Obstentrics_Williams

Obstentrics_Williams. Usually a disease of aging, aortic stenosis in younger women is most likely a congenital lesion. Since the decline in rheumatic disease incidence, aortic stenosis is less common, and the most frequent cause in the United States is a bicuspid valve (Friedman, 2008). A normal aortic valve has an area of 3 to 4 cmr, with a pressure gradient <5 mm Hg. If the valve area is < 1 cmr, there is severe obstruction to flow and a progressive pressure overload on the left ventricle (Roeder, 2011). Concentric left ventricular hypertrophy follows, and if it is severe, enddiastolic pressures become elevated, ejection fraction declines, and cardiac output is reduced (see Table 49-6). Characteristic manifestations develop late' and include chest pain, syncope, heart failure, and sudden death from arrhythmias. Life expectancy averages only 5 years after exertional chest pain develops, and valve replacement is indicated for symptomatic patients.


Obstentrics_Williams

Obstentrics_Williams. Clinically significant aortic stenosis is infrequent during pregnancy. Mild-to-moderate degrees of stenosis are well tolerated, however, severe disease is life-threatening. he principal underlying hemodynamic problem is the ixed cardiac output associated with severe stenosis. During pregnancy, several common events acutely lower preload further and thus aggravate the ixed cardiac output. hese include vena caval occlusion from the gravid uterus, regional analgesia, and hemorrhage. Importantly, these also decrease cardiac, cerebral, and uterine perfusion. It follows that severe aortic stenosis may be extremely dangerous during pregnancy. From the earlier-cited Canadian study, complication rates were higher if the aortic valve area measured < 1.5 cmr(Siu, 2001 b). And in the report by Hameed and associates (2001), the maternal mortality rate with aortic stenosis was 8 percent. Women with valve pressure gradients > 100 mm Hg appear to be at greatest risk.


Obstentrics_Williams

Obstentrics_Williams. For asymptomatic women with aortic stenosis, no treatment except close observation is required. Management of a symptomatic woman includes strict limitation of activity and prompt treatment of infections. If symptoms persist despite bed rest, surgical intervention may be considered. Catheter-based valvuloplasty is associated with risks to both the mother and fetus and is not very efective in the long term (Pessel, 2014; Reich, 2004). The aortic valve can again narrow or new aortic regurgitation may develop. he alternative surgical approach-valve replacement-is associated with significant risk of fetal demise due to the efects of cardiac bypass (Dart, 2010). Accordingly, the American College of Cardiology, the American Heart Association, and the European Society of Cardiology recommend delaying conception until after surgical correction for severe aortic stenosis (Bonow, 2008).


Obstentrics_Williams

Obstentrics_Williams. For women with critical aortic stenosis, intensive monitoring during labor is essential. Pulmonary arteY catheterization may be helpful because of the narrow margin separating fluid overload from hypovolemia. Women with aortic stenosis are dependent on adequate end-diastolic ventricular filling pressures to maintain cardiac output and systemic perfusion. Abrupt drops in end-diastolic volume may result in hypotension, syncope, myocardial infarction, and sudden death. hus, avoiding diminished ventricular preload and maintaining cardiac output are key. During labor and delivery, afected women are best managed on the "wet" side. his provides a margin of safety in intravascular volume in anticipation of possible hemorrhage. In women with a competent mitral valve, pulmonary edema is rare.


Obstentrics_Williams

Obstentrics_Williams. During labor, narcotic epidural analgesia seems ideal and avoids potentially hazardous hypotension. Easterling and coworkers (1988) studied the efects of epidural analgesia in ive women with severe stenosis and demonstrated immediate and profound efects from decreased illing pressures. Xia and associates (2006) emphasize slow administration of dilute local anesthetic agents into the epidural space. In hemodynamically stable women, forceps or vacuum delivery is used for standard obstetrical indications.


Obstentrics_Williams

Obstentrics_Williams. Aortic valve regurgitation or insuiciency allows diastolic Bow of blood from the aorta back into the let ventricle. Frequent causes of abnormal insuiciency are rheumatic fever, connective tissue abnormalities, and congenital lesions. With Marfan syndrome, the aortic root may dilate and create regurgitation (p. 967). Acute insuiciency may also develop with bacterial endocarditis or aortic dissection (pp. 965 and 967). Last, aortic and mitral vlve insuiciency have both been linked to the appetite suppressants fenBuramine and dexfenBuramine and to the ergot-derived dopamine agonists cabergoline and pergolide (Gardin, 2000; Schade, 2007; Zanettini, 2007). With chronic insuiciency, let ventricular hypertrophy and dilation develop and are followed by slow-onset fatigue, dyspnea, and pulmonary edema, although rapid deterioration usually follows (see Table 49-6).


Obstentrics_Williams

Obstentrics_Williams. Aortic insuiciency is generally well tolerated during pregnancy. Like mitral valve insuiciency, diminished vascular resistance is thought to improve hemodynamic function. If symptoms of heart failure develop, diuretics are given and bed rest is encouraged. his lesion is usually congenital and also may be associated with Fallot tetralogy or Noonan syndrome. The greater hemodynamic burden of pregnancy can precipitate right-sided heart failure or atrial arrhythmias in women with severe stenosis. Surgical correction ideally is done before pregnancy, but if symptoms progress, a balloon valvuloplasty may be necessary antepartum (Galal, 2015; Siu, 2001a).


Obstentrics_Williams

Obstentrics_Williams. In studying pregnancy outcomes, Drenthen and colleagues (2006) found infrequent cardiac complications in a group of 81 pregnancies in 51 Dutch women with pulmonic stenosis. The NHA classification worsened in two women, and nine experienced palpitations or arrhythmias. No changes in pulmonary valvular function or other adverse cardiac events were reported. However, non cardiac complication rates were significant-17 percent had preterm delivery, 15 percent had hypertension, and 4 percent developed thromboembolism.


Obstentrics_Williams

Obstentrics_Williams. The incidence of congenital heart disease in the United States approximates 11 per 1000 liveborn neonates (Egbe, 2014). With modern surgeries, approximately 90 percent of those born with congenital heart disease survive to childbearing age, and it is now the most common type of heart disease encountered during pregnancy (Brickner, 2014; Lindley, 2015). Specifically, analysis from the United States Nationwide Inpatient Sample database shows a linear rise in the prevalence of congenital heart disease between 2000 and 2010-from 6.4 to 9.0 per 10,000 women admitted for delivery (Thompson, 2015).


Obstentrics_Williams

Obstentrics_Williams. Of pregnancy outcomes in women with congenital heart disease compared with those without, the odds of cardiovascular and obstetrical complications were 10.5 to 35.5 and 1.2 to 2.1 times higher, respectively (Thompson, 2015). Moreover, maternal mortality rates were greater for women with congenital heart disease than for unafected gravidas-17.8 and 0.7 per 10,000 deliveries, respectively. Opotowsky and coworkers (2012) reported similar risks.


Obstentrics_Williams

Obstentrics_Williams. Approximately one fourth of all adults has a patent foramen ovale (Miller, 2015). Most atrial septal defects (ASDs) are asymptomatic until the third or fourth decade. he secundumtype defect accounts for 70 percent, and associated mitral valve myxomatous abnormalities with prolapse are common. Most recommend repair if ASD is discovered in adulthood. Pregnancy is well tolerated unless pulmonary hypertension has developed, but this is uncommon (Geva, 2014). Treatment of ASD during pregnancy is indicated for congestive heart failure or an arrhythmia. Based on their review, liaga and colleagues (2003) concluded that the risk of endocarditis with an ASD is negligible.


Obstentrics_Williams

Obstentrics_Williams. With the potential to shunt blood from right to let, aparadoxical embolism, that is, entry of a venous thrombus through the septal defect and into the systemic arterial circulation, is possible and may cause an embolic stroke (Erkut, 2006; Miller, 2015). In asymptomatic women with ASD, thromboembolism prophylaxis is problematic, and the heterogeneous recommendations have been summarized by Kizer and Devereux (2005). Compression stockings and prophylactic heparin have also been recommended for a pregnant woman with an ASD who is immobile or has another risk factor for thromboembolism (Head, 2005).


Obstentrics_Williams

Obstentrics_Williams. These lesions close spontaneously during childhood in 90 percent of cases. Most defects are paramembranous, and the degree of left-to-right shunt and associated physiological derangements are related to lesion size. In general, if the defect mea sures < 1.25 cmr, pulmonary hypertension and heart failure do not develop. If the efective defect size exceeds that of the aortic valve orifice, symptoms rapidly develop. For these reasons, most children undergo surgical repair before pulmonary hypertension develops. Adults with unrepaired large defects develop left ventricular failure and pulmonary hypertension and have a high incidence of bacterial endocarditis (Brickner, 2000, 2014).


