Elevated blood pressure and risk of mitral regurgitation: A longitudinal cohort study of 5.5 million United Kingdom adults.
Elevated blood pressure and risk of mitral regurgitation: A longitudinal cohort study of 5.5 million United Kingdom adults.
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血压升高与二尖瓣反流风险：一项针对550万英国成年人的纵向队列研究
DOI：
10.1371/journal.pmed.1002404
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发表时间：
2017-10
期刊：
影响因子：
15.8
通讯作者：
MacMahon S
中科院分区：
文献类型：
--
作者：
Rahimi K;Mohseni H;Otto CM;Conrad N;Tran J;Nazarzadeh M;Woodward M;Dwyer T;MacMahon S
在既往无心脏病的人群中，二尖瓣返流被认为是一种退行性疾病，没有确定的预防风险因素。我们的目的是检验收缩压（SBP）升高与二尖瓣返流风险升高相关的假设。我们使用了1990年1月1日至2015年12月31日英国临床实践研究数据链（CPRD）的链接电子健康记录。CPRD覆盖了目前英国人口的约7%，并广泛代表了年龄，性别和种族的人口。约550万基线时无已知心血管或瓣膜疾病的英国患者纳入本队列研究。我们使用考克斯回归模型研究了血压（BP）与二尖瓣返流风险之间的关系。我们的主要暴露变量是SBP，我们的主要结局是二尖瓣返流的事件报告，这些事件报告从出院报告或初级护理记录中确定。在CPRD中符合我们入选标准的5，553，984例患者中，在10年随访期间，28，655例（0.52%）被诊断为二尖瓣返流，另有1，262例（0.02%）被诊断为二尖瓣狭窄。SBP与二尖瓣返流风险持续相关，没有证据表明最低值降至115 mmHg（p < 0.001）。SBP每增加20 mmHg，二尖瓣返流风险增加26%（风险比[HR] 1.26; CI 1.23，1.29）。观察到的相关性部分由随访期间影响左心室的疾病（心肌梗死[MI]、缺血性心脏病[IHD]、心肌病和心力衰竭）介导。然而，这些继发性二尖瓣返流的近因介导的过度风险（PERM）百分比仅为13%（CI 6.1%，20%），并且对SBP和二尖瓣返流之间的长期相关性影响不大（中介校正HR 1.22; CI 1.20，1.25; p < 0.001）。舒张压（DBP）每增加10 mmHg（p < 0.001）或脉压（PP）每增加15 mmHg（p < 0.001）的相关性相似。相比之下，SBP与二尖瓣狭窄风险之间无相关性（HR每升高20 mmHg SBP 1.03; CI 0.93，1.14; p = 0.58）。这些分析基于从健康记录中常规收集的数据，这些数据可能对测量误差敏感，并且观察到的相关性可能无法推广到二尖瓣返流的不太严重和亚临床病例。长期暴露于整个范围内的血压升高与原发性和继发性二尖瓣返流的风险增加相关。这些结果表明，血压控制可能是重要的，在预防二尖瓣返流。利用英国临床实践研究数据链的数据，Kazem Rahimi及其同事研究了血压升高是否与二尖瓣返流的风险增加有关。血压升高（BP）是一系列心血管疾病的主要危险因素。在既往无心脏病的人群中，二尖瓣返流被认为是一种退行性疾病，没有确定的预防风险因素。尚不清楚血压升高是否也是二尖瓣返流的危险因素。约550万基线时无已知心血管或瓣膜疾病的英国患者被纳入该队列研究，并随访约10年。这项研究显示，血压升高与二尖瓣返流（但不是二尖瓣狭窄）风险之间存在明确的对数线性相关性，没有明显的阈值低于或高于该阈值，该关系不再存在。这种关联仅部分由继发性二尖瓣返流的既定原因介导，表明血压升高对瓣膜退行性变有直接和独立的影响。这项研究的结果表明，二尖瓣返流不是衰老的必然结果，其风险可能通过既定的干预措施进行修改。未来的研究应该建立所观察到的相关性的因果关系，并测试血压降低是否可能降低二尖瓣返流的风险。
Mitral regurgitation in people without prior cardiac disease is considered a degenerative disease with no established risk factors for its prevention. We aimed to test the hypothesis that elevated systolic blood pressure (SBP) across its usual spectrum is associated with higher risk of mitral regurgitation. We used linked electronic health records from the United Kingdom Clinical Practice Research Datalink (CPRD) from 1 January 1990 to 31 December 2015. CPRD covers approximately 7% of the current UK population and is broadly representative of the population by age, sex, and ethnicity. About 5.5 million UK patients with no known cardiovascular or valve disease at baseline were included in this cohort study. We investigated the relationship between blood pressure (BP) and risk of mitral regurgitation using Cox regression models. Our primary exposure variable was SBP and our primary outcome was incident reports of mitral regurgitation, which were identified from hospital discharge reports or primary care records. Of the 5,553,984 patients in the CPRD that met our inclusion criteria, during the 10-year follow-up period, 28,655 (0.52%) were diagnosed with mitral regurgitation and a further 1,262 (0.02%) were diagnosed with mitral stenosis. SBP was continuously related to the risk of mitral regurgitation with no evidence of a nadir down to 115 mmHg (p < 0.001). Each 20 mmHg increment in SBP was associated with a 26% higher risk of mitral