Pewowaruk Ryan, Jaeger Byron C, Hughes Timothy M, Upadhya Bharathi, Kitzman Dalane W, Supiano Mark A, Gepner Adam D
Ryan Pewowaruk Research Consulting, Madison, WI (R.P.).
Wake Forest University School of Medicine, Department of Biostatistics and Data Science, Winston-Salem, NC (B.C.J.).
Hypertension. 2025 Jun;82(6):1004-1011. doi: 10.1161/HYPERTENSIONAHA.124.24816. Epub 2025 Apr 22.
The longitudinal impact of blood pressure (BP) control on the components of arterial stiffness has not been studied.
The SPRINT (Systolic BP Intervention Trial) compared an intensive systolic BP goal (<120 mm Hg) to a standard goal (<140 mm Hg). Carotid-femoral pulse wave velocity (PWV) was measured in a subset of participants (n=605) at 0, 1, 2, and 3 years after randomization. Structural stiffening due to remodeling of the vessel wall and load-dependent stiffening, from changes in BP, were calculated by adjusting PWV to a 120/80 mm Hg reference BP with participant-specific models. The effect of intensive BP control on BP and arterial stiffness components over time was evaluated using generalized least squares regression.
Intensive BP control slowed the progression of PWV (total stiffness) compared with standard BP control at 3-year follow-up (-0.49 [-0.02 to -0.96] m/s, =0.042). Differences in total stiffness between treatment groups over 3 years of follow-up were driven by intensive BP control reducing load-dependent PWV (-0.71 [-0.58 to -0.85] m/s, <0.001), not structural PWV (+0.20 [-0.26 to +0.66], =0.40). Load-dependent PWV was lower in the intensive treatment group at 1 year and remained lower throughout the follow-up. In contrast, structural PWV was similar between the 2 groups and increased throughout the follow-up period.
Intensive BP control slowed the progression of total arterial stiffness by decreasing load-dependent stiffness, but not through reduced structural stiffness. Future investigations are needed to determine if load-dependent PWV may have potential utility as a biomarker to monitor the efficacy of treatment and guide BP management strategies.
URL: https://www.clinicaltrials.gov; Unique identifier: NCT01206062.
血压(BP)控制对动脉僵硬度各组成部分的纵向影响尚未得到研究。
收缩压干预试验(SPRINT)将强化收缩压目标(<120 mmHg)与标准目标(<140 mmHg)进行了比较。在随机分组后的0、1、2和3年,对一部分参与者(n = 605)测量了颈股脉搏波速度(PWV)。通过使用参与者特异性模型将PWV调整至120/80 mmHg的参考血压,计算出血管壁重塑导致的结构硬化以及血压变化引起的负荷依赖性硬化。使用广义最小二乘回归评估强化血压控制随时间对血压和动脉僵硬度各组成部分的影响。
在3年随访时,与标准血压控制相比,强化血压控制减缓了PWV(总僵硬度)的进展(-0.49 [-0.02至-0.96] m/s,P = 0.042)。在3年随访期间,治疗组之间总僵硬度的差异是由于强化血压控制降低了负荷依赖性PWV(-0.71 [-0.58至-0.85] m/s,P<0.001),而非结构PWV(+0.20 [-0.26至+0.66],P = 0.40)。强化治疗组在1年时的负荷依赖性PWV较低,且在整个随访期间一直较低。相比之下,两组之间的结构PWV相似,且在整个随访期间均增加。
强化血压控制通过降低负荷依赖性僵硬度减缓了总动脉僵硬度的进展,但并非通过降低结构僵硬度。需要进一步研究以确定负荷依赖性PWV是否可能作为一种生物标志物,用于监测治疗效果并指导血压管理策略。