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Obstentrics_Williams. Krieger EV, Landzberg M], Economy E, et al: Comparison of risk of hypertensive complications of pregnancy among women with versus without coarctation of the aorta. Am] Cardiolt107:1529, 2011 Krul SP, van der Smagt]], van den Berg MP, et al: Systematic review of pregnancy in women with inherited cardiomyopathies. Euro ] Heart Failure 13:584,t2011 Kulas T, Habek D: Infective puerperal endocarditis caused by Escherichia coli. ] Perinat Med 34:342, 2006 Kuleva M, Youssef A, Maroni E, et al: Maternal cardiac function in normal twin pregnancy: a longitudinal study. Ultrasound Obstet Gynecol 38:575, 201t1 Ladner HE, Danielser B, Gilbert WM: Acute myocardial infarction in pregnancy and the puerperium: a population-based study. Obstet Gynecol 105:480, 2005 Lane CR, Trow TK: Pregnancy and pulmonary hypertension. Clin Chest Med 32:165,t2011 LaRue 5, Shanks A, Wang IW, et al: Let ventricular assist device in pregnancy. Obstet Gynecol 118:426,t2011


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Obstentrics_Williams. Lane CR, Trow TK: Pregnancy and pulmonary hypertension. Clin Chest Med 32:165,t2011 LaRue 5, Shanks A, Wang IW, et al: Let ventricular assist device in pregnancy. Obstet Gynecol 118:426,t2011 Lawley CM, Lain 5], lgert CS, et al: Prosthetic heart valves in pregnancy, outcomes for women and their babies: a systematic review and meta-analysis. B]OG 122(11):1446,t2015 Lee LC, Bathgate SL, Macri C]: Arrhythmogenic right ventricular dysplasia in pregnancy. A case report.] Reprod Med 51:725, 2006 Ldniak-Sobelga A, Tracz W, Kostkiewicz M, et al: Clinical and echocardiographic assessment of pregnant women with valvular heart disease-maternal and fetal outcome. Int] Cardiol 94: 15, 2004


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Obstentrics_Williams. Leyh RG, Fischer 5, Ruhpatwar A, et al: Anticoagulation for prosthetic heart valves during pregnancy: is low-molecular-weight heparin an alternative? Eur] Cardiothorac Surg 21:577,t2002 Leyh RG, Fischer 5, Ruhpatwar A, et al: Anticoagulation therapy in pregnant women with mechanical valves. Arch Gynecol Obstet 268: 1, 2003 Li W, Li H, Long Y: Clinical characteristics and long-term predictors of persistent left ventricular systolic dysfunction in peripartum cardiomyopathy. Can] CardioIt32:362, 2016 Lin LT, Tsui KH, Change R, et al: Management of recurrent and refractory ventricular tachycardia in pregnancy. Taiwan] Obstet Gynecol 54(3):319,t2015 Lindley K], Conner SN, Cahill AG: Adult congenital heart disease in pregnancy. Obstet Gynecol Surv 70(6):397,t2015 Link MS: Evaluation and initial treatment of supraventricular tachycardia. N Engl] Med 367:1438, 2012 Lu CW, Shih ]C, Chen SY, et al: Comparison of 3 risk estimation methods for predicting cardiac outcomes in pregnant women with


Obstentrics_Williams

Obstentrics_Williams. treatment of supraventricular tachycardia. N Engl] Med 367:1438, 2012 Lu CW, Shih ]C, Chen SY, et al: Comparison of 3 risk estimation methods for predicting cardiac outcomes in pregnant women with congenital heart disease. Circt] 79(7):1609, 2015 Lupton M, Oteng-Ntim E, Ayida G, et al: Cardiac disease in pregnancy. Curr Opin Obstet GynecoIt14:137, 2002 Maron B]: Hypertrophic cardiomyopathy: an important global disease. Amt] Med 116:63, 2004 Maron B], Towbin ]A, Thiene G, et al: Contemporary deinitions and classification of the cardiomyopathies an merican Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research nd Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation 113:1807,2006


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Obstentrics_Williams. Martin RB, Nelson DB, Stewart R, et al: Impact of pregnancy on maternal cardiac atria. Abstract No. 508, Am] Obstet Gynecol 216:5632, 2017 McLintock C: Anticoagulant therapy in pregnant women with mechanical prosthetic heart valves: no easy option. hromb Res 127:556,t2011 McLintock C: Thromboembolism in pregnancy: challenges and controversies in the prevention of pregnancy-associated venous thromboembolism and management of anticoagulation in women with mechanical prosthetic heart valves. Best Pract Res Clin Obstet GynecoIt28(4):519, 2014 McNamara DM, Elkayam U, Alharethi R, et al: Clinical outcomes for peripartum cardiomyopathy in North America: results of the IPAC study (investigations of pregnancy-associated cardiomyopathy). ] Am Coll Cardiol 66(8):905, 2015 Meijboom L], Drenthen W, Pieper PG, et al: Obstetric complications in Marfan syndrome. Intit] Cardiol 110:53, 2006


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Obstentrics_Williams. Meijboom L], Drenthen W, Pieper PG, et al: Obstetric complications in Marfan syndrome. Intit] Cardiol 110:53, 2006 Melchiorre K, Sharma R, Khalil A, et al: Maternal cardiovascular function in normal pregnancy: evidence of maladaptation to chronic volume overload. Hypertension 67(4):754, 2016 Meng ML, Landau R, Viktorsdottir 0, et al: Pulmonary hypertension in pregnancy: a report of 49 cases at four tertiary North American sites. Obstet GynecoIt129(3):511,t2017 Miller BR, Strubian D, Sundararajan 5: Stroke in the young: patent foramen ovale and pregnancy. Stroke 46(8):e181, 2015 Miniero R, Tardivo I, Centofanti P, et al: Pregnancy in heart transplant recipients. ] Heart Lung Transplant 23:898, 2004 Mohamed-Ahmed 0, Nelson-Piercy C, Bramham K, et al: Pregnancy outcomes in liver and cardiothoracic transplant recipients: a UK national cohort study. PLoS One 9(2):e89151, 2014 Moioli M, Mendada MV, Bentivoglio G, et al: Peripartum cardiomyopathy. Arch Gynecol Obstet 281:183, 2010


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Obstentrics_Williams. Moioli M, Mendada MV, Bentivoglio G, et al: Peripartum cardiomyopathy. Arch Gynecol Obstet 281:183, 2010 Mousa A, McKinley CA, hongt]: Acute postpartum myocardial infarction after ergometrine administration in a woman with familial hypercholesterolaemia. B]OG 107:939,t2000 Mul TFM, van Herwerden A, Cohen-Overbeek TE, et al: Hypoxic-ischemic fetal insult resulting from maternal aortic root replacement, with normal fetal heart rate at term. Am ] Obstet Gynecol 179:825, 1998 Murray ML, Pepin M, Peterson 5, et al: Pregnancy-related deaths and complications in women with vascular Ehlers-Danlos syndrome. Genet Med 16(12):874,t2014 Nanna M, Stergiopoulos K: Pregnancy complicated by valvular heart disease: an update.t] Am Heart Assoc 3:e000712, 2014 Nappi F, Spadaccio C, Chello M, et al: Impact of structural valve deterioration on outcomes in the cryopreserved mitral homograft valve. ] Card Surg 29(5):616,t2014


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Obstentrics_Williams. Nappi F, Spadaccio C, Chello M, et al: Impact of structural valve deterioration on outcomes in the cryopreserved mitral homograft valve. ] Card Surg 29(5):616,t2014 Nelson DB, Martin R, Stewart D, et al: The forgotten ventricle. Right ventricular remodeling across pregnancy and postpartum. Abstract No. 641. Am] Obstet GynecoIt216;S376, 2017 Newman T, Cafardi ]M, Warshak CR: Human immunodeiciency virusassociated pulmonary arterial hypertension diagnosed postpartum. Obstet Gynecol 125(1):193,t2015 Nishimura A, Otto CM, Bonow RO, et al: 2014 AHNACC guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiologyl American Heart Association Task Force on Practice Guidelines.] Thorac Cardiovasc 148(1):e1, 2014


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Obstentrics_Williams. Nishimura A, Otto CM, Bonow RO, et al: 2017 AHIACC focused update of the 2014 AHAIACC Guideline for the Management of Patients with Valvular Heart Disease: A Report of the American College of Cardiologyl American Heart Association Task Force on Clinical Practice Guidelines. Circulation 135(25):el159, 2017 Ntusi NB, Badri M, Gumedze F, et al: Pregnancy-associated heart failure: a comparison of clinical presentation and outcome berween hypertensive heart failure of pregnancy and idiopathic peripartum cardiomyopathy. PLoS One 10(8):e0133466, 2015 Obican SG, Cleary KL: Pulmonary arterial hypertension in pregnancy. Semin Perinatol 35(5):289, 2014 O'Gara PT, Greenfield A], Afridi NA, et al: Case 12-2004: a 38-yearold woman with acute onset of pain in the chest. N Engl ] Med 350:16, 2004 OosterhofT, Meijboom F], Vliegen HW, et al: Long-term follow-up of homograft function after pulmonary valve replacement in patients with tetralogy of Fallor. Eur Heart] 27: 1478, 2006


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Obstentrics_Williams. OosterhofT, Meijboom F], Vliegen HW, et al: Long-term follow-up of homograft function after pulmonary valve replacement in patients with tetralogy of Fallor. Eur Heart] 27: 1478, 2006 Opotowsky AR, Siddiqi OK, D'Souza B, et al: Maternal cardiovascular events during childbirth among women with congenital heart disease. Heart 98:145,t2012 Pacheco LD, Saade GR, Hankins GD: Acute myocardial infarction during pregnancy. Clin Obstet Gynecol 57(4):835, 2014 Page RL, ]oglar ]A, Caldwell MA, et al: 2015 ACCIAHAlHRS guideline for the management of adult patients with supraventricular tachycardia: executive summary. Circulation 133:e471, 2015 Papatsonis DNM, Heetkamp A, van den Hombergh C, et al: Acute type A aortic dissection complicating pregnancy at 32 weeks: surgical repair after cesarean section. Am] Perinatol 26: 153, 2009


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Obstentrics_Williams. Papatsonis DNM, Heetkamp A, van den Hombergh C, et al: Acute type A aortic dissection complicating pregnancy at 32 weeks: surgical repair after cesarean section. Am] Perinatol 26: 153, 2009 Pappone C, Santinelli V, Manguso F, et al: A randomized study of prophylactic catheter ablation in asymptomatic patients with the Wolf-Parkinson-Whi te syndrome. N Englt] Med 349: 1803, 2003 Patten IS, Rana S, Shahul S, et al: Cardiac angiogenic imbalance leads to peripartum cardiomyopathy. Nature 485:333,t2012 Pearson GD, Veille Jc, Rahimtoola S, et al: Peripartum cardiomyopathy. National Heart, Lung, and Blood Institute and Oice of Rare Diseases (National Institutes of Health) workshop recommendations and review. ]AMA 283: 1183, 2000 Penning S, Robinson KD, Major CA, er al: A comparison of echocardiography and pulmonary artery catheterization for evaluation of pulmonary artery pressures in pregnant patients with suspected pulmonary hypertension. Am ] Obstet Gynecol 184:1568,t2001


