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Acquired Heart Disease in Pregnancy
OBSTETRICS OBSTETRICS
HEART DISEASE IN PREGNANCY 3
Acquired Heart Disease in Pregnancy Gregory A.L. Davies, MD, FRCSC, FACOG,1 William N.P. Herbert, MD, FACOG2 1
Professor and Chair, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynaecology, Queen’s University, Kingston ON
2
William Norman Thornton Professor and Chair, Department of Obstetrics and Gynecology University of Virginia, Charlottesville VA USA
Abstract The incidence of rheumatic heart disease in most industrialized countries is decreasing. Those women who have regurgitant lesions will commonly experience an improvement in symptoms, and therapy is required only in the most severe cases. Women with mild to moderate stenotic lesions can usually expect a good outcome to pregnancy, but women with severe stenotic lesions require close monitoring by both their obstetricians and their cardiologists, especially during the third trimester, labour and delivery, and the early postpartum period. This is the third in a series of five articles reviewing in detail the assessment and management of specific cardiac disorders in pregnancy.
Résumé L’incidence de la cardiopathie rhumatismale est en baisse dans la plupart des pays industrialisés. Les femmes qui présentent des lésions à reflux connaîtront généralement une amélioration des symptômes; le traitement n’est requis que dans les cas les plus graves. Les femmes qui présentent des lésions sténosées allant de légères à modérées peuvent habituellement s’attendre à de bonnes issues de grossesse; toutefois, les femmes qui présentent de graves lésions sténosées nécessitent un suivi étroit de la part de leurs obstétriciens et de leurs cardiologues, particulièrement pendant le troisième trimestre, le travail et l’accouchement, et les débuts de la période post-partum. Il s’agit du troisième article d’une série de cinq analysant en détail l’évaluation et la prise en charge de troubles cardiaques particuliers au cours de la grossesse. J Obstet Gynaecol Can 2007;29(6):507–509
Key Words: Cardiac disease, pregnancy, rheumatic heart disease, mitral stenosis, aortic stenosis Competing Interests: None declared. Received on December 6, 2006 Accepted on March 28, 2007
RHEUMATIC HEART DISEASE
onsistent with a reduced incidence of rheumatic fever, the incidence of rheumatic heart disease has declined over the last 40 years.1 The prevalence of rheumatic heart disease in pregnancy has decreased in developed countries such that the previous ratio of rheumatic to congenital heart disease of 3–4:1 has essentially been reversed.2,3 However, a resurgence of rheumatic fever has been reported in some areas of the United States.4
C
In patients with rheumatic heart disease, the mitral valve is most commonly affected. Mitral stenosis occurs in approximately 90% of patients and mitral regurgitation in 7%. The aortic valve is the second most commonly affected valve, although to a lesser degree; aortic regurgitation is present in 2.5% of patients and aortic stenosis in only 1%.5 Although the tricuspid and pulmonic valves may also be affected, such involvement is almost always combined with mitral or aortic disease.6,7 MITRAL STENOSIS
Many patients with mild mitral stenosis are asymptomatic until they become pregnant.8 At that time the prenatal physiologic changes contribute to an increase in left atrial pressure and subsequent symptoms of dyspnea and eventually tachypnea, orthopnea, and paroxysmal nocturnal dyspnea.1,9 Management of mitral stenosis in pregnancy depends on the level of symptoms. Patients who are asymptomatic may continue, within reason, their normal activities of living. Patients who develop dyspnea with exercise must restrict their activities and, depending on the severity, may require continuous bed rest. Other treatments include sodium restriction to less than 2 g/day1,7,10 or oral b-adrenergic blockers to decrease maternal tachycardia, thereby creating a longer diastolic filling time.10,11 For JUNE JOGC JUIN 2007 l
507
OBSTETRICS
patients who develop atrial fibrillation, digoxin therapy has been recommended.7,9 Digoxin is also recommended by some11 as prophylaxis for atrial fibrillation in mitral stenosis during pregnancy. Diuretic therapy, usually with furosemide, is recommended by some, but others caution against use in patients with severe mitral stenosis without the concurrent use of invasive hemodynamic monitoring, because sudden death has been reported.11,12 For patients with marked symptoms before pregnancy, relief of the stenosis should be considered.10 Patients with severe symptoms during pregnancy that cannot be controlled by medical therapy have been successfully treated by balloon valvuloplasty13–16 or open or closed mitral valvotomy.7,10,13,17,18 Intrapartum