Emily Gelson

To estimate the effect of maternal heart disease on fetal growth and neonatal outcomes. A retrospective cohort study of all women with congenital and acquired heart disease admitted at Chelsea and Westminster Hospital between 1994 and 2010 was performed. The women who delivered immediately before and immediately after each index pregnancy were used as controls. Data were obtained from medical and obstetric notes. Birth weight percentiles were calculated using a customized birth weight percentile program, and neonatal complications (preterm birth, perinatal mortality, and recurrence of congenital heart disease) were noted. Median birth weight percentile was significantly lower in the heart disease group (31) compared with the control group (49;P.001 Mann-Whitney U test [corrected].The rate of neonatal complications was significantly higher in the heart disease group (34% compared with 15%). Preterm birth occurred in 42 (13%) pregnancies, of which 67% were iatrogenic. Eighty-one (25%) newborns in the heart disease group were small for gestational age, and there were four stillbirths and four neonatal deaths (perinatal mortality rate 20 per 1,000). This cohort study suggests a significant reduction in fetal growth rates associated with maternal heart disease, which is also associated with preterm delivery and reduced birth weight. The presence of maternal cyanosis and a reduced cardiac output are the most significant predictors. II.

Does pregnancy affect valvular heart disease?Changes that occur in pregnancy pose a substantial demand on cardiac function in women with valvular disease. By eight weeks' gestation, systemic vascular resistance falls by 30-70% of its preconception value, initiating a 30-50% increase in cardiac output, an increase of 10-20 beats/min in heart rate, and a 30-50% increase in blood volume. Systemic vascular resistance falls by 30-70% of its preconception value. Labour, particularly the second stage, is associated with a further increase in cardiac output. Pain induces a sympathetic response causing an increase in heart rate. Stroke volume is augmented by autotransfusion during contractions. After delivery, the return of uterine blood into the systemic circulation results in a further increase in cardiac output. Stroke volume, heart rate, and cardiac output remain high for 24 hours after delivery, with rapid intravascular volume shifts in the first two weeks postpartum. Mitral stenosisIn mitral stenosis, the increase in cardiac output is limited by the amount of blood that can flow through the narrowed valve during diastole. The pregnancy induced increase in the maternal heart rate shortens diastole, reducing left ventricular filling.2 In some cases, this leads to reduced cardiac output, increased left atrial pressure, and overt cardiac failure. About 40% of women with mitral stenosis experience some symptomatic decline in cardiac function in pregnancy.3 Typically, patients develop shortness of breath with exertion in the second trimester, progressing to orthopnoea and paroxysmal nocturnal dyspnoea as pregnancy advances. Often the deterioration is acute, typically due to an arrhythmia, usually atrial fibrillation secondary to stretch of the left atrium.Several reports have highlighted the dangers to the mother of pregnancy in the presence of mitral stenosis.2 3 4w2 Maternal outcomes are favourable in women with mild mitral stenosis, but not in women with moderate or severe mitral stenosis, who have a high rate of morbidity (such as pulmonary oedema, arrhythmias, the need to start or increase cardiac medication, and the need for admission to hospital). Predictors of adverse maternal outcome include the severity of mitral stenosis (valve area <1.5 cm2) and New York Health Association (NYHA) functional class (box 1).5 The prepregnancy risk of maternal mortality in the presence of severe mitral stenosis has been quoted at 1-5%6 and is also associated with NYHA functional class.7 No data are available on the long term effects of pregnancy on maternal cardiac function in mitral stenosis.Box 1 New York Health Association classification • Class I: Patients with no limitation of activities and no symptoms from ordinary activities • Class II: Patients with slight, mild limitation of activity who are comfortable at rest or with mild exertion • Class III: Patients with marked limitation of activity who are comfortable only at rest • Class IV: Patients who should be at complete rest, confined to bed or chair, and in whom any physical activity brings on discomfort and symptoms occur at rest Aortic stenosisIn young women aortic stenosis is usually congenital. The limited ability of the left ventricle to augment cardiac output results in an abnormal rise in left ventricular systolic and filling pressures, leading to a compensatory left ventricular hypertrophy. In pregnancy the increase in stroke volume and fall in systemic vascular resistance lead to an increase in the gradient across the aortic valve.2 The clinical consequences of the increased aortic gradient depend on the degree of pre-existing left ventricular hypertrophy and left ventricular systolic function. When compensatory changes in the left ventricle are inadequate to meet the demands imposed by the need for increased cardiac output late in pregnancy, symptoms develop. Moderate to severe aortic stenosis (valve area <1.5 cm2) substantially affects pregnancy outcome. Studies from the 1970s show a high incidence (17.4%) of maternal mortality.w3 More recent studies report no maternal or neonatal deaths; however, moderate to severe aortic stenosis is associated with significant maternal morbidity, including heart failure, arrhythmia, and syncope.4 8w4 Pregnancy seems to have a long term effect on the clinical course of aortic stenosis, with a 31% rate of cardiac surgery reported within a three year follow-up period.4Aortic and mitral regurgitation Pregnancy is usually well tolerated in women with chronic left sided valve regurgitation without left ventricular dysfunction. This tolerance is due to the fall in systemic vascular resistance and reduced left ventricular afterload. Symptoms may occur in women with severe lesions, particularly in labour, delivery, and the early postpartum period and include dyspnoea on exertion, orthopnoea, and paroxysmal nocturnal dyspnoea.2