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背景高血压导致血管事件的机制尚不清楚。有关诊断和治疗指南仅关注平均血压。我们针对血压、血压最高值、未经治疗阵发性高血压随诊差异,及经治疗后残留差异确立预示意义。方法我们确定脑卒中风险与随诊血压差异(用标准差和不依赖于平均血压的参数表达),曾有短暂性脑缺血发作(TIA;UK-TIA试验和3项定群研究)和经治疗的高血压病人(英国-斯堪的纳维亚心脏预后试验血压控制分组研究[ASCOT-BPLA])的最高血压相关。ASCOT-BPLA也做了24 h动态血压监测(ABPM)研究。发现每项TIA定群研究,随诊SBP差异可作为发生脑卒中强预示因子[如,UK-TIA试验,>7次随诊SDSBP 10%HR:6.22,95%CI(4.16,9.29),P<0.0001],不依赖于平均SBP,但是依赖于精确测量[>10次随诊,脑卒中top10%HR:12.08(7.40,19.72),P<0.0001]。SBP最高值也为脑卒中强预示因子[>7次随诊,校正平均SBP后top 10%HR:15.01(6.56,34.38),P<0.0001]。ASCOT-BPLA试验,治疗中SBP随诊残留差异也为脑卒中和冠脉事件强预示因子[如脑卒中top 10%HR:3.25(2.32,4.54),P<0.0001],不依赖临床或ABPM。ABPM差异为较弱预示因子,但所有差异测量,用于年轻病人和各人群平均SBP较低(<中位数)病人最有预示性。解释SBP和最高SBP值随诊差异为脑卒中强预示因子,不依赖于平均SBP。做高血压治疗病人,SBP残留差异增加与血管事件高风险相关。
Background The mechanism by which hypertension causes vascular events is unclear. The diagnosis and treatment guidelines focus solely on the mean blood pressure. We aim at the highest blood pressure, blood pressure, untreated patients with paroxysmal hypertension follow-up differences, and after treatment to establish the significance of residual differences. Methods We determined differences in stroke risk and follow-up blood pressure (expressed as standard deviation and parameters independent of mean blood pressure), transient ischemic attacks (TIA; UK-TIA and 3 population studies) and Treated hypertensive patients (British-Scandinavian Heart Prognosis Trial Blood Pressure Control Study [ASCOT-BPLA]). ASCOT-BPLA also conducted a 24-h ambulatory blood pressure monitoring (ABPM) study. For each TIA cohort, differences in SBP follow-up were found to be strongly predictors of stroke (eg, UK-TIA,> 7 visits followed by SDSBP 10% HR: 6.22, 95% CI 4.16, 9.29, P <0.0001], independent of mean SBP, but relies on accurate measurements [> 10 follow-ups, stroke top10% HR: 12.08 (7.40, 19.72), P <0.0001]. The highest SBP was also a strong predictor of stroke [> 7 visits, corrected for top 10% HR after SBP: 15.01 (6.56, 34.38), P <0.0001]. ASCOT-BPLA trial, residual SBP after treatment was also a strong predictor of stroke and coronary events (eg top 10% HR in stroke: 3.25 (2.32, 4.54), P <0.0001), independent of clinical or ABPM. ABPM differences are weaker predictors, but all differences measures are most predictive of lower (median) SBP for younger patients and for each population. Interpretation SBP and the highest SBP value followed up as a strong predictor of stroke, independent of the mean SBP. In hypertensive patients, increased residual SBP is associated with a higher risk of vascular events.