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Obstentrics_Williams. Pepin M, Schwarze U, Superti-Furga A, et al: Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type. N Engl J Med 342:6 3, 2000 Pessel C, Bonanno C: Valve disease in pregnancy. Semin Perinatal 38(5):273, 20t14 Pierce D, Calkins BC, hornton K: Infectious endocarditis: diagnosis and treatment. Am Fam Physician 85:981, 2012 Pijuan-Domenech A, Galian L, Goya M, et al: Cardiac complications during pregnancy are better predicted with the modiied WHO risk score. Int ] Cardiol 195:149,t2015 Pinski SL, Trohman RG: Interference in implanted cardiac devices, part II. Pacing Clin Electrophysiol 25(10):1496, 2002 Pitton A, Petolillo M, Munegato E, et al: Hypertrophic obstructive cardiomyopathy and pregnancy: anesthesiological observations and clinical series. Minerva Anesthesiol 73:313,t2007


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Obstentrics_Williams. Pitton A, Petolillo M, Munegato E, et al: Hypertrophic obstructive cardiomyopathy and pregnancy: anesthesiological observations and clinical series. Minerva Anesthesiol 73:313,t2007 Pombar X, Strassner HT, Fenner PC: Pregnancy in a woman with class H diabetes mellitus and previous coronary artery bypass graft: a case report and review of the literature. Obstet Gynecol 85:825, 1995 Pyatt ]R, Dubey G: Peripartum cardiomyopathy: current understanding, comprehensive management review and new developments. Postgrad Med ] 87:34,t2011 Raman AS, Sharma S, Hariharan: Minimal use of luoroscopy to reduce fetal radiation exposure. Tex Heart Inst] 42(2):152,t2015 Ramzyt], New G, Cheong A, et al: Iatrogenic anterior myocardial infarction secondary to ergometrine-induced coronary artery spasm during dilation and curettage for an incomplete miscarriage. Int J Cardiol 198: 154, 2015


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Obstentrics_Williams. Rashba E], Zareba W, Moss A], et al: Inluence of pregnancy on the risk for cardiac events in patients with hereditary QT syndrome. Circulation 97:451, 1998 Ray WA, Murray KT, Hall K, et al: Azithromycin and the risk of cardiovascular death. N Engl ] Med 366: 1881, 2012 Redield MM: Heart failure with preserved ejection fraction. N Englt] Med 375(19):1868,t2016 Reich 0, Tax P, Marek ], et al: Long term results of percutaneous balloon valvoplasty of congenital aortic stenosis: independent predictors of outcome. Heart 90:70, 2004 Rich S, McLaughlin W: Pulmonary hypertension. In Zipes DP (ed): Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed. Philadelphia, Saunders, 2005 Robins K, Lyons G: Supraventricular tachycardia in pregnancy. Br ] Anaesth 92: 140, 2004 Roden DM: Drug-induced prolongation of the QT interval. N Engl ] Med 350:1013,t2004 Roden DM: Long-QT syndrome. N Engl] Med 358:169, 2008


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Obstentrics_Williams. Roden DM: Drug-induced prolongation of the QT interval. N Engl ] Med 350:1013,t2004 Roden DM: Long-QT syndrome. N Engl] Med 358:169, 2008 Roeder HA, Kuller ]A, Barker PC, et al: Maternal valvular heart disease in pregnancy. Obstet Gynecol Surv 66:561,t2011 Rowan ]A, McCowan LM, Raudkivi P], et al: Enoxaparin treatment in women with mechanical heart valves during pregnancy. m ] Obstet Gynecol 185:633,t2001 Russo ML, Gandhi M, Morris SA: Aortic dissection in pregnancy-a Texas population-based study. Abstract No. 769. Am] Obstet GynecoI216:S445, 2017 Ruys TP, Roos-Hesselinkt]W, Hall R, et al: Heart failure in pregnant women with cardiac disease: data from the ROPAC. Heart 100(3):231,t2014 Ruys TP, Roos-Hesselink ]W, Pijuan-Domenech A, et l: Is a planned caesarean section in women with cardiac disease beneicial? Heart 101(7):530, 2015


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Obstentrics_Williams. Ruys TP, Roos-Hesselink ]W, Pijuan-Domenech A, et l: Is a planned caesarean section in women with cardiac disease beneicial? Heart 101(7):530, 2015 Savu 0, ]urcuf R, Giu§ca S, et al: Morphological and functional adaptation of the maternal heart during pregnancy. Circ Cardiovasc Imaging 5:289,t2012 Sawhney H, Aggarwal N, Suri V, et al: Maternal and perinatal outcome in rheumatic heart disease. Intt] Gynaecol Obstet 80:9, 2003 Schade R, Andersohn F, Suissa S, et al: Dopamine agonists and the risk of cardiac-valve regurgitation. N Engl] Med 356:29, 2007 Schinkel AF: Pregnancy in women with hypertrophic cardiomyopathy. Cardio Rev 22(5):217,t2014 Schulte-Sasse U: Life threatening myocardial ischaemia associated with the use of prostaglandin EI to induce abortion. B]OG 107:700,t2000 Seaworth B], Durack DT: Infective endocarditis in obstetric and gynecologic practice. Am] Obstet Gynecol 154: 180, 1986


Obstentrics_Williams

Obstentrics_Williams. Seaworth B], Durack DT: Infective endocarditis in obstetric and gynecologic practice. Am] Obstet Gynecol 154: 180, 1986 Seeburger ], Wilhelm-Mohr F, Falk V: Acute type A dissection at 17 weeks of gestation in a Marfan patient. Ann Thorac Surg 83:674, 2007 Seshadri S, Oakeshott P, Nelson-Piercy C, et al: Prepregnancy care. BM] 344:34,t2012 Seth R, Moss A], McNitt S, et al: Long QT syndrome and pregnancy. ] Am ColI Cardiol 49: 1 092, 2007 Sheield ]S, Cunningham FG: Diagnosing and managing peripartum cardiomyopathy. Contemp Ob/Gyn 44:74, 1999 Sheield ]S, Cunningham FG: Thyrotoxicosis and heart failure that complicate pregnancy. Am] Obstet GynecoIt190:211, 2004 Sherer DM: Coarctation of the descending thoracic aorta diagnosed during pregnancy. Obstet Gynecol 100: 1 094, 2002 Shivvers SA, Wians FH ]r, Kefer ]H, et al: Maternal cardiac troponin I levels during normal labor and delivery. Am] Obstet Gynecol 180: 122, 1999


Obstentrics_Williams

Obstentrics_Williams. Shivvers SA, Wians FH ]r, Kefer ]H, et al: Maternal cardiac troponin I levels during normal labor and delivery. Am] Obstet Gynecol 180: 122, 1999 Shrof H, Benenstein R, Freedberg R, et al: Mitral valve Libman-Sacks endocarditis visualized by real time three-dimensional transesophageal echocardiography. Echocardiography 29:E 100, 2012 Silversides CK, Harris L, Haberer K, et al: Recurrence rates of arrhythmias during pregnancy in women with previous tachyarrhythmia and impact on fetal and neonatal outcomes. n1 ] Cardiol 97: 1206, 2006 Simpson LL: Matenal cardiac disease: update for the clinician. Obstet Gynecol 119:345,t2012 Sims DB, Vinkt], Uriel N, et al: A successful pregnancy during mechanical circulatory device support.] Heart Lung Transplant 30:1065,t2011 Siu SC, Colman ]M: Congenital heart disease: heart disease and pregnancy. Heart 85:710, 2001a


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Obstentrics_Williams. Siu SC, Colman ]M: Congenital heart disease: heart disease and pregnancy. Heart 85:710, 2001a Siu Sc, Sermer M, Colman ]M, et al: Prospective multicenter study of pregnancy outcomes in women with heart disease. Circulation 104:515, 200t1b Siva A, Shah AM: Moderate mitral stenosis in pregnancy: the haemodynamic impact of diuresis. Heart 91t:e3, 2005 Sliwa K, Blauwet L, Tibazarwa K, et al: Evaluation of bromocriptine in the treatment of acute severe peripartum cardiomyopathy: a proof-of-concept pilot study. Circulation 121:1465,t2010 Small M), James AH, Kershaw T, et al: Near-miss maternal mortality: cardiac dysfunction as the principal cause of obstetric intensive care unit admissions. Obstet Gynecol 119:250, 2012 Smith I), Gillham MJ: Fulminant peripartum cardiomyopathy rescue with extracorporeal membranous oxygenation. Int) Obstet Anesth 18: 186, 2009 Smok DA: Aortopathy in pregnancy. Semin PerinatoIt38(5):295, 2014


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Obstentrics_Williams. Smok DA: Aortopathy in pregnancy. Semin PerinatoIt38(5):295, 2014 Stergiopoulos K, Shiang E, Bench T: Pregnancy in patients with pre-existing cardiomyopathies.t) m Coli Cardiol 58:337, 2011 Stewart RD, Nelson DB, Matulevicious SA, et al: Cardiac magnetic resonance imaging to assess the impact of maternal habitus on cardiac remodeling during pregnancy. m) Obstet Gynecol 214(5):640.e1, 2016 Sutaria N, O'Toole L, Northridge 0: Postpartum acute MI following routine ergometrine administration treated successfully by primary PTCA. Heart 83:97,t2000 Thaman R, Varnava A, Hamid MS, et al: Pregnancy related complications in women with hypertrophic cardiomyopathy. Heart 89:752, 2003 hompson )L, Kuklina EV, Bateman BT, et al: Medical and obstetric outcomes among pregnant women with congenital heart disease. Obstet Gynecol 126(2):346,t20t15 Thorne S, MacGregor A, Nelson-Piercy C: Risks of contraception and pregnancy in heart disease. Heart 92(10):152, 2006


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Obstentrics_Williams. Thorne S, MacGregor A, Nelson-Piercy C: Risks of contraception and pregnancy in heart disease. Heart 92(10):152, 2006 Thurman R, Zafar N, Sayyer P, et al: Labour profile and outcomes in pregnant women with heart disease. Abstract No. 799. Amt) Obstet Gynecol 216:S459,t2017 Trigas V, Nagdyman N, Pildner von Steinburg S, et al: Pregnancy-related obstetric and cardiologic problems in women after atrial switch operation for transposition of the great arteries. Circ) 78(2):443, 2014 Tuzcu V, Gul EE, Erdem A, et al: Cardiac interventions in pregnant patients without luoroscopy. Pediatr Cardiol 36(6): 1304,t2015 Van Hagen 1M, Roose-Hesselink)W, Ruys TP, et al: Pregnancy in women with a mechanical heart valve: data of the European Society of Cardiology Registry of Pregnancy and Cardiac Disease (ROPAC). Circulation 132(2):132,t2015 Vashisht A, Katakam N, Kausar S, et al: Postnatal diagnosis of maternal congenital heart disease: missed opportunities. BM) Case Rep, 2015. pii: bcr2015209938


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Obstentrics_Williams. Vinatier 0, Virelizier S, Depret-Mosser S, et al: Pregnancy after myocardial infarction. Eur) Obstet Gynecol Reprod Bioi 56:89, 1994 Vitarelli A, Capotosto L: Role of echocardiography in the assessment and management of adult congenital heart disease in pregnancy. Int ) Cardiovasc Imaging 27:843,t201t1 Vos R, Ruttens 0, Verleden SE, et al: Pregnancy ater heart and lung transplantation. Best Pract Res Clin Obstet Gynecol 28(8): 1146, 2014 Wang H, Zhang W, Liu T: Experience of managing pregnant women with Eisenmenger's syndrome: maternal and fetal outcome in 13 cases. ) Obstet Gynaecol Res 37:64,t2011 Ware )S, Seidman )G, Arany Z: Shared genetic predisposition in peripartum and dilated cardiomyopathies. N Engl) Med 374(26):2601,t2016 Warnes CA: Pregnancy and delivery in women with congenital heart disease. Circ) 79(7):1416, 2015 Watkins H, Ashrafian H, Redwood C: Inherited cardiomyopathies. N Englt) Med 364:1643, 2011