Obstentrics_Williams

Obstentrics_Williams. Pregnancy is well tolerated with small-to-moderate sized shunts. If pulmonary arterial pressures reach systemic levels, however, there is reversal or bidirectional Bow-Eisenmenger syndrome (p. 960). When this develops, the maternal and fetal mortality rates are signiicantly higher, and thus, pregnancy is not generally advisable. Bacterial endocarditis is more common with unrepaired defects, and antimicrobial prophylaxis is often required (p. 965). As shown in Table 49-4, 10 to 16 percent of ofspring born to these women also have a ventricular septal defect.


Obstentrics_Williams

Obstentrics_Williams. These account for approximately 3 percent of all congenital cardiac malformations and are distinct from isolated atrial or ventricular septal defects. An atrioventricular (A V) septal defect is characterized by a common, ovoid A V junction. his defect is associated with aneuploidy, Eisenmenger syndrome, and other malformations (Altin, 2015). Compared with simple septal defects, complications are more frequent during pregnancy. In a review of 48 pregnancies in 29 afected women, complications included persistent deterioration of NA class in 23 percent, signiicant arrhythmias in 19 percent, and heart failure in 2 percent (Drenthen, 2005b). Congenital heart disease was identiied in 15 percent of the ofspring.


Obstentrics_Williams

Obstentrics_Williams. The ductus connects the proximal left pulmonary artery to the descending aorta just distal to the left subclavian artery. Functional closure of the ductus from vasoconstriction occurs shortly after term birth. he physiological consequences with its persistence are related to its size. Most signiicant lesions are repaired in childhood, but for individuals who do not undergo repair, the mortality rate is high after the ifth decade (Brickner, 2014). In some younger women with an unrepaired ductus during pregnancy, however, pulmonary hypertension, heart failure, or cyanosis will develop if systemic blood pressure falls and leads to shunt reversal of blood from the pulmonary artery into the aorta (Vashisht, 2015). A sudden blood pressure decline at delivery-such as with regional analgesia or hemorrhage-may lead to fatal collapse. Accordingly, hypotension is ideally avoided but treated vigorously if it develops. Prophylaxis for bacterial endocarditis is indicated at delivery for unrepaired


Obstentrics_Williams

Obstentrics_Williams. lead to fatal collapse. Accordingly, hypotension is ideally avoided but treated vigorously if it develops. Prophylaxis for bacterial endocarditis is indicated at delivery for unrepaired defects (p. 965). As shown in Table 49-4, the incidence of inheritance approximates 4 percent.


Obstentrics_Williams

Obstentrics_Williams. When congenital heart lesions produce right-to-Ieft shunting of blood past the pulmonary capillary bed, cyanosis develops. The classic and most commonly encountered lesion in adults and during pregnancy is the Fallot tetraloy (Lindley, 2015). his is characterized by a large ventricular septal defect, pulmonary stenosis, right ventricular hypertrophy, and an overriding aorta that receives blood from both the right and left ventricles. The magnitude of the shunt varies inversely with systemic vascular resistance. Hence, during pregnancy, when peripheral resistance declines, the shunt increases and cyanosis worsens.


Obstentrics_Williams

Obstentrics_Williams. Generally, women with cyanotic heart disease do poorly during pregnancy. With uncorrected Fallot tetralogy, maternal mortality rates approach 10 percent. here is a relationship between chronic hypoxemia, polycythemia, and pregnancy outcomes such as miscarriage and perinatal morbidity. When hypoxemia is intense enough to stimulate a rise in hematocrit above 65 vol umes percent, pregnancy wastage is virtually 100 percent.


Obstentrics_Williams

Obstentrics_Williams. Although not all cyanotic lesions are repairable, with satis factory surgical correction before pregnancy, maternal and fetal outcomes are much improved. In a review of 197 pregnancies in 99 women with surgically corrected Fallot tetralogy, preg nancy was usually well tolerated, and no mothers died. Still, almost 9 percent of pregnancies were complicated by adverse and heart failure (Balci, 2011; Kamiya, 2012). For women with a pulmonary valve replacement, pregnancy does not adversely afect graft function (Oosterhof, 2006). Prior to or after con ception, women with Fallot tetralogy are ofered genetic coun seling and evaluation for 22q 11 deletion syndrome (Lindley, 2015).


Obstentrics_Williams

Obstentrics_Williams. Some women with Ebstein anomay, characterized by a mal positioned and malformed tricuspid valve, may reach reproduc tive age. Right ventricular failure from volume overload and cyanosis are common during pregnancy. In the absence of cya nosis, heart failure, or signiicant arrhythmias, afected women usually tolerate pregnancy well (Brickner, 2014). Transposition of the Great Vessels


Obstentrics_Williams

Obstentrics_Williams. Pregnancy following surgical correction of transposition has prominent risks. Canobbio (2006) and Drenthen (2005a), each with their colleagues, described outcomes of 119 pregnancies in 68 women-90 percent had a prior Mustard procedure and 10 percent a previous Senning procedure. During pregnancy, one fourth had arrhythmias, 12 percent developed heart failure, and one subsequently required cardiac transplantation. One woman died suddenly a month after delivery, and another died 4 years later. A third of the newborns were delivered preterm. In another report of 60 pregnancies in 34 women who had undergone transposition repair, approximately a fourth ended in miscarriage or abortion, and another fourth delivered preterm (Trigas, 2014). Deterioration in functional class occurred in seven women, and documented deterioration in systolic function occurred in four women. Finally, two women required resuscitation during delivery, and one experienced supraventricular tachycardia during labor.


Obstentrics_Williams

Obstentrics_Williams. and documented deterioration in systolic function occurred in four women. Finally, two women required resuscitation during delivery, and one experienced supraventricular tachycardia during labor. Of other defects, in women with previously repaired truncus arteriosus and doubleoutlet right ventricle, successful-although eventful-pregnancies have also been described (Drenthen, 2008; Hoendermis, 2008).


Obstentrics_Williams

Obstentrics_Williams. With hypoplastic lt heart syndrome, almost 70 percent of afected women are now expected to survive into adulthood and frequently become pregnant (Feinstein, 2012). Those who have undergone a Fontan repair are at particularly high risk for complications. In brief, this procedure involves diverting blood via a surgical anastomosis from the vena cava to the pulmonary artery without passing through the right ventricle. Blood Bows passively to the pulmonary vasculature. Thus, patients with a Fontan palliation are very preload dependent (Lindley, 2015). lead to pulmonary


Obstentrics_Williams

Obstentrics_Williams. lead to pulmonary FIGURE 49-4 Eisenmenger syndrome due to a ventricular septal defect (VSD). A. Substantialolet-to-right shunting through the VSD leads to morphological changes in the smaller pulmonary arteries and arterioles. Specifically, medial hypertrophy, intimal cellular proliferations, and fibrosis lead to narrowing or closure of the vessel lumen. These vascular changes create pulmonary hypertension and a resultant reversal of the intracardiac shunt (8). With sustained pulmonary hypertension, extensive atherosclerosis and calcification often develop in the large pulmonary arteries. Although a VSD is shown here, Eisenmenger syndrome may also develop in association with a large atrial septal defect or patent ductus arteriosus.


Obstentrics_Williams

Obstentrics_Williams. Of outcomes, one review of 14 women conceiving after a Fontan repair found that six spontaneously aborted all pregnancies, and eight others carried 14 pregnancies to viability (Cauldwell, 2016). Cardiac complications included arrhythmias and thromboembolism. Ten newborns delivered preterm, and eight neonates were small for gestational age. Similar complications attend a maternal systemic right ventricle, that is, one in which the right ventricle rather than the left pumps blood to the systemic circulation (Khan, 2015).


Obstentrics_Williams

Obstentrics_Williams. his describes secondary pulmonary hypertension that arises from any cardiac lesion. The syndrome develops when pulmonary vascular resistance exceeds systemic resistance and leads to concomitant right-to-Ieft shunting. The most common underlying defects are atrial or ventricular septal defects and persistent ductus arteriosus (Fig. 49-4). Patients are asymptomatic for years, but eventually pulmonary hypertension becomes severe enough to cause this shunting (Greutmann, 2015).


