Blood Pressure Therapy Intensity Correlates With Cardiac Function in ACDHF

Intensification of blood pressure-lowering therapy correlates with improved outcomes among hospitalized patients with concomitant acutely decompensated chronic heart failure (ADCHF) and essential hypertension, according to a new report.¹

Patients with therapeutic intensification of pharmacological pressure-unloading therapy had marked improvements in cardiac load, the study found, as demonstrated by reductions in N-terminal pro-B-type natriuretic peptide (NT-proBNP). The study was published in BMC Cardiovascular Disorders.

Essential hypertension can add complexity to the treatment of ADCHF, the authors explained.

“Hypertension not only contributes to the development and progression of heart failure, but also complicates its management during acute decompensation,” they wrote.

Heart failure therapies can help lower blood pressure, but the investigators noted that this is not their primary purpose. Treating such patients, then, requires a delicate balancing act, they said.

“Overly aggressive reduction (of blood pressure) may precipitate hypotension and hypoperfusion,” they wrote, “while insufficient control can exacerbate myocardial stress and remodeling.”²

There is currently little clarity regarding the optimal intensity of blood pressure modulation for people with heart failure, the authors noted, and current approaches to the problem tend to rely solely on blood pressure values, “which may not fully capture the overall pharmacologic burden or the dose-response relationship of the administered regimen.”¹

The use of a standardized metric like therapeutic intensity score (TIS) can offer a benefit compared to blood pressure values because it incorporates drug classes, doses, and combinations. Therefore, the authors aimed to determine if there is a correlation between in-hospital TIS and cardiac-function improvement among patients with ADCHF and essential hypertension.

To find out, they retrospectively analyzed 517 patients who were hospitalized with hypertension, including 257 with ADCHF with hypertension and 260 with hypertension but normal cardiac function. The latter cohort served as the control group.

The primary exposure in the study was change in TIS from admission to discharge. The primary outcome was change in NT-proBNP, they said.

Notably, the patients with heart failure had lower median TIS at hospital admission, with scores of 0.50 versus 0.75 (P < .001). The only exception was in the subgroup of patients with stage 1 or with very short-duration hypertension, they explained.

“This points to a potential gap in baseline blood pressure management prior to hospitalization for ADCHF, aligning with prior reports of suboptimal hypertension control in patients presenting with acute heart failure,” they said.

However, TIS increased in patients with heart failure as their hospitalizations continued. As it did, NT-proBNP levels decreased (β = 0.384; 95% CI, 0.108-0.660; P = .007) after adjusting for covariates such as age and left ventricular ejection fraction (LVEF). This association between TIS intensification and NT-proBNP reduction was uniform across heart failure phenotypes, the investigators said, including among patients with preserved ejection fraction.

“This observed dose-dependent response relationship suggests that structured escalation of pharmacologic pressure-unloading therapy during acute decompensation may facilitate cardiac unloading, irrespective of baseline LVEF,” they said.

The authors noted that their findings align with the findings of the STRONG-HF trial, which showed that rapidly up-titrating guideline-directed medical therapy prior to discharge can reduce the risk of rehospitalization or death in the 6 months following discharge.³

While the data in this study suggested that TIS intensification is associated with NT-proBNP reduction, the investigators said future studies are warranted to determine whether using TIS to guide therapy will lead to improved clinical outcomes.

“Future prospective studies should integrate standardized imaging protocols alongside biomarker assessment to more fully characterize the hemodynamic and structural response to therapy,” they wrote.

References

1. Zhang Z, Fan Z, Liu Y, Han L. Correlation between pharmacologic blood pressure-lowering intensity and improvement in cardiac function in patients with acutely decompensated heart failure. BMC Cardiovasc Disord. Published online February 11, 2026. doi:10.1186/s12872-026-05610-5

2. Iglesias J, Ghetiya S, Ledesma KJ, Patel CS, Levine JS. Interactive and potentially independent roles of renin-angiotensin-aldosterone system blockade and the development of cardiorenal syndrome type 1 on in-hospital mortality among elderly patients admitted with acute decompensated congestive heart failure. Int J Nephrol Renovasc Dis. 2019;12:33-48. doi:10.2147/IJNRD.S185988

3. Mebazaa A, Davison B, Chioncel O, et al. Safety, tolerability and efficacy of up-titration of guideline-directed medical therapies for acute heart failure (STRONG-HF): a multinational, open-label, randomised, trial. Lancet. 2022;400(10367):1938-1952. doi:10.1016/S0140-6736(22)02076-1