care of patients with severe mitral stenosis should include invasive hemodynamic monitoring. Pulmonary capillary wedge pressures may be misleading in patients with mitral stenosis. Clark recommends that severe mitral stenosis be managed with high-normal or elevated pulmonary capillary wedge pressures to maintain adequate ventricular filling pressure and cardiac output.11 Epidural anaesthesia should be used to reduce stress-induced tachycardia.11,14 Delivery by Caesarean section should be reserved for obstetrical indications.11,14 Close monitoring for the first 48 hours after delivery is advised, as this remains a time of high risk for pulmonary edema secondary to the normal postpartum increase in cardiac output.10 Silversides et al. described a series of 74 women with mitral stenosis who experienced 80 pregnancies. Eighty-nine percent of the women were classified as New York Heart Association (NYHA) functional class I, and the remainder were class II at the beginning of pregnancy. Fifty-three percent had mild mitral stenosis, 36% had moderate, and 11% had severe mitral stenosis. Forty percent of pregnancies were associated with a worsening of the women’s NYHA functional classification by two or more classes. Thirty-five percent of these women experienced pulmonary edema, arrhythmias (mild 26%, moderate 38%, severe 67%), or both. The mean gestational age when pulmonary edema developed was 30 weeks. In women who developed arrhythmias, atrial fibrillation was the most common (70%), followed by supraventricular tachycardia (30%). An adverse fetal or neonatal outcome occurred in 30% of pregnancies; the most common was preterm birth. Seventy-four percent of deliveries were vaginal. Only one of the 21 Caesarean sections was performed for cardiac indications. By the time of discharge following delivery, 68% of women were receiving digoxin, b-adrenergic blockers, or diuretics. There were no maternal deaths, and none of the symptomatic women failed to respond to medical therapy.8 508
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The maternal mortality associated with mitral stenosis is stratified by NYHA classification: class I, 0.1%; class II, 0.3%; class III, 5.5%; and class IV, 6.0%.1 Most patients are in class I or II at presentation, but 12% to 25% of patients are in class III or IV.19 MITRAL REGURGITATION
Mitral regurgitation occurs in 7% of patients with rheumatic heart disease.5 Many patients have associated mitral stenosis and should be treated and counselled as described above. Although rheumatic heart disease is not the most common cause of mitral regurgitation in pregnancy,14 it represents the most clinically significant lesions.11 Pregnancy is generally well tolerated by patients with mitral regurgitation, and it has been theorized that mitral regurgitation may actually improve in pregnancy because of the physiologic reduction in systemic vascular resistance.9 Previously asymptomatic women may worsen immediately after delivery because of sudden increases in systemic vascular resistance.20 It has also been suggested that these patients are at increased risk of left atrial enlargement and subsequent atrial fibrillation.11 For this reason, prophylactic digoxin has been suggested for patients with severe regurgitation.11 Lesniak-Sobelga et al.21 described the pregnancies of 44 women with isolated mitral regurgitation. Six women had severe regurgitation and the remainder had moderate regurgitation. All six women with severe regurgitation and one with moderate regurgitation experienced cardiac complications. Three required diuresis for pulmonary edema, and four required antiarrhythmic therapy for supraventricular tachycardia. Eighty-nine percent of women delivered vaginally. One baby was born prematurely, and three others had intrauterine growth restriction.21 AORTIC STENOSIS
Aortic stenosis in pregnancy is described in detail in the article on congenital heart disease.22 Most patients with aortic stenosis of rheumatic origin also have associated mitral stenosis.10 Some authors have found that a higher maternal mortality is associated with aortic stenosis of rheumatic origin than with aortic stenosis of congenital origin.11 The rate of maternal mortality associated with severe aortic stenosis in pregnancy is most commonly cited as 17%, with a fetal mortality of 32%.23 This series also identified a maternal mortality of 40% associated with termination of pregnancy.23 This widely quoted statistic was derived from a description of two maternal deaths in five patients undergoing termination of pregnancy and may not represent the total population with aortic stenosis. Decisions regarding anaesthesia and mode of delivery for patients with aortic stenosis must be individualized on the basis of severity of symptoms and urgency of delivery.
