(rad or millirad [mrad])
(rem or millirem [mrem])
(rem or millirem [mrem])
Ionizing radiation exposure to the fetus can manifest its deleterious effects in three main ways:
1. Cell death and teratogenesis (deterministic effect)
2. Carcinogenesis (stochastic effect)
3. Genetic effects or mutations in germ cells, for which there are no long-term data.
Exposure to extremely high-dose radiation (1000–2000 mGy) in pregnant animals results in teratogenic effects in all. During the time of active organogenesis (up to 42 days), radiation exposure may cause severe structural abnormalities. The greatest risk of central nervous system effects occurs at 8–15 weeks of gestation. It can be stated confidently that the fetal risks of malformation, growth restriction, resorption, or miscarriage are not increased with radiation doses of <50 mGy, and most cardiac interventional procedures will produce a total exposure to the woman of much less than 50 mGy.[35–37]
Unlike the deterministic radiation effects for malformation or growth restriction, there is not, by definition, a radiation dose threshold level below which one can state there is no increased risk of carcinogenesis.[35,36] The risk of childhood cancers, principally leukemias, from in utero exposure is estimated to be about 0.06% per 10 mSv, which is an increase of 1.5- to 2-fold over the natural incidence.[35] However, the longer term adult risk of developing cancer is unknown and believed to be greater since solid cancers are more prevalent than induced leukemias and occur much later in life.[35,36] The risk of inducing hereditary effects has been estimated at one excess case per million for every 0.1 mGy absorbed dose to the gonads.[35,38] Although this relationship has been used to predict heritable abnormalities in the offspring of irradiated fetuses, it probably only applies to women in the active reproductive phase of life, and not to in utero life when the gonads are inactive.
The harmful doses referred to herein are those received by the fetus, and the relationship between the dose to the mother and the dose received by the fetus must be understood. The uterus receives only the radiation scattered from the irradiated area. This represents only a small fraction of the total target site dose delivered, typically <2%.[35] Generally speaking, interventional procedures above the diaphragm are unlikely to deliver dangerous doses to the fetus. During its most susceptible early developmental stage, the fetus is very small and far away from the diaphragm. A study of estimated fetal dose during typical cardiac electrophysiological ablation reported doses of 0.1–0.2 mGy in the first trimester, 0.3 mGy in the second trimester, and 0.55 mGy in the third trimester.[38] Based on current understanding, doses of this magnitude will not pose significant risks to the fetus or measurably increase the risk of childhood cancers. The excess lifetime risk of fatal cancer would not exceed 50 cases per million fetuses exposed to such a dose level.
Nevertheless, everything must still be done to minimize fetal exposure to ionizing radiation. The first step is to ensure that there is no medical alternative to the procedure being contemplated and that there is no imaging alternative to the X-rays.[35,36] Transesophageal echocardiography has been used in combination with fluoroscopy to reduce the amount of radiation exposure during PBMV and percutaneous balloon aortic valvuloplasty (PBAV) in pregnancy,[39] and this has been used as the exclusive imaging technique for some cases of PBMV.[40] Transesophageal echocardiography has also been used as the only imaging technique in pacemaker [41] and implantable cardioverter defibrillator insertions in pregnant women,[33] and to close an atrial septal communication during pregnancy.[42] Magnetic resonance imaging (MRI) has been used in pregnancy for the diagnosis of maternal and fetal lesions and is generally considered to be safe to the fetus.[43,44] Recent developments suggest that the use of MRI-guided cardiovascular interventions will increase.[45] Recently, catheter ablation of arrhythmia using remote magnetic navigation has been shown to be sufficiently safe and feasible in young adults and is an attractive alternative to conventional ablation techniques for pregnant women because it significantly lowers fluoroscopy exposure, especially when preprocedural three-dimensional (3D) imaging, e.g. noncontrast magnetic resonance imaging, is used to guide the procedure in complex congenital patients.[46]
