Maternal Cardiovascular Function in Normal Pregnancy

Understanding cardiovascular physiological adaptation to pregnancy is particularly important in elucidating the pathophysiology and management of hypertensive disorders of pregnancy—still one of the most common causes of maternal morbidity and mortality worldwide. Functional changes of the heart in pregnancy have been widely investigated during the last few decades with relatively inconsistent results. Some studies demonstrated an enhancement of cardiac function in pregnancy, whereas others showed depressed cardiac function, and a few, unchanged functional status. The most likely reason for these conflicting results is that complex data on maternal cardiac function has not been interpreted in the context of heart geometry, loading conditions, and maternal anthropometric factors, which are all modified from as early as the time of conception and continue to change continuously throughout pregnancy. Furthermore, in the majority of previous studies, cardiac data were usually expressed as single echocardiographic indices compared across gestation without clear delineation between normal and abnormal function. Hence, an important limitation of previous work is the lack of distinction between physiological cardiac adaptation to pregnancy and cardiac dysfunction as a consequence of the pregnancy. Cardiac function is a generic and nonspecific concept that, by necessity, varies depending on the clinical context— alterations in function may simply reflect the effect of hemodynamic changes, altered cardiac geometry or body size on heart function, or indicate true cardiac dysfunction. Cardiac function is conventionally measured by assessing cardiac chamber size, ventricular mass, and function. However, for systolic or diastolic dysfunction to occur to a clinically relevant degree, there would first have to be impaired myocardial contractility and relaxation. Consequently, only an integrated approach using parallel techniques and multiple indices can provide results that reflect the intrinsic myocardial functional status of the heart. The aim of this study is to understand maternal cardiac adaptation to pregnancy from myocardium to chamber, using a comprehensive approach taking into account the simultaneous Abstract—The aim of this study was to investigate cardiac functional status in pregnancy using a comprehensive approach taking into account the simultaneous changes in loading and geometry, as well as maternal age and anthropometric indices. This was a prospective cross-sectional study of 559 nulliparous pregnant women assessed at 4 time points during pregnancy and at 1 year postpartum. All women underwent conventional echocardiography and tissue Doppler velocities and strain rate analysis at multiple cardiac sites. Mean arterial pressure and total vascular resistance index significantly decreased (both P<0.001) during the first 2 trimesters of pregnancy and increased thereafter. Stroke volume index and cardiac index showed the opposite trend compared with mean arterial pressure and total vascular resistance index (both P<0.05). Myocardial and ventricular function were significantly enhanced in the first 2 trimesters but progressively declined thereafter. By the end of pregnancy, significant chamber diastolic dysfunction and impaired myocardial relaxation was evident in 17.9% and 28.4% of women, respectively, whereas myocardial contractility was preserved. There was full recovery of cardiac function at 1 year postpartum. Cardiovascular changes during pregnancy are thought to represent a physiological adaptation to volume overload. The findings of a drop in stroke volume index, impaired myocardial relaxation with diastolic dysfunction, and a tendency toward eccentric remodeling in a significant proportion of cases at term are suggestive of cardiovascular maladaptation to the volume-overloaded state in some apparently normal pregnancies. These unexpected cardiovascular findings have important implications for the management of both normal and pathological pregnancy states. (Hypertension. 2016;67:754-762. DOI: 10.1161/HYPERTENSIONAHA.115.06667.) • Online Data Supplement