Increased risks of circulatory diseases in late pregnancy and puerperium.

We studied a nationwide Swedish cohort with 654,957 women who had 1,003,489 deliveries from 1987 through September 1995 to assess late pregnancy and puerperal risks of circulatory diseases. We used standardized incidence rate ratios to calculate relative risks [with 95% confidence intervals (CIs)]. Compared with unexposed (nonpregnant and early pregnant) women, relative risks of venous thrombosis and pulmonary embolism during the third trimester were 6.7 (95% CI = 5.7--7.8) and 2.7 (95% CI = 1.7--4.2), respectively. Around delivery (from 2 days before to 1 day after delivery), the relative risks of all assessed circulatory diseases were dramatically increased: venous thrombosis, 115.1 (95% CI = 96.4--137.0); pulmonary embolism, 80.7 (95% CI = 53.9--117.9); subarachnoid hemorrhage, 46.9 (95% CI = 19.3--98.4); intracerebral hemorrhage, 95.0 (95% CI = 42.1--194.8); cerebral infarction, 33.8 (95% CI = 10.5--84.0); and myocardial infarction, 27.0 (95% CI = 0.6--180.0). During the rest of the first 6 weeks postpartum, the risks declined but were still substantially increased for all diseases, with the exception of subarachnoid hemorrhage. The results suggest that the increased risk for circulatory diseases related to pregnancy is mainly confined to a few days around delivery.

Genetic effects on the liability of developing pre-eclampsia and gestational hypertension.

Genetic factors are known to be important in the etiology of pre-eclampsia and possibly also gestational hypertension, but the degree of genetic influence has not been quantified. To estimate the genetic and environmental effects on the liability of developing pre-eclampsia and gestational hypertension, we cross-linked the population-based Swedish Twin Register and the Swedish Medical Birth Register. We included female twin pairs with known zygosity, both of whom gave birth in Sweden from 1973 through 1993; in all 917 monozygotic and 1,199 dizygotic twin pairs. For pre-eclampsia, the estimates of heritability and nonshared environmental effect were 0. 54 (95% confidence interval 0-0.71) and 0.46 (0.29-0.67), respectively; corresponding estimates for gestational hypertension were 0.24 (0-0.53) and 0.76 (0.47-1.00), respectively. When considering both diseases as a single entity (pregnancy-induced hypertensive diseases), the heritability estimate was 0.47 (0.13-0. 61). These results suggest that genetic factors are important in the development of pre-eclampsia as well as gestational hypertension. The heritability estimates can be of importance when planning genetic linkage studies. In efforts to identify women with elevated risk of developing pre-eclampsia during pregnancy, a question about family history of pre-eclampsia should be included.