Obstentrics_Williams

Obstentrics_Williams. Pregnant women with Eisenmenger syndrome tolerate hypotension poorly, and death usually is caused by right ventricular failure with cardiogenic shock. In a review of 44 cases through 1978, maternal and perinatal mortality rates approximated 50 percent (Gleicher, 1979). In a later review of 73 pregnancies, Weiss and associates (1998) cited a 36-percent maternal death rate. Three of 26 deaths were antepartum, and the remainder of women died intrapartum or within a month of delivey. In a subsequent study of 13 gravidas, one mother died 17 days after delivery, and there were ive perinatal deaths (Wang, 2011). Given such poor outcomes or both mother and etus, Eisenmenger syndrome is considered to be an absolute contraindication to pregnancy (Brickner, 2014; Lindley, 2015; Meng, 2017; Warnes, 2015). Management of those who do become pregnant has recently been detailed by Broberg (2016) and is discussed in the next section.


Obstentrics_Williams

Obstentrics_Williams. Normal resting mean pulmonary artery pressure is 12 to 16 mm Hg. Pulmonary vascular resistance in late pregnancy approximates 80 dyne/sec/cm-5, which is 34-percent less than the nonpregnant value of 120 dyne/sec/cm-5 (Clark, 1989). Pulmonay hypertension is deined in nonpregnant individuals as a resting mean pulmonary pressure >25 mm Hg. he current clinical classification system, shown in Table 49-7, includes five groups of disorders that cause pulmonary hypertension (Galie, 2016). There are important prognostic and therapeutic distinctions between group 1 pulmonary arterial hypertension and the other groups. Group 1 indicates that a specific disease afects pulmonary arterioles. It includes idiopathic or primary pulmonary arterial hypertension as well as those cases secondary to a known cause such as connective tissue disease. For example, approximately one third of women with scleroderma and 10 percent with systemic lupus erythematosus


Obstentrics_Williams

Obstentrics_Williams. TABLE 49-7. Comprehensive Clinical Classification of Pulmonary Hypertension 1. Pulmonary arterial hypertension Drug and toxin induced Associated with connective tissue disease, HIV infections, portal hypertension, congenital heart diseases, schistosomiasis Drugs, toxins and radiation induced Associated with connective tissue disease, HIV infection I" Persistent pulmonary hypertension of the newborn 2. Pulmonary hypertension due to let heart disease 3. Pulmonary hypertension due to lung diseases and/or hypoxia Other pulmonary diseases with mixed restrictive and obstructive pattern Sleep-disoriented breathing Chronic exposure to high altitude 4. Chronic thromboembolic pulmonary hypertension/other pulmonary artery obstructions Other pulmonary artery obstructions, i.e., tumors, arteritis, pulmonary stenosis, parasites 5. Pulmonary hypertension with unclear and/or multifactorial mechanisms


Obstentrics_Williams

Obstentrics_Williams. Other pulmonary artery obstructions, i.e., tumors, arteritis, pulmonary stenosis, parasites 5. Pulmonary hypertension with unclear and/or multifactorial mechanisms Hematological disorders: chronic hemolysis, myeloproliferative disorders, splenectomy Systemic disorders: sarcoidosis, pulmonary histiocytosis, neurofibromatosis Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid disorders Others: fibrosing mediastinitis, chronic renal failure HIV = human immunodeficiency virus. Adapted from Galie, 2016. have pulmonary hypertension (Rich, 2005). Other causes in young women are human immunodeiciency virus (HI) infection, sickle-cell disease, and thyrotoxicosis (Newman, 2015; Sheield, 2004).


Obstentrics_Williams

Obstentrics_Williams. have pulmonary hypertension (Rich, 2005). Other causes in young women are human immunodeiciency virus (HI) infection, sickle-cell disease, and thyrotoxicosis (Newman, 2015; Sheield, 2004). In pregnant women, group 2 disorders are the most common. hese are secondary to pulmonary venous hypertension caused by left-sided atrial, ventricular, or valvular disorders. A typical example is mitral stenosis discussed earlier (p. 955). In contrast, groups 3 through 5 are seen infrequently in young healthy women .


Obstentrics_Williams

Obstentrics_Williams. Symptoms may be vague, and dyspnea with exertion is the most frequent. With group 2 disorders, orthopnea and nocturnal dyspnea are also usually present. Angina and syncope occur when right ventricular output is ixed, and they suggest advanced disease. Chest radiography often shows enlarged pulmonary hilar arteries and attenuated peripheral markings. It also may disclose parenchymal causes of hypertension. N oninvasive echocardiography can provide an estimate of pulmonary artery pressures, although cardiac catheterization remains the standard for measurement. In two studies with a combined 51 pregnant women who underwent both echo cardiography and cardiac catheterization, pulmonary artery pressures were significantly overestimated by echocardiography in approximately one third of cases (Penning, 2001; Wylie, 2007).


Obstentrics_Williams

Obstentrics_Williams. Regardless of the etiology, the inal common pathway of pulmonary hypertension is right heart failure and death. he average survival length after diagnosis is <4 years (Krexi, 2015). That said, longevity depends on the severity and cause of pulmonary hypertension at discovery. As discussed later, some disorders respond to medical interventions, which may improve quality of life. Preconceptional and contraceptive counseling are imperative (Gei, 2014).


Obstentrics_Williams

Obstentrics_Williams. he maternal mortality rate is appreciable in afected women, and this is especially so with idiopathic pulmonary hypertension. In the past, there were frequently poor distinctions in identiying both causes and severity of hypertension. hus, although most severe cases of idiopathic pulmonary arterial hypertension had the worst prognosis, it was erroneously assumed that all types of pulmonary hypertension were equally dangerous. With widespread use of echocardiography, lesssevere lesions with a better prognosis are now discernible. Bedard and coworkers (2009) reported that maternal mortality rate statistics improved during the decade ending in 2007 (25 percent) compared with those for the decade ending in 1996 (38 percent). Importantly, almost 80 percent of the deaths were during the first month postpartum. More recently, Meng and associates (2017) reported mortality rates of 23 percent with group 1 and 5 percent with the other groups. Mortality was related to pulmonary hypertension


Obstentrics_Williams

Obstentrics_Williams. month postpartum. More recently, Meng and associates (2017) reported mortality rates of 23 percent with group 1 and 5 percent with the other groups. Mortality was related to pulmonary hypertension severity.


Obstentrics_Williams

Obstentrics_Williams. As discussed, pregnancy is contraindicated with severe disease, especially in women with pulmonary arterial changesmost cases in group 1. With milder disease from other causes-group 2 being the most common-the prognosis is better (Meng, 2017). With the more frequent use of echocardiography and pulmonary artery catheterization in young women with heart disease, we have identified women with mild-to-moderate pulmonary hypertension who tolerate pregnancy, labor, and delivery well. One example described by Sheield and Cunningham (2004) is that of pulmonary hypertension that develops with thyrotoxicosis but is reversible with treatment. Similarly, Boggess and colleagues (1995) described nine women with interstitial and restrictive lung disease with varying degrees of pulmonary hypertension, and all tolerated pregnancy reasonably well.


Obstentrics_Williams

Obstentrics_Williams. Treatment of symptomatic pregnant women includes activity limitation and avoidance of the supine position later in gestation. Diuretics, supplemental oxygen, and pulmonary vasodilator drugs are standard therapy for symptoms. Some recommend anticoagulation (Hsu, 2011). Several reports describe the successful use of intravenous pulmonary artery vasodilators (Badalian, 2000; Garabedian, 2010; Goya, 2014). Prostacyclin analogues that can be administered parenterally include epoprostenol and treprostinil, whereas iloprost is inhaled. Each has been used in gravidas. Inhaled nitric oxide is an option that has been employed in cases of acute cardiopulmonary decompensation (Lane, 2011). As reviewed by Obiean and Cleary (2014), phosphodiesterase-5 inhibitors, such as sildenail, cause vasodilation of both the pulmonary and systemic vascular beds and have an inotropic efect on the hypertrophic right ventricle. his also has been used to advantage during pregnancy (Goland, 2010; Hsu, 2011; Meng,


Obstentrics_Williams

Obstentrics_Williams. of both the pulmonary and systemic vascular beds and have an inotropic efect on the hypertrophic right ventricle. his also has been used to advantage during pregnancy (Goland, 2010; Hsu, 2011; Meng, 2017). Bosentan, an endothelin-receptor antagonist, is teratogenic in mice and contraindicated in pregnancy (Obican, 2014).