Acquired Heart Disease in Pregnancy
AORTIC REGURGITATION
As with aortic stenosis, most patients with aortic regurgitation of rheumatic origin have associated mitral valve disease.11 Their clinical course, therefore, is probably determined more by the extent of their mitral valve disease than by their aortic regurgitation. When aortic regurgitation is the predominant lesion, pregnancy is usually well tolerated.9 It has been suggested that aortic regurgitation may actually improve in pregnancy because of the decrease in systemic vascular resistance.9 Also, the physiologic tachycardia of pregnancy may reduce regurgitant flow as diastolic filling times are shortened.1,11 It has also been recognized that the murmurs normally associated with both aortic and mitral regurgitation may be reduced in pregnancy.24 For patients with severe aortic regurgitation and symptoms of left-sided heart failure, the mainstay of therapy is decreasing cardiac work. Patients should limit their activity, and bed rest may be necessary. Sodium restriction may also be helpful.10 Diuresis and inotropic therapy with digitalis have been suggested in difficult cases.14 Despite aggressive medical therapy, some patients will require aortic valve replacement in pregnancy.25,26 Case reports suggest that pulsatile perfusion at bypass may help preserve placental hemodynamic function.27–29 REFERENCES 1. Brady K, Duff P. Rheumatic heart disease in pregnancy. Clin Obstet Gynecol 1989;32:21–40. 2. Pitkin RM, Perloff JK, Koos BJ, Beall MH. Pregnancy and congenital heart disease. Ann Intern Med 1990;112:445–54. 3. McFaul PB, Dornan JC, Lamki H, Boyle D. Pregnancy complicated by maternal heart disease. A review of 519 women. Br J Obstet Gynaecol 1988;95:861–7. 4. Veasy LG, Wiedmeier SE, Orsmond GS, Ruttenberg HD, Boucek MM, Roth SJ, et al. Resurgence of acute rheumatic fever in the intermountain area of the United States. N Engl J Med 1987;316:421–7. 5. Szekely P, Turner R, Snaith L. Pregnancy and the changing pattern of rheumatic heart disease. Br Heart J 1973;35:1293–303. 6. Robbins SL, Cotran RS, Kumar V. Robbin’s pathologic basis of disease. 4th ed. Philadelphia: WB Saunders, 1989:597. 7. Hess DB, Hess LW. Management of cardiovascular disease in pregnancy. Obstet Gynecol Clin North Am 1992;19:679–95. 8. Silversides CK., Colman JM, Sermer M, Farine D, Siu SC. Early and intermediate-term outcomes of pregnancy with congenital aortic stenosis. Am J Cardiol 2003;91:1386–9. 9. Burlew BS. Managing the pregnant patient with heart disease. Clin Cardiol 1990;13:757–62. 10. Lang RM, Borow KM. Pregnancy and heart disease. Clin Perinatol 1985;12: 551–69.