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Obstentrics_Williams. Warnes CA: Pregnancy and delivery in women with congenital heart disease. Circ) 79(7):1416, 2015 Watkins H, Ashrafian H, Redwood C: Inherited cardiomyopathies. N Englt) Med 364:1643, 2011 Weiss BM, Zemp L, Seifert B, et al: Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 1978 through 1996. ) m Coll CardioIt31:1650, 1998 Wilson W, Taubert A, Gewitz M, et al: Prevention of infective endocarditis. Guidelines from the American Heart Association. Circulation 116: 1736, 2007 World Health Organization: Medical eligibility for contraceptive use, 4th ed. 2009. Geneva, World Health Organization, 2010 Wylie B), Epps KC, Gaddipati S, et al: Correlation of transthoracic echocardiography and right heart catheterization in pregnancy. ) Perinat Med 35(6):497, 2007


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Obstentrics_Williams. Wylie B), Epps KC, Gaddipati S, et al: Correlation of transthoracic echocardiography and right heart catheterization in pregnancy. ) Perinat Med 35(6):497, 2007 Xia W, Messerlian AK, Mackleyt), et al: Successful epidural anesthesia for cesarean section in a parturient with severe aortic stenosis and a recent history of pulmonary edema-a case report. ) Clin Anesth 18: 142, 2006 YangX, Wang H, Wang Z, et al: Alteration and signiicance of serum cardiac troponin I and cystatin C in preeclampsia. Clin Chim Acta 374: 168, 2006 Yu M, Yi K, Zhou L, et al: Pregnancy increases heart rates during paroxysmal supraventricular tachycardia. Can) Cardiol 31(6):820.e5, 2015 Zanettini R, Antonini A, Gatto G, et al: Valvular heart disease and the use of dopamine agonists for Parkinson's disease. N Englt) Med 356:39, 2007 Zeeman GG: Obstetric critical care: a blueprint for improved outcomes. Crit Care Med 34:S208, 2006


Obstentrics_Williams

Obstentrics_Williams. Zeeman GG: Obstetric critical care: a blueprint for improved outcomes. Crit Care Med 34:S208, 2006 Zwiers WJ, Blodgett TM, Vallejo MC, et al: Successful vaginal delivery for a parturient with complete aortic coarctation.) Clin Anesth 18:300,t2006 GENERAL CONSIDERATIONS ..................... 975 DIAGNOSIS AND EVALUATION IN PREGNANCY ...... 977 ADVERSE PREGNANCY EFFECTS ...................978 ANTIHYPERTENSIVE DRUGS ....i....i....i....i.......... 980 ANTIHYPERTENSIVE TREATMENT IN PREGNANCY ... 981 SUPERIMPOSED PREECLAMPSIA .................. 983 FETAL ASSESSMENT ....i.........i............... 983 DELIVERY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 983 POSTPARTUM CARE ............................ 984 A smal proportion of women suiringrom chronic nephritis had eclampsia. For the most part, autopsy wil reveal the presence of renal changes usualy of acute nephritis, though occasionaly it may be engrafied upon a chronic process.


Obstentrics_Williams

Obstentrics_Williams. -J. Whitridge Williams (1903) At the time of Wiliams Obstetrics' first edition, little attention was paid to blood pressure changes, even with "toxemia." At that time, chronic hypertension was designated "senile" and thought to develop only in older individuals (Lindheimer, 2015). Indeed, chronic hypertension is not mentioned, per se, in Williams' 1903 textbook, except for some deference given to chronic anatomical renal changes occasionally associated with eclampsia. It is now apparent that chronic hypertension is one of the most common serious complications encountered during pregnancy. his is not surprising because, according to the National the Centers for Disease Control and Prevention (2011), the prevalence of hypertension in women aged 18 to 39 years approximates 7 percent.


Obstentrics_Williams

Obstentrics_Williams. he incidence of chronic hypertension complicating pregnancy varies depending on population vicissitudes. In a study of more than 56 million births from the Nationwide Patient Sample, the incidence was 1.8 percent (Bateman, 2012). And, in more than 878,000 pregnancies from the Medicaid Analytic Extract, 2.3 percent were complicated by chronic hypertension (Bateman, 2015). Despite this substantive prevalence, optimal management has not been well studied. It is known that chronic hypertension usually improves during early pregnancy. his is followed by variable behavior later in pregnancy and, importantly, by the unpredictable development of superimposed preeclampsia. The latter carries increased risks for maternal and perinatal morbidity and mortality.


Obstentrics_Williams

Obstentrics_Williams. To define chronic hypertension, the range of normal blood pressure must irst be established. This is not a simple task because, like all polygenically determined biological variants, blood pressure norms difer between populations. And, within these norms, wide variations are found between individuals. Moreover, numerous epigenetic factors inluence presentation. For example, not only do blood pressures vary between races and genders, but pressures-especially systolic-rise directly with increasing age and weight. Thus, pragmatically, normal adults have a broad range of blood pressures, but so do those with chronic hypertension. And finally, resting blood pressure measurements do not reflect daily activities.


Obstentrics_Williams

Obstentrics_Williams. After these variables are acknowledged, important considerations for any population are the attendant risks of chronic hypertension. It is a leading cause of death and accounts for nearly 15 percent of mortality worldwide. Approximately 65 million Americans have hypertension, and this number is growing concurrently with epidemic obesity (Kotchen, 2015). Hypertension increases substantively the risk of cardiovascular disease, coronary heart disease, congestive heart failure, stroke, renal failure, and peripheral arterial disease (Forouzanfar, 2017).


Obstentrics_Williams

Obstentrics_Williams. For the foregoing reasons, chronic hypertension would logically be deined as some level of sustained resting blood pressure that is associated with acute or long-term adverse efects. In this regard, most consider 140/90 mm Hg as the upper limit of normal for blood pressure values. But, in the United States, these values are based primarily on actuarial tables constructed using data derived from white adult males and compiled by life insurance companies. These "norms" disregard interrelated factors such as ethnicity, gender, and other important covariants. he importance of race, for example, was emphasized by Kotchen (2015), who cites the incidence of hypertensiondeined as blood pressurea> 140/90 mm Hg-to be 34 percent in blacks, 29 percent in whites, and 21 percent in Mexican Americans.


Obstentrics_Williams

Obstentrics_Williams. For many years, the Joint National Committee has promulgated guidelines for diagnosis, classification, and management of chronic hypertension. In 2008, the National Heart, Lung, and Blood Institute discontinued these guidelines, and the Joint National Committee 8 GNC 8) was instead asked to provide an evidence-based review Games, 2014). Findings pertinent to caring for young women with chronic hypertension are summarized in Table


Obstentrics_Williams

Obstentrics_Williams. Proven benefits accrue with treatment of otherwise normal adults who have sustained hypertension. Numerous studies evaluating many combinations of antihypertensive therapy have been conducted. Importantly, these trials evaluated monotherapy versus combination therapeutic regimens and their ethnospecific beneits. Most evaluated cardiovascular outcomes, but many also confirmed risk reductions in rates of cerebrovascular accident, renal insuficiency, and mortality. Because of these incontrovertible beneits, the JNC 8 recommends the management outlined in Table 50-1.


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Obstentrics_Williams. Thus, even for mildly elevated blood pressure, interventions to reduce these sequelae are beneficial (SPRINT Research Group, 2015). Moreover, antihypertensive therapy in nonpregnant reproductive-aged women with sustained diastolic pressures ::90 mm Hg is considered standard. Not clear from these observations, however, is what constitutes the best management for women being treated who contemplate pregnancy, for those undergoing treatment who become pregnant, or for those first identified to have chronic hypertension during pregnancy (August, 2015). In these women, the benefits and safety of instituting antihypertensive therapy are less clear, as subsequently discussed on page 981.


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Obstentrics_Williams. Women with chronic hypertension are ideally counseled before pregnancy. The duration of hypertension, degree of blood pressure control, and current therapy are ascertained. hose women who require multiple medications for control or those who are poorly controlled carry greater risk for adverse pregnancy outcomes. Home measurement devices are checked for accuracy. General health, daily activities, and dietary habits are also assessed (Table 50-2). For hypertensive women with disease lasting longer than 5 years or with comorbid diabetes, cardiovascular and renal function is assessed (August, 2015; Gainer, 2005). Women with evidence for organ dysfunction or those with prior adverse events such as a stroke, myocardial infarction (MI), arrhythmias, or ventricular failure are at markedly higher risk for a recurrence or worsening dysfunction during pregnancy. Renal function is evaluated by serum creatinine measurement. Also, if


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Obstentrics_Williams. TABLE 50-1. Eighth Joint National Committee (JNC 8}-2014 Chronic Hypertension Guidelines and Recommendations Lifestyle modifications endorsed from the Lifestyle Work Group (Eckel, 2013) Recommend selection among four specific medication classes: angiotensin-converting enzyme inhibitors (ACE-I), angiotensin-receptor blockers (ARB), calcium-channel blockers, or diuretics: General population: <60 years old-initiate pharmacological therapy to lower diastolic pressure :;90 mm Hg and systolic pressuren:;140 mm Hg Diabetics: lower pressure to < 140/90 mm Hg Chronic kidney disease: lower pressure to < 140/90 mm Hg. Also add ACE-lnor ARB to improve outcomes


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Obstentrics_Williams. Chronic kidney disease: lower pressure to < 140/90 mm Hg. Also add ACE-lnor ARB to improve outcomes General non black population: initial therapy should include thiazide-type diuretic, calcium-channel blocker, ACE-I, or ARB General black population: primary antihypertensive therapy should include thiazide-type diuretic or calcium-channel blocker Assess monthly, and after 1 month, if goals not met, then increase primary drug dose or add second drug. If no response, increase either or add third drug; then if no response, refer to hypertension specialist Summarized from James, 201a4. TABLE 50-2. Lifestyle Modifications for Hypertensive Patients Consume a dietary pattern that emphasizes intake of vegetables, fruits, and whole grains; includes low-fat dairy products, poultry, fish, legumes, nontropical vegetable oils, and nuts; limits sweets and red meats. Examples are DASH, USDA Food Pattern, or the AHA Diet


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Obstentrics_Williams. Engage in aerobic physical activity three to four sessions per week, lasting on average 40 minutes per session, and involving moderate-to-vigorous intensity physical activity Moderation of alcohol consumption AHA = American Heart Association; DASH = Dietary Approaches to Stop Hypertension; USDA = United States Department of Agriculture. Summarized from Eckel, 2013; Kotchen, 2015. a urine spot protein/creatinine ratio is abnormally high (>0.3), proteinuria is further quantified with a 24-hour urine collection (Hladunewich, 2011; Kuper, 2016; Morgan, 2016a). The Working Group Report on High Blood Pressure in Pregnancy (2000) of the National Heart, Lung, and Blood Institute concluded that the risks of fetal loss and accelerated renal disease deterioration are increased if the serum creatinine level is above 1.4 mg/dL (Chap. 53, p. 1034).


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Obstentrics_Williams. Although pregnancy is considered by many to be contraindicated in women with severe, poorly controlled hypertension, there is no consensus. Certainly, women who maintain persistent diastolic pressures ::110 mm Hg despite therapy; require multiple antihypertensives; have a serum creatinine level > 2 mg/ dL; or have a history of prior stroke, MI, or cardiac failure must be counseled as to the marked risks to themselves and to their pregnancy outcome.


