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Belfort 3 1 Scotsdale Healthcare, Scottsdale, Arizona and Department of Obstetrics and Gynecology, University of Arizona College of Medicine, Tucson, AZ, USA 2 Department of Cardiology, Marshfi eld Clinic, Marshfi eld, WI, USA 3 Department of Obstetrics and Gynecology, Division of Maternal - Fetal Medicine, University of Utah School of Medicine, Salt Lake City, UT and HCA Healthcare, Nashville, TN, USA Introduction Although cardiac disease complicates only 1 – 4% of all pregnan- cies in the United States, such conditions continue to account for up to 10 – 25% of maternal mortality [1 – 5] . Similar fi ndings are seen elsewhere. In the recently published Confi dential Enquiry into maternal deaths, Why Mothers Die , 2000 – 2002, heart disease has now become the leading cause of indirect maternal death in the UK. In contrast to the very distant past, rheumatic fever and its valvular sequelae of heart failure is no longer the most common cause of maternal mortality. Both maternal congenital heart disease and acquired maternal heart disease such as myocardial infarction and cardiomyopathy now are the predominant causes of maternal death. With advances in the treatment of congenital heart disease in newborns and children, more young women are reaching reproductive age and attempting pregnancy. As a con- sequence, congenital heart disease is a common form of heart disease complicating pregnancy in North American women. On the other end of the spectrum, more women are postponing pregnancy until the fourth or fi fth decade of life – a time where underlying medical conditions such as hypertension and diabe- tes, coupled with advancing maternal age, may exacerbate the incidence of acquired heart disease (such as myocardial infarction or cadiomyopathy) complicating pregnancy. Indeed, in the UK, maternal mortality rates from congenital causes have remained stable but those from ischemia/cardiomyopathy have risen. The long held belief that pregnancy is absolutely contraindi- cated in maternal cardiovascular diasease is no longer justifi able using evidenced - based medicine. There are some conditions in which pregnancy is contraindicated and a high maternal risk and poor fetal outcome can be predicted. However, in many women with heart disease a more favorable maternal and fetal outcome will be expected.This chapter, therefore, will focus on the precari- ous interaction between cardiac disease and pregnancy. Counseling the p regnant c ardiac p atient Maternal outcome in the cardiac patient is dependent upon the type of cardiac disease, myocardial function, maternal functional status, presence and severity of cyanosis, pulmonary vascular pressures/resistance and prior surgical procedures along with any uncorrected lesions and residuae or sequelae of repair. Of these, maternal functional status, the degree of cyanosis along with accompanying pulmonary vascular pressure/resistance, and the type of current maternal cardiac disease are the most predictive of an adverse outcome. Siu et al [6] have reported a method of assessing risk and outcomes in women with cardiac disease using (i) functional status, (ii) left heart dysfunction, (iii) prior cardiac events, and (iv) left heart obstruction as indicators of who is at a level of risk that can safely allow delivery at a community hospital. Before 1973, the Criteria Committee of the New York Heart Association (NYHA) recommended a classifi cation of cardiac disease based on clinical function (classes I – IV). Table 20.1 out- lines the specifi cs of the NYHA classifi cation system. Such a clas- sifi cation is useful in discussing the pregnant cardiac patient, although patients who begin pregnancy as functional class I may develop congestive heart failure and pulmonary edema during the course of gestation. Other classifi cations including the Canadian Cardiovascular Society Functional Classifi cation (classes I – IV) and Specifi c Activity Scale have been used in other countries and have similar grades of disability. This functional classifi cation system, although somewhat anti- quated, remains most useful when comparing the performance of individuals with uniform etiologic and anatomic defects. In general, most women who begin pregnancy as a functional class NYHA I or II have an improved outcome as compared with those classifi ed as class III or IV [7] . Counseling the pregnant cardiac patient regarding her prog- nosis for successful pregnancy is further complicated by recent advances in medical and surgical therapy, fetal surveillance, and neonatal care. Such advances render invalid many older estimates of maternal mortality and fetal wastage. Table 20.2 represents a Cardiac Disease 257 Currently available data suggest that today