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Acquired heart disease and pregnancy

Carol A Waksmonski, MD
Anita LaSala, MD
Michael R Foley, MD
Section Editors
Catherine M Otto, MD
Charles J Lockwood, MD, MHCM
Deputy Editor
Susan B Yeon, MD, JD, FACC


Although cardiac disease complicates a small percentage of all pregnancies in developed countries (eg, only 1 to 4 percent of pregnancies in the United States), maternal cardiac disease is a major cause of non-obstetric maternal morbidity and mortality (figure 1). Care of the high-risk patients requires a team approach including a maternal-fetal medicine specialist, cardiologist, and obstetrical anesthesiologist.

In the past, rheumatic heart disease was the most common form of cardiac disease in pregnant women; it still predominates in developing countries and in immigrant populations in the United States. Congenital heart disease is now the most common form of heart disease complicating pregnancy in the United States, in part because advances in the treatment of congenital heart disease have made it possible for more affected children to reach adulthood and attempt pregnancy. (See "Pregnancy in women with congenital heart disease: General principles" and "Pregnancy and Marfan syndrome".)

In addition, many women are postponing childbearing until the fourth and fifth decades of life [1,2]; with advancing maternal age, underlying medical conditions such as hypertension, diabetes, and hypercholesterolemia become more common and increase the incidence of acquired heart disease complicating pregnancy.


Pregnancy is associated with several cardiocirculatory changes that can significantly impact underlying cardiac disease. These changes begin early in pregnancy (within the first five to eight weeks), reach their peak during the late second trimester, and then remain relatively constant until delivery [3]. Knowledge of these cardiovascular adaptations is required to correctly interpret hemodynamic and cardiovascular tests in the gravida, to predict the effects of pregnancy on the woman with underlying cardiac disease, and to understand how the fetus will be affected by maternal cardiac disorders. (See "Maternal cardiovascular and hemodynamic adaptations to pregnancy".)

Antepartum hemodynamic changes

Cardiac output — The cardiac output rises 30 to 50 percent above baseline during normal pregnancy [4,5]. The degree of change is acutely influenced by posture, as the cardiac output is higher when the pregnant woman is in the left lateral decubitus position, particularly in the latter part of pregnancy [6,7]. In comparison, assumption of the supine position can lower the output by as much as 25 to 30 percent due to compression of the inferior cava by the gravid uterus, leading to a substantial reduction in venous return to the heart.

The increased cardiac output is the result of changes in three important factors that determine cardiac performance: preload is increased due to the associated rise in blood volume; afterload is reduced due to the decline in systemic vascular resistance; and the maternal heart rate rises by 15 to 20 beats/min [4]. The direct effect of pregnancy on left ventricular contractility remains controversial [8].

Regardless of the mechanism, the stress induced by the increase in cardiac output can cause patients with underlying and often asymptomatic heart disease to decompensate during the latter half of pregnancy. This was illustrated in a series of 51 pregnant or postpartum women who developed acute pulmonary edema: 13 (25 percent) had cardiac disease and 6 of the 13 had occult structural lesions [9]. (See "Management of heart failure during pregnancy".)


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Literature review current through: Sep 2016. | This topic last updated: Jul 11, 2014.
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