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.

BACKGROUND: As a result of antenatal screening, abortion of fetuses with Down syndrome has become increasingly common. Little is known about the cardiovascular phenotype in infants with Down syndrome born today.

The risk of a very preterm delivery in successive pregnancies is increased primarily among women with a previous very preterm delivery. Changes in smoking habits influence the risk of preterm delivery as well.

The ingestion of caffeine may increase the risk of an early spontaneous abortion among non-smoking women carrying fetuses with normal karyotypes.

Context During pregnancy, serum levels of estrogen, progesterone, and other hormones are markedly higher than during other periods of life. Pregnancy hormones primarily are produced in the placenta, and signs of placental impairment may serve as indirect markers of hormone exposures during pregnancy. During pregnancy, these markers have been inconsistently associated with subsequent risk of breast cancer in the mother. Objective To examine associations between indirect markers of hormonal exposures, such as placental weight and other pregnancy characteristics, and maternal risk of developing breast cancer. Design and Setting Population-based cohort study using data from the Swedish Birth Register, the Swedish Cancer Register, the Swedish Cause of Death Register, and the Swedish Register of Population and Population Changes. Participants Women included in the Sweden Birth Register who delivered singletons between 1982 and 1989, with complete information on date of birth and gestational age. Women were followed up until the occurrence of breast cancer, death, or end of follow-up (December 31, 2001). Cox proportional hazards models were used to estimate associations between hormone exposures and risks of breast cancer. Main Outcome Measure Incidence of invasive breast cancer. Results Of 314 019 women in the cohort, 2216 (0.7%) developed breast cancer during the follow-up through 2001, of whom 2100 (95%) were diagnosed before age 50 years. Compared with women who had placentas weighing less than 500 g in 2 consecutive pregnancies, the risk of breast cancer was increased among women whose placentas weighed between 500 and 699 g in their first pregnancy and at least 700 g in their second pregnancy (or vice versa) (adjusted hazard ratio, 1.82; 95% confidence interval [CI], 1.07-3.08), and the corresponding risk was doubled among women whose placentas weighed at least 700 g in both pregnancies (adjusted hazard ratio, 2.05; 95% CI, 1.15-3.64). A high birth weight (Ն4000 g) in 2 successive births was associated with an increased risk of breast cancer before but not after adjusting for placental weight and other covariates (adjusted hazard ratio, 1.10; 95% CI, 0.76-1.59). Conclusions Placental weight is positively associated with maternal risk of breast cancer. These results further support the hypothesis that pregnancy hormones are important modifiers of subsequent maternal breast cancer risk.