maternal mortality is almost exclusively seen in patients with pulmonary hyperten- sion, cardiac valvular disease (acquired or congenital) and includ- ing endocarditis, coronary artery disease, cardiomyopathy, and sudden cardiac arrhythmia death. DeSwiet, reporting on mater- nal mortality from heart disease in the United Kingdom between 1985 and 1987, stated that all deaths occurred due to endocarditis (22%), pulmonary hypertension (30%), coronary artery disease (39%), and cardiomyopathy or myocarditis (9%) [2] . Similarly, a review of maternal mortality in Utah from 1982 to 1994 revealed 13 cardiac deaths, 4 (31%) due to pulmonary hypertension, 4 secondary to cardiomyopathy (31%), 2 due to coronary artery disease (15%), and 3 (23%) due to sudden arrhythmia [9] . In a smaller series of maternal deaths from West Virginia between 1985 and 1989, the two cardiac deaths described were due to cardiomyopathy [10] . Clark et al [11] reported on 95 maternal deaths within a large USA community hospital system in which 1.46 million deliveries occurred over a 6 - year period (2000 – 2006). Cardiac disease accounted for 11% of all deaths (n = 10) and was the fourth most common cause of death after complications of pre - eclampsia, amniotic fl uid embolism, and obstetric hemor- rhage). Of interest is that 50% of the cardiac deaths were associ- ated with myocardial infarction in women with no prior history of ischemic heart disease. In a study of 252 pregnancies in women with cardiac disease the following independent predictors of cardiac events (conges- tive heart failure, arrhythmia, and stroke) were identifi ed [12] : • NYHA functional class III or IV • maternal cyanosis • history of prior arrhythmia • pulmonary vascular disease • myocardial dysfunction (ejection fraction < 40%) • left heart obstruction. The same authors then prospectively applied these risk predic- tors to another cohort of women with congenital or acquired cardiac disease and found that the four predictors of having cardiac events were: • left ventricular systolic dysfunction (LVEF < 40%) • poor functional status/cyanosis • previous cardiac event (heart failure, stroke, transient ischemic attack) • left - sided cardiac valvular lesions (mitral valve area < 2.0 cm 2 , aortic valve area < 1.5 cm 2 ) . One point was given for each fi nding. Not suprisingly, those with scores of 0 and no specifi c risk issue had the lowest risk of developing pulmonary edema, stroke, arrhythmia necessitating treatment, cardiac arrest or death. In a study by Presbitero et al. [13] , looking at the outcome of the mother and the fetus in pregnancies complicated by cyanotic congenital heart disease, the adverse impact of low maternal oxygen saturation was clearly illustrated. The likelihood of a live birth was less frequent (12%) if the mother ’ s resting oxygen satu- ration was below 85% as compared to a resting oxygen saturation of greater than 85% (63%). It would appear, however, that with synthesis of maternal risk estimates for various types of cardiac disease that was initially developed for the fi rst edition of this text in 1987. Counseling of the pregnant cardiac patient, as well as general management approaches, were based on this classifi ca- tion [8] . Category I included conditions that, with proper man- agement, were associated with negligible maternal mortality (1%). Cardiac lesions in category II traditionally carried a 5 – 15% risk of maternal mortality. Patients with cardiac lesions in group III were, and probably remain, subject to a mortality risk exceed- ing 25%. In all but exceptional cases, this risk is unacceptable, and prevention or interruption of pregnancy is generally recommended. Table 20.1 New York Heart Association ( NYHA ) functional classifi cation system. Class I No limitations of physical activity, ordinary physical activity does not precipitate cardiovascular symptoms such as dyspnea, angina, fatigue, or palpitations Class II Slight limitation of physical activity. Ordinary physical activity will precipitate cardiovascular symptoms. Patients are comfortable at rest Class III Less than ordinary physical activity precipitates symptoms that markedly limit activity. Patients are comfortable at rest Class IV Patients have discomfort with any physical activity. Symptoms are present at rest Table 20.2 Maternal risk associated with pregnancy. Group I: Minimal risk of complications (mortality < 1%) Atrial septal defect * Ventricular septal defect * Patent ductus arteriosus * Pulmonic/tricuspid disease Corrected tetralogy of Fallot Bioprosthetic valve Mitral stenosis, New York Heart Association (NYHA) classes I and II Marfan syndrome with normal aorta Group II: Moderate risk of complications (mortality 5 – 15%) Mitral stenosis with atrial fi brillation † Artifi cial valve * † Mitral stenosis, NYHA classes III and IV Aortic stenosis Coarctation of aorta, uncomplicated Uncorrected tetralogy of Fallot Previous myocardial infarction Group III: Major risk of complications or death (mortality > 25%) Pulmonary hypertension Coarctation of aorta, complicated Marfan syndrome with aortic involvement * If unassociated with pulmonary hypertension. † If anticoagulation with heparin, rather than coumadin, is elected. Chapter 20 258 tion) at a time when optimum anticoagulation with coumarin derivatives may have adverse fetal consequences. Table 20.4 out- lines the relative changes in the coagulation factors and inhibitors associated with normal pregnancy. For women receiving any type of therapeutic anticoagulation, the risk of serious postpartum hemorrhage is also increased. 4 Marked fl uctuations in cardiac output normally occur in preg- nancy, particularly during labor and delivery [16] . Such changes increase progressively from the fi rst stage of labor, reaching, in appropriate obstetric care, the presence or absence of the afore- mentioned secondary complications of cardiomyopathy, pulmo- nary hypertension, endocarditis, and sudden arrhythmias play a much more important role in determining ultimate maternal outcome than the primary structural nature of the cardiac lesion itself. Physiologic c onsiderations The unique problems encountered by the pregnant woman with cardiac disease are secondary to four principal physiologic changes [14] . 1 A 50% increase in intravascular volume is seen in normal preg- nancy. Figure 20.1 illustrates the changes in total blood volume, plasma volume, and red cell volume during normal pregnancy. In patients whose cardiac output is limited by intrinsic myocar- dial dysfunction, valvular lesions, or ischemic cardiac disease, volume overload will be poorly tolerated and may lead to conges- tive failure or worsening ischemia. In patients with an anatomic predisposition, such volume expansion may result in aneurysm formation or dissection (e.g. Marfan syndrome). Even in women with multiple pregnancies, the heart is able to withstand repeti- tive episodes of gestational volume overload without lasting det- rimental structural or functional changes [15] . 2 Decreased systemic vascular resistance (SVR) becomes especially important in patients with the potential for right to left shunts, which will invariably be increased by a falling SVR during preg- nancy. Such alterations in cardiac afterload also complicate adap- tion to pregnancy in patients with certain types of valvular disease. Table 20.3 summarizes the central hemodynamic changes associated with normal term pregnancy. 3 The hypercoagulability associated with pregnancy heightens the need for adequate anticoagulation in patients at risk for arterial thrombosis (artifi cial valves and some subsets of atrial fi brilla- 5,000 4,000 3,000 2,000 1,000 8 1216 202428323640 Weeks of pregnancy Total blood volume Plasma volume Red blood cell volume Volume (mL) Figure 20.1 Changes in total blood volume, plasma volume, and red cell volume in normal pregnancy (Reproduced by permission from Shnider SM, Levinson G. Anesthesia for Obstetrics , 3rd edn. Lippincott, Williams & Wilkins, 1993.) Non - pregnant Pregnant Percent change * Cardiac output (L/min) 4.3 ± 0.9 6.2 ± 1.0 +43 Heart rate (bpm) 71 ± 10.0 83 ± 1.0 +17 Systemic vascular resistance (dyne/cm/sec 5 ) 1,530 ± 520 1,210 ± 266 − 21 Pulmonary vascular resistance (dyne/cm/sec 5 ) 119 ± 47.0 78 ± 2 2 − 34 Colloid oncotic pressure (mmHg) 20.8 ± 1.0 18.0 ± 1.5 − 14 COP − PCWP (mmHg) 14.5 ± 2.5 10.5 ± 2.7 − 28 Mean arterial pressure (mmHg) 86.4 ± 7.5 90.3 ± 5.8 − NSC Pulmonary capillary wedge pressure (mmHg) 6.3 ± 2.1 7.5 ± 1.8 − NSC Central venous pressure (mmHg) 3.7 ± 2.6 3.6 ± 2.5 NSC Left ventricular stroke work index (g/m/m 2 ) 41 ± 8 4 8 ± 6 +NSC * NSC = no statistically signifi cant change. COP − PCWP = colloid oncotic pressure − pulmonary capillary wedge pressure (mmHg). (Reproduced by permission from Clark SL, et al: Central hemodynamic assessment of normal term pregnancy. Am J Obstet Gynecol 1989;161:1439.) Table 20.3 Central hemodynamic changes associated with normal term pregnancy. . 3 1 Scotsdale Healthcare, Scottsdale, Arizona and Department of Obstetrics and Gynecology, University of Arizona College of Medicine, Tucson, AZ, USA 2 Department of Cardiology, Marshfi. 270 Adams et al. Guidelines for the early management of adults with ischemic stroke . Stroke 2007 ; 38 : 1676 . 271 Caplan LR . The evaluation of stroke . UpToDate 2007 ; 15.1. 256 Critical. Int Care Med 2003 ; 29 : 2323 – 2326 . 152 Konstantinopoulos PA , Mousa S , Khairallah R , Mtanos G . Postpartum cerebral angiopathy: an important diagnostic consider- ation in the postpartum