基线舒张压和降压对心血管预后及全因死亡率的影响:一项 Meta 分析。

IF 10.3 1区 医学 Q1 UROLOGY & NEPHROLOGY
Amara Sarwal, Robert E Boucher, Sydney E Hartsell, Guo Wei, Jincheng Shen, Glenn M Chertow, Paul K Whelton, Alfred K Cheung, John William McEvoy, Tom Greene, Srinivasan Beddhu
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引用次数: 0

摘要

背景:对舒张压过低的人降低血压可能有害。因此,我们对五项大型降压试验进行了荟萃分析,研究基线舒张压是否会改变降压对临床结果的影响:在基于收缩压干预试验(N = 9361)、糖尿病血压控制心血管风险行动(N = 2362)、皮质下小卒中二级预防(N = 3020)、非裔美国人肾脏病研究(N = 3020)的个体参与者数据的研究水平荟萃分析中,研究人员发现,舒张压基线是否会改变降压对临床结果的影响、在非裔美国人肾脏病和高血压研究(N = 1094)和肾脏病饮食调整(N = 840)研究中,我们使用 DerSimonian-Laird 随机效应模型来检验降压干预对心血管、全因死亡率和肾脏结果的影响是否依赖于基线舒张压。研究结果平均基线年龄为 65 ± 10 岁。平均基线收缩压和舒张压分别为 141 ± 17 毫米汞柱和 79 ± 12 毫米汞柱。加强血压控制可降低心血管综合结果风险(HR 0.79,95% CI 0.72,0.87)和全因死亡率风险(HR 0.86,95% CI 0.75,0.99),但无证据表明血压干预效果因基线舒张压水平而异(心血管综合结果的交互作用 p = 0.76,全因死亡率的交互作用 p = 0.85)。基线舒张压最低四分位数和最高四分位数的平均基线舒张压分别为 65 ± 6 mm Hg 和 84 ± 9 mm Hg,但降压干预对两组结果的影响相似。此外,没有证据表明降压干预与基线舒张压对肾脏结果有交互作用:结论:在所纳入的舒张压范围内,没有证据表明基线舒张压会改变强化降压的有益效果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Baseline Diastolic BP and BP-Lowering Effects on Cardiovascular Outcomes and All-Cause Mortality: A Meta Analysis.

Background: Lowering blood pressure (BP) in persons with low diastolic BP could be harmful. Hence, we examined whether baseline diastolic BP modifies the effects of BP lowering on clinical outcomes in a meta-analysis of five large BP lowering trials.

Methods: In a study-level meta-analysis based on individual participant data of the Systolic Blood Pressure Intervention Trial (N = 9361), the Action to Control Cardiovascular Risk in Diabetes Blood Pressure (N = 2362), the Secondary Prevention of Small Subcortical Strokes (N = 3020), the African American Study of Kidney Disease and Hypertension (N = 1094) and the Modification of Diet in Renal Disease (N = 840) studies, we used DerSimonian-Laird random-effects models to examine the dependence of the effect of the BP lowering intervention on baseline diastolic BP for cardiovascular, all-cause mortality and kidney outcomes.

Results: Mean baseline age was 65 ± 10 years old. Mean baseline systolic and diastolic BP were 141 ± 17 and 79 ± 12 mm Hg, respectively. More intensive BP control resulted in lower risk of composite cardiovascular outcome (HR 0.79, 95% CI 0.72, 0.87) and all-cause mortality (HR 0.86, 95% CI 0.75, 0.99) without evidence that the BP intervention effects differed by level of baseline diastolic BP (interaction p = 0.76 for cardiovascular composite and 0.85 for all-cause mortality). The mean baseline diastolic BP in the lowest and the upper three quartiles of baseline diastolic BP were 65 ± 6 mm Hg and 84 ± 9 mm Hg, respectively but the effects of the BP interventions on the outcomes were similar in both groups. Furthermore, there was no evidence of interaction of the BP intervention and baseline diastolic BP for kidney outcomes.

Conclusions: Within the included diastolic BP range, there was no evidence that baseline diastolic BP modified the beneficial effects of intensive BP lowering.

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来源期刊
Journal of The American Society of Nephrology
Journal of The American Society of Nephrology 医学-泌尿学与肾脏学
CiteScore
22.40
自引率
2.90%
发文量
492
审稿时长
3-8 weeks
期刊介绍: The Journal of the American Society of Nephrology (JASN) stands as the preeminent kidney journal globally, offering an exceptional synthesis of cutting-edge basic research, clinical epidemiology, meta-analysis, and relevant editorial content. Representing a comprehensive resource, JASN encompasses clinical research, editorials distilling key findings, perspectives, and timely reviews. Editorials are skillfully crafted to elucidate the essential insights of the parent article, while JASN actively encourages the submission of Letters to the Editor discussing recently published articles. The reviews featured in JASN are consistently erudite and comprehensive, providing thorough coverage of respective fields. Since its inception in July 1990, JASN has been a monthly publication. JASN publishes original research reports and editorial content across a spectrum of basic and clinical science relevant to the broad discipline of nephrology. Topics covered include renal cell biology, developmental biology of the kidney, genetics of kidney disease, cell and transport physiology, hemodynamics and vascular regulation, mechanisms of blood pressure regulation, renal immunology, kidney pathology, pathophysiology of kidney diseases, nephrolithiasis, clinical nephrology (including dialysis and transplantation), and hypertension. Furthermore, articles addressing healthcare policy and care delivery issues relevant to nephrology are warmly welcomed.
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