11. Clark SL. Cardiac disease in pregnancy. Obstet Gynecol Clin North Am 1991; 18:237–56. 12. Christianson R, Page EW. Diuretic drugs and pregnancy. Obstet Gynecol 1976; 48:647–52. 13. Oakley CM. Cardiovascular disease in pregnancy. Can J Cardiol 1990;6:3B–9B. 14. Gianopoulos JG. Cardiac disease in pregnancy. Med Clin North Am 1989;73: 639–50. 15. Esteves CA, Ramos AIO, Braga SL, Harrison JK, Sousa JE. Effectiveness of percutaneous balloon mitral valvotomy during pregnancy. Am J Cardiol 1991;68:930–4. 16. Chow W, Chow T, Wat M, Cheung KL. Percutaneous balloon mitral valvotomy in pregnancy using the Inoue balloon catheter. Cardiology 1992;81:182–5. 17. Abid A, Abid F, Zargouni N, Khayati A. Closed mitral valvotomy in pregnancy—a study of seven cases. Int J Cardiol 1990;26:319–21. 18. Wu J, Chern M, Yeh K, Chen YC, Fu M, Hung JS. Urgent/emergent percutaneous transvenous mitral commissurotomy. Cathet Cardiovasc Diagn 1994;31:18–22. 19. Veray FX, Hernandez–Cibes JJ, Pelegrina I. Heart disease in pregnancy. Obstet Gynecol 1968;32:424–31. 20. Khanlou H. Khanlou N. Eiger G. Relationship between mitral valve regurgitant flow and peripartum change in systemic vascular resistance. South Med J 2003;96:308–9. 21. Lesniak-Sobelga A, Tracz W, KostKiewicz M, Podolec P, Pasowicz M. Clinical and echocardiographic assessment of pregnant women with valvular heart diseases-maternal and fetal outcome. Int J Cardiol 2004;94:15–23. 22. Davies GAL, Herbert WNP. Congenital heart disease in pregnancy. J Obstet Gynaecol Can 2007;29(5):409–414. 23. Arias F, Pineda J. Aortic stenosis and pregnancy. J Reprod Med 1978;20: 229–32. 24. Marcus FI, Ewy GA, O’Rourke RA, Walsh B, Bleich AC. The effect of pregnancy on the murmurs of mitral and aortic regurgitation. Circulation 1970;41:795–805. 25. Tehrani H, Masroor S, Lombardi P, Rosenkranz E, Salerno T. Beating heart aortic valve replacement in a pregnant patient. J Cardiac Surg 2004;19:57–8. 26. Martin TC, Idahosa V, Ogunbiyi A, Fevrier-Roberts G, Winter A. Successful pregnancy and delivery after pulmonary autograft operation (Ross procedure) for rheumatic aortic valve insufficiency. West Ind Med J 2003;52:62–4. 27. Tripp HF, Stiegel RM, Coyle JP. The use of pulsatile perfusion during aortic valve replacement in pregnancy. Ann Thoracic Surg 1999;67:1169–71. 28. Golden LP. Aortic valve repair and arch replacement during pregnancy: a case report. AANA J 1996;64:243–54. 29. Khan N, Pumphrey C, Clarke J, Jahangiri M. Aortic root replacement in pregnancy. J Royal Soc Med 2003;96:551–2.
JUNE JOGC JUIN 2007 l
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HEART DISEASE IN PREGNANCY 3
Acquired Heart Disease in Pregnancy Gregory A.L. Davies, MD, FRCSC, FACOG,1 William N.P. Herbert, MD, FACOG2 1
Professor and Chair, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynaecology, Queen’s University, Kingston ON
2
William Norman Thornton Professor and Chair, Department of Obstetrics and Gynecology University of Virginia, Charlottesville VA USA
Abstract The incidence of rheumatic heart disease in most industrialized countries is decreasing. Those women who have regurgitant lesions will commonly experience an improvement in symptoms, and therapy is required only in the most severe cases. Women with mild to moderate stenotic lesions can usually expect a good outcome to pregnancy, but women with severe stenotic lesions require close monitoring by both their obstetricians and their cardiologists, especially during the third trimester, labour and delivery, and the early postpartum period. This is the third in a series of five articles reviewing in detail the assessment and management of specific cardiac disorders in pregnancy.
