Eyal Cohen

and 6 more

Objective: To compare the interpregnancy weight gain in women whose first infant had a major congenital anomaly vs. those without an affected child. Design: Nationwide cohort study Setting: Denmark Population: All primigravid women with two consecutive singleton births between January 2004 and December 2017. Main Outcome Measure: Inter-pregnancy weight difference Methods: Multivariable linear regression compared women whose infant had an anomaly vs. those whose infant did not, adjusting for interpregnancy time interval, demographics, smoking and health status at the first pregnancy. Results: Of the 199,536 women, 4035 (2.0%) had a child with an anomaly at the first birth. The mean (SD) maternal BMI at the start of the first pregnancy was 24.2 (4.9) and 23.8 (4.6) kg/m2 in women with, and without, an anomaly-affected newborn. By the start of the second pregnancy, their interpregnancy weight gain was 4.7% and 4.2%, respectively – an adjusted absolute higher gain of 0.34% (95% CI 0.11 to 0.58) or 0.13 kg (95% CI 0.01 to 0.26) in women with an anomaly-affected first-born infant. Compared to those with an unaffected pregnancy, the interpregnancy weight gain difference was greatest in women whose first-born infant had a multi-organ anomaly (0.73%, 95% CI -0.10 to 1.57). Weight gain was more pronounced in women whose infants spent >30 days in hospital between pregnancies. Conclusions: Mothers of an infant with a major congenital anomaly have higher weight gain after pregnancy. Strategies are needed to support a healthy lifestyle in these women.

Mohab Basem

and 4 more

Purpose To examine whether low-density lipoprotein cholesterol (LDL-C) levels influence the cardiovascular risk associated with non-aspirin non-steroidal anti-inflammatory drug (NSAID) use after myocardial infarction (MI). Methods Using Danish health registries, we conducted a population-based cohort study of all adult patients with first-time MI during 2010–2020 with an LDL-C value before discharge. Based on the latest LDL-C value, we categorized patients into a low and a high LDL-C group (<3.0 vs. ≥3.0 mmol/L). We used time varying Cox regression to compute hazard ratios (HRs) with 95% confidence intervals of the association between NSAID use and a major adverse cardiovascular event (MACE: recurrent MI, ischemic stroke, and all-cause death). Results We followed 50,573 patients for a median of 3.1 years. While exposed, 521 patients experienced a MACE: 312 in the low LDL-C group and 209 in the high LDL-C group. The HRs for MACE comparing NSAID use with non-use were 1.21 (1.11–1.32) overall, 1.19 (1.06–1.33) in the low LDL-C group, and 1.23 (1.07–1.41) in the high LDL-group. The HRs for recurrent MI and ischemic stroke were comparable between the LDL-C subgroups. The HRs for all-cause death were 1.22 (1.07–1.39) in the low LDL-C group and 1.54 (1.30–1.83) in the high LDL-C group. Changing the cut-off value for LDL-C to 1.8 and 1.4 mmol/L showed consistent results. Conclusion In patients with MI, LDL-C levels did not influence the increased risk of MACE associated with NSAID use, but might influence the association between NSAID use and all-cause death.