背景:高血压可能导致靶器官损伤(TOD)。在某些情况下,目标血压(BP)管理可能不合适。
目的:我们旨在评估重度高血压患者的针对性血压管理对肾性TOD的影响。
方法:这是一项前瞻性队列研究,涉及因严重高血压(BP>180/120)与任何症状相关而入院的患者。该研究涉及2017年8月至2018年2月期间在我们的三级中心转诊至ICU的患者。所有患者均根据近期指南进行目标BP治疗。Hs-肌钙蛋白T(hs-TNT)和血清肌酐(s。在所有患者入院时和24小时后测量creat)。患者分为A组(初始hs-TNT正常)和B组(初始hs-TNT高)。主要结果是院内肾脏相关发病率(包括肾衰竭)。
结果:四百七十例连续的高血压危象患者参与了这项研究。B组住院死亡率(4例)和肾脏TOD(急性肾功能不全)的发生率明显高于A组(P值分别为0.001和0.000)。B组入院时的初始s.creat值与随访s.creat值之间存在显着差异,在接下来的24小时内s.creat显着升高(P=0.002),而A组差异不显著(P=0.34)。hs-TNT与随访结果呈显著正相关(P=0.004)。
结论:在重度HTN中,hs-TNT可能由于明显的后负荷而升高。重度HTN和高hs-TNT患者的s.creat值较高,如果他们的血压急剧下降至指南目标血压,则与肾衰竭和院内死亡率的风险增加相关。在遵循临床指南之前,应考虑在急诊HTN管理期间使用生物标志物。然而,我们的发现强调了hs-TNT作为重度或急诊HTN患者危险分层指标的潜在效用.
BACKGROUND: Hypertension may cause target organ damage (TOD). Target blood pressure (BP) management may not be appropriate in some conditions.
OBJECTIVE: We aim to assess the impact of targeted BP management in severe hypertension on renal TOD.
METHODS: This is a prospective cohort study involving patients admitted due to severe hypertension (BP > 180/120) associated with any symptoms. The study involved patients referred to the ICU in our tertiary center during the period between August 2017 and February 2018. All patients underwent target BP treatment according to recent
guidelines. Hs-Troponin T (hs-TNT) and serum creatinine (s.creat) were measured in all patients on admission and 24 h later. Patients were divided into Group A (with initial normal hs-TNT) and Group B (with initial high hs-TNT). The main outcome was in-hospital renal-related morbidity (including renal failure).
RESULTS: Four hundred seventy consecutive patients with hypertensive crises were involved in the study. Group B had a significantly higher incidence of in-hospital mortality (4 patients) and renal TOD (acute renal dysfunction) than Group A (P value = 0.001 and 0.000 respectively). There was a significant difference between initial s.creat on admission and follow-up s.creat values in Group B with significant elevation of their s.creat on the following 24 h (P = 0.002), while this difference is insignificant in Group A (P = 0.34). There was a significant positive correlation between hs-TNT and the follow-up s.creat (P = 0.004).
CONCLUSIONS: In severe HTN, hs-TNT may be elevated due to marked afterload. Patients with severe HTN and high hs-TNT have higher s.creat values, which are associated with an increased risk of renal failure and in-hospital mortality if their BP decreases acutely to the
guideline-target BP. Using biomarkers during the management of emergency HTN should be considered before following clinical
guidelines. However, our findings do underscore the potential utility of hs-TNT as an indicator for risk stratification in patients with severe or emergency HTN.