Obstentrics_Williams

Obstentrics_Williams. During labor and delivery, these women are at greatest risk when venous return and right ventricular filling are diminished. To avoid hypotension, assiduous attention is given to epidural analgesia induction and to blood loss prevention and treatment at delivery (Meng, 2017).


Obstentrics_Williams

Obstentrics_Williams. The American Heart Association defines these as a heterogeneous group of myocardial diseases associated with mechanical and/ or electrical dysfunction. Afected women usually-but not invariably-have inappropriate ventricular hypertrophy or dilation. Cardiomyopathies stem from varied causes, some of which are genetic (Maron, 2006). Of the two major divisions, primay cardiomyopathies are solely or predominantly conined to heart muscle. Examples are hypertrophic cardiomyopathy, dilated cardiomyopathies, and peripartum cardiomyopathy. Secondary cardiomyopathies result from generalized systemic disorders that produce pathological myocardial involvement. Diabetes, systemic lupus erythematosus, chronic hypertension, and thyroid disorders are representative conditions.


Obstentrics_Williams

Obstentrics_Williams. Epidemiological studies suggest that this disorder is common, afecting approximately 1 in 500 adults (Herrey, 2014; Maron, 2004). Characterized by cardiac hypertrophy, myocyte disarray, and interstitial ibrosis, the condition is caused by mutations in anyrone of more than a dozen genes that encode cardiac sarcomere proteins in up to 60 percent of afected patients. In such cases, inheritance is autosomal dominant, and genetic screening is complex (Elliott, 2014). Other genetic and nongenetic causes account for 5 to 10 percent of cases, and the cause is unknown in approximately 25 percent. The myocardial muscle abnormality is typified by let ventricular myocardial hypertrophy with a pressure gradient against let ventricular outflow. Diagnosis is established by echocardiographic identification of a hypertrophied and nondilated left ventricle in the absence of other cardiovascular conditions.


Obstentrics_Williams

Obstentrics_Williams. Most afected women are asymptomatic, but dyspnea, anginal or atypical chest pain, syncope, and arrhythmias may develop. Complex arrhythmias may progress to sudden death, which is the most frequent cause of death. Asymptomatic patients with runs of ventricular tachycardia are especially prone to sudden death. Symptoms usually worsen with exercise. lthough limited reports suggest that pregnancy is well tolerated, adverse cardiac events are frequent. In one analysis of 271 pregnancies in 127 afected women, there were no maternal deaths. However, more than a fourth had at least one adverse cardiac symptom-including dyspnea, chest pain, or palpitations (Thaman, 2003). Based on one systematic review that included 237 women with hypertrophic cardiomyopathy who had a combined 408 pregnancies, Schinkel (2014) calculated a maternal mortality rate of 0.5 percent. Worsening of symptoms or other complications occurred in 29 percent, and 26 percent delivered preterm.


Obstentrics_Williams

Obstentrics_Williams. Management is similar to that for aortic stenosis. Strenuous exercise is prohibited during pregnancy. Abrupt positional changes are avoided to prevent reflex vasodilation and decreased preload. Likewise, drugs that evoke diuresis or diminish vascular resistance are generally not used. If symptoms develop, especially angina, 3-adrenergic or calcium-channel blocking drugs are given. The delivery route of the fetus is determined by obstetrical indications. Choice of anesthesia is controversial, and some authors consider general anesthesia the safest (Pitton, 2007). Neonates rarely demonstrate inherited lesions at birth.


Obstentrics_Williams

Obstentrics_Williams. This is characterized by left and/or right ventricular enlargement and reduced systolic function in the absence of coronary, valvular, congenital, or systemic disease known to cause myocardial dysfunction. Although there are many known causes of dilated cardiomyopathy-both inherited and acquired, the etiology remains undefined in approximately half of cases (Stergiopoulos, 2011). Some result from viral infections, including myocarditis and HIV (Barbaro, 1998; Felker, 2000). Other causes, which are potentially reversible, include alcoholism, cocaine abuse, and thyroid disease. Watkins and coworkers (2011) reviewed the many complex genetic mutations associated with inherited forms of dilated cardiomyopathy.


Obstentrics_Williams

Obstentrics_Williams. This disorder is similar to other forms of nonischemic dilated cardiomyopathy except for its unique relationship with pregnancy (Pyatt, 2011). Indeed, peripartum cardiomyopathy shares a genetic predisposition with both familial and sporadic idiopathic dilated cardiomyopathy (Ware, 2016). Currently, it is a diagnosis of exclusion following a concurrent evaluation for peripartum heart failure. Although the term peripartum cardiomyopathy has been used widely, at least until recently, little evidence supported a unique pregnancy-induced cardiomyopathy. Pearson (2000) reported findings of a workshop of the National Heart, Lung, and Blood Institute that established the following diagnostic criteria: 1. Development of cardiac failure in the last month of pregnancy or within 5 months after delivery, 2. Absence of an identifiable cause for the cardiac failure, 3. Absence of recognizable heart disease prior to the last month of pregnancy, and 4.


Obstentrics_Williams

Obstentrics_Williams. Absence of an identifiable cause for the cardiac failure, 3. Absence of recognizable heart disease prior to the last month of pregnancy, and 4. Left ventricular systolic dysfunction demonstrated by classic echocardiographic criteria, such as depressed ejection fraction or fractional shortening along with a dilated left ventricle (Fig. 49-5). he etiology of peripartum cardiomyopathy remains unknown, and proposed causes include viral myocarditis, abnormal immune response to pregnancy, aberrant response to the greater hemodynamic burden of pregnancy, hormonal interactions, malnutrition, inflammation, and apoptosis (Elkayam, 2011). Another suggests that oxidative stress during late pregnancy leads to the proteolytic cleavage of prolactin (Hilfiker-Kleiner, 2014). The resulting 16-kDa prolactin


Obstentrics_Williams

Obstentrics_Williams. FIGURE 49-5 Peripartum cardiomyopathy with mild pulmonary edema. Anterior-posterior projection chest radiograph of a woman with an abnormally enlarged heart and mild perihilar opacification consistent with dilated cardiomyopathy. fragment is cardiotoxic and can impair cardiomyocyte metab olism and contractility. Bromocriptine therapy has been suggested because it inhibits prolactin secretion. In one pre liminary study, bromocriptine improved recovery of afected women, and a randomized trial is currently recruiting patients (Haghikia, 2015; Sliwa, 2010).


Obstentrics_Williams

Obstentrics_Williams. Hypertensive disorders frequently coexist with peripartum cardiomyopathy, and another proposed mechanism links peripartum cardiomyopathy to preeclampsia (Cunningham, 2012; Fong, 2014; Patten, 2012). Antiangiogenic factors-already known to be associated with preeclampsia-can induce peripartum cardiomyopathy in susceptible mice. hus, cardiomyopathy may be precipitated by antiangiogenic factors in a host made susceptible because of insuicient proangiogenic factors. Several investigators describe a common pathway linking these suggested etiologies (Arany, 2016; Hiliker-Kleiner, 2014). Specifically, unbalanced oxidative stress and a high level of prolactin leads to production of the 16-kDa prolactin fragment that seems to both initiate and propagate the disease. The fragment, which mainly afects the endothelium, together with additional antiangiogenic factors might disturb the angiogenic balance during the puerperium and thereby impair cardiac function.


Obstentrics_Williams

Obstentrics_Williams. With no proven etiology, the diagnosis of peripartum cardiomyopathy currently requires that other causes of cardiac dysfunction be excluded. Biiltmann and coworkers (2005) studied endomyocardial biopsy specimens from 26 women with peripartum cardiomyopathy and reported that more than half had histological evidence of "borderline myocarditis." hey noted viral genomic material for parvovirus B 19, human herpesvirus 6, Epstein-Barr virus, and cytomegalovirus. From Parland Hospital, otherwise "idiopathic" heart failure was found to be caused by hypertensive heart disease, clinically silent mitral stenosis, obesity, or viral myocarditis (Cunningham, 1986). Indeed, 20 percent of women with treated chronic hypertension in pregnancy have concentric hypertrophy (Ambia, 2017).


Obstentrics_Williams

Obstentrics_Williams. N tusi and associates (2015) analyzed the clinical features of 30 women with peripartum cardiomyopathy compared with 53 women with hypertensive heart failure. With cardiomyopathy, the symptoms began postpartum in all women, whereas symptoms began antepartum in 85 percent of women with hypertensive heart failure. Peripartum cardiomyopathy was significantly linked with twin gestation, smoking, and echo cardiographic abnormalities. In contrast, hypertensive heart failure patients more often had a family history of hypertension, hypertension and preeclampsia in a prior pregnancy, tachycardia, and left ventricular hypertrophy on echo cardiography.