regurgitation (hazard ratio [HR] 1.26; CI 1.23, 1.29). The observed association was partially mediated by diseases affecting the left ventricle during follow-up (myocardial infarction [MI], ischaemic heart disease [IHD], cardiomyopathy, and heart failure). However, the percentage of excess risk mediated (PERM) by these proximate causes of secondary mitral regurgitation was only 13% (CI 6.1%, 20%), and accounting for them had little effect on the long-term association between SBP and mitral regurgitation (mediator-adjusted HR 1.22; CI 1.20, 1.25; p < 0.001). Associations were similar for each 10 mmHg increment in diastolic blood pressure (DBP) (p < 0.001) or each 15 mmHg increment in pulse pressure (PP) (p < 0.001). By contrast, there was no association between SBP and risk of mitral stenosis (HR per 20 mmHg higher SBP 1.03; CI 0.93, 1.14; p = 0.58). These analyses are based on routinely collected data from health records which may be sensitive to measurement errors, and the observed associations may not be generalizable to less severe and subclinical cases of mitral regurgitation. Long-term exposure to elevated BP across its whole spectrum is associated with an increased risk of primary and secondary mitral regurgitation. These findings suggest that BP control may be of importance in the prevention of mitral regurgitation. Using data from the UK Clinical Practice Research Datalink, Kazem Rahimi and colleagues examine whether elevated blood pressure is associated with greater risk of mitral regurgitation. Elevated blood pressure (BP) is a major risk factor for a range of cardiovascular conditions. Mitral regurgitation in people without prior cardiac disease is considered a degenerative disease with no established risk factors for its prevention. Whether elevated BP is also a risk factor for mitral regurgitation is unknown. About 5.5 million UK patients with no known cardiovascular or valve disease at baseline were included in this cohort study and were followed up for about 10 years. This study shows a clear log-linear association between elevated BP and risk of mitral regurgitation (but not mitral stenosis) with no apparent threshold below or above which the relationship ceased to exist. The association was only partially mediated by conditions that are established causes of secondary mitral regurgitation, suggesting that elevated BP has a direct and independent effect on valve degeneration. The findings from this study suggest that mitral regurgitation is not an inevitable consequence of ageing and that its risk might be modifiable with established interventions. Future studies should establish the causality of the observed associations and test whether BP lowering might reduce the risk of mitral regurgitation.
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DOI：
10.1136/bmj.h4865
发表时间：
2015-09-29
期刊：
BMJ (Clinical research ed.)
影响因子：
--
作者：
Emdin CA;Anderson SG;Callender T;Conrad N;Salimi-Khorshidi G;Mohseni H;Woodward M;Rahimi K
通讯作者：
Rahimi K
影响因子：
5.7
作者：
Coffey, Sean;Cairns, Benjamin J.;Iung, Bernard
通讯作者：
Iung, Bernard
影响因子：
168.9
作者：
Nishimura, Rick A.;Vahanian, Alec;Mack, Michael J.
通讯作者：
Mack, Michael J.
影响因子：
20.1
作者：
Rahimi, Kazem;Emdin, Connor A.;MacMahon, Stephen
通讯作者：
MacMahon, Stephen
影响因子：
2.8
作者：
Singh, JP;Evans, JC;Benjamin, EJ
通讯作者：
Benjamin, EJ