Contrary to popular belief and practice, external shielding of the pelvis and abdomen of the mother during procedures involving the head or chest is of limited protective value to the fetus.[35,36,38] The radiation dose absorbed by the fetus without external shielding has been found to be only 3% higher at all stages of gestation.[38] Most fetal exposure is caused by internally scattered radiation from directly exposed structures.[36] Previously described principles of limiting radiation to all cardiac patients must also be applied in these cases: minimizing beam-on time, the use of pulsed fluoroscopy, optimal beam collimation, optimal positioning, and using the least magnification possible.[35,36] There are also other maneuvers that may help reduce fetal radiation dose. Since the dose to the small first-trimester fetus is strongly related to fetal position, imaging the mother with her bladder empty will result in the smallest absorbed fetal dose.[38] A transradial approach for coronary intervention during pregnancy has been described and hypothesized to reduce fetal radiation exposure.[47]
Animal studies have shown no evidence of teratogenic effects from iodinated radiocontrast agents, but there is a potential risk of fetal hypothyroidism for procedures performed when the fetal thyroid becomes active (after 25 weeks of gestation). However, these risks have been shown to be minimal.[36,48] Of course, consideration must still be given to the potential for adverse effects (renal dysfunction, anaphylaxis) in the mother.
Key points regarding radiation risk for cardiac interventional procedures during pregnancy
1. The mother should be counseled that there are radiation risks to the fetus but that a dose of <50 mGy has not been associated with any increase in fetal anomalies or pregnancy loss, and that the risk of abnormality at this dose level is negligible in comparison with the other risks of pregnancy, and certainly negligible in comparison with the risks of not undertaking the intervention. Most interventional cardiac procedures would produce a total exposure to the woman of significantly <50 mGy (usually 1–10 mGy), and a dose to the fetus of <1 mGy.[36,37] Such a dose would not be expected to materially increase the offspring’s risk of childhood cancers. It will be necessary to help the mother keep these risks in perspective and not let the fear of fetal anomalies divert from the appropriate planned management and its benefits.
2. It should be ensured that there are no other therapeutic maneuvers or imaging techniques that can be used instead of an X-ray-guided intervention.[36,37]
Valvar heart disease
Valvar heart disease, both acquired and congenital, is the most common indication for cardiac intervention during pregnancy. General issues in valvar heart disease in pregnancy are dealt with in Chapters 11 and 13, and in extensive recent reviews.[29,49–51] This discussion will focus on the indications for, and the management of, cardiac intervention for valvar lesions in pregnant women.
Mitral valve stenosis
The greatest number of cardiac interventions in pregnancy involve mitral stenosis. Most experience has been in developing countries with higher incidences of rheumatic heart disease.[3] Worldwide, mitral stenosis is the most common symptomatic valvar abnormality seen in pregnancy.[29] The pregnancy-associated rise in circulating volume and HR results in a corresponding increase in the pressure gradient across the narrowed mitral valve, which can result in heart failure and pulmonary edema. Additionally, the rise in atrial pressure may give rise to atrial arrhythmias, with increased HR and/or loss of atrial contraction further exacerbating the unfavorable hemodynamics and worsening the heart failure. Recent reports confirm the high incidence (65%) of arrhythmias and heart failure in pregnant women with severe mitral stenosis, as well as an increased risk of fetal mortality and morbidity.[3,51,52] Despite these high rates of maternal complications with severe mitral stenosis, no maternal deaths were reported in these series. However, fetal morbidity was related to the severity of the mitral stenosis, with a 33–44% rate of preterm delivery and a 33% incidence of fetal growth restriction.
