Expert Review of Obstetrics & Gynecology
ISSN: 1747-4108 (Print) 1747-4116 (Online) Journal homepage: http://www.tandfonline.com/loi/ierb20
Effect of maternal heart disease on pregnancy outcomes Emily Gelson & Mark Johnson To cite this article: Emily Gelson & Mark Johnson (2010) Effect of maternal heart disease on pregnancy outcomes, Expert Review of Obstetrics & Gynecology, 5:5, 605-617, DOI: 10.1586/ eog.10.49 To link to this article: http://dx.doi.org/10.1586/eog.10.49
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Effect of maternal heart disease on pregnancy outcomes Expert Rev. Obstet. Gynecol. 5(5), 605–617 (2010)
Emily Gelson†1 and Mark Johnson1 Department of Obstetrics and Gynaecology, Imperial College London, Chelsea and Westminster Hospital, 369 Fulham Road, London, SW10 9NH, UK † Author for correspondence: Tel.: +44 208 846 7892 Fax: +44 208 846 7796
[email protected] 1
The presence of maternal heart disease has an adverse effect on pregnancy outcomes. The most recent triennial confidential enquiry confirmed that heart disease is now the most common cause of maternal death in the UK. Maternal and neonatal morbidity are also significant. This article details the causes of heart disease and why maternal mortality is increasing. The marked physiological changes to the cardiovascular system during pregnancy are outlined. The effects of pregnancy on heart disease are discussed for specific cardiac lesions/conditions, and basic management principles are described. Keywords : arrhythmia • cardiomyopathy • congenital heart disease • ischemic heart disease • pregnancy • valvular heart disease
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Learning objectives Upon completion of this activity, participants should be able to:
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Identify causes of cardiac morbidity and death in pregnancy, including predictors of primary cardiac events during pregnancy in women with heart disease
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Examine appropriate anticoagulation regimens in pregnancy for women with mechanical heart valves and strategies for their incorporation into management
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Describe effects of maternal heart disease and its treatment on fetal outcomes
10.1586/EOG.10.49
© 2010 Expert Reviews Ltd
ISSN 1747-4108
605
Review
CME
Gelson & Johnson
Financial & competing interests disclosure
Editor Elisa Manzotti, Editorial Director, Future Science Group, London, UK. Disclosure: Elisa Manzotti has disclosed no relevant financial relationships. CME Author Désirée Lie, MD, MSEd Clinical Professor; Director of Research and Faculty Development, Department of Family Medicine, University of California, Irvine, Orange, California, USA. Disclosure: Désirée Lie, MD, MSEd, has disclosed the following relevant financial relationship: she served as a nonproduct speaker for: ‘Topics in Health’ for Merck Speaker Services. Authors and Credentials Emily Gelson, BSc (Hons) Department of Obstetrics and Gynaecology, Imperial College London, Chelsea and Westminster Hospital, 369 Fulham Road, London, SW10 9NH, UK. Disclosure: Emily Gelson has disclosed no relevant financial relationships. Mark Johnson, PhD Department of Obstetrics and Gynaecology, Imperial College London, Chelsea and Westminster Hospital, 369 Fulham Road, London, SW10 9NH, UK. Disclosure: Mark Johnson has disclosed no relevant financial relationships.
