Parity and aortic dimensions in healthy women

Cardiac output and blood volume increase dramatically during the course of normal pregnancy, peaking around the time of parturition1. In addition to hemodynamic stress, high levels of circulating gestational hormones and angiogenic factors may contribute to increased risk for aortic dissection in late pregnancy, especially in women with Marfan or Turner syndromes2. It is unknown whether repeated pregnancies may result in enduring enlargement of aortic diameter in healthy women. Therefore, in this cross-sectional study we investigated the relation between ascending and descending aortic diameters and parity history in 51 healthy female volunteers. Parity was defined as the number of live births. All subjects provided written informed consent for voluntary participation in an IRB-approved protocol. Women with hypertension, congenital or acquired cardiac disease, diabetes, renal or liver disease and history of pregnancy complications such as pre-eclampsia or multiple gestations were excluded from study. Ascending and descending aortic diameters (AAD, DAD) were measured at the level of the pulmonary artery bifurcation by magnetic resonance (Fig. 1). Age, BSA, and blood pressure were similar in low and high parity groups (Table 1). However, AAD was 13% greater (P = .001) and DAD was 10% greater (P = .001) in the multiparous group. Multivariable analysis showed that age (P < .001), BSA (P = .004) and parity (P = .002) each contributed significantly to variation in AAD, while age (P < .001) and BSA (P < .001, but less so parity (P = .072) correlated with descending aortic diameter. Figure 1 Intraluminal, end-systole aortic diameters were measured on T-1 weighted black blood images at the level of the pulmonary artery bifurcation as previously described 8. Cross-sectional measurements were made perpendicular (AP) and parallel (RL) to the ... Table 1 Aortic Diameters Stratified by Parity Group The fact that both ascending and descending aortic diameters are larger in healthy multiparous women compared to null or uniparous women suggests the experience of normal pregnancies and births causes enduring changes in the wall structure of the thoracic aorta. High levels of circulating angiogenic factors involved in vascular development of the placenta and embryo3 may also induce remodeling of the maternal vasculature to accommodate the increased blood volume of pregnancy. High estrogen and progesterone levels in pregnant women are associated with histological changes in the aortic wall, including fragmentation of reticulin fibers, diminished acid mucopolysaccharides, disruption of elastic fibers, and hypertrophy and hyperplasia of smooth muscle cells5. It thus seems plausible that a summation of hormonal and hemodynamic stresses after repeated pregnancies might result in enduring aortic enlargement 6. Our sample by design excluded confounders affecting aortic size such as HTN and diabetes7. Thus, we were able to discern statistically significant and biologically plausible effects of multiparity on aortic dimensions. However, these observations most likely underestimate the effects of pregnancy on aortic dimensions in the general population with its high prevalence of obesity, diabetes and hypertension. Our findings are important for expanding knowledge about ways in which gender-specific physiological factors such as normal pregnancy may influence cardiovascular biology, and are relevant to assessing pregnancy risks in women that have preexisting conditions associated with aortic complications such as Marfan and Turner syndromes, and bicuspid aortic valve.