Women with severe mitral stenosis who wish to become pregnant need to be counseled about the risks of the pregnancy to them and to the child, and should be offered therapeutic choices. PBMV prior to pregnancy has been successfully used to minimize pregnancy-associated clinical deterioration in such women and reduce the requirement for medication (with its attendant fetal risks) or cardiac intervention during the pregnancy.[29] If the presence of severe calcification or associated mitral regurgitation make the woman an unsuitable candidate for PBMV, then mitral valve replacement can be considered. Despite the maternal and fetal risks in pregnant women who have had mitral valve replacement prior to pregnancy,[49] the series by Bhatla et al. demonstrated that only 3% of those who had had valve replacement surgery deteriorated into New York Heart Association (NYHA) functional class III–IV compared with 26% of those who had had either valvotomy or no prior intervention.[3] Furthermore, there were fewer fetal growth-restricted and low-birthweight infants born to mothers with prosthetic valves. However, such an approach does raise the issue of whether tissue valves (needing a further replacement in 10–15 years) or metal valves (raising problems of anticoagulation in pregnancy) should be used (see Chapter 11).
The surgical approach to mitral stenosis in developed countries focuses on open mitral valvuloplasty and mitral valve replacement, both of which require the use of cardiopulmonary bypass with its attendant risks to the fetus (see above). De Souza et al. reported on 24 pregnant women who underwent open mitral valvuloplasty for refractory severe heart failure due to mitral stenosis.[53] There was only one maternal death but six fetal and two neonatal deaths. In another report of 73 women undergoing mitral valve replacement or open mitral valvuloplasty, there was 1 maternal death and 10 fetal deaths.[8]
Closed mitral valvotomy surgery has been performed for more than six decades and is often the preferred approach to severe mitral stenosis for patients in developing countries. Because there is no need for cardiopulmonary bypass, closed mitral valvotomy may have some advantages in pregnant women. Audits of closed mitral valvotomy in pregnancy in developing countries have reported no maternal mortality and fetal mortality rates of 0–12%.[28,54] However, there is a significant likelihood of re-stenosis and a need for repeat surgery. Furthermore, the closed procedure can be used only for isolated mitral stenosis, with no left atrial thrombus, no heavy calcification, and a reasonably well-preserved valvar/subvalvar apparatus. In developed countries, closed mitral valvotomy has been abandoned in favor of open mitral commissurotomy and mitral valve replacement because of better hemodynamic and long-term results with these procedures. Therefore, in these countries, cardiac surgeons are no longer being trained in the technique of closed mitral valvotomy and it cannot be considered a realistic option in that context.
PBMV has been practiced for more than 20 years with excellent results. In a series of 2773 nonpregnant patients, there was a technical failure rate of 1.2% and an in-hospital death rate of 0.4%. Good results (mitral valve area >1.5 cm2 and no regurgitation more than grade 2 out of 4) were obtained in 90% of patients, with only 4.7% having to undergo mitral surgery within the first month after the percutaneous procedure.[55] Increasingly, PBMV is being used in pregnancy for women in NYHA functional class III–IV refractory to medical therapy and the experience of its use in pregnancy has been equally positive. The technique using the Inoue balloon has been well described.[56] There has now been extensive experience of the use of PBMV to treat medically refractory symptomatic mitral stenosis in pregnancy.[4,31,53,57] Symptomatic, hemodynamic, and echocardiographic improvement is seen in the vast majority of treated women. The excellent results achieved are probably related to the underlying valvar pathology. The valves in these young mothers are unlikely to be heavily calcified or to have significant subvalvar thickening. Commissural fusion is the major pathology, and this makes them good candidates for PBMV. Maternal mortality has been very low (<0.3%), as has fetal/neonatal mortality (0–5%).[31,57]