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Obstentrics_Williams. he hypertensive disorders that uniquely complicate pregnancy are discussed in Chapter 40 (p. 710). Women are diagnosed with chronic hypertension if it is documented to precede pregnancy or ifhypertension is identified before 20 weeks' gestation. Evidence also supports that prehypertension may herald adverse outcomes similar to those in women with chronic hypertension (Rosner, 2017). In some women without overt chronic hypertension, a history of repeated pregnancies complicated by gestational hypertension, with or without the preeclampsia syndrome, may be elicited. Each is a risk marker for latent chronic hypertension, and this is especially so for preeclampsia, and in particular early-onset preeclampsia. In many ways, gestational hypertension is analogous to gestational diabetes in that such women have a chronic hypertensive diathesis, in which heredity and environment playaa major role.


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Obstentrics_Williams. Although uncommon, secondary causes of hypertension are always a possibility in afected women. Thus, consideration is given to underlying chronic renal disease, connective-tissue disease, primary aldosteronism, Cushing syndrome, pheochromocytoma, and myriad other causes. That said, most pregnant women with antecedent hypertension will have otherwise uncomplicated disease. Several factors increase the likelihood that pregnant women will have chronic hypertension. hree of those most frequently cited are ethnicity, obesity, and diabetes. As previously dis cussed, chronic hypertension has a population incidence that women (Kotchen, 2015). Related to this, hundreds of blood identified, including candidate genes for preeclampsia and chronic hypertension (Cowley, 2006; Ward, 2015).


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Obstentrics_Williams. The metabolic syndrome is a clinical cluster that includes hypertension, high blood sugar, excess fat at the waist, and abnormal cholesterol or triglyceride levels. This constellation is a risk marker for superimposed preeclampsia and for persistent postpartum hypertension Qeyabalan, 2015; Spaan, 2012). This is not surprising because obesity may increase the prevalence of chronic hypertension tenfold (Chap. 48, p. 938). In addition, obese women are more likely to develop superimposed preeclampsia. Diabetes is also prevalent in chronically hypertensive women, and its interplay with obesity and preeclampsia is overwhelming (Leon, 2016). In aforementioned study from the Nationwide Patient Sample, the most frequent comorbidities associated with chronic hypertension were pregestational diabetes-6.6 percent, thyroid disorders-4.1 percent, and collagen-vascular disease-0.6 percent (Bateman, 2012). Similar comorbidities were described by Cruz and associates (201a1). • Efects of Pregnancy on


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Obstentrics_Williams. • Efects of Pregnancy on Blood pressure drops in early pregnancy in most women with chronic hypertension, and it rises again during the third trimester (Fig. According to studies by Tihtonen and coworkers (2007), women with chronic hypertension have persistently elevated vascular resistance and possibly reduced intravascular volume expansion. Adverse outcomes in these women are dependent largely on whether superimposed preeclampsia develops. This may be related to observations reported by Hibbard and colleagues (2005, 2015) that arterial mechanical properties are most marked in women with superimposed preeclampsia. .120 Chronic hypertension )..:ln 100 n (yellow) compared with blood pressures across pregnancy in 4589 healthy nulliparas (blue). (Data from August, 2015; Levine, 1997; Sibai, 1990a.)


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Obstentrics_Williams. .120 Chronic hypertension )..:ln 100 n (yellow) compared with blood pressures across pregnancy in 4589 healthy nulliparas (blue). (Data from August, 2015; Levine, 1997; Sibai, 1990a.) Chronic hypertension is associated with several adverse maternal and perinatal outcomes listed in Table 50-3. In sum, these adversities are directly related to severity and duration of hypertension before pregnancy and whether superimposed preeclampsia develops, especially early in gestation. Importantly, in women with mild chronic hypertension, outcomes are also related to blood pressure levels during pregnancy. At this time, however, there are no proven benefits of "tight" versus "lesstight" control of chronic hypertension during pregnancy, as discussed later (p. 982) (Magee, 2015).


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Obstentrics_Williams. Most women whose chronic hypertension is well controlled with therapy before pregnancy will do well. Even these women, however, are at increased risk for adverse outcomes. Complications are more likely with severe baseline hypertension and TABLE 50-3. Some Adverse Efects of Chronic Hypertension on Maternal and Perinatal Outcomes HELLP = hemolYSiS, elevated liver enzyme levels, low platelet cou nt.


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Obstentrics_Williams. TABLE 50-3. Some Adverse Efects of Chronic Hypertension on Maternal and Perinatal Outcomes HELLP = hemolYSiS, elevated liver enzyme levels, low platelet cou nt. especially with documented end-organ damage (Czeizel, 2011; Odibo, 2013). In a study of pregnancy outcomes in nearly 30,000 chronically hypertensive women, Gilbert and associates (2007) reported markedly increased rates of maternal morbidity that included stroke, pulmonary edema, and renal failure. hese observations were verified in the report from the Nationwide Patient Sample by Bateman and colleagues (2012). In this latter study, hypertension complications included stroke-2.7 per 1000, acute renal failure-5.9 per 1000, pulmonary edema-1.5 per 1000, mechanical ventilation-3.8 per 1000, and in-house maternal mortality-O.4 per 1000. he contribution of hypertension to pregnancy-related strokes is discussed in Chapter 60 (p. 1160) and to hypertensive and idiopathic peripartum cardiomyopathy in Chapter 49 (p. 963).


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Obstentrics_Williams. Pregnancy-aggravated hypertension may be due to gestational hypertension or to superimposed preeclampsia. In either instance, blood pressures can be dangerously elevated. As emphasized by Clark and Hankins (2012), systolic pressure :::160 mm Hg or diastolic pressure :::110 mm Hg will rapidly cause renal or cardiopulmonary dysfunction or cerebral hemorrhage. With superimposed severe preeclampsia or eclampsia, the maternal prognosis is poor unless the pregnancy is ended. Placental abruption is a common and serious complication (Chap. 41, p. 767). In addition to hypertensive heart failure mentioned above, aortic dissection was described by Weissman-Brenner and coworkers (2004) and is discussed in Chapter 49 (p. 967).


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Obstentrics_Williams. In aggregate, chronic hypertension is associated with a fivefold risk for maternal death (Gilbert, 2007). his is emphasized by the report by Creanga and colleagues (2015) describing 3358 pregnancy-related deaths in the United States from 2006 through 2010. Hypertensive disorders, including chronic hypertension and preeclampsia syndrome, accounted for 9.4 percent of these deaths. Undoubtedly related were other causes of death such as cardiovascular conditions-14.6 percent, cerebrovascular conditions-6.2 percent, and cardiomyopathy-11.8 percent. Moodley (2007) reported similar indings with 3406 maternal deaths from South Africa.


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Obstentrics_Williams. Because superimposed preeclampsia is not precisely defined in women with chronic hypertension, the reported incidence varies from 13 to 40 percent (American College of Obstetricians and Gynecologists, 2013; Bramham, 2016; Kim, 2016b; Moussa, 2017). August and colleagues (2015) posit that this predilection may stem from similar genetic, biochemical, and metabolic abnormalities. For example, the risk for superimposed preeclampsia is directly related to the severity of baseline hypertension (Ankumah, 2014; Morgan, 2016b). In a Maternal-Fetal Medicine Units (MFMU) Network trial, Caritis and coworkers (1998) identiied superimposed preeclampsia in 25 percent of hypertensive gravidas. he rate was 29 percent in a California database study (Yanit, 2012). And, women whose hypertension becomes severe enough to warrant chronic antihypertensive therapy during pregnancy are at inordinately high risk for superimposed preeclampsia (Morgan, 2016a). And, this risk is even higher if there is baseline


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Obstentrics_Williams. enough to warrant chronic antihypertensive therapy during pregnancy are at inordinately high risk for superimposed preeclampsia (Morgan, 2016a). And, this risk is even higher if there is baseline proteinuria. Finally, and women at high risk for preeclampsia (Henderson, 2014). The recommendation to initiate 81 mg between 12 and 28 weeks' gestation and continue therapy until delivery was adopted by the American College of Obstetricians and Gynecologists (2016b). In addition to chronic hypertension, indications for aspirin prophylaxis for those at high-risk of preeclampsia include a history ofpreeclampsia, multifetal gestation, diabetes, renal disease, and autoimmune disease.


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Obstentrics_Williams. Antioxidants to prevent preeclampsia have been studied. with chronic hypertension to treatment with vitamins C and E or with a placebo. A similar number in both groups developed preeclampsia-17 versus 20 percent, respectively. FIGURE 50-2 Blood pressure trends in treated, chronically hypertensive women with and without superimposed preeclampsia. Mean maternal pressures (MAPs) at entry (p = 0.002) and throughout gestation (p <0.001) are significantly diferent for each group. MAP nadir at 23.3 weeks (95% CI, 22.5-24.1) for superimposed preeclampsia versus 26.4 weeks (95% CI, 22.5-27.6) for those without preeclampsia is significant (3.1 weeks, 95% (I, 2.3-4.3). (Data from Morgan, 2016a.) shown in Figure 50-2, chronically hypertensive women destined to develop severe superimposed preeclampsia have higher initial blood pressures that nadir earlier than those of women who do not develop severe disease.


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Obstentrics_Williams. Thus far, clinical prognostic and predictive tests for superimposed preeclampsia have been disappointing (CondeAgudelo, 2015). Di Lorenzo and colleagues (2012) studied serum markers for Down syndrome to predict preeclampsia and calculated a sensitivity of 60 percent, with a 20-percent false-positive rate. Similar results were found using antiangiogenic factors to discriminate among chronic hypertension, gestational hypertension, and preeclampsia (Costa, 2016; Sibai, 2008). According to Anton and coworkers (2013), microRNA assays may prove valuable as predictors of pregnancy-associated hypertension. Trials ofvarious medications to prevent preeclampsia in women with chronic hypertension have generally been disappointing and


Obstentrics_Williams

Obstentrics_Williams. Trials ofvarious medications to prevent preeclampsia in women with chronic hypertension have generally been disappointing and Chronic hypertension augments the risk two-to threefold for premature placental separation. he general obstetrical population risk is 1 in 200 to 300 pregnancies, and this rises to 1 in 60 to 120 pregnancies in women with chronic hypertension (Ankumah, 2014; Cruz, 2011; Magee, 2015). he abruption risk is elevated further if the woman smokes. Most abruptions are in women with worsening gestational hypertension or superimposed preeclampsia. The abruption risk is highest with severe hypertension, and Vigil-De Gracia and colleagues (2004) reported it to be 8.4 percent. From medical record data from the Norwegian Birth Registry, folic acid and/or multivitamin supplements slightly lowered the abruption incidence in women with chronic hypertension (Nilsen, 2008).


