are the most common presenting symptom, are usually intermit- tent and only rarely indicate a serious problem. From the history, the inter- mittent thumping and missed beats caused by ectopic beats can be readily distinguished from the rapid palpitation of tachycardia. Ectopic beats that are most noticeable at rest but disappear during physical exertion are benign. [...]... doses in patients with underlying sinus node disease Intermittent sinus bradycardia may be seen in cases of sinoatrial disease, or occur with heightened vagal tone in patients susceptible to vasovagal syncope Sinus bradycardia and sinus pauses may occur in patients with obstructive sleep apnea Congenital complete heart block is usually detected in childhood, and asymptomatic patients with a mean heart. .. beats/min is not uncommon during pregnancy and a rate that is persistently in excess of 110/min should prompt consideration of underlying causes of secondary tachycardia, including infection, in ammatory disease, thyrotoxicosis and cardiomyopathy A Holter monitor may be helpful to differentiate the normal circadian variation in heart rate of a sinus tachycardia from the virtually fixed heart rate of incessant... thromboembolism in pregnancy (Table 17. 1) Virchow’s three postulates remain valid Pregnancy induces both a hypercoagulable state and alterations in blood flow Endothelial factors are released with delivery, especially when it is surgical The plasma concentration of clotting factors (fibrinogen and factors VII, VIII and X) increases and fibrinolytic activity diminishes in pregnancy as a result of an increased... with cyanotic congenital heart disease who frequently need bedrest in pregnancy Pulmonary embolism 245 Thrombophilias Thrombophilias may be inherited or acquired Afflicted individuals may declare themselves with a first-ever thrombotic episode in pregnancy or the puerperium Inherited abnormalities in the coagulation syndrome include deficiency of protein C, protein S or antithrombin III Congenital or acquired... arrhythmia Infrequently, a patient may have 12-lead ECG abnormalities indicative of primary ‘electrical’ disease, such as frequent ectopic beats or Wolff–Parkinson–White syndrome (Figure 16.2) In patients with suspected bradycardia, abnormalities that should be sought include evidence of sinus node disease such as resting sinus bradycardia or intermittent pauses, and conduction system disease causing prolongation... baby References 1 Anderson MH Rhythm disorders In: Oakley C (ed.), Heart Disease in Pregnancy London: BMJ Publishing, 19 97: pp 248–81 2 Conti JB, Curtis AB Arrhythmias during pregnancy In: Saksena S, Camm AJ (eds), Electrophysiological Disorders of the Heart Philadelphia: Elsevier, 2005: pp 5 17 32 3 Ferrero S, Colombo BM, Ragni N Maternal arrhythmias during pregnancy Arch Gynecol Obstet 2004;269:244–53... ventricle, causing patchy posterobasal infarction In the clinical context of major PE, raised cardiac markers including troponins do not indicate a concomitant coronary artery event.21 Diagnosis Clinical presentation Pulmonary embolism presents in diverse ways, which vary from non-specific to catastrophic (Table 17. 2) Early surgical studies showed that two-thirds of fatal cases die within an hour of... faintness Pleuritic chest pain Non-pleuritic chest pain Hemoptysis Leg swelling or pain Tachypnea Tachycardia Chest tenderness Raised jugular venous pressure Right ventricular heave and gallop Deep vein thrombosis problem is that a complaint of shortness of breath is common in pregnancy A high index of suspicion is needed and PE should be excluded in any pregnant or parturient patient with unexplained... Implantable cardioverter-defibrillators and pregnancy: a safe combination? Circulation 19 97; 96:2808–12 17 Rashba EJ, Zareba W, Moss AJ et al In uence of pregnancy on the risk for cardiac events in patients with hereditary long QT syndrome LQTS Investigators Circulation 1998; 97: 451–6 18 Kloeck W, Cummins RO, Chamberlain D et al Special resuscitation situations: an advisory statement from the International Liaison... led to a fall in the number of postpartum deaths during the past few decades More recently, the proportion of antepartum deaths has risen with up to half of all the deaths occurring during pregnancy, the numbers distributed throughout, but the most dangerous period still being the first 24 hours after delivery (vaginal or surgical), and the heightened risk continuing although diminishing over the next . infarc- tion induced by ergonovine administration. Intern Med 2003;42:983–6. 38 Ruch A, Duhring JL. Postpartum myocardial infarction in a patient receiving bromocriptine. Obstet Gynecol 1989 ;74 :448–9. 39. arrhythmia during pregnancy include: • Resting 12-lead ECG • ECG recorded during tachycardia, 12-lead if at all possible • Echocardiogram • Thyroid function tests. Heart Disease in Pregnancy, Second. rather than inca- pacitating or life threatening. Advice about appropriate actions during sympto- matic episodes, together with reassurance, is usually all that is needed. In the remaining minority