Parental genetically predicted liability for coronary heart disease and risk of adverse pregnancy outcomes: a cohort study.
Parental genetically predicted liability for coronary heart disease and risk of adverse pregnancy outcomes: a cohort study.
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DOI：
10.1186/s12916-023-03223-9
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发表时间：
2024-01-25
期刊：
影响因子：
9.3
通讯作者：
Magnus, Maria Christine
中科院分区：
文献类型：
--
作者：
Hernaez, Alvaro;Skara, Karoline H.;Page, Christian M.;Mitter, Vera R.;Hernandez, Marta H.;Magnus, Per;Njolstad, Pal R.;Andreassen, Ole A.;Corfield, Elizabeth C.;Havdahl, Alexandra;Naess, Oyvind;Brumpton, Ben;Asvold, Bjorn Olav;Lawlor, Deborah A.;Fraser, Abigail;Magnus, Maria Christine
不良妊娠结局（APO）可能会暴露或加剧女性患冠心病（CHD）的潜在风险。我们估计了母亲和父亲对CHD的遗传预测责任与APO终身风险的关系。我们假设，协会将被发现的妇女，但不是他们的男性伴侣（阴性对照）。我们研究了83,969名女性来自挪威母亲、父亲和儿童队列研究或Trøndelag健康研究的患者（以及多达55，568名男性伴侣），具有基因分型数据和妊娠期间任何APO的终生病史（1967-2019）挪威医学出生登记处（流产、死产、妊娠期高血压疾病、妊娠期糖尿病、小于胎龄儿、大于胎龄儿和自发性早产）。使用148个基因变异（p值< 5 × 10−8，不处于连锁不平衡）生成母亲和父亲CHD遗传风险评分（GRS）。分别在每个队列中使用逻辑回归确定CHD的GRS与每种载脂蛋白O之间的关联，调整基因组主成分，并使用固定效应荟萃分析进行合并。女性冠心病GRS高一个标准差与任何妊娠期高血压疾病（比值比[OR] 1.08，95%置信区间[CI] 1.05-1.10）、先兆子痫（OR 1.08，95% CI 1.05-1.11）和小于胎龄儿（OR 1.04，95% CI 1.01-1.06）的风险增加相关。与小于胎龄儿（OR 0.98，95%CI 0.96-1.00）和死产（OR 1.04，95%CI 0.98-1.11）的低风险相关性不精确。在调整了总怀孕次数和男性伴侣的GRS并将分析限制在稳定的夫妇之后，这些发现仍然一致。其他APO的相关性接近于零。有微弱的证据表明，父亲的先天性心脏病的遗传预测与自发性早产的女性伴侣（OR 1.02，95%CI 0.99-1.05），但不与其他APO。妊娠期高血压疾病、小于胎龄儿和死产可能会暴露出遗传预测的CHD倾向。父亲遗传预测CHD风险与女性伴侣自发性早产的关系需要进一步探讨。在线版本包含补充材料，可通过10.1186/s12916-023-03223-9获得。
Adverse pregnancy outcomes (APO) may unmask or exacerbate a woman’s underlying risk for coronary heart disease (CHD). We estimated associations of maternal and paternal genetically predicted liability for CHD with lifelong risk of APOs. We hypothesized that associations would be found for women, but not their male partners (negative controls). We studied up to 83,969 women (and up to 55,568 male partners) from the Norwegian Mother, Father and Child Cohort Study or the Trøndelag Health Study with genotyping data and lifetime history of any APO in their pregnancies (1967–2019) in the Medical Birth Registry of Norway (miscarriage, stillbirth, hypertensive disorders of pregnancy, gestational diabetes, small for gestational age, large for gestational age, and spontaneous preterm birth). Maternal and paternal genetic risk scores (GRS) for CHD were generated using 148 gene variants (p-value < 5 × 10−8, not in linkage disequilibrium). Associations between GRS for CHD and each APO were determined using logistic regression, adjusting for genomic principal components, in each cohort separately, and combined using fixed effects meta-analysis. One standard deviation higher GRS for CHD in women was related to increased risk of any hypertensive disorders of pregnancy (odds ratio [OR] 1.08, 95% confidence interval [CI] 1.05–1.10), pre-eclampsia (OR 1.08, 95% CI 1.05–1.11), and small for gestational age (OR 1.04, 95% CI 1.01–1.06). Imprecise associations with lower odds of large for gestational age (OR 0.98, 95% CI 0.96–1.00) and higher odds of stillbirth (OR 1.04, 95% CI 0.98–1.11) were suggested. These findings remained consistent after adjusting for number of total pregnancies and the male partners’ GRS and restricting analyses to stable couples. Associations for other APOs were close to the null. There was weak evidence of an association of paternal genetically predicted liability for CHD with spontaneous preterm birth in female partners (OR 1.02, 95% CI 0.99–1.05), but not with other APOs. Hypertensive disorders of pregnancy, small for gestational age, and stillbirth may unmask women with a genetically predicted propensity for CHD. The association of paternal genetically predicted CHD risk with spontaneous preterm birth in female partners needs further exploration. The online version contains supplementary material available at 10.1186/s12916-023-03223-9.
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DOI：
10.1161/hypertensionaha.116.07099
发表时间：
2016-06
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
--
作者：
Egeland GM;Klungsøyr K;Øyen N;Tell GS;Næss Ø;Skjærven R
通讯作者：
Skjærven R
DOI：
10.1016/j.xgen.2022.100193
发表时间：
2022-10-12
期刊：
CELL GENOMICS
影响因子：
--
作者：
Brumpton, Ben M.;Graham, Sarah;Surakka, Ida;Skogholt, Anne Heidi;Loset, Mari;Fritsche, Lars G.;Wolford, Brooke;Zhou, Wei;Nielsen, Jonas Bille;Holmen, Oddgeir L.;Gabrielsen, Maiken E.;Thomas, Laurent;Bhatta, Laxmi;Rasheed, Humaira;Zhang, He;Kang, Hyun Min;Hornsby, Whitney;Moksnes, Marta Riise;Coward, Eivind;Melbye, Mads;Giskeodegard, Guro F.;Fenstad, Jorn;Krokstad, Steinar;Naess, Marit;Langhammer, Arnulf;Boehnke, Michael;Abecasis, Goncalo R.;Asvold, Bjorn Olav;Hveem, Kristian;Willer, Cristen J.
通讯作者：
Willer, Cristen J.
影响因子：
16.2
作者：
Black MH;Sacks DA;Xiang AH;Lawrence JM
通讯作者：
Lawrence JM
影响因子：
7.2
作者：
通讯作者：
--
影响因子：
4.3
作者：
Markovitz, Amanda Rose;Haug, Eirin Beate;Rich-Edwards, Janet W.
通讯作者：
Rich-Edwards, Janet W.