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Obstentrics_Williams. Rates of almost all adverse perinatal outcomes are greater in women with chronic hypertension than in nonafected controls. As expected, for the entire group of hypertensive women, those who developed preeclampsia have substantially higher adverse outcome rates compared with those without preeclampsia. As shown in Figure 50-3, adverse outcome rates rise incrementally with rising blood pressures. Evidence also supports that chronic hypertension-treated or untreated-is associated with show little or no benefit. Low-dose aspirin has been evaluated 55


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Obstentrics_Williams. FIGURE 50-3 Frequency of selected adverse maternal and perinaLa! uuLcomes by blood stratification in women with mild chronic hypertension. SGA = small for gestational age. (Data Ankumah,o2014.) most frequently (Mol, 2016; Sta, 2015). In the MFMU Network study by Caritis (1998) cited above, the incidence ofsuperimposed preeclampsia, fetal-growth restriction, or both is similar in women given low-dose aspirin or placebo. Using the same database, Moore and associates (2015) found that early administration of low-dose aspirin « 17 weeks' gestation) resulted in a significant 41-percent lower frequency of superimposed preeclampsia in chronically hypertensive women-18 versus 31 percent. Duley (2007) and Meads (2008) and their colleagues performed systematic reviews and noted that low-dose aspirin was beneicial in some high-risk women. Moderate beneits were also found from a metaanalysis by Askie and coworkers (2007). In a secondary analysis, Poon and associates (2017) noted that aspirin was


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Obstentrics_Williams. was beneicial in some high-risk women. Moderate beneits were also found from a metaanalysis by Askie and coworkers (2007). In a secondary analysis, Poon and associates (2017) noted that aspirin was inefective to reduce the incidence ofpreterm preeclampsia.


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Obstentrics_Williams. he U.S. Preventive Services Task Force recommends treatment with low-dose aspirin for chronically hypertensive congenital anomalies. Bateman and coworkers (2015) from the Medicaid Analytic Extract cited earlier found an elevated risk for severe congenital malformations-especially cardiac defects. Moreover, severe hypertension and fetal esophageal atresia or stenosis have been associated (Binhidy, 2011; Van Gelder, 2015).


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Obstentrics_Williams. The stillbirth frequency with chronic hypertension is substantively greater in most reports (Chap. 35, p. 646). In the Nationwide Patient Sample study, the stillbirth rate was 15.1 per 1000 births (Bateman, 2012). This is similar to that of 18 per 1000 from a Norwegian study by Ahmad and coworkers (2012) and of 24 per 1000 births from a Network study reported by Ankumah and colleagues (2014) and described on page 982. Low-birthweight neonates are also common. hey are due to fetal-growth restriction, preterm delivery that is largely clinically indic�ted, or both (see Fig. 50-3). In the California database study noted earlier, a fourth of fetuses were delivered preterm (Yanit, 2012).


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Obstentrics_Williams. These and other studies attest to the elevated risk for fetalgrowth restriction, and the incidence averages 20 percent. Zetterstrom and coworkers (2006) reported a 2.4-fold risk for fetal-growth restriction in 2754 chronically hypertensive Swedish women compared with the risk in normotensive women. Broekhuijsen and associates (2012) found a 1.3-fold increased risk for 1609 Dutch nulliparas with chronic hypertension compared with that in normotensive controls. As with other complications, fetal-growth dysfunction is more likely in chronically hypertensive women who develop superimposed preeclampsia. In one study, the incidence of growth-restricted fetuses born to women with superimposed preeclampsia was almost 50 percent compared with only 21 percent in chronically hypertensive women without preeclampsia (Chappell, 2008). Finally, women with chronic hypertension severe enough to warrant treatment had an II-percent incidence of fetal-growth restriction to a degree yielding birthweights


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Obstentrics_Williams. preeclampsia (Chappell, 2008). Finally, women with chronic hypertension severe enough to warrant treatment had an II-percent incidence of fetal-growth restriction to a degree yielding birthweights ;3rd percentile (Morgan, 2016a). For all of these reasons, neonates born to these women have a correspondingly high rate of intensive-care nursery admission.


Obstentrics_Williams

Obstentrics_Williams. All of these adverse perinatal efects of chronic hypertension contribute to the greater perinatal mortality rate, which is threeto fourfold higher than the rate in nonafected gravidas (American College of Obstetricians and Gynecologists, 2013). In the Network study by Ankumah (2014) referenced in Figure 50-3, the perinatl death rate was 31 per 1000 births with mild hypertension, 72 per 1000 births with moderate disease, and 100 per 1000 births in women with severe chronic hypertension. And, in the study from Parkland Hospital by Morgan (20 16a), the perinatal mortality rate was 32 per 1000 births in women who were treated for their chronic hypertension. Again, as expected, the highest rates are in women who develop superimposed preeclampsia, for whom the risk doubled from 4 to 8 percent. Finally, if diabetes coexists with chronic hypertension, then preterm delivery, fetalgrowth restriction, and perinatal mortality rates are increased even more (Gonzalez-Gonzalez, 2008; Yanit, 2012).


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Obstentrics_Williams. he diagnosis of chronic hypertension in pregnancy should be confirmed. The American College of Obstetricians and Gynecologists (2013) recommends use of ambulatory monitoring to exclude suspected white-coat hypertension before initiating antihypertensive therapy. Goals for chronic hypertension management include rate reductions of adverse maternal or perinatal outcomes just discussed. Treatment is targeted to prevent moderate or severe hypertension and to delay or dampen the severity of pregnancy-aggravated hypertension. To some extent, these goals can be achieved pharmacologically. Blood pressure self-monitoring is encouraged, but for accuracy, automated devices must be properly calibrated (Brown, 2004; Staessen, 2004). Personal health modification includes dietary counseling and reduction of behaviors such as tobacco, alcohol, cocaine, or other substance use (see Table 50-2). A low-sodium diet is not required (American College of Obstetricians and Gynecologists, 2013).


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Obstentrics_Williams. Some women-especially those with long-term or untreated hypertension-have complications that increase the risk of adverse pregnancy events. For example, in one study, a fourth of gravidas with chronic hypertension also had concentric ventricular hypertrophy (Ambia, 2017; Kim, 20 16a). Thus, if not already accomplished, assessment during pregnancy is done for the cardiovascular and renal systems (Morgan, 2016a,b).


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Obstentrics_Williams. As concluded by the American College of Obstetricians and Gynecologists (2013, 2016a), treatment of hypertension during pregnancy has included every drug class, but information is still limited regarding safety and eicacy (Czeizel, 2011; Podymow, 2011). lthough many studies indicate greater perinatal adverse efects in gravidas requiring treatment, it is still not known whether this is due to cause or efect (Orbach, 2013). The following summary of antihypertensive drugs is abstracted from several sources, including the 2016 Physicians' Desk Rf erence. Many of these drugs are also discussed throughout Chapter 12 (p. 241) and have been reviewed by Umans and associates (2015).


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Obstentrics_Williams. PeripheraLy acting 3-adrenergic-receptor blockers cause a generalized decline in sympathetic tone and decreased cardiac output. Examples are propranolol, metoprolol, and atenolol. Labetalol is a popular and commonly used QJ3-adrenergic blocker that is considered safe. Some adrenergic-blocking drugs act centraLy by reducing sympathetic outflow to efect a generalized decreased vascular tone. These include clonidine and a-methyldopa. Drugs in this class most frequently used in pregnancy to treat hypertension are methyldopa or an a-or 3-receptor blocking agent such as labetalol.


Obstentrics_Williams

Obstentrics_Williams. hese drugs are divided into three subclasses based on their modiication of calcium entry into cells and interference with binding sites on voltage-dependent calcium channels. Common agents include nifedipine-a dihydropyridine, and verapamil-a phenylalkyl amine derivative. These agents have negative inotropic efects and thus can worsen ventricular dysfunction and congestive heart failure. Theoretically, they may potentiate the vasoactive actions of magnesium sulfate that is given for eclampsia neuroprophylaxis. Although data are limited regarding their use during pregnancy, they appear to be safe therapy for chronic hypertension (Briggs, 2015; U mans, 2015).


Obstentrics_Williams

Obstentrics_Williams. hiazide diuretics are sulfonamides, and these were the first drug group used to successfully treat chronic hypertension (Beyer, 1982). hese agents and loop-acting diuretics such as furosemide are commonly used in nonpregnant hypertensive patients. In the short term, they provide sodium and water diuresis with volume depletion. But with time, there is sodium escape, and volume depletion is partially corrected. Some aspect of lowered peripheral vascular resistance likely contributes to their efectiveness in reducing long-term morbidity (Umans, 2015).


Obstentrics_Williams

Obstentrics_Williams. Thiazide drugs may be mildly diabetogenic, and expected volume expansion may be curtailed in pregnant women. Sibai and colleagues (1984) showed that plasma volume expanded only about 20 percent over time in hypertensive pregnant women who continued diuretic therapy compared with a 50-percent expansion in women who discontinued treatment. lthough perinatal outcomes were similar in these women, such concerns have led to practices of withholding diuretics as irst-line therapy for chronic hypertension, particularly after 20 weeks' gestation (Working Group Report, 2000). Even so, in a Cochrane review, Churchill and associates (2007) reported no diferences in perinatal outcomes in 1836 nonhypertensive women randomly assigned to a thiazide diuretic or placebo for primary preeclampsia prevention. Overall, thiazide diuretics are considered safe in pregnancy (Briggs, 2015). But for preeclampsia treatment, they are considered to be inefective (Umans, 2015).


Obstentrics_Williams

Obstentrics_Williams. Hydralazine relaxes arterial smooth muscle and has been used parenterally for decades to safely treat severe peripartum hypertension (Chap. 40, p. 739). Oral hydralazine mono therapy for chronic hypertension is not generally used because of its weak antihypertensive efects and resultant tachycardia. It may be an efective adjunct for long-term use with other antihypertensives, especially if there is chronic renal insuiciency. In one study, vasodilator treatment of chronically hypertensive women was associated with a twofold rise in rates of low-birthweight and growth-restricted neonates (S u, 2013).


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Obstentrics_Williams. These drugs inhibit the conversion of angiotensin-I to the potent vasoconstrictor angiotensin-II. They can cause severe fetal malformations when given in the second and third trimesters. These include oligohydramnios, hypocalvaria, and renal dysfunction (Chap. 12, p. 241). Some preliminary studies also suggest teratogenic efects, and because of this, they are not recommended at any time during pregnancy (Briggs, 2015; Podymow, 2011). Angiotensin-receptor blockers act in a similar manner. But, instead of blocking the production of angiotensin-II, they inhibit binding to its receptor. They are presumed to have the same fetal efects as angiotensin-converting enzyme inhibitors and thus are also contraindicated.


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Obstentrics_Williams. The prognosis for pregnancy outcome with chronic hyperten sion is somewhat dependent on the severity of disease ante dating pregnancy. This may be related to indings that many women with severe hypertension have renal disease-as either cause or efect (Cunningham, 1990; Morgan, 2016a). It fol lows that women whose hypertension is severe enough to require antihypertensive therapy are at inordinately high risk for superimposed preeclampsia.


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Obstentrics_Williams. pregnancies in women whose blood pressure at 6 to 11 weeks' gestation was 2170/110 mm Hg. All were given oral treat ment with a-methyldopa and hydralazine to maintain pres sures < 160/1a10 mm Hg. Of the 44 pregnancies, superimposed preeclampsia developed in half, and all adverse perinatal out comes were in this group. Moreover, all neonates of women in the superimposed group were delivered preterm, nearly 80 percent were also growth restricted, and 48 percent sufered perinatal death. Conversely, those women with severe chronic had reasonably good outcomes. There were no perinatal deaths, and only 5 percent of fetuses were growth restricted. Webster and colleagues (2017) found labetalol and nifedipine to be equally efective for chronic hypertension in pregnant women.