Balloon inflation has been reported to cause a transient decrease in maternal blood pressure and fetal HR, with a return to baseline levels within a few seconds of balloon deflation.[57] The woman is recumbent for the procedure and pressure from the uterus may result in maternal hypotension and hinder the passage of catheters.[48] The rate of reported complications has been low but maternal complications do include cardiac tamponade, residual atrial septal defect, excessive blood loss, venous thrombosis, transient atrial fibrillation, deterioration in degree of mitral regurgitation, and systemic embolization. Furthermore, PBMV has precipitated uterine contractions and resulted in preterm labor.[29,58] Tocolytics have been used to suppress labor precipitated by the procedure but tocolytic agents may have significant cardiovascular effects and must be used with caution.[18]
The other concern remains the radiation risk. In some centers, therapeutic terminations of pregnancy have been offered to women who had PBMV before 18 weeks of gestation. However, early follow-up reports of children born after the procedure found no evidence of abnormal growth or development, although these studies included follow-up of <8 years.[31,59] Mishra et al. reviewed fluoroscopy exposure times from several series and reported that 95% of the procedures had <16 min of fluoroscopy time and that the average fluoroscopy time for their own group of 85 women was 3.6±3.2 min.[4] Such exposure times would not be expected to materially affect fetal risk. Even so, all measures should be taken to limit radiation risks to the fetus, including use of the Inoue balloon, which requires less procedural time,[29,60] and increased use of transesophageal echocardiography to reduce fluoroscopy time.[39,40,59] Because of the increased sensitivity to radiation effects in early pregnancy, PBMV should be avoided in the first trimester if possible. Fortunately, the hemodynamic changes of pregnancy are such that most women with mitral stenosis do not deteriorate clinically until the second or third trimester.
PBMV by the Inoue balloon technique is probably the ideal treatment for significant symptomatic mitral stenosis in pregnant women.[60] Although, to date, there have been no direct comparative studies of PBMV and mitral valve surgery in pregnancy (and such a future study is unlikely), cumulative descriptive reports have shown lower maternal and fetal/neonatal mortality rates and an acceptable rate of complications with the percutaneous approach.[4,31,53,57,59] However, there are the unknown risks of future problems from radiation exposure, and the risks of precipitating premature labor. Therefore, this procedure must be limited to those symptomatic women for whom medical therapy has not been successful. PBMV is no substitute for expert management during pregnancy, labor, and delivery. The procedure cannot be performed in women with more than moderate mitral regurgitation, left atrial thrombus, marked calcification, or absence of commissural fusion. If such women with severe mitral stenosis cannot be controlled medically,[51] they will need careful assessment for mitral valve surgery, keeping in mind the higher fetal loss associated with the cardiopulmonary bypass necessary for such surgery.
Aortic valve stenosis
Severe aortic valve stenosis was traditionally considered a contraindication to pregnancy, with increased maternal mortality and morbidity, as well as concerns about clinical deterioration, leading to preterm delivery and fetal morbidity.[29,52] However, recent reports suggest a more optimistic outcome for this group of women. Of 70 pregnancies with aortic stenosis reviewed by Tzemos et al. 71% had moderate or severe aortic stenosis.[50] There were no cardiac complications in the women with mild aortic stenosis. There were seven pregnancies (four with severe aortic stenosis and three with moderate aortic stenosis) that were complicated by pulmonary edema (two pregnancies), supraventricular tachycardia (one pregnancy), and worsening of NYHA functional class by >2 (four pregnancies). Of the four patients with severe aortic stenosis, two had refractory symptoms and required balloon valvuloplasty. No patient required cardiac surgery. There were no maternal deaths and all 70 pregnancies resulted in live births.