Résumé L’incidence de la cardiopathie rhumatismale est en baisse dans la plupart des pays industrialisés. Les femmes qui présentent des lésions à reflux connaîtront généralement une amélioration des symptômes; le traitement n’est requis que dans les cas les plus graves. Les femmes qui présentent des lésions sténosées allant de légères à modérées peuvent habituellement s’attendre à de bonnes issues de grossesse; toutefois, les femmes qui présentent de graves lésions sténosées nécessitent un suivi étroit de la part de leurs obstétriciens et de leurs cardiologues, particulièrement pendant le troisième trimestre, le travail et l’accouchement, et les débuts de la période post-partum. Il s’agit du troisième article d’une série de cinq analysant en détail l’évaluation et la prise en charge de troubles cardiaques particuliers au cours de la grossesse. J Obstet Gynaecol Can 2007;29(6):507–509
Key Words: Cardiac disease, pregnancy, rheumatic heart disease, mitral stenosis, aortic stenosis Competing Interests: None declared. Received on December 6, 2006 Accepted on March 28, 2007
RHEUMATIC HEART DISEASE
onsistent with a reduced incidence of rheumatic fever, the incidence of rheumatic heart disease has declined over the last 40 years.1 The prevalence of rheumatic heart disease in pregnancy has decreased in developed countries such that the previous ratio of rheumatic to congenital heart disease of 3–4:1 has essentially been reversed.2,3 However, a resurgence of rheumatic fever has been reported in some areas of the United States.4
C
In patients with rheumatic heart disease, the mitral valve is most commonly affected. Mitral stenosis occurs in approximately 90% of patients and mitral regurgitation in 7%. The aortic valve is the second most commonly affected valve, although to a lesser degree; aortic regurgitation is present in 2.5% of patients and aortic stenosis in only 1%.5 Although the tricuspid and pulmonic valves may also be affected, such involvement is almost always combined with mitral or aortic disease.6,7 MITRAL STENOSIS
Many patients with mild mitral stenosis are asymptomatic until they become pregnant.8 At that time the prenatal physiologic changes contribute to an increase in left atrial pressure and subsequent symptoms of dyspnea and eventually tachypnea, orthopnea, and paroxysmal nocturnal dyspnea.1,9 Management of mitral stenosis in pregnancy depends on the level of symptoms. Patients who are asymptomatic may continue, within reason, their normal activities of living. Patients who develop dyspnea with exercise must restrict their activities and, depending on the severity, may require continuous bed rest. Other treatments include sodium restriction to less than 2 g/day1,7,10 or oral b-adrenergic blockers to decrease maternal tachycardia, thereby creating a longer diastolic filling time.10,11 For JUNE JOGC JUIN 2007 l
507
OBSTETRICS
patients who develop atrial fibrillation, digoxin therapy has been recommended.7,9 Digoxin is also recommended by some11 as prophylaxis for atrial fibrillation in mitral stenosis during pregnancy. Diuretic therapy, usually with furosemide, is recommended by some, but others caution against use in patients with severe mitral stenosis without the concurrent use of invasive hemodynamic monitoring, because sudden death has been reported.11,12 For patients with marked symptoms before pregnancy, relief of the stenosis should be considered.10 Patients with severe symptoms during pregnancy that cannot be controlled by medical therapy have been successfully treated by balloon valvuloplasty13–16 or open or closed mitral valvotomy.7,10,13,17,18 Intrapartum care of patients with severe mitral stenosis should include invasive hemodynamic monitoring. Pulmonary capillary wedge pressures may be misleading in patients with mitral stenosis. Clark recommends that severe mitral stenosis be managed with high-normal or elevated pulmonary capillary wedge pressures to maintain adequate ventricular filling pressure and cardiac output.11 Epidural anaesthesia should be used to reduce stress-induced tachycardia.11,14 Delivery by Caesarean section should be reserved for obstetrical indications.11,14 Close monitoring for the first 48 hours after delivery is advised, as this remains a time of high risk for pulmonary edema secondary to the normal postpartum increase in cardiac output.10 Silversides et al. described a series of 74 women with mitral stenosis who experienced 80 pregnancies. Eighty-nine percent of the women were classified as New York Heart Association (NYHA) functional class I, and the remainder were class II at the beginning of pregnancy. Fifty-three percent had mild mitral stenosis, 36% had moderate, and 11% had severe mitral stenosis. Forty percent of pregnancies were associated with a worsening of the women’s NYHA functional classification by two or more classes. Thirty-five percent of these women experienced pulmonary edema, arrhythmias (mild 26%, moderate 38%, severe 67%), or both. The mean gestational age when pulmonary edema developed was 30 weeks. In women who developed arrhythmias, atrial fibrillation was the most common (70%), followed by supraventricular tachycardia (30%). An adverse fetal or neonatal outcome occurred in 30% of pregnancies; the most common was preterm birth. Seventy-four percent of deliveries were vaginal. Only one of the 21 Caesarean sections was performed for cardiac indications. By the time of discharge following delivery, 68% of women were receiving digoxin, b-adrenergic blockers, or diuretics. There were no maternal deaths, and none of the symptomatic women failed to respond to medical therapy.8 508
