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Pregnancy in most women with heart disease has a favourable maternal and fetal outcome. With the exception of patients with Eisenmenger syndrome, pulmonary vascular obstructive disease, and Marfan syndrome with aortopathy, maternal death during pregnancy in women with heart disease is rare.1-4 However, pregnant women with heart disease do remain at risk for other complications including heart failure, arrhythmia, and stroke. Women with congenital heart disease now comprise the majority of pregnant women with heart disease seen at referral centres. The next largest group includes women with rheumatic heart disease. Peripartum cardiomyopathy, though infrequent, will be discussed in view of its unique relation to pregnancy. Two groups of conditions not discussed further are coronary artery disease, infrequently encountered, and isolated mitral valve prolapse, which generally has an excellent outcome.
Cardiovascular physiology and pregnancy
Hormonally mediated increases in blood volume, red cell mass, and heart rate result in a major increase in cardiac output during pregnancy; cardiac output peaks during the second trimester, and remains constant until term. Gestational hormones, circulating prostaglandins, and the low resistance vascular bed in the placenta result in concomitant decreases in peripheral vascular resistance and blood pressure. During labour and delivery, pain and uterine contractions result in additional increases in cardiac output and blood pressure. Immediately following delivery, relief of caval compression and autotransfusion from the emptied and contracted uterus produce a further increase in cardiac output. Most haemodynamic changes of pregnancy resolve by two weeks postpartum.5
Outcomes associated with specific cardiac lesions
Congenital heart lesions
Left to right shunts
The effect of increase in cardiac output on the volume loaded right ventricle in atrial septal defect (ASD), or the left ventricle in ventricular septal defect (VSD) and patent ductus arteriosus, is counterbalanced by the decrease in peripheral vascular resistance. Consequently, the increase in volume overload is attenuated. In the absence of pulmonary hypertension, pregnancy, labour and delivery are well …
Footnotes
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