Intensive Blood Pressure Control Reduces Risk for Heart Failure, Mortality


Intensive systolic blood pressure control led to a large absolute difference in death and HF among patients with abnormal biomarker levels of hscTnT and NTproBNP.

Jarett D. Berry, MD

Jarett D. Berry, MD

Elevated high-sensitivity cardiac troponin T (hscTnT) and N-terminal pro-B-type natriuretic peptide (NTproBNP) are shown to identify individuals with and without prevalent cardiovascular disease (CVD) at high risk for heart failure (HF) and mortality.

However, a lack of randomized clinical data has shown it is unknown if this risk is modifiable with an increased intensive systolic blood pressure (SBP) control treatment strategy.

Investigators, led by Jarett D. Berry, MD, Division of Cardiology, University of Texas Southwestern Medical Center, observed intensive SBP control led to a large absolute difference in death and HF among patients with abnormal levels of hscTnT and NTproBNP, showing modifiable risk with intensive blood pressure control.


The Systolic Blood Pressure Intervention Trial (SPRINT) was a randomized clinical, open-label trial that was conducted in 9361 patients at 102 sites in the United States from October 2010 - August 2015. Participants were required to be ≥50 years of age with elevated blood pressure with increased CVD risk. Exclusions included patients with diabetes.

In the study, participants were randomized to either intensive (<120 mm Hg) or usual care (<140 mm Hg) SBP lowering. Primary endpoints were considered a composite of all-cause mortality and HF, with secondary endpoints including all-cause mortality, a composite CVD endpoint, and composite CVD endpoint and total mortality.

Samples obtained at enrollment of study helped investigators measure high-sensitivity cardiac troponin T and NTproBNP levels. They defined elevated levels of 14 ng/L for hscTnT and 125 pg/mL for NT proNBP.

Investigators performed statistical analysis on an intention-to-treat basis from September 2019 - July 2021.


A total of 9361 participants were enrolled in SPRINT, with 8828 patients (5578 men, 63.2%; mean age, 68.0 years) having serum measures of hscTnT at baseline. Data show the median concentration of hscTnT was 9.4 ng/L (IQR 6.4 - 14.1 ng/L) with 2262 patients (25.6%), having values of 14 ng/L or more.

Moreover, 8836 patients (5585 men, 63.2%; SD age, 68.0 years) had measured NTproBNP levels and 3371 of patients (38.2%) had values of 125 pg/mL or more. The median concentration of NTproBNP was 86 pg/mL (IQR, 37 - 197 pg/mL).

A total of 1411 patients (16.0%) had both biomarker levels elevated and in comparison to participants with no elevated biomarkers, demographic data show the patients were older (SD, 75.6 years versus 64.2 years) and more likely to be male (1028 of 1411 patients versus 2968 of 4609 patients).

Data show randomization to the intensive SBP group led to a 4.9% (95% CI, 1.7% - 7.5%) absolute risk reduction (ARR) in death and HF (421 events) for patients with elevated hscTnT, in comparison to a 1.7% (95% CI, 0.7% - 2.5%) ARR for patients without elevated levels.

In addition, patients with elevated NTproBNP show an ARR for death and HF over 4 years was 4.6% (95% CI, 2.3% - 6.5%) in comparison to 1.8% (95% CI, 0.9% - 2.5%) in patients without elevated levels.

In patients with elevated levels of both biomarkers, data show the ARR for death and HF over 4 years was 7.8% (95% CI, 3.3% - 11.3%) compared to 1.7% (95% CI, 0.8% - 2.3%) in patients with neither biomarker.


Investigators concluded the elevated baseline risk translated into large ARR for mortality with intensive SBP control.

“Our data suggest the hypothesis that integrating widely available biomarker tests with these types of systems-level interventions could represent an efficient and effective approach to identifying patients at the highest risk for CVD,” investigators wrote.

The study, “Associations of High-Sensitivity Troponin and Natriuretic Peptide Levels With Outcomes After Intensive Blood Pressure Lowering: Findings From the SPRINT Randomized Clinical Trial,” was published online in JAMA Cardiology.

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