Obstentrics_Williams

Obstentrics_Williams. Morgan and coworkers (2016a) reported 447 women whose chronic hypertension required treatment beginning prior to 20 weeks. More than half of these women developed superimposed severe preeclampsia. he rate of preeclampsia was 53 percent for those whose 24-hour protein excretion was <300 mg. But for those with antecedent baseline proteinuriaa> 300 mg/day, 79 percent developed severe preeclampsia. Continuing prepregnancy antihypertensive treatment during pregnancy is debatable for those with mild or moderate hypertension. Although blood pressure reduction certainly beneits the mother long term, it at least theoretically can reduce uteroplacental perfusion. In older observational reports, most pregnancy outcomes in women with mild to moderate hypertension generally were good without treatment and unless superimposed preeclampsia developed (Chesley, 1978; Umans, 2015).


Obstentrics_Williams

Obstentrics_Williams. N ewer data are accruing that address potential salutary efects on pregnancy outcomes by simply lowering blood pressure. Earlier studies were relatively small and had widely varying inclusion and outcome criteria. In a Cochrane review of 49 of these studies that included a total of 4723 women with mild to moderate hypertension, Abalos and coworkers (2014) conirmed that the risk for subsequent severe hypertension was lowered with therapy. Compared with untreated women, the frequencies of superimposed preeclampsia, eclampsia, abruption, preterm birth, fetal-growth restriction, and perinatal or maternal mortality did not difer. This latter Cochrane review raised concerns for fetal-growth restriction with 3-blocking TABLE 50-4. Selected Pregnancy Outcomes in Women with Chronic Hypertension Treated During Pregnancy with and without Baseline Proteinuriaa


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Obstentrics_Williams. TABLE 50-4. Selected Pregnancy Outcomes in Women with Chronic Hypertension Treated During Pregnancy with and without Baseline Proteinuriaa Superimposed preeclampsia 79% 49% <0.001 Abruption 0 1% 0.45 EGA at delivery (mean)b 35.1 ± 4.3 wks 37.2 ± 3.3 wks <0.001 ;30 weeks 18% 6% 0.001 ;34 weeks 34% 17% 0.005 ;37 weeks 48% 26% 0.002 Birthweight (mean)b 2379 ± 1028 g 2814 ± 807 g <0.001 ;3rd percentile 20% 9% 0.01 ; 10th percentile 41 % 22% <0.001 Perinatal mortality 36/1000 31/1000 0.47 aDefined as ::300 mgld protein excretion before 20 weeks' gestation. bMean ± standard deviations. EGA = estimated gestational age. Data from Morgan, 2016b.


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Obstentrics_Williams. Perinatal mortality 36/1000 31/1000 0.47 aDefined as ::300 mgld protein excretion before 20 weeks' gestation. bMean ± standard deviations. EGA = estimated gestational age. Data from Morgan, 2016b. drugs, ,notably atenolol. It is not resolved, however, because diminished placental perfusion secondary to lowered maternal blood pressure is confounded by the fact that worsening blood pressure itself is associated with abnormal fetal growth. Some also posit that the drugs have a direct fetal action (Umans, 2015). In two of the larger randomized trials, however, the incidence of growth restriction was not altered in women randomly assigned to treatment (Gruppo di Studio Ipertensione in Gravidanza, 1998; Sibai, 1990a).


Obstentrics_Williams

Obstentrics_Williams. he observations of Morgan and colleagues (20 16a) support the findings of the Cochrane review by Abalos. Specifically, they reported that despite therapy for chronic h) pertension, there was frequent superimposed preeclampsia, fetal-growth restriction, preterm delivery, and perinatal mortality. Moreover, and as shown in Table 50-4, women with baseline proteinuria >300 mg/ d had even worse obstetrical outcomes.


Obstentrics_Williams

Obstentrics_Williams. During the past decade, the concept of tight control of blood pressure has been espoused as a means of optimizing maternal and perinatal outcomes. Such control is analogous to that of glycemic control for management of the pregnant diabetic patient. he observational study by Ankumah (2014) noted earlier lends credence to tighter control of blood pressure. hese investigators showed that the risk of adverse pregnancy outcomes in 759 women with chronic hypertension was lower when blood pressures before 20 weeks were < 140 mm Hg compared with higher pressure categories and increasing blood pressures. Unfortunately, this did not hold up when less-tight was compared with tight control. Speciically, Magee and coworkers (2015) randomized 987 women with chronic hypertension or gestational hypertension to either one of these two management schemes. Except for a lower rate of severe hypertension in the tightly controlled group, they found no signiicant diferences between these two groups' other


Obstentrics_Williams

Obstentrics_Williams. to either one of these two management schemes. Except for a lower rate of severe hypertension in the tightly controlled group, they found no signiicant diferences between these two groups' other adverse pregnancy outcomes (Table 50-5). Tight control was also not more costly (Ahmed, 2016). These and similar findings prompted an ongoing randomized controlled trial-Project CHAP (ClinicaITrials.gov, 2016)-to answer this question.


Obstentrics_Williams

Obstentrics_Williams. Until there are data to conirm any salutary efects of treatment of uncomplicated mild to moderate chronic hypertension in pregnancy, it seems reasonable to follow the guidelines of the American College of Obstetricians and Gynecologists (2013) and the Society for Maternal-Fetal Medicine (2015). Pregnant women with severe hypertension must be treated for maternal neuro-, cardio-, and renoprotection. Treatment is ap <0.001, all other comparisons p >0.05. HELLP = hemolysis, elevated liver enzyme levels, low platelet count. Data from Magee, 201n5. also mandatory for women with prior adverse outcomes such as strokes, MIs, and evidence for cardiac or renal dysfunction. With end-organ dysfunction, treatment to diastolic pressure level ;90 mm Hg is reasonable to mitigate further organ damage. For most women with mild to moderate hypertension, the


Obstentrics_Williams

Obstentrics_Williams. With end-organ dysfunction, treatment to diastolic pressure level ;90 mm Hg is reasonable to mitigate further organ damage. For most women with mild to moderate hypertension, the College recommends that treatment be withheld as long as systolic blood pressure is < 160 mm Hg and diastolic blood pressure is < 105 mm Hg. Some find it reasonable to begin women with persistent systolic pressuresa> 150 mm Hg or dia stolic pressures of95 to 100 mm Hg or greater (August, 2015; Working Group Report, 2000). At Parkland Hospital we initi ate treatment with antihypertensive agents for blood pressures of 150/100 mm Hg or higher. Our preferred regimens include mono therapy with a 3-blocking drug such as labetalol or a calcium-channel blocking agent such as amlodipine. For women in the first half of pregnancy, therapy with a thiazide diuretic seems reasonable. This is especially true in black women, in whom there is a high prevalence of salt-sensitive chronic hypertension.


Obstentrics_Williams

Obstentrics_Williams. It is controversial whether or not women who present early in pregnancy and who are already taking antihypertensive drugs should continue to take these (Rezk, 2016). According to the American College of Obstetricians and Gynecologists (2013) and the Society for Maternal-Fetal Medicine (2015), for women with mild to moderate hypertension, it is reasonable to discontinue medications during the irst trimester and to restart them if blood pressures approach the severe range. Our practice at Parkland Hospital is to continue treatment if the woman is already taking drugs when she presents for prenatal care. Exceptions are discontinuation of angiotensin-converting enzyme inhibitors and receptor blockers.


Obstentrics_Williams

Obstentrics_Williams. Some women will have persistently worrisome hypertension despite usual therapy (Samuel, 2011; Sibai, 1990a). In these women, primary attention is given to the likelihood of pregnancy-aggravated hypertension, with or without superimposed preeclampsia. Other possibilities include inaccurate blood-pressure measurements, suboptimal treatment, and antagonizing substances such as chronic ingestion of nonsteroidal antiinlammatory drugs (NSAIDs) (Moser, 2006; Sowers, 2005). As discussed, the frequency of superimposed preeclampsia for women with chronic hypertension varies depending on the study population and hypertension severity (Ankumah, 2014). Importantly, in 40 to 50 percent of chronically hypertensive women, superimposed preeclampsia develops before 37 weeks (Chappell, 2008; Harper, 2016). This proportion is even higher in women who required hypertension treatment during pregnancy (Morgan, 20 16a).


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Obstentrics_Williams. The diagnosis may be diicult to make, especially in women with hypertension who have underlying renal disease with chronic proteinuria (Cunningham, 1990; Morgan, 2016b). As discussed in Chapter 40 (p. 712), conditions that support the diagnosis of superimposed preeclampsia include worsening hypertension, new-onset proteinuria, neurological symptoms such as severe headaches and visual disturbances, generalized edema, oliguria, and certainly, convulsions or pulmonary edema. Making the diagnosis based on worsening proteinuria in women with baseline proteinuria is problematic. Supporting laboratory abnormalities are rising serum creatinine or hepatic transaminase levels, thrombocytopenia, or any of the facets of


Obstentrics_Williams

Obstentrics_Williams. HELLP (hemolysis, �levated liver enzyme levels, low 2latelet count) syndrome. For women with chronic hypertension and superimposed preeclampsia with severe features, magnesium sulfate for maternal neuroprophylaxis is recommended (Ameri can College of Obstetricians and Gynecologists, 2013). Severe hypertension is treated as described in Chapter 40 (p. 738). Some pregnant women with chronic hypertension have worsening hypertension with no other findings of superim posed preeclampsia. This is most commonly encountered near the end of the second trimester. In the absence of other supporting criteria for superimposed preeclampsia, this likely represents the higher end of the normal blood-pressure curve shown in Figure 50-1. In such women, if preeclampsia can be confidently excluded, it is reasonable to begin or to increase the dose of antihypertensive therapy.


Obstentrics_Williams

Obstentrics_Williams. Women with well-controlled chronic hypertension who have no complicating factors can generally be expected to have a good pregnancy outcome. Because even those with mild hypertension have a greater risk of superimposed preeclampsia and fetal-growth restriction, serial antepartum assessment of fetal well-being is recommended by many. That said, according to the American College of Obstetricians and Gynecologists (2013), with the exception of sonographic fetal-growth monitoring, described in Chapter 44 (p. 852), no conclusive data address either benefit or harm associated with various antepartum surveillance strategies. • Expectant Management of Early-Onset


Obstentrics_Williams

Obstentrics_Williams. • Expectant Management of Early-Onset Given that many women with chronic hypertension develop superimposed preeclampsia before term, considerations for expectant management may be reasonable in some cases. In a study from Magee-Women's Hospital, 41 careully selected women with a median gestational age of 31.6 weeks were expectantly managed (Samuel, 2011). Despite liberal criteria to mandate delivery, 17 percent developed either placental abruption or pulmonary edema. The latency period was extended by a mean of 9.7 days. There were no perinatal deaths, however, salutary outcomes were similar. These investigators recommend randomized trials to study expectant management before this becomes usual care.


Obstentrics_Williams

Obstentrics_Williams. For chronically hypertensive women who have complications such as fetal-growth restriction or superimposed preeclampsia, the decision to deliver is made by clinical judgment. The route of delivery is dictated by obstetrical factors. Certainly, most women with superimposed severe preeclampsia are better delivered even when the fetus is markedly preterm. Increased risk for placental abruption, cerebral hemorrhage, and peripartum heart failure attend delivery delays (Cunningham, 1986, 2005; Martin, 2005). For women with chronic hypertension without preeclampsia, expectant management at later gestational ages was reported recently by Harper and colleagues (2016). They concluded that expectant management beyond 39 weeks' gestation was associated with an increasing incidence of severe preeclampsia and that planned delivery before 37 weeks was associated with a rise in rates of adverse neonatal outcomes.