This more recent experience exemplifies the current management of severe aortic stenosis in pregnant women.[50] Most reports consider severe aortic stenosis to be present if the aortic valve area is <1 cm2 with a peak systolic velocity of 4 m/s or higher.[50] Attempts should be made to identify preconception those women with severe aortic stenosis and consider valve surgery or balloon valvotomy before pregnancy. The choice of valve replacement becomes important because of the increased risks in pregnancy for women with prosthetic valves (Chapter 11). For women with aortic stenosis, an attractive alternative to bioprosthetic or mechanical valves may be the pulmonary autograft (Ross procedure).[61] For women with severe aortic stenosis who present already pregnant, discussion needs to focus on the risks of the pregnancy for mother and child, and include termination, continuing medical management, and the need for intervention, either surgical or balloon valvuloplasty.[29] These women should also be advised that even if they deliver successfully without cardiac intervention, there is a significant likelihood of a need for such intervention postpartum.[50]
Women who develop symptoms may respond to medical therapy that includes bed rest, diuretics, and close monitoring, generally in a hospital environment.[29] Failure to respond to medical management requires decisions about termination, early delivery, or cardiac intervention. Cardiac intervention must be limited to women with clinical deterioration. A high gradient across the aortic valve during pregnancy is not a sufficient reason for intervention.[39] Aortic valve surgery has been successfully carried out in pregnancy for decades but the number of reported cases has been small. Because of the small numbers, most case series on cardiac surgery in pregnancy have not separately reported the mortality or morbidity results for only the women undergoing aortic surgery.[2,9,16] Two separate reviews from 1994 and 1996 reported no maternal mortality but fetal losses of 30–38% in two small groups of 18 and 15 women.[5,23] There have been no recent large series of aortic valve replacement in pregnancy, but in 2003 Jahangiri et al. did report replacement of the aortic valve in four women: one with congenital aortic stenosis, two with aortic regurgitation, and one with mitral and aortic stenosis.[22] All four women did very well during surgery and three women delivered a normal baby at 38 weeks by cesarean section. The fetus in the fourth case showed evidence of hydrops a week after surgery and the pregnancy was terminated 2 weeks after surgery. Although there have been no large series of pregnant women undergoing aortic valve surgery, it is clear that fetal mortality remains a major concern. It is for this reason that balloon aortic valvotomy has been performed in pregnant women with aortic stenosis refractory to medical therapy. There have been only a few cases of PBAV in pregnancy reported in the literature.[39,50,62] In all reported cases, there has been a reduction in valvar gradient and an improvement in the clinical situation, without fetal loss.
Unlike PBMV, PBAV in nonpregnant adults has been considered a palliative procedure because the improvement in hemodynamics has been transient and there has been no demonstrated improvement in long-term survival. Its use has therefore been relegated to the elderly with severe aortic stenosis who are not considered candidates for aortic valve replacement, and it has been used as a “bridge to surgery” for those in cardiogenic shock or for those who require urgent noncardiac surgery. It cannot be considered an alternative to aortic valve replacement in the adult. Complications of PBAV have included embolic phenomena, marked aortic regurgitation, hemopericardium, and aortic rupture but none of these has yet been reported with PBAV during pregnancy.[48,62] It should not be performed in the setting of already significant aortic regurgitation or a heavily calcified valve. It carries the risk of radiation exposure to mother and fetus but the increasing use of transesophageal echocardiography during PBAV does reduce fluoroscopy times.[39]
There have been no reported series of PBAV in pregnancy and certainly no comparative studies with aortic valve surgery. Given the rarity of the need for intervention, such future series are unlikely. PBAV must be considered palliative; the woman must understand that she will require definitive aortic valve surgery in the future and that the sole purpose of the PBAV is to allow her pregnancy to continue. There is no role for transcatheter aortic valve replacement in the pregnant patient with aortic stenosis.
Pulmonary valve stenosis
Pulmonary stenosis during pregnancy is most probably due to congenital obstruction at the valvar, subvalvar, or supravalvar level but has also been described in the setting of stenosis in a homograft that had been part of a previous Ross procedure.[29,63] Unlike with mitral stenosis or aortic stenosis, even severe pulmonary stenosis does not appear to have an adverse effect on maternal or fetal morbidity and mortality.[48,64] Balloon valvuloplasty for pulmonary stenosis has been performed in nonpregnant patients but only a handful of cases of balloon valvuloplasty during pregnancy have been reported.[48] These resulted in significant improvements and no complications, but experience is limited and the procedure should be considered only for rare women with severe symptomatic valvar pulmonary valve stenosis that is refractory to medical management.
