This diagnosis implies the presence of a pathological connective tissue disorder-often termed myxomatous degenerationwhich may involve the valve lealets themselves, the annulus, or the chordae tendineae. Mitral insuiciency may develop. Most women with mitral valve prolapse are asymptomatic and are diagnosed during routine examination or echocardiography. he few women with symptoms have anxiety, palpitations, atypical chest pain, dyspnea with exertion, and syncope (Guy, 2012).
Pregnant women with mitral valve prolapse rarely have cardiac complications. Hypervolemia may even imptove alignment of the mitral valve, and women without pathological myxomatous degeneration generally have excellent pregnancy outcomes (LdniakSobelga, 2004). For women who are symptomatic, �-blocking drugs diminish sympathetic tone, relieve chest pain and palpitations, and reduce the risk of life-threatening arrhythmias.
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.
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.
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).