Obstentrics_Williams

Obstentrics_Williams. For women with mild to moderate chronic hypertension who continue to have an uncomplicated pregnancy, the merican College of Obstetricians and Gynecologists (2013) recommends delivery not be pursued until 38°17 weeks. The consensus committee indings by Spong and associates (2011) recommend consideration for delivery at 38 to 39 weeks, that is, :::37 completed weeks. A trial of labor induction is preferable, and many of these women respond favorably and will be delivered vaginally (Alexander, 1999; Atkinson, 1995).


Obstentrics_Williams

Obstentrics_Williams. For women with severe preeclampsia, peripartum management is the same as described in Chapter 40 (p. 729). Epidural analgesia for labor and delivery is optimal with the caveat that it is not given to treat hypertension (Lucas, 2001). hat said, women with severe superimposed preeclampsia are more sensitive to the acute hypotensive efects of epidural analgesia (Vricella, 2012). Also in this group, magnesium sulfate neuroprophylaxis is initiated for prevention of eclampsia. Severe hypertension-diastolic blood pressure :::110 mm Hg or systolic pressurea:::160 mm Hg-is treated with either intravenous hydralazine or labetalol. Some prefer to treat women when the diastolic pressure reaches 100 to 105 mm Hg. Vigil-De Gracia and colleagues (2006) randomly assigned 200 women to intravenous hydralazine or labetalol to acutely lower severe high blood pressure in pregnancy. Outcomes were similar except for significantly more maternal palpitations and tachycardia with hydralazine and signiicantly


Obstentrics_Williams

Obstentrics_Williams. or labetalol to acutely lower severe high blood pressure in pregnancy. Outcomes were similar except for significantly more maternal palpitations and tachycardia with hydralazine and signiicantly more neonatal hypotension and bradycardia with labetalol.


Obstentrics_Williams

Obstentrics_Williams. In most respects, postpartum observation, prevention, and management of adverse complications are similar in women with severe chronic hypertension and in those with severe preeclampsia-eclampsia. For persistent severe hypertension, consideration is given for a cause such as pheochromocytoma or Cushing disease (Sibai, 2012). And, in women with chronic end-organ damage, certain complications are more common. These include cerebral or pulmonary edema, heart failure, renal dysfunction, or cerebral hemorrhage, especially within the irst 48 hours after delivery (Martin, 2005; Sibai, 1990b, 2012). hese frequently are preceded by sudden elevations"spikes"-of mean arterial blood pressure and of the systolic component (Cunningham, 2000, 2005).


Obstentrics_Williams

Obstentrics_Williams. Following delivery, as maternal peripheral resistance rises, left ventricular workload also grows. This elevation is further aggravated by appreciable and pathological amounts of interstitial luid that are mobilized to be excreted as endothelial disruption from preeclampsia resolves. In these women, sudden hypertension-either moderate or severe-may exacerbate diastolic dysfunction, cause systolic dysfunction, and lead to pulmonary edema (Cunningham, 1986; Gandhi, 2001). Prompt hypertension control, along with furosemide-evoked diuresis, usually quickly resolves pulmonary edema.


Obstentrics_Williams

Obstentrics_Williams. he antihypertensive regimen given antepartum can be restarted in the puerperium. It is also possible in many women to forestall postpartum hypertension by administering intravenous or oral furosemide to augment the normal postpartum diuresis. In one study, 20-mg oral furosemide given daily for 5 days to postpartum women with severe preeclampsia aided blood pressure control (Ascarelli, 2005). Daily weights are helpful in this regard. On average, a woman should weigh 15 pounds less immediately after delivery. Excessive extracellular fluid can then be estimated. Other studies are in progress to determine aspects of postpartum blood pressure management (Cursino, 2015). Some evidence supports that chronic ingestion ofNSAIDs in the puerperium elevates blood pressure in women with severe preeclampsia (Vigil-De Gracia, 2017). his may not be problematic if these drugs are given only as needed (Wasden, 2014).


Obstentrics_Williams

Obstentrics_Williams. Women with chronic hypertension have special considerations for contraceptive and sterilization choices. These are discussed in detail throughout Chapters 38 and 39. Ultimately, women with chronic hypertension are at high risk for lifetime cardiovascular complications, especially when accompanied by diabetes, obesity, and the metabolic syndrome. Recent evidence also suggests that these women are at greater risk to develop cardiomyopathy remote from pregnancy (Behrens, 2016). Abalos E, Duley L, Steyn OW, et al: Antihypertensive drug therapy for mild to moderate hypertension during pregnancy. Cochrane Database Syst Rev 2:CD002252,t2014 Ahmad AS, Samuelsen SO: Hypertensive disorders in pregnancy and fetal death at diferent gestational lengths: a population study of2 121 371 pregnancies. BJOG 119(12):1521,t2012 Ahmed RJ, Gafni A, Hutton EK, et al: The cost implications ofless tight versus tight control of hypertension in pregnancy (CHIPS Trial). Hypertension 68(4):1049,t2016


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Obstentrics_Williams. Ahmed RJ, Gafni A, Hutton EK, et al: The cost implications ofless tight versus tight control of hypertension in pregnancy (CHIPS Trial). Hypertension 68(4):1049,t2016 Alexander JM, Bloom SL, Mcintire DO, et al: Severe preeclampsia and the very low birth weight infant: is induction of labor harmful? Obstet Gynecol 93:485, 1999 Ambia M, Morgan JL, Wilson L, et al: Frequency and consequences of ventricular hypertrophy in pregnant women with treated chronic hypertension. Am J Obstet GynecoIt217:467.e1, 2017 American College of Obstetricians and Gynecologists: Chronic hypertension in pregnancy and superimposed preeclampsia. In: Hypertension in Pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy. 2013


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Obstentrics_Williams. American College of Obstetricians and Gynecologists: Hypertension. In Clinical Updates in Women's Health Care, Volume V, No. I, January 2016a American College of Obstetricians and Gynecologists: Practice advisory on lowdose aspirin and prevention of preeclampsia: updated recommendations. 2016b. Available at: http://ww.acog.org/About-ACOG/News-Room/ Practice-Advisories/Practice-Advisory-Low-Dose-Aspirin-and-Preventionof-Preeclampsia-U pdated-Recommendations. Accessed January 5, 2017 Ankumah NA, Cantu J, Jauk V, et al: Risk of adverse pregnancy outcomes in women with mild chronic hypertension before 20 weeks of gestation. Obstet Gynecol 123(5):966,t2014 Anton L, Olarerin-George AO, Schwartz N, et al: miR-210 inhibits trophoblast invasion and is a serum biomarker for preeclampsia. Am J Pathol 183(5):1437,t2013 Ascarelli MH, Johnson V, McCreary H, et al: Postpartum preeclampsia management with furosemide: a randomized clinical trial. Obstet Gynecol 105(1):29,t2005


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Obstentrics_Williams. Ascarelli MH, Johnson V, McCreary H, et al: Postpartum preeclampsia management with furosemide: a randomized clinical trial. Obstet Gynecol 105(1):29,t2005 Askie LM, Duley L, Henderson-Smart OJ, et al: Antiplatelet agents for prevention of pre-eclampsia: a meta-analysis of individual patient data. Lancet 369(9575):1791,t2007 Atkinson MW, Guinn 0, Owen J, et al: Does magnesium sulfate afect the length of labor induction in women with pregnancy-associated hypertension? Am J Obstet GynecoIt173(4):1219, 1995 August P, Jeyabalan A, RobertS JM: Chronic hypertension and pregnancy. In: Taylor N, RobertS JM, Cunningham FG, et al (eds): Chesley's Hypertensive Disorders in Pregnancy. Amsterdam, Academic Press, 2015 Banhidy F, Acs N, Puh6 EH, et al: Chronic hypertension with related drug treatment of pregnant women and congenital abnormalities in their ofspring: a population-based study. Hypertens Res 34(2):257, 2011


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Obstentrics_Williams. Broekhuijsen K, Langeveld J, van den Berg P, et al: Maternal and neonatal outcomes in pregnancy in women with chronic hypertension. Am J Obstet GynecoIt206:S344,t20t12 Brown M, McHugh L, Mangos G, et al: Automated self-initiated blood pressure or 24-hour ambulatory blood pressure monitoring in pregnancy? BJOG 111 :38, 2004 Caritis S, Sibai B, Hauth J, et al: Low-dose aspirin to prevent preeclampsia in women at high risk. N EnglJ Med 338(11):701,t1998 Centers for Disease Control and Prevention: Vital signs: prevalence, treatment, and control of hypertension-United States, 1999-2002 and 2005-2008. MMWR 60(4):1,t2011 Chappell LC, Enye S, Seed P, et al: Adverse perinatal outcomes and risk factors for preeclampsia in women with chronic hypertension: a prospective study. Hypertension 51(4):1002, 2008


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Obstentrics_Williams. Chappell LC, Enye S, Seed P, et al: Adverse perinatal outcomes and risk factors for preeclampsia in women with chronic hypertension: a prospective study. Hypertension 51(4):1002, 2008 Chesley LC: Superimposed preeclampsia or eclampsia. In Chesley LC (ed): Hypertensive Disorders in Pregnancy. New York, Appleton-Century-Crots, 1978 Churchill 0, Beevers GO, Meher S, et al: Diuretics for preventing pre-eclamp sia. Cochrane Database Syst Rev 1 :CD004451, 200 Clark SL, Hankins GO: Preventing maternal death. 10 clinical diamonds. Obstet Gynecol 119(2):360,t2012 ClinicalTrials.gov: Chronic Hypertension and Pregnancy (CHAP) Project. 2016. Available at: https:llclinicaltrials.gov/ct2/show/NCT02299414. Accessed JanualY 5,t2017 Conde-Agudelo A, Romero R, RobertS ltvl: Tests to predict preeclampsia. In Taylor N, RobertS JM, Cunningham FG, et al (eds): Chesley's Hypertensive Disorders in Pregnancy, 4th ed. Amsterdam, Academic Press, 20t15


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Obstentrics_Williams. Costa A, Hoshida MS, Alves A, et al: Preeclampsia and superimposed preeclampsia: the same disease? he role of angiogenic biomarkers. Hypertens Pregnancy 35(2): 139,t2016 Cowley AW Jr: he genetic dissection of essential hypertension. Nat Rev Genet 7:829,t2006 Creanga A, Berg CJ, Syverson C, et al: Pregnancy-related mortality in the United States, 2006-2010. Obstet Gynecol 125(1):5,t2015 Cruz MO, Gao W, Hibbard JU: Obstetrical and perinatal outcomes among women with gestational hypertension, mild preeclampsia, and mild chronic hypertension. Am J Obstet GynecoIt205:260.el, 2011 Cunningham FG: Severe preeclampsia and eclampsia: systolic hypertension is also important. Obstet Gynecol 105:237,t2005 Cunningham FG, Cox SM, Harstad W, et al: Chronic renal disease and pregnancy outcome. Am J Obstet Gynecol 163:453, 1990


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Obstentrics_Williams. Cunningham FG, Cox SM, Harstad W, et al: Chronic renal disease and pregnancy outcome. Am J Obstet Gynecol 163:453, 1990 Cunningham FG, Pritchard JA, Hankins GO, et al: Idiopathic cardiomyopathy or compounding cardiovascular events? Obstet GynecoI67:157, 1986 Cunningham FG, Twickler 0: Cerebral edema complicating eclampsia. Am J Obstet Gynecol 182(1):94,t2000 Cursino T, Katz L, Coutinho I, et al: Diuretics vs. placebo for postpartum blood pressure control in preeclampsia (DIUPRE): a randomized clinical trial. Reprod Health 12:66,t2015 Czeizel AE, Banhidy F: Chronic hypertension in pregnancy. Curr Opin Obstet Gynecol 23(2):76, 2011 Di Lorenzo G, Ceccarello M, Cecotti V, et al: First trimester maternal serum PIGF, free b-hCG, PAPP-A, PP-13, uterine artery Doppler and maternal history for the prediction of preeclampsia. Placenta 33(6):495, 2012