Heart disease is now the leading cause of maternal mortality in the UK with a mortality rate of 2.27 per 100,000 maternities; double that reported in 1990 [1] . However, the incidence of heart disease during pregnancy has remained constant at 0.9% over several decades [2] , implying that the severity of heart disease and/or the risk it poses during pregnancy is increasing. The main cause of this appears to be an increased incidence in previously undiagnosed ischemic heart disease. This is due to lifestyle changes, with increasing numbers of pregnancies in women with risk factors such as obesity, diabetes and smoking, and also pregnancies in older women. In addition, women with complex pre-existing heart disease are surviving into adulthood and considering pregnancy. Pregnancy in women with heart disease not only poses a risk of maternal death but also of serious morbidity such as heart failure, stroke and cardiac arrhythmia. The fetus is not spared, with neonatal morbidity and mortality due to fetal growth retardation and prematurity also markedly increased. The causes of maternal heart disease are diverse and its management complex. Causes of maternal heart disease
In the developed world, congenital heart disease is now more common in the pregnant population than acquired heart disease. This reflects the fact that with advances in cardiac surgery and medication, 85% of infants with congenital heart disease now survive into adult life [3,4] . In the UK, the prevalence of congenital heart disease at birth remains constant at seven per 1000 live infants but the number of adults with congenital heart disease is increasing by 1600 per year with a 50% increase in those with complex disease [5] . By contrast, the rates of maternal death related to structural congenital heart disease have declined progressively, suggesting that the level of awareness may have increased and, thus, may have led to improved management of pregnant women with various congenital heart defects [6,7] . Ischemic heart disease is rapidly increasing in the pregnant population and is now the commonest cause of cardiac death in pregnancy in the UK [2] . This is likely due to increased maternal age, smoking, the adoption of a sedentary lifestyle and poor 606
diet leading to greater rates of obesity, diabetes and hypertension. Acute myocardial infarction accounts for the majority of deaths and is most commonly due to coronary atherosclerosis, although coronary artery dissection and consequent occlusion is also relatively frequent [8] . The risk of an acute myocardial infarction during pregnancy is small but increasing, with an estimated incidence of one in 35,700 deliveries between 1991 and 2000 [9] and one in 16,100 deliveries between 2000 and 2002 [10] . Consistent with the decline in rheumatic fever in the developed world, the prevalence of pregnancies complicated by rheumatic heart disease in the UK has significantly decreased. Rheumatic heart disease remains prevalent in many developing countries [101] . The current level of immigration to the UK means that we are experiencing a resurgence in these cases and it seems inevitable that the number of pregnant women with rheumatic heart disease will increase over the coming years. Indeed, the latest confidential enquiry reported the first maternal deaths due to rheumatic heart disease since 1991–1993 and both were in recent immigrants [1] . Pregnancy-induced cardiomyopathy is a disorder in which left ventricular systolic dysfunction and heart failure present in the last month of pregnancy and the first 5 months postdelivery, in the absence of all other causes of dilated cardiomyopathy with heart failure. It is a rare condition with an estimated incidence of 1 case per 5000–10,000 live births [11] . However, it is one of the most common causes of maternal death in the UK [1] . Cardiac arrhythmias are also an important cause of maternal morbidity. Pregnancy increases the incidence of cardiac arrhythmia. This is due to hormonal changes, alterations in autonomic tone, increased hemodynamic demands and mild hypokalemia. These factors act to precipitate cardiac arrhythmias not present prior to pregnancy or exacerbate pre-existing arrhythmias. The risk is highest during labor and delivery. Physiological changes in normal pregnancy
During normal pregnancy there are dramatic alterations in cardiovascular physiology, initiated by a fall in systemic vascular resistance to 30–70% of its preconception value by 8 weeks of Expert Rev. Obstet. Gynecol. 5(5), (2010)
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Effect of maternal heart disease on pregnancy outcomes
gestation (Box 1) [12] . The mechanism(s) responsible for triggering such widespread vasodilatation is unclear but increased circulating levels of estrogens, vasodilatory peptides or factors such as nitric oxide and calcitonin gene-related peptide have all been suggested to be responsible. The fall in systemic vascular resistance results in fluid retention and an increased blood volume. Since there is a relatively greater expansion in plasma volume, this results in a fall in hematocrit and plasma osmolality. The increase in cardiac output is secondary to a greater stroke volume and higher heart rate. It rises to a peak between the 20th and 24th weeks and remains stable until term. Arterial blood pressure falls until mid pregnancy, gradually returning to prepregnancy levels late in the second trimester. Prolonged volume overload results in progressive physiological left ventricular hypertrophy. Labor, particularly the second stage, is associated with a further increase in cardiac output. Pain induces a sympathetic response causing an increase in heart rate. Stroke volume is augmented by autotransfusion during contractions. Following delivery the return of uterine blood into the systemic circulation results in a further increase in cardiac output. Stroke volume, heart rate and cardiac output remain high for 24 h postdelivery with rapid intravascular volume shifts in the first 2 weeks postpartum. Thus, the later stages of labor and early postpartum are periods of high risk of pulmonary edema.