Obstentrics_Williams

Obstentrics_Williams. he incidence of peripartum cardiomyopathy varies considerably and depends on the diligence for the search of a cause. In a review of the Nationwide Inpatient Sample database, the incidence rose from 1 in 1181 live births in 2004 to 1 in 849 in 2011 (Kolte, 2014). Two other large population-based studies cite a frequency of 1 in 2000 to 2800 live births (Gunderson, 2011; Harper, 2012). In an earlier study from Parkland Hospital, we identified idiopathic cardiomyopathy in only approximately 1 in 15,000 deliveries-an incidence similar to that of idiopathic cardiomyopathy in young nonpregnant women (Cunningham, 1986).


Obstentrics_Williams

Obstentrics_Williams. Approximately half of women sufering from peripartum cardiomyopathy recover baseline ventricular function within 6 months of delivery. But in those with persistent cardiac failure, the mortality rate approaches 85 percent over 5 years (Moioli, 2010). In a group of 100 women with newly diagnosed peripartum cardiomyopathy, 72 percent had a left ventricular ejection fraction ::50 percent, and 93 percent had event-free survival (McNamara, 2015). However, six women experienced nine major events that included four deaths, four left ventricular assist device implantations, and one heart transplantation. Recovery to a left ventricular ejection fraction ::50 percent occurred in almost 90 percent of women whose baseline ejection fraction was at least 30 percent. This compared with <40 percent in women whose baseline ventricular ejection fraction was < 30 percent. Recovery was also related to the baseline left ventricular end-diastolic diameter. Li and colleagues (2016) also found that a


Obstentrics_Williams

Obstentrics_Williams. in women whose baseline ventricular ejection fraction was < 30 percent. Recovery was also related to the baseline left ventricular end-diastolic diameter. Li and colleagues (2016) also found that a baseline left ventricular ejection fraction <34 percent and a brain natriuretic peptide (BNP) level > 1860 pg/ mL were associated with an approximately threefold greater risk of persistent left ventricular systolic dysfunction.


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Obstentrics_Williams. From the largest studies on the topic, approximately one third of women with a history of peripartum cardiomyopathy will sufer relapse with worsening of symptoms and deterioration of left ventricular function during another pregnancy (Elkayam, 20 14a). The risk of relapse in women with persistent left ventricular dysfunction is substantially higher than in those who have developed normal ventricular function before a subsequent pregnancy (Hiliker-Kleiner, 2017). But, normalization of let ventricular function does not guarantee an uncomplicated pregnancy, because approximately 20 percent of these women are at risk for deterioration in left ventricular function.


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Obstentrics_Williams. Arrhythmogenic right ventricular dysplasia is a unique cardiomyopathy defined histologically by progressive replacement of right ventricular myocardium with adipose and fibrous tissue. It has an estimated population prevalence of 1 in 5000, predisposes to ventricular tachyarrhythmias, and is a cause of sudden death, particularly in younger individuals (Agir, 2014; Elliott, 2008). The additional risk of pregnancy in women with arrhythmogenic right ventricular cardiomyopathy is unknown, however, based on their systematic review, Krul and coworkers (2011) counsel against pregnancy.


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Obstentrics_Williams. Restrictive cardiomyopathy is probably the least common type. This inherited cardiomyopathy is characterized by a ventricular illing pattern in which worsening myocardial stifness raises ventricular pressure precipitously and al�ows only a small filling volume (Elliott, 2008). Because of the severe clinical course and poor prognosis in general, pregnancy is not advised (Krul, 2011). Takotsubo cardiomyopathy is a rare form of acute reversible left ventricular apical wall ballooning (Kraft, 2017).


Obstentrics_Williams

Obstentrics_Williams. Regardless of the underlying condition that causes cardiac dysfunction, women who develop peripartum heart failure almost always have obstetrical complications that either contribute to or precipitate heart failure. For example, preeclampsia is common and may precipitate afterload failure. Indeed, indings from the Registry on Pregnancy and Cardiac Disease indicate that women with preexisting heart disease who develop preeclampsia have a 30-percent risk of developing heart failure during pregnancy (Ruys, 2014). Moreover, high-output states caused by hemorrhage and acute anemia elevate cardiac workload and magniy the physiological efects of compromised ventricular function. Similarly, infection and sepsis syndrome raise cardiac output and oxygen utilization and depress myocardial function.


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Obstentrics_Williams. In many populations, chronic hypertension with superimposed preeclampsia is the most frequent cause of heart failure in pregnancy. Many of these women have concentric let ventricular hypertrophy (Ambia, 2017). In some, mild antecedent undiagnosed hypertension causes covert cardiomyopathy, and when superimposed preeclampsia develops, together they may cause otherwise inexplicable peripartum heart failure. Obesity is a frequent cofactor with chronic hypertension, and it too is associated with ventricular hypertrophy (Kenchaiah, 2002).


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Obstentrics_Williams. Congestive heart failure can have a gradual onset or may present as acute "flash" pulmonary edema. Heart failure onset is most likely at the end of the second/beginning of the third trimester and peripartum (Ruys, 2014). Of symptoms, dyspnea is universal and others are orthopnea, palpitations, substernal chest pain, a sudden decline in the ability to complete usual duties, and nocturnal cough. Clinical findings include persistent basilar rales, hemoptysis, progressive edema, tachypnea, and tachycardia (Sheield, 1999). Hallmark radiographic findings usually are cardiomegaly and pulmonary edema (see Fig. 49-5). Acutely, there is usually systolic failure, and echocardiography shows an ejection fraction <0.45 or a fractional shortening <30 percent, or both, and an end-diastolic dimensionr> 2.7 cm/m2 (Hibbard, 1999). Coincidental diastolic failure may also be found, depending on the underlying cause (Redfield, 2016).


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Obstentrics_Williams. with diuretic administration to reduce preload. Hypertension is common, and afterload reduction is accomplished with hydralazine or another vasodilator. Because of marked fetal efects, angiotensin-converting enzyme inhibitors are withheld until after delivery. With chronic heart failure, the incidence of associated thromboembolism is high, and thus prophylactic heparin is often recommended. Lt ventricular assist devices are now employed more fre quently for acute and chronic heart failure treatment. A few reports describe their use during pregnancy (LaRue, 2011; Sims, 2011). Extracorporeal membrane oxygenation (ECMO) was reported to be lifesaving in a woman with fulminating peri partum cardiomyopathy, and it may be used in women with pulmonary hypertension (Meng, 2017; Smith, 2009).


Obstentrics_Williams

Obstentrics_Williams. In the United States, those at greatest risk for endocarditis are those with congenital heart lesions, intravenous drug use, degenerative valve disease, and intracardiac devices (Karchmer, 2015). Subacute bacterial endocarditis usually stems from a low-virulence bacterial infection superimposed on an underlying structural lesion. These are usually native valve infections. Organisms that cause indolent endocarditis are most often viridans-group streptococci or Staphylococcus or Enterococcus species. Among intravenous drug abusers and those with catheter-related infections, Staphylococcus aureus predominates. With prosthetic valve infections, Staphylococcus epidermidis is a frequent cause. Streptococcus pneumoniae and Neisseria gonorrhoeae may occasionally cause acute, fulminating disease. Others have reported Neisseria sicca and N mucosa, group B streptococcus, and Escherichia coli endocarditis during pregnancy or peripartum (Cox, 1988; Deger, 1992; Kangavari, 2000; Kulas, 2006).


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Obstentrics_Williams. Infective endocarditis symptoms vary and often develop insidiously. Fever, often with chills, is seen in 80 to 90 percent of cases, a murmur is heard in up to 85 percent, and anorexia, fatigue, and other constitutional symptoms are common (Karchmer, 2015). Clinical clues are anemia, proteinuria, and manifestations of embolic lesions that include petechiae, focal neurological changes, chest or abdominal pain, and ischemia in an extremity. In some cases, heart failure develops. Symptoms may persist for several weeks before the diagnosis is found, and a high index of suspicion is necessary.