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The maternal mortality associated with mitral stenosis is stratified by NYHA classification: class I, 0.1%; class II, 0.3%; class III, 5.5%; and class IV, 6.0%.1 Most patients are in class I or II at presentation, but 12% to 25% of patients are in class III or IV.19 MITRAL REGURGITATION
Mitral regurgitation occurs in 7% of patients with rheumatic heart disease.5 Many patients have associated mitral stenosis and should be treated and counselled as described above. Although rheumatic heart disease is not the most common cause of mitral regurgitation in pregnancy,14 it represents the most clinically significant lesions.11 Pregnancy is generally well tolerated by patients with mitral regurgitation, and it has been theorized that mitral regurgitation may actually improve in pregnancy because of the physiologic reduction in systemic vascular resistance.9 Previously asymptomatic women may worsen immediately after delivery because of sudden increases in systemic vascular resistance.20 It has also been suggested that these patients are at increased risk of left atrial enlargement and subsequent atrial fibrillation.11 For this reason, prophylactic digoxin has been suggested for patients with severe regurgitation.11 Lesniak-Sobelga et al.21 described the pregnancies of 44 women with isolated mitral regurgitation. Six women had severe regurgitation and the remainder had moderate regurgitation. All six women with severe regurgitation and one with moderate regurgitation experienced cardiac complications. Three required diuresis for pulmonary edema, and four required antiarrhythmic therapy for supraventricular tachycardia. Eighty-nine percent of women delivered vaginally. One baby was born prematurely, and three others had intrauterine growth restriction.21 AORTIC STENOSIS
Aortic stenosis in pregnancy is described in detail in the article on congenital heart disease.22 Most patients with aortic stenosis of rheumatic origin also have associated mitral stenosis.10 Some authors have found that a higher maternal mortality is associated with aortic stenosis of rheumatic origin than with aortic stenosis of congenital origin.11 The rate of maternal mortality associated with severe aortic stenosis in pregnancy is most commonly cited as 17%, with a fetal mortality of 32%.23 This series also identified a maternal mortality of 40% associated with termination of pregnancy.23 This widely quoted statistic was derived from a description of two maternal deaths in five patients undergoing termination of pregnancy and may not represent the total population with aortic stenosis. Decisions regarding anaesthesia and mode of delivery for patients with aortic stenosis must be individualized on the basis of severity of symptoms and urgency of delivery.
Acquired Heart Disease in Pregnancy
AORTIC REGURGITATION
As with aortic stenosis, most patients with aortic regurgitation of rheumatic origin have associated mitral valve disease.11 Their clinical course, therefore, is probably determined more by the extent of their mitral valve disease than by their aortic regurgitation. When aortic regurgitation is the predominant lesion, pregnancy is usually well tolerated.9 It has been suggested that aortic regurgitation may actually improve in pregnancy because of the decrease in systemic vascular resistance.9 Also, the physiologic tachycardia of pregnancy may reduce regurgitant flow as diastolic filling times are shortened.1,11 It has also been recognized that the murmurs normally associated with both aortic and mitral regurgitation may be reduced in pregnancy.24 For patients with severe aortic regurgitation and symptoms of left-sided heart failure, the mainstay of therapy is decreasing cardiac work. Patients should limit their activity, and bed rest may be necessary. Sodium restriction may also be helpful.10 Diuresis and inotropic therapy with digitalis have been suggested in difficult cases.14 Despite aggressive medical therapy, some patients will require aortic valve replacement in pregnancy.25,26 Case reports suggest that pulsatile perfusion at bypass may help preserve placental hemodynamic function.27–29 REFERENCES 1. Brady K, Duff P. Rheumatic heart disease in pregnancy. Clin Obstet Gynecol 1989;32:21–40. 2. Pitkin RM, Perloff JK, Koos BJ, Beall MH. Pregnancy and congenital heart disease. Ann Intern Med 1990;112:445–54. 3. McFaul PB, Dornan JC, Lamki H, Boyle D. Pregnancy complicated by maternal heart disease. A review of 519 women. Br J Obstet Gynaecol 1988;95:861–7. 4. Veasy LG, Wiedmeier SE, Orsmond GS, Ruttenberg HD, Boucek MM, Roth SJ, et al. Resurgence of acute rheumatic fever in the intermountain area of the United States. N Engl J Med 1987;316:421–7. 5. Szekely P, Turner R, Snaith L. Pregnancy and the changing pattern of rheumatic heart disease. Br Heart J 1973;35:1293–303. 6. Robbins SL, Cotran RS, Kumar V. Robbin’s pathologic basis of disease. 4th ed. Philadelphia: WB Saunders, 1989:597. 7. Hess DB, Hess LW. Management of cardiovascular disease in pregnancy. Obstet Gynecol Clin North Am 1992;19:679–95. 8. Silversides CK., Colman JM, Sermer M, Farine D, Siu SC. Early and intermediate-term outcomes of pregnancy with congenital aortic stenosis. Am J Cardiol 2003;91:1386–9. 9. Burlew BS. Managing the pregnant patient with heart disease. Clin Cardiol 1990;13:757–62. 10. Lang RM, Borow KM. Pregnancy and heart disease. Clin Perinatol 1985;12: 551–69.