Mitral or aortic regurgitation
Mitral regurgitation during pregnancy may be due to mitral valve prolapse or rheumatic mitral disease. It may also occur as a consequence of valvuloplasty for mitral stenosis. Aortic regurgitation is likely to be due to a bicuspid aortic valve, rheumatic disease, or an enlarged aortic annulus.[29] Because of the physiological decrease in systemic vascular resistance, both of these lesions are generally well tolerated during pregnancy. For those pregnant women with symptoms and left ventricular dysfunction, there is well-established, effective medical management with diuretics, digoxin, and vasodilator therapy. Although angiotensin-converting enzyme (ACE) inhibitors are contraindicated during pregnancy, nitrates and hydralazine are effective substitutes when vasodilatation is the required effect.[29] Because women with valvar regurgitation generally do well during pregnancy (see Chapter 13), and because prosthetic valves carry particular risks during pregnancy, there is no recommendation for prepregnancy prophylactic replacement of mitral or aortic valves in women with severe regurgitation but no other established indications for surgery. Intervention during pregnancy should be undertaken only for severely symptomatic women who are refractory to optimal medical therapy. When surgery is needed, it is usually because of sudden deterioration, such as in endocarditis or dissection. Some adaptations to cardiopulmonary bypass techniques may help lower the risk of fetal death,[21] but at this time there is no percutaneous alternative to open heart surgical cardiopulmonary bypass repair for mitral regurgitation or aortic regurgitation. Preliminary work on percutaneous aortic valve replacement and mitral valve repair is at much too early a stage to predict its future role in interventions during pregnancy.
Prosthetic valves
The challenges of management of a pregnant woman with a prosthetic valve are discussed in Chapter 11. Interventions in pregnant women with a prosthetic valve may be considered in the setting of valve thrombosis, endocarditis, or degeneration of a bioprosthetic valve or homograft. Thromboembolism is common owing to pregnancy-related thrombophilia, as well as problems with inadequate anticoagulation during pregnancy.[65] Prosthetic valve thrombosis poses special problems in pregnancy because of the relative contraindications to thrombolysis in pregnancy,[47,49] the high operative risks of surgical thrombectomy, and the high fetal loss in any cardiac surgery with cardiopulmonary bypass. Salazar et al. reported five patients with prosthetic valve thrombus who underwent surgery: thrombectomy in one patient and valve replacement in the other four. The maternal mortality rate was 20% and there was only one live baby, delivered preterm at 31 weeks.[66] Despite its relative contraindications, thrombolysis has been successfully used for the treatment of prosthetic valve thrombus in pregnancy.[67] In a 2013 series of 25 pregnancies complicated by valve thrombosis, low-dose slow infusion of tissue-type plasminogen activator resulted in complete thrombus lysis in all patients. There was one episode of placental hemorrhage with a preterm live birth at week 30 and one minor bleed. There were five spontaneous miscarriages, all in patients who had been treated in the first trimester. The thrombolytic sessions were carried out under transesophageal echocardiographic guidance. Thrombolytic therapy should be considered first for valve thrombosis, reserving high-risk surgery for women at a particularly high risk of bleeding or when thrombolysis has failed.[69] If surgery becomes necessary, it should be noted that successful reported surgical procedures have used simple thrombectomy, valve replacement with conventional cardiopulmonary bypass, or a beating-heart technique for valve replacement.[21]
Endocarditis
Antibiotic prophylaxis has not generally been recommended for uncomplicated labor and delivery. However, recent reports have indicated a significant incidence of bacteremia during normal labor and delivery,[29] as well as high rates of maternal (22.1%) and fetal (14.7%) mortality associated with endocarditis during pregnancy.[68] Antibiotic prophylaxis is thus now more frequently recommended even for uncomplicated labor in particularly high-risk women with valvar heart disease, prosthetic valves, or congenital lesions that predispose them to endocarditis.[29,69] Successful operative procedures have been reported for endocarditis complications during pregnancy but, in the light of the high morbidity and mortality rates for mother and fetus, it has been recommended that early delivery of the fetus should be considered, if at all possible, to allow intensive medical and surgical therapy of the infection.[68,70]