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Obstentrics_Williams. Diagnosis is made using the Duke criteria, which include positive blood cultures for typical organisms and evidence of endocardial involvement (Hoen, 2013; Pierce, 2012). Echocardiography may be diagnostic, but lesions <2 mm or those on the tricuspid valve may be missed. If uncertain, transesophageal echocardiog raphy is accurate and informative. Importantly, a negative echo cardiographic study does not exclude endocarditis. Treatment is primarily medical, and ascertainment of the infecting organism and its sensitivities is imperative for antimi crobial selection. Guidelines for appropriate antibiotic treatment (Habib, 2015; Karchmer, 2015). Recalcitrant bacteremia and heart failure due to valvular dysfunction are but a few reasons that persistent valvular infection may require replacement.


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Obstentrics_Williams. Infective endocarditis is uncommon during pregnancy and the puerperium. During a 7 -year period, the incidence of endocarditis at Parkland Hospital approximated 1 in 16,000 births, and two of seven women died (Cox, 1988). Matenal and fetal mortality rates range from 25 to 35 percent (Habib, 2015; Seaworth, 1986). In a systematic review of infective endocarditis during pregnancy, risk factors were intravenous drug use (14 percent), congenital heart disease (12 percent), and rheumatic heart disease (12 percent) (Kebed, 2014). he most common pathogens were streptococcal (43 percent) and staphylococcal (26 percent) species. Among 51 pregnancies, the maternal mortality rate was 11 percent.


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Obstentrics_Williams. For years, patients with heart valve problems were given peri procedural antibiotics for endocarditis prophylaxis. Currently, however, recommendations are more stringent. The American Heart Association recommends prophylaxis for dental procedures in those with: (1) a prosthetic valve or prosthetic material used in a valve repair, (2) prior endocarditis, (3) unrepaired cyanotic heart defect or repaired lesion with residual defect at prosthetic sites, and (4) valvulopathy ater heart transplantation (Nishimura, 2017). The American College of Obstetricians and Gynecologists (2016) does not recommend endocarditis prophylaxis for either vaginal or cesarean delivery in the absence of pelvic infection except with the lesions cited above. Women at highest risk for endocarditis are those with cyanotic cardiac disease, prosthetic valves, or both. When indicated, and for women not already receiving intrapartum antimicrobial therapy for another indication that would also provide coverage against


Obstentrics_Williams

Obstentrics_Williams. cardiac disease, prosthetic valves, or both. When indicated, and for women not already receiving intrapartum antimicrobial therapy for another indication that would also provide coverage against endocarditis, prophylactic regimens are shown in Table 49-8. hese are administered as close to 30 to 60 minutes before the anticipated delivery time as is feasible.


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Obstentrics_Williams. Both preexisting and new-onset cardiac arrhythmias are often encountered during pregnancy, labor, delivery, and the puerperium Qoglar, 2014; Knotts, 2014). In a study of73 women with a history of supraventricular tachycardia (ST) , paroxysmal atrial flutter or fibrillation, or ventricular tachycardia, recurrence rates during pregnancy were 50, 52, and 27 percent, respectively (Silversides, 2006). The mechanism(s) responsible for the higher incidence of arrhythmias during pregnancy are TABLE 49-8. Antibiotic Prophylaxis for Infective Endocarditis in High-Risk Patients American College of Obstetricians and Gynecologist (2016) Standard (IV): ampicillin 2 9 or cefazolin or ceftriaxone 1 9 Penicillin-allergic (IV): cefazolin or ceftriaxone 1 9 or clindamycin 600 mg Oral: amoxicillin 2 9 American Heart Association/European Society of Cardiology (Karchmer, 201n5)a


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Obstentrics_Williams. American Heart Association/European Society of Cardiology (Karchmer, 201n5)a Standard: amoxicillin 2 9 PO or ampicillin 2 9 IV or 1M Penicillin-allergic: clarithromycin or azithromycin 500 mg PO; cephalexin 2 gnPO; clindamycin 600 mg PO, IV, or 1M; or cefazolin or ceftriaxone 1 9 IV or 1M 1M = intramuscularly; IV = intravenously. aCefazolin r ceftriaxone given 30 minutes and all others given 1 hour prior to procedure. not well elucidated. From some studies, estradiol and progesterone are proarrhythmic. Estrogen augments the number of adrenergic receptors in the myocardium, and adrenergic responsiveness seems to be greater in pregnancy (Enriquez, 2014). Perhaps the normal but mild hypokalemia of pregnancy and/or the physiological rise in heart rate serves to induce arrhythmias. Alternatively, detection of arrhythmias may be greater because of the frequent visits typical of routine prenatal care.


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Obstentrics_Williams. Slow heart rhythms, including complete heart block, are compatible with a successful pregnancy outcome (Keepanasseril, 2015). Some women with complete heart block have syncope during labor and delivery, and occasionally temporary cardiac pacing is necessary (Hidaka, 2006). In our experiences and from others, women with permanent artificial pacemakers usually tolerate pregnancy well (Hidaka, 2011; Jafe, 1987). With ixed-rate devices, cardiac output apparently is increased by augmented stroke volume.


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Obstentrics_Williams. Patients with pacemakers or other electrical implants require special precautions during surgery. Stray current may be interpreted as an intracardiac signal by the implanted device and lead to pacing changes. In addition, myocardial burns may result from conduction of current through the pacing electrode rather than through the grounding pad (Pinski, 2002). With these devices, preventive steps include cardiology consultation; bipolar electrosurgery or Harmonic scalpel use rather than mono polar current; if needed, minimal monopolar settings; continuous cardiac and pulse oximetry monitoring; contingency plans for arrhythmias; and close proximity of electrosurgery active and return electrodes (Crossley, 2011).


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Obstentrics_Williams. The most common arrhythmia seen in reproductive-aged women is paroxysmal SVT. The prevalence during pregnancy is 24 cases per 100,000 hospital admissions, and approximately 20 percent will experience symptomatic exacerbations during pregnancy (Enriquez, 2014). Interestingly, the mean heart rate of pregnant women with paroxysmal SVT is faster compared with nonpregnant women-184 versus 166 bpm, respectively (Yu, 2015). From Hungary, BGnhidy and associates (2015) found that approximately half of women with paroxysmal SVT had an initial onset during pregnancy. Notably, maternal paroxysmal SVT was associated with a twofold greater risk of septal cardiac defects, particularly secundum atrial septal defects, in their ofspring.


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Obstentrics_Williams. In contrast, rarely do atrial ibrilation and atrial lutter present for the irst time during pregnancy. Indeed, new-onset atrial ibrillation should prompt a search for underlying etiologies that include cardiac anomalies, hyperthyroidism, pulmonary embolism, drug toxicity, and electrolyte disturbances (DiCarloMeacham, 2011). Major complications include embolic stroke, and when associated with mitral stenosis, pulmonary edema may develop in later pregnancy if the ventricular rate is increased.


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Obstentrics_Williams. For acute treatment, vagal maneuvers, which include Valsalva maneuver, carotid sinus massage, bearing down, and immersion of the face in ice water, raise vagal tone and block the atrioventricular node (Link, 2012; Page, 2015). Intravenous adenosine is a short-acting endogenous nucleotide that also blocks atrioventricular nodal conduction. Our experiences are similar to those of others in that adenosine is safe and efective for cardioversion in hemodynamically stable gravidas (Page, 2015; Robins, 2004). Transient fetal bradycardia has been described with adenosine (Dunn, 2000).


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Obstentrics_Williams. If pharmacological therapy is inefective or contraindicated, the merican College of Cardiology and the merican Heart Association recommend synchronized cardioversion in pregnant women with hemodynamically unstable SVT (Page, 2015). And although electrical cardioversion with standard energy settings is not contraindicated in pregnancy, vigilance is important. Barnes and colleagues (2002) described a case in which direct current cardioversion led directly to a sustained uterine contraction and fetal bradycardia. As an aside, pregnancy has no efect on the operation of implantable cardioverter-defibrillator devices (Boule, 2014). If cardioversion fails or is unsafe because of concurrent thrombus, then long-term anticoagulation and heart rate control with medication are necessary (DiCarlo-1eacham, 2011). Other treatment options recommended by the American College of Cardiology and the American Heart Association (Page, 2015) include:


Obstentrics_Williams

Obstentrics_Williams. Intravenous metoprolol or propranolol when adenosine is inefective or contraindicated Intravenous verapamil when adenosine and 3-blocking agents are inefective or contraindicated Intravenous amiodarone with potentially life-threatening SVT and when other therapies are inefective or contraindicated. Pregnancy may predispose otherwise asymptomatic women with WoffParkinson-White (WP) syndrome to exhibit arrhythmias. In a study of 25 women who had SVT diagnosed before pregnancy, three of 12 women with WPW syndrome and six of 13 without the condition developed SVT during pregnancy (Pappone, 2003). In some patients, accessory pathway ablation may be indicated. Driver and coworkers (2015) have provided a review.