11. Clark SL. Cardiac disease in pregnancy. Obstet Gynecol Clin North Am 1991; 18:237–56. 12. Christianson R, Page EW. Diuretic drugs and pregnancy. Obstet Gynecol 1976; 48:647–52. 13. Oakley CM. Cardiovascular disease in pregnancy. Can J Cardiol 1990;6:3B–9B. 14. Gianopoulos JG. Cardiac disease in pregnancy. Med Clin North Am 1989;73: 639–50. 15. Esteves CA, Ramos AIO, Braga SL, Harrison JK, Sousa JE. Effectiveness of percutaneous balloon mitral valvotomy during pregnancy. Am J Cardiol 1991;68:930–4. 16. Chow W, Chow T, Wat M, Cheung KL. Percutaneous balloon mitral valvotomy in pregnancy using the Inoue balloon catheter. Cardiology 1992;81:182–5. 17. Abid A, Abid F, Zargouni N, Khayati A. Closed mitral valvotomy in pregnancy—a study of seven cases. Int J Cardiol 1990;26:319–21. 18. Wu J, Chern M, Yeh K, Chen YC, Fu M, Hung JS. Urgent/emergent percutaneous transvenous mitral commissurotomy. Cathet Cardiovasc Diagn 1994;31:18–22. 19. Veray FX, Hernandez–Cibes JJ, Pelegrina I. Heart disease in pregnancy. Obstet Gynecol 1968;32:424–31. 20. Khanlou H. Khanlou N. Eiger G. Relationship between mitral valve regurgitant flow and peripartum change in systemic vascular resistance. South Med J 2003;96:308–9. 21. Lesniak-Sobelga A, Tracz W, KostKiewicz M, Podolec P, Pasowicz M. Clinical and echocardiographic assessment of pregnant women with valvular heart diseases-maternal and fetal outcome. Int J Cardiol 2004;94:15–23. 22. Davies GAL, Herbert WNP. Congenital heart disease in pregnancy. J Obstet Gynaecol Can 2007;29(5):409–414. 23. Arias F, Pineda J. Aortic stenosis and pregnancy. J Reprod Med 1978;20: 229–32. 24. Marcus FI, Ewy GA, O’Rourke RA, Walsh B, Bleich AC. The effect of pregnancy on the murmurs of mitral and aortic regurgitation. Circulation 1970;41:795–805. 25. Tehrani H, Masroor S, Lombardi P, Rosenkranz E, Salerno T. Beating heart aortic valve replacement in a pregnant patient. J Cardiac Surg 2004;19:57–8. 26. Martin TC, Idahosa V, Ogunbiyi A, Fevrier-Roberts G, Winter A. Successful pregnancy and delivery after pulmonary autograft operation (Ross procedure) for rheumatic aortic valve insufficiency. West Ind Med J 2003;52:62–4. 27. Tripp HF, Stiegel RM, Coyle JP. The use of pulsatile perfusion during aortic valve replacement in pregnancy. Ann Thoracic Surg 1999;67:1169–71. 28. Golden LP. Aortic valve repair and arch replacement during pregnancy: a case report. AANA J 1996;64:243–54. 29. Khan N, Pumphrey C, Clarke J, Jahangiri M. Aortic root replacement in pregnancy. J Royal Soc Med 2003;96:551–2.
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