Dissection of the aorta
Acute dissection of the aorta is a life-threatening situation. Left untreated, it has a 50% mortality rate in the first 48 h.[71] Aortic dissection in women aged under 40 years is rare; however, about half of the dissections in women in this age range occur during pregnancy and it is important to consider this rare but life-threatening diagnosis in any pregnant woman presenting with chest or interscapular discomfort.[72] A review of pregnant women with aortic dissection reported in the literature between 1983 and 2002 identified 45 women with Stanford type A dissection (involving the ascending aorta) and 12 with Stanford type B (not involving the ascending aorta).[73] Maternal mortality for type A dissections was 15% and for type B was 0%. Fetal mortality was 32% for type A and 43% for type B. The high fetal mortality rate in type B dissection occurred despite the fact that these women usually did not undergo immediate surgery, and probably occurred because the dissection extended down into the iliac vessels and caused decreased placental flow. Of the 45 women with type A dissection, 20 had either Marfan or Ehlers–Danlos syndrome, 9 had hypertension, and 4 had a bicuspid aortic valve. The average size of the aortic root at time of presentation was 4.8±0.9 cm.
Changes in the structure of arteries and veins have been described in pregnancy, and estrogen receptors have been found in human aortic tissue. Hormonal changes during pregnancy lead to gradual dilatation of the aorta and of the renal and placental vessels in an effort to improve perfusion during pregnancy.[73] These changes occur with every pregnancy but dissection occurs only rarely and under special circumstances. The aortas of Marfan and Ehlers–Danlos syndrome patients already have connective tissue defects. In addition, abnormal elastic properties have been described in the aortas of patients with bicuspid aortic valve and those with repaired tetralogy of Fallot.[74] Coarctation of the aorta has also been associated with an intrinsic aortopathy, thus placing these individuals at risk of dissection. In a series of 50 pregnant women with coarctation, there was 1 episode of Stanford type A dissection that resulted in death.[75]
Every effort should be made to identify women with Marfan or Ehlers–Danlos syndrome, bicuspid aortic valve, coarctation, and hypertension before pregnancy and to assess the aortic root size. Asymptomatic women with a dilated aorta should be considered for elective aortic root replacement before pregnancy because this can now be done with relatively low mortality and morbidity risks.[73] Unfortunately, prophylactic aortic root replacement does not guarantee freedom from dissection at another portion of the aorta during pregnancy.[76] In pregnant women, close clinical and echocardiographic surveillance is warranted and beta-blockers should be considered if the aortic root is larger than 4 cm or is enlarging during the pregnancy (keeping in mind that a small amount of physiological enlargement of the aorta can often be observed during pregnancy [73,77]). Hypertension and preeclampsia should be controlled as well as possible. High-risk women can be admitted to hospital at between 28 and 32 weeks of gestation with plans for aortic root surgery shortly after delivery. Such an admission should be to a facility with a surgical, obstetric, and neonatal team experienced in cardiac surgery during pregnancy. It has been recommended that if dissection occurs before 30 weeks, then emergency surgery should be undertaken with the fetus in utero.[71,73,76] After 30 weeks, immediate cesarean section followed by the aortic surgery is preferred, keeping in mind the increased risk of bleeding from the delivery site. (Dealing with a postpartum hemorrhage at the same time as cardiac surgery puts the woman at a particularly high risk; a delay of 24 h between the two procedures may be advisable if considered safe from the cardiac point of view.) There have been no serious complications reported from the use of this type of approach.[73,78] Of course, there will be crisis situations in which it will not be possible to undertake delivery prior to aortic surgery and the fetus will be exposed to all the previously discussed risks of cardiopulmonary bypass.
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