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Obstentrics_Williams. This form of arrhythmia is uncommon in healthy young women without underlying heart disease. Brodsky and associates (1992) described seven pregnant women with new-onset ventricular tachycardia and reviewed 23 reports. Most of these women were not found to have structural heart disease. In 14 cases, tachycardia was precipitated by physical exercise or psychological stress. Abnormalities found included two cases of myocardial infarction, two of prolonged QT interval, and one of anesthesia-provoked tachycardia. They concluded that pregnancy events precipitated the tachycardia and recommended 3-blocking agents for control. As previously discussed (p. 964), arrhythmogenic right ventricular dysplasia will result occasionally in ventricular tachyarrhythmias (Lee, 2006). If unstable, emergency cardioversion is indicated, and standard adult energy settings are adequate Qeejeebhoy, 2011; Lin, 2015).


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Obstentrics_Williams. This conduction anomaly may predispose individuals to a potentially fatal ventricular arrhythmia known as torsades de pointes (Roden, 2008) . Two studies comprised of 502 pregnant women with long QT syndrome both reported a signiicant increase in cardiac events postpartum but not during pregnancy (Rashba, 1998; Seth, 2007). The normal rise in heart rate during pregnancy may be partially protective. Paradoxically, 3-blocking agents-preferably propranolol-lower the risk of torsades de pointes in patients with long QT syndrome and should be continued throughout pregnancy and the puerperium (Enriquez, 2014; Seth, 2007). Importantly, many medications, including some used during pregnancy such as azithromycin, erythromycin, and clarithromycin, may predispose to QT prolongation (Ray, 2012; Roden, 2004).


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Obstentrics_Williams. vlarfan syndrome and coarctation are two aortic diseases that place the pregnant woman at increased risk for aortic dissection (Russo, 2017). Indeed, half of dissection cases in young women are related to pregnancy (O'Gara, 2004). Other risk factors are bicuspid aortic valve and Turner or Noonan syndrome. A high rate of aortic dissection or rupture is also reported in patients with Ehlers-Danlos syndrome (Murray, 2014; Pepin, 2000). Although the mechanism(s) involved are unclear, the initiating event is a tear in the intimal layer of the aorta, followed by hemorrhage into the media, and finally rupture.


Obstentrics_Williams

Obstentrics_Williams. In most cases, aortic dissection presents with severe chest pain described as ripping, tearing, or stabbing. Diminution or loss of peripheral pulses coupled with a recently acquired aor tic insuiciency murmur is an important physical inding. he diferential diagnosis of aortic dissection in pregnancy includes myocardial infarction, pulmonary embolism, pneumothorax, aortic valve rupture, and obstetrical catastrophes, especially placental abruption and uterine rupture. More than 90 percent of patients with aortic dissection have an abnormal chest radiograph. Aortic angiography is the most definitive method for diagnosis confirmation. However, sonog raphy, computed tomography, and MR imaging are used more frequently depending on the urgency of the clinical situation. Initial medical treatment is given to lower blood pressure.


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Obstentrics_Williams. Initial medical treatment is given to lower blood pressure. Proximal dissections most often need to be resected, and the aortic valve replaced if necessary. Distal dissections are more complex, and many may be treated medically. Among non pregnant patients, survival is not improved by immediate elec tive repair compared with surveillance and delayed repair of abdominal aortic aneurysms <5.5 cm. But, Karthikesalingam and colleagues (2016) suggest that the size threshold for aneu rysm repair should be revisited.


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Obstentrics_Williams. This autosomal dominant connective tissue disorder has an incidence of 2 to 3 cases per 10,000 individuals and is without racial or ethnic predilection (Ammash, 2008). As discussed in Chapter 59 (p. 1151), Marfan syndrome is characterized by generalized tissue weakness that can result in dangerous cardiovascular complications. Because all tissues are involved, other defects are frequent and include joint laxity and scoliosis. Progressive aortic dilation causes aortic valve insuiciency, and there may be infective endocarditis and mitral valve prolapse with insuiciency. Aortic dilation and dissecting aneurysm are the most serious abnormalities. Early death is due either to valvular insuiciency and heart failure or to a dissecting aneurysm.


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Obstentrics_Williams. Of outcomes, a study using the Nationwide Inpatient Sample from 2003 to 2010 found 339 deliveries in women with Marfan syndrome. There was one maternal death and six (1.8 percent) aortic dissections (Hassan, 2015). Russo and associates (2017) used Texas obstetrical discharge data and found that eight of 47 women with aortic dissection had Marfan syndrome. A study from the United ingdom reported similar results (Curry, 2014).


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Obstentrics_Williams. The aortic root usually measures approximately 2 cm, and during normal pregnancy, it expands slightly (Easterling, 1991). With Marfan syndrome, aortic root repair is recommended at diameters of 4.0 to 4.5 cm (Smok, 2014). The guidelines of the American College of Cardiology, the American Heart Association, and the merican Association of horacic Surgeons advise prophylactic aortic repair in women considering pregnancy if the diameter of the ascending aorta exceeds 4 cm (Hiratzka, 2010). The guidelines of the European Society of Cardiology (2011) advise repair of the aorta at diameters :::4.5 cm. Because shorter patients have dissection at a smaller diameter, surgical repair is also considered using a formula indexed to height (Bradley, 2014; Smok, 2014).


Obstentrics_Williams

Obstentrics_Williams. For pregnant women with known thoracic aortic root or ascending aortic dilation, monthly or bimonthly echocardiographic measurements of the ascending aortic dimensions are recommended to detect expansion (Hiratzka, 2010). Prophylactic 3-blocking agents have become standard for pregnant women with �1arfan syndrome because they reduce hemodynamic stress on the ascending aorta and slow the dilation rate (Simpson, 2012). Ideally, pregnant women with aortic aneurysms are delivered at facilities in which cardiothoracic surgery is available. Vaginal delivery with regional analgesia and an assisted second stage seem safe for women with an aortic root diameter < 4 cm.


Obstentrics_Williams

Obstentrics_Williams. When the aortic root measures 4 to 5 cm or greater, elective cesarean delivery is recommended with consideration of postpartum replacement of the proximal aorta with a prosthetic graft (Simpson, 2012). Successful aortic root replacement during pregnancy has been described, but the surgery has also been associated with fetal hypoxic-ischemic encephalopathy (Mul, 1998; Seeburger, 2007). Several case reports describe emergency cesarean deliveries in women with acute type A dissections that were repaired successfully at the time of delivery (Guo, 2011; Haas, 2011; Papatsonis, 2009). To evaluate obstetrical outcomes, investigators for one study of 63 women with Marfan syndrome analyzed their 142 pregnancies. Of 111 pregnancies progressing past 20 weeks' gestation, 15 percent delivered preterm, and 5 percent had preterm prematurely ruptured membranes (vleijboom, 2006). here were eight perinatal deaths, and half of the neonatal survivors were subsequently diagnosed with Marfan syndrome.


Obstentrics_Williams

Obstentrics_Williams. In this relatively rare lesion, the aorta is abnormally narrowed and is often accompanied by abnormalities of other large arteries. A fourth of afected patients have a bicuspid aortic valve, and another 10 percent have cerebral artery aneurysms. Other associated lesions are persistent ductus arteriosus, septal defects, and Turner syndrome. he collateral circulation arising above the coarctation remodels and expands, often strikingly, to cause localized erosion of rib margins by hypertrophied intercostal arteries. Typical indings include hypertension in the upper extremities but normal or reduced pressures in the lower extremities. Authors have described diagnosis during pregnancy using MR imaging (Sherer, 2002; Zwiers, 2006). Moreover, Jimenez-Juan and associates (2014) found that aortic diameter measured by �1R and the risk of adverse events during pregnancy were inversely correlated. Of note, no adverse outcomes occurred if the minimum diameter at the coarctation exceeded 15 mm.


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Obstentrics_Williams. Major complications with aortic coarctation include congestive heart failure after long-standing severe hypertension, bacterial endocarditis of the bicuspid aortic valve, and aortic rupture. Because hypertension may worsen in pregnancy, antihypertensive therapy using 3-blocking drugs is usually required. Aortic rupture is more likely late in pregnancy or early puerperium. Cerebral hemorrhage from circle of Wiis aneurysms may also occur.


