BACKGROUND:Given the important role of cardiac injury and neurohormonal activation in the pathways leading from hypertension to heart failure and strong associations observed between hypertension and its sequelae on hs-cTnT (high-sensitivity cardiac troponin T) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) levels, we hypothesized that intensive systolic blood pressure (SBP) lowering would decrease levels of hs-cTnT and NT-proBNP.METHODS:hs-cTnT and NT-proBNP were measured at baseline and 1 year from stored specimens in SPRINT (Systolic Blood Pressure Intervention Trial). Changes in biomarkers were evaluated continuously on the log scale and according to categories (≥50% increase, ≥50% decrease, or <50% change). The effect of intensive SBP lowering on continuous and categorical changes in biomarker levels were assessed using linear and multinomial logistic regression models, respectively. The association between changes in biomarkers on heart failure and death was assessed using multivariable-adjusted Cox proportional hazards models.RESULTS:Randomization to intensive SBP lowering (versus standard SBP management) resulted in a 3% increase in hs-cTnT levels over 1-year follow-up (geometric mean ratio, 1.03 [95% CI, 1.01–1.04]) and a higher proportion of participants with ≥50% increase (odds ratio, 1.47 [95% CI, 1.13, 1.90]). In contrast, randomization to intensive SBP lowering led to a 10% decrease in NT-proBNP (geometric mean ratio, 0.90 [95% CI, 0.87–0.93]) and a lower probability of ≥50% increase in NT-proBNP (odds ratio, 0.57 [95% CI, 0.46–0.72]). The association of randomized treatment assignment on change in hs-cTnT was completely attenuated after accounting for changes in estimated glomerular filtration rate over follow-up, whereas the association of treatment with NT-proBNP was completely attenuated after adjusting for change in SBP. Increases in hs-cTnT and NT-proBNP from baseline to 1 year were associated with higher risk for heart failure and death, with no significant interactions by treatment assignment.CONCLUSIONS:Intensive SBP lowering increased hs-cTnT, mediated by the effect of SBP lowering on reduced kidney filtration. In contrast, intensive SBP lowering decreased NT-proBNP, a finding that was explained by the drop in SBP. These findings highlight the importance of noncardiac factors influencing variation in cardiac biomarkers and raise questions about the potential role of hs-cTnT as a surrogate marker for heart failure or death in SBP-lowering studies.

中文翻译：

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强化血压控制对肌钙蛋白和利尿钠肽水平的影响：SPRINT 的研究结果

背景：考虑到心脏损伤和神经激素激活在高血压导致心力衰竭的途径中的重要作用，以及观察到高血压与其后遗症 hs-cTnT（高敏心肌肌钙蛋白 T）和 NT-proBNP（N 端）之间的密切关联，前 B 型利尿钠肽）水平，我们假设强化收缩压 (SBP) 降低会降低 hs-cTnT 和 NT-proBNP 的水平。方法：在基线和 1 年后测量 hs-cTnT 和 NT-proBNP将样本保存在 SPRINT（收缩压干预试验）中。根据类别（增加≥50%、减少≥50%或变化<50%）连续评估生物标志物的变化。分别使用线性和多项逻辑回归模型评估强化收缩压降低对生物标志物水平连续和分类变化的影响。使用多变量调整的 Cox 比例风险模型评估心力衰竭生物标志物变化与死亡之间的关联。结果：随机化强化 SBP 降低（与标准 SBP 管理相比）导致 1 年内 hs-cTnT 水平增加 3%随访（几何平均比，1.03 [95% CI，1.01-1.04]），并且增加≥50%的参与者比例较高（比值比，1.47 [95% CI，1.13，1.90]）。相比之下，随机化强化 SBP 降低导致 NT-proBNP 降低 10%（几何平均比，0.90 [95% CI，0.87–0.93]），NT-proBNP 增加 ≥50% 的可能性较低（比值比） ，0.57 [95% CI，0.46–0.72]）。在考虑了随访期间估计肾小球滤过率的变化后，随机治疗分配与 hs-cTnT 变化的关联完全减弱，而在调整 SBP 变化后，NT-proBNP 治疗的关联完全减弱。hs-cTnT 和 NT-proBNP 从基线到 1 年的增加与心力衰竭和死亡风险较高相关，治疗分配之间没有显着的相互作用。结论：强化 SBP 降低会增加 hs-cTnT，这是由 SBP 降低效应介导的肾脏滤过减少。相比之下，强烈降低 SBP 会降低 NT-proBNP，这一发现可以用 SBP 下降来解释。这些发现强调了影响心脏生物标志物变化的非心脏因素的重要性，并提出了关于 hs-cTnT 在降低 SBP 的研究中作为心力衰竭或死亡替代标志物的潜在作用的问题。