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).
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.
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.
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).
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).