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Obstentrics_Williams. Duley L, Henderson-Smarr OJ, Meher S, et al: Antiplatelet agents for preventing pre-eclampsia and its complications. Cochrane Database Syst Rev 2:CD004659, 2007 Eckel RH, Jakicic JM, Ard JD, et al: 2013 AHAIACC guidelines on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiologyl American Heart Association Task Force on Practice Guidelines. Circulation 129(25 Suppl 2):S76, 2013 Forouzanfar MH, Liu P, Roth GA, et al: Global burden of hypertension and sysrolic blood pressure of at least 110 to 115 mm Hg, 1990-2015. JM1A 317:165,t2017 Gainer J, Alexander J, Mclntire 0, et al: Maternal echocardiogram findings in pregnant patients with chronic hypertension. Presented at the 25th Annual Meeting of the Society for Maternal-Fetal Medicine, Reno, February 7-12, 2005


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Obstentrics_Williams. Gandhi SK, Powers JC, Nomeir A, et al: The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med 344(1): 17, 2001 Gilbert M, YoungAL, Danielsen B: Pregnancy-outcomes in women with chronic hypertension: a population-based study. J Reprod Med 52(11): 1 046, 2007 Gonzalez-Gonzalez NL, Ramirez 0, Mozas J, et al: Factors inluencing pregnancy outcomes in women with type 2 versus type 1 diabetes mellitus. Acta Obstet Gynecol Scand 87(1):43, 2008 Gruppo di Studio Iperrensione in Gravidanza: Nifedipine versus expectant management in mild to moderate hypertension in pregnancy. BJOG 105(7): 718, 1998 Harper LM, Biggio JR, Anderson S, et al: Gestational age of delivery in pregnancies complicated by chronic hypertension. Obstet Gynecol 127(6):1101,t2016


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Obstentrics_Williams. Harper LM, Biggio JR, Anderson S, et al: Gestational age of delivery in pregnancies complicated by chronic hypertension. Obstet Gynecol 127(6):1101,t2016 Henderson JT, Whitlock EP, O'Connor E, et al: Low-dose aspirin for prevention of morbidity and mortality from preeclampsia: a systematic evidence review for the U.S. Preventive Services Task Force. Ann Intern Med 160(10): 695,t2014 Hibbard JU, Korcarz CE, Nendaz GG, et al: The arterial system in pre-eclampsia and chronic hypertension with superimposed pre-eclampsia. BJOG 112(7):897,t2005 Hibbard JU, Shrof SG, Cunningham FG: Cardiovascular alterations in pregnancy and preeclamptic pregnancy. In Taylor RN, Roberts JM, Cunningham FG, et al (eds): Chesley's Hypertensive Disorders in Pregnancy. Amsterdam, Academic Press, 2015 Hladunewich MA, Schaefer F: Proteinuria in special populations: pregnant women and children. Adv Chronic Kidney Dis 18(4):267,t2011


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Obstentrics_Williams. Hladunewich MA, Schaefer F: Proteinuria in special populations: pregnant women and children. Adv Chronic Kidney Dis 18(4):267,t2011 James PA, Oparil S, Carter BL, et al: 2014 evidence-based guidelines for the management of high blood pressure in adults. Report from the panel members appointed to the Eighth Joint National Committee ONC 8). JAMA 311(5):507,t2014 Jeyabalan A, Hubel CA, Roberts JM: Metabolic syndrome and preeclampsia. In Taylor RN, RobertS JM, Cunningham FG, et al (eds): Chesley's Hyper tensive Disorders in Pregnancy, 4th ed. Amsterdam, Academic Press, 2015 Kim MJ, Seo J, Cho Kl, et al: Echocardiographic assessment of structural and hemodynamic changes in hypertension-related pregnancy. J Cardiovasc Ultrasound 24:28, 2016a Kim SA, Park JB: OS 23-03 Midtrimester risk prediction of superimposed pre-eclampsia in pregnant women with chronic hypertension. J Hypertens 34 Suppl 1:e241, 2016b


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Obstentrics_Williams. Kim SA, Park JB: OS 23-03 Midtrimester risk prediction of superimposed pre-eclampsia in pregnant women with chronic hypertension. J Hypertens 34 Suppl 1:e241, 2016b Kotchen TA: Hypertensive vascular disease: In Kasper DL, Fauci AS, Hauser SL, et al (eds): Harrison's Principles of Internal Medicine, 19th ed. New York, McGraw-Hill Education, 20t15 Kuper SG, Tita AT, Youngstrom ML, et al: Baseline renal function tests and adverse outcomes in pregnant patients with chronic hypertension. Obstet Gynecol 128:93,t2016 Leon MG, Moussa HN, Longo M, et al: Rate of gestational diabetes mellitus and pregnancy outcomes in patients with chronic hypertension. Am J PerinatoIt33(8):745,t2016 Levine RJ, Hauth JC, Curet LB, et al: Trial of calcium to prevent preeclampsia. N Engl J Med (2):69, 199


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Obstentrics_Williams. Levine RJ, Hauth JC, Curet LB, et al: Trial of calcium to prevent preeclampsia. N Engl J Med (2):69, 199 Lindheimer MD, Taylor RN, Roberts JM et al: Introduction, history, controversies, and deinitions. In Taylor RN, Roberts JM, Cunningham FG, et al (eds): Chesley's Hypertensive Disorders in Pregnancy, 4th ed. Amsterdam, Academic Press, 2015 Lucas M), Sharma SK, McIntire DD, et al: A randomized trial of labor analgesia in women with pregnancy-induced hypertension. Amt) Obstet Gynecol 185(4):970,t2001 Magee A, von Dadelszen P, Rey E, et al: Less-tight versus tight control of hypertension in pregnancy. N Engl) Med 2(5):407,t2015 Martin )N )r, Thigpen BD, Moore RC, et al: Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure. Obstet Gynecol 105(2):246, 2005


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Obstentrics_Williams. Martin )N )r, Thigpen BD, Moore RC, et al: Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure. Obstet Gynecol 105(2):246, 2005 Meads CA, Cnossen )S, Meher S, et al: Methods of prediction and prevention of pre-eclampsia: systematic reviews of accuracy and efectiveness literature with economic modelling. Health Technol Assess 12(6):1,t2008 Mol BW, Roberts CT, Thangaratinam S, et al: Pre-eclampsia. Lancet 387(10022):999,t2016 Moodley): Maternal deaths due to hypertensive disorders in pregnancy: Saving Mothers report 2002-2004. Cardiovasc) Afr 18:358,t2007 Moore GS, Allshouse A, Post AL. et al: Early initiation of/ow-dose aspirin for reduction in preeclampsia risk in high-risk women: a secondary analysis of the MFMU high-risk aspirin study.) Perinatol 35(5):328,t2015 Morgan )L, Nelson DB, RobertS SW, et al: Blood pressure profiles across pregnancy in women with chronic hypertension. Am) PerinatoI33(12): 1128, 2016a


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Obstentrics_Williams. Morgan )L, Nelson DB, RobertS SW, et al: Blood pressure profiles across pregnancy in women with chronic hypertension. Am) PerinatoI33(12): 1128, 2016a Morgan )L, Nelson DB, Roberts SW, et al: The association of baseline proteinuria and adverse pregnancy outcomes in pregnant women with treated chronic hypertension. Obstet Gynecol 128:270, 2016b Moser M, Setaro )F: Resistant or diicult-to-control hypertension. N Engl ) Med 355:385, 2006 Moussa HN, Leon MG, Marti A, et al: Pregnancy outcomes in women with preeclampsia superimposed on chronic hypertension with and without severe features. Am) PerinatoIt34(4):403, 2017 Nilsen RM, Vollset SE, Rasmussen SA, et al: Folic acid and multivitamin supplement use and risk of placental abruption: a population-based registry study. Am) Epidemiol 167(7):867,t2008


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Obstentrics_Williams. Physicians' Desk Reference, 70th ed. Chestertown, PDR Network, 2016 Podymow T, August P: Antihypertensive drugs in pregnancy. Semin Nephrol 31(1):70,t2011 Poon LC, Wright D, Rolnik DL, et al: Aspirin for evidence-based preeclampsia prevention trial: efect of aspirin in prevention of preterm preeclampsia in subgroups of women according to their characteristics and medical and obstetrical history. Am ) Obstet Gynecol August 4, 2017 [Epub ahead of print] Rezk M, Eliakwa H, Gamal A, Emara M: Maternal and fetal morbidiry following discontinuation of antihypertensive drugs in mild to moderate chronic hypertension: a 4-year observational study. Pregnancy Hypertens 6:291, 2016 Rosner )Y, Gutierrez M, Dziadosz M, et al: Prehypertension in early pregnancy: what is the signiicance? Am) PerinatoIt34(2):1l7, 2017


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Obstentrics_Williams. Rosner )Y, Gutierrez M, Dziadosz M, et al: Prehypertension in early pregnancy: what is the signiicance? Am) PerinatoIt34(2):1l7, 2017 Samuel A, Lin C, Parviainen K, et al: Expectant management of preeclmpsia superimposed on chronic hypertension. ) Matern Fetal Neonatal Med 24(7) :907, 2011 Sibai BM: Etiology and management of postpartum hypertension-preeclampsia. Amt) Obstet Gynecol 206(6):470, 2012 Sibai BM, Anderson GD: Pregnancy outcome of intensive therapy in severe hypertension in irst trimester. Obstet Gynecol 67(4):517, 1986 Sibai BM, Grossman A, Grossman HG: Efects of diuretics on plasma volume in pregnancies with long-term hypertension. Am ) Obstet Gynecol 150(7):831, 1984 Sibai BM, Koch vA, Freire S, et al: Serum inhibin A and angiogenic factor levels in pregnancies with previous preeclampsia andlor chronic hypertension: are they useful markers for prediction of subsequent preeclampsia? Am ) Obstet Gynecol 199(3):268.e 1, 2008


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Obstentrics_Williams. Sibai BM, Mabie We, Shamsa F, et al: A comparison of no medication versus methyldopa or labetalol in chronic hypertension during pregnancy. Am ) Obstet Gynecol 162(4):960, 1990a Sibai BM, Villar A, Mabie BC: Acute renal failure in hypertensive disorders of pregnancy. Pregnancy outcome and remote prognosis in thirry-one consecutive cases. Am) Obstet GynecoIt162(3): 7, 1990b Sociery for Maternal-Fetal Medicine: SMFM statement: beneit of antihypertensive therapy for mild-to-moderate chronic hypertension during pregnancy remains uncertain. Am) Obstet GynecoIt213(1):3, 2015 Sowers )R, White WB, Pitt B, et al: he efects of cyclooxygenase-2 inhibitors and nonsteroidal anti-inflammatory therapy on 24-hour blood pressure in patients with hypertension, osteoarthritis, and rype 2 diabetes mellitus. Arch Intern Med 165(2):161,t2005 Spaan JJ, Sep S), van Balen VL, et al: Metabolic syndrome as a risk factor for hypertension after preeclampsia. Obstet Gynecol 120(2 Pt 1):311, 2012


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