Obstentrics_Williams

Obstentrics_Williams. Cerebral hemorrhage from circle of Wiis aneurysms may also occur. Of outcomes from 188 pregnancies, a third of women had hypertension that was related to significant coarctation gradients, and one woman died from dissection at 36 weeks' gestation (Beauchesne, 2001). Of nearly 700 deliveries in women with coarctation from the Nationwide Inpatient Sample, hypertensive complications of pregnancy were increased threeto fourfold (rieger, 2011). Importantly, almost 5 percent of women with coarctation had an adverse cardiovascular outcome-maternal death, heart failure, arrhythmia, cerebrovascular or other embolic event-compared with only 0.3 percent of controls. Of women with coarctation, 41 percent underwent cesarean delivery compared with 26 percent of controls.


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Obstentrics_Williams. Congestive heart failure demands vigorous eforts to improve cardiac function and may warrant pregnancy interruption. Some authors recommend that resection of the coarctation be undertaken during pregnancy to protect against the possibility of a dissecting aneurysm and aortic rupture. This poses significant perfusion risk, especially for the fetus, because all the arterial collaterals must be clamped for variable periods.


Obstentrics_Williams

Obstentrics_Williams. Pregnant women with coronary artery disease commonly have the classic risk factors of diabetes, smoking, hypertension, hyperlipidemia, and obesity Games, 2006). Although relatively rare, the risk of acute myocardial infarction is approximately threefold higher in pregnant women compared with nonpregnant women of similar age (Elkayam, 2014b). From more than 50 million hospitalizations in the United States between 1998 and 2009, rates of acute myocardial infarction approximated 2 per 100,000 delivery hospitalizations and 4 per 100,000 postpartum hospitalizations (Callaghan, 2012). Ladner and colleagues (2005) reported a similar rate of 2.7 per 100,000 deliveries.


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Obstentrics_Williams. The mortality rate with myocardial infarction in pregnancy is higher compared with age-matched nonpregnant women. In a Nationwide Inpatient Sample study totaling 859 pregnancies complicated by acute infarction, the death rate was 5.1 percent Games, 2006). Women who sustain an infarction <2 weeks before delivery are at especially high risk of death due to the greater myocardial demand of labor and delivery (Esplin, 1999).


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Obstentrics_Williams. In a systematic review of 150 cases, most women developed an acute myocardial infarction (MI) during the third trimester or postpartum (Elkayam, 2014b). Approximately three fourths presented with ST segment-elevation MI (STEMI). he leading mechanisms of acute infarction included spontaneous coronary dissection (43 percent) and atherosclerotic disease (27 percent). Signiicant complications included heart failure/cardiogenic shock (38 percent), recurrent angina or infarction (19 percent), and ventricular arrhythmias (12 percent). he maternal and fetal mortality rates were 7 and 5 percent, respectively. Of other potential antecedents, coronary artery occlusion in two pregnant smokers with hypercholesterolemia has been described following ergometrine administration (Mousa, 2000; Ramzy, 2015; Sutaria, 2000). Schulte-Sasse (2000) reported myocardial ischemia associated with prostaglandin Ervaginal suppositories given for 1 labor induction.


Obstentrics_Williams

Obstentrics_Williams. Diagnosis of acute myocardial infarction during pregnancy does not difer from that in nonpregnant patients and is based on clinical presentation, characteristic ECG changes, and evidence of myocardial necrosis relected by elevated serum troponin levels (Pacheco, 2014). Of note, troponin I levels are undetectable near term in normal pregnancy and do not rise following either vaginal or cesarean delivery (Koscica, 2002; Shivvers, 1999). Importantly, however, troponin I levels are higher in preeclamptic women compared with normotensive controls (Atalay, 2005; Yang, 2006). With spontaneous coronary artery dissection, establishing the diagnosis requires a high index of suspicion in the gravida presenting with chest pain (Codsi, 2016). For this condition, coronary angiography is considered the diagnostic gold standard and should be expediently performed if acute coronary syndrome-deined as myocardial infarction or unstable angina-is present.


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Obstentrics_Williams. Treatment of acute myocardial infarction is similar to that for nonpregnant patients (Pacheco, 2014). An algorithm summarizing one approach to its management during pregnancy is shown in Figure 49-6. Several reports describe successful percutaneous transluminal coronary angioplasty and stent placement during pregnancy (Balmain, 2007; Duarte, 2011; FIGURE 49-6 Initial management of acute myocardial infarction during pregnancy. Risk stratification refers to the risk ofdeveloping recurrent symptoms despite optimal medical management. (Adapted with permission from Pacheco LO, Saade GR, Hankins GO: Acute myocardial infarction during pregnancy, (lin Obstet Gynecol. 2014 Oec;S7(4):83S-843.) Dwyer, 2005). Cardiopulmonary resuscitation may be required, as described in Chapter 47 (p. 931). If the infarct has healed suiciently, cesarean delivery is reserved for obstetrical indications, and epidural analgesia is ideal for labor (Esplin, 1999).


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Obstentrics_Williams. • Pregnancy with Prior Ischemic Heart Disease he advisability of pregnancy after a myocardial infarction is unclear. Ischemic heart disease is characteristically progressive, and because it is usually associated with hypertension or diabetes, pregnancy in most of these women seems inadvisable. In a review of 30 pregnancies in women who had sustained an inarction remoterompregnancy, none of the women died, four had congestive heart failure, and four had worsening angina during pregnancy (Vinatier, 1994). Pombar and coworkers (1995) evaluated outcomes of women with diabetes-associated ischemic heart disease and infarction. Three had undergone coronary artery bypass grafting before pregnancy. Of 17 women, eight died during pregnancy. Certainly, pregnancy raises cardiac workload, and these investigators concluded that ventricular performance should be assessed using ventriculography, radionuclide studies, echocardiography, or coronary angiography before conception. Without signiicant


Obstentrics_Williams

Obstentrics_Williams. investigators concluded that ventricular performance should be assessed using ventriculography, radionuclide studies, echocardiography, or coronary angiography before conception. Without signiicant ventricular dysfunction, pregnancy will likely be tolerated. For the woman who becomes pregnant before these studies are performed, echocardiography is done. Exercise tolerance testing may be indicated, and radionuclide ventriculography exposes the fetus to minimal radiation.


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Obstentrics_Williams. Abdalla M, Mancini OM: Management of pregnancy in the post-cardiac transplant patient. Semin Perinatal 38(5):318, 2014 Agir A, Bozyel 5, Celikyurt U: Arrhythmogenic right ventricular cardiomyopathy in pregnancy. Int Heart J 55(4):372, 2014 Aliaga L, Santiago FM, Marti J, et al: Right-sided endocarditis complicating an atrial septal defect. Am J Med Sci 325:282, 2003 Altin FH, Yildiz 0, Karacalilar M: Complete atrioventricular septal defects and pulmonary stenosis diagnosed in a 49-year-old woman after 10 uneventful births. Tex Heart Inst J 42(2):166, 2015 Ambia M, Morgan JL, Wilson L, et al: Frequency and consequences ofconcentric hypertrophy in pregnant women with treated chronic hypertension. Abstract No. 808, mJ Obstet Gynecol 216:5463, 2017 American College of Obstetricians and Gynecologists: Thromboembolism in pregnancy. Practice Bulletin No. 123, September 2011, Reairmed 2017


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Obstentrics_Williams. American College of Obstetricians and Gynecologists: Thromboembolism in pregnancy. Practice Bulletin No. 123, September 2011, Reairmed 2017 American College ofObstetricians and Gynecologists: Use ofprophylactic antibiotics in labor and delivery. Practice Bulletin No. 120, June 2011, Reafirmed 2016 Ammash NM, Sundt TM, Connolly HM: Marfan syndrome-diagnosis and management. Curr Prabl Cardiol 33: ,t2008 Angeli F, Angeli E, Verdecchia P: Electrocardiographic changes in hypertensive disorders of pregnancy. Hypertens Res 3 (11):973,t2014 Arany Z, Elkayam U: Peripartum cardiomyopathy. Circulation 133(14): 1397, 2016 Armenti T, Radomski ]5, Moritz MJ, et al: Report from the National Transplantation Pregnancy Registry (NTPR): outcomes of pregnancy after transplantation. Clin Transpl 121t:30,t2002 Atalay C, Erden G, Turhan T, et al: he efect ofmagnesium sulfate treatment on serum cardiac troponin I levels in preeclamptic women. Acta Obstet Gynecol Scand 84:617, 2005


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