Systolic Blood Pressure and Risk of Valvular Heart Disease: A Mendelian Randomization Study
Systolic Blood Pressure and Risk of Valvular Heart Disease: A Mendelian Randomization Study
复制标题
DOI：
10.1001/jamacardio.2019.2202
复制
发表时间：
2019-08-01
期刊：
影响因子：
24
通讯作者：
Rahimi, Kazem
中科院分区：
文献类型：
--
作者：
Nazarzadeh, Milad;Pinho-Gomes, Ana-Catarina;Rahimi, Kazem
要点问题收缩压升高是重大瓣膜性心脏病的危险因素吗？研究结果在这项针对 329237 名个体的孟德尔随机研究中，与遗传相关的收缩压升高 20 毫米汞柱似乎与主动脉瓣狭窄、主动脉瓣反流和二尖瓣反流的较高风险相关。意味着终生处于收缩压升高可能与严重瓣膜性心脏病的风险增加有关，这表明降低血压可能是预防这种疾病的有效策略。重要性瓣膜性心脏病的可改变危险因素仍然很大程度上未知，这限制了预防和治疗。目的评估收缩压（BP）与主要瓣膜性心脏病之间的关联。设计、设置和参与者英国生物银行基于人口的队列由 502602 名基线年龄为 40 至 96 岁的男性和女性组成，通过孟德尔随机化使用个体参与者数据进行评估。纳入标准是有效的遗传数据和血压测量值。参与者是在 2006 年至 2010 年期间招募的；数据分析于 2018 年 6 月至 2019 年 1 月进行。暴露在临床评估期间测量收缩压，并从独立的变异中识别出高血压遗传效应的工具（r（2）的连锁不平衡阈值）
Key PointsQuestionIs elevated systolic blood pressure a risk factor for major valvular heart disease? FindingsIn this mendelian randomization study of 329237 individuals, genetically associated 20-mm Hg increments of elevated systolic blood pressure appeared to be associated with a higher risk of aortic stenosis, aortic regurgitation, and mitral regurgitation. MeaningLifetime exposure to elevated systolic blood pressure may be associated with an increased risk of major valvular heart disease, suggesting that blood pressure lowering might be a useful strategy for prevention of this condition.ImportanceModifiable risk factors for valvular heart disease remain largely unknown, which limits prevention and treatment. ObjectiveTo assess the association between systolic blood pressure (BP) and major valvular heart disease. Design, Setting, and ParticipantsA UK Biobank population-based cohort of 502602 men and women aged 40 to 96 years at baseline was evaluated through mendelian randomization using individual participant data. Inclusion criteria were valid genetic data and BP measurements. The participants were recruited between 2006 and 2010; data analysis was performed from June 2018 to January 2019. ExposuresSystolic BP was measured during clinical assessment and instruments for the genetic effect of high BP were identified from variants that were independently (linkage disequilibrium threshold of r(2)