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Box 1. Physiological changes in normal pregnancy. • Decreased systemic and pulmonary vascular resistance • Increased blood volume • Initial fall in blood pressure to 20 weeks followed by an increase until term • Increased heart rate • Increased stroke volume • Increased cardiac output • Physiological cardiac hypertrophy • Pulmonary capillary wedge pressure unchanged
Pregnancy in specific conditions Left to right shunts
In pregnancy, increased cardiac output and blood volume are counterbalanced by a decrease in peripheral vascular resistance. Left-to-right shunting in patients with atrial septal defects (ASDs), ventricular septal defects and patent ductus arteriosus is therefore reduced. In the absence of pulmonary hypertension, pregnancy, labor and delivery are well tolerated [23] . Patients with ASDs are at risk of atrial arrhythmia and paradoxical embolism. As such there is a low threshold for prophylaxis with either aspirin alone or with heparin if other risk factors are present. Right-sided heart lesions
Effect of pregnancy on heart disease
In the presence of maternal heart disease, such a dramatic alteration in the cardiovascular system may ultimately lead to cardiac decompensation or death. Risk to the mother with heart disease appears to be determined primarily by the ability of their cardiovascular system to adapt to pregnancy. As such, different cardiac lesions carry specific mortality risks, dependent on current hemodynamic status, previous operations and anatomical features [13] . The cardiac conditions of highest risk are pulmonary vascular disease, Marfan syndrome with a dilated aortic root, left-sided obstructive lesions and a dilated poorly functioning left ventricle. Pregnancy also poses the risk of serious maternal morbidity. The only large prospective study of pregnancy outcomes in women with congenital heart disease to date identified 546 women with congenital heart disease with 599 pregnancies. This showed a combined maternal, fetal and neonatal mortality of 3% [6] . The rate of primary cardiac event, the most common of which was pulmonary edema, was 13%. In a multivariate analysis, the most significant predictor of morbidity and mortality was the presence of left ventricular dysfunction. Predictors of adverse maternal outcomes are listed in Box 2 . Other studies combining congenital and acquired heart disease have mainly arisen from the developing world, where rheumatic heart disease is the most predominant cardiac lesion encountered [14–22] . These retrospective studies demonstrate a high rate of cardiac complication ranging from 11.11 to 30% and a maternal mortality rate of 2–3.3%. Higher rates of both maternal morbidity and mortality were seen in women with poorer cardiac New York Heart Assiciation (NYHA) functional class at baseline [14–16] . www.expert-reviews.com
Right-sided heart lesions lead to abnormal loading of the right ventricle (Table 1) . During pregnancy, increased blood volume and heart rate put a considerable strain on the right side of the heart, leading to enlargement of the right ventricle [24] . Pulmonary stenosis
Isolated pulmonary stenosis is usually well tolerated during pregnancy [25] . However, the increased cardiac output of pregnancy can lead to increased right-ventricular pressure and, in severe pulmonary stenosis, this may lead to right-ventricle failure and/or atrial arrhythmia. Tetralogy of Fallot
Tetralogy of Fallot (TOF) is the most common form of cyanotic congenital heart disease. It is characterized by a nonrestrictive ventricular septal defect, aortic override, pulmonary stenosis and right-ventricular hypertrophy. In developed countries, TOF is usually corrected surgically in infancy, well before pregnancy Box 2. Predictors of adverse maternal outcomes. • Prior cardiac event (heart failure, transient ischemic attack or stroke) or arrhythmia • Baseline New York Heart Association class greater than II or cyanosis • Left heart obstruction (mitral valve area
