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Arterial Hypertension: Highlights from the European Society of Cardiology 2025 Congress

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Disclosure: MLM has received honoraria from Recordati and Neopharmed and travel support from Servier and Menarini, and is on the European Cardiology Review editorial board; this did not affect peer review.

Correspondence: Maria Lorenza Muiesan, Department of Clinical and Experimental Sciences, Division of Internal Medicine, ASST Spedali Civili Brescia, University of Brescia, 25121 Brescia, Italy. E: marialorenza.muiesan@unibs.it

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© The Author(s). This work is open access and is licensed under CC-BY-NC 4.0. Users may copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly.

Several hotline trials were presented at the European Society of Cardiology Congress 2025 that examined different treatment options for hypertensive patients. This article discusses two of these trials, RETREAT-FRAIL (Deprescribing in older frail patients) and Bax-HTN (a new drug for treatment of uncontrolled/resistant hypertension).

Both studies are clinically relevant: the first addresses the effect on all-cause death of stepping down antihypertensive therapy in older residents in nursing homes; the second evaluates the antihypertensive efficacy and safety of an aldosterone-synthase inhibitor, baxdrostat, in resistant and uncontrolled hypertensive patients.

RETREAT-FRAIL

The RETREAT-FRAIL trial, presented on 29 August 2025 by Prof Athanase Benetos, professor of geriatric medicine at the University Hospital of Nancy-Lorraine in France, is a multicentre, randomised trial conducted in France.1

In the study, 1,048 nursing home residents aged ≥80 years with blood pressure (BP) <130 mmHg and treated with at least two antihypertensive therapies were randomly assigned to a protocol-driven strategy of step-down therapy or usual care. The median number of antihypertensive therapies fell from 2.6 to 1.5 in the step-down arm and from 2.5 to 2.0 in the usual care arm.

It is important to underline that several precautionary measures were implemented to minimise the risks associated with the withdrawal of some drugs with compelling indications. Before randomisation, it was established which antihypertensive drug could be discontinued or not according to medical necessity.

Increases in systolic and diastolic BP (of 4.1 mmHg and 1.8 mmHg, respectively) were observed among those in the step-down arm relative to the usual care arm.

At the end of the follow-up (median of 38.4 months) all-cause mortality was 61.7% in the step-down group and 60.2% in the usual care group, with similar Kaplan–Meier curves. No statistically significant differences were observed regarding major cardiovascular events or non-cardiovascular death between the two groups.

In addition, no significant between-group differences in adverse events, including in relative changes on standardised tests measuring cognition, balance, activities of daily living or quality of life were reported.

Subgroup analysis, carried out according to the severity of frailty scale, showed a non-significant decrease of risk of death in participants with a high frailty score and de-prescribing treatment.

The results of this study fill a knowledge gap. The findings of the RETREAT-FRAIL study conflict with previous observational studies, such as PARTAGE, OPTiMiSE and DALTON, which showed lower rates of death and of adverse events during de-intensification of BP-lowering drugs in frail older adults with and without dementia.1–4 The characteristics of patients in the RETREAT-FRAIL study are similar to those in previous studies and allow generalisability of these findings.

A possible limitation of the study, acknowledged by Benetos et al., is the open-label design, which might have diluted the differences between the step-down and usual care arms during the study. In addition, the lack of discontinuation of drugs prescribed according to compelling indication in the step-down group might have reduced the difference in outcome.

These findings show that, in older and frail patients, an antihypertensive medication step-down strategy and subsequent mild increase in BP are unlikely to have a relevant, beneficial effect on all-cause mortality, but, at the same time, do not cause additional harm. This evidence further suggests an individualised approach should be taken to older and frail patients living in nursing homes.

BaxHTN

The BaxHTN trial investigated the efficacy and safety of baxdrostat, a selective aldosterone synthase inhibitor (ASI), in patients with uncontrolled or treatment-resistant hypertension.5

The results were presented by principal investigator Prof Bryan Williams from University College London at the hotline session of 30 August.

This phase III study, conducted at 214 clinical sites across multiple countries, enrolled adults with ≥140 mmHg and <170 mmHg seated systolic BP despite treatment with maximally tolerated doses of two antihypertensives (uncontrolled hypertension 27%) or at least three antihypertensives (resistant hypertension 73%), including a diuretic.

In both uncontrolled and resistant hypertensives, the screening phase lasted 4 weeks. In the first part of the study, 796 patients (mean age of 62 years and 39% women) were randomised 1:1:1 to receive baxdrostat 1 mg, baxdrostat 2 mg or placebo once daily for a 12-week double-blind period.

In the second part of the study, patients were randomised to receive baxdrostat 2 mg (n=483) or standard of care (n=245) for a 12-week, open-label period.

During the third part of the study, patients were randomised again to a double-blind withdrawal period, in which 257 of those in the baxdrostat 2 mg group were re-randomised 2:1 to baxdrostat 2 mg or placebo for 8 weeks.

Finally, part 4, an open-label period from week 32 to week 52 to assess longer-term safety, is ongoing.

The primary efficacy endpoint of the study, i.e. the placebo-adjusted reductions in seated systolic BP from baseline were −8.7 mmHg for the 1 mg dose and −9.8 mmHg for the 2 mg dose (both p<0.0001).

Changes in systolic BP with baxdrostat therapy were consistent in all the prespecified subgroups and were confirmed by an exploratory analysis of 24 hours of BP monitoring.

The proportions of controlled patients (with systolic BP <130 mmHg) were 39.4% with baxdrostat 1 mg, 40% with baxdrostat 2 mg and 18.7% with placebo.

The change in seated systolic BP was maintained at the end of the second part in all patients treated with baxdrostat 2 mg.

At the end of part 3, patients treated according to the standard of care had an increase in seated systolic BP, while a further reduction of systolic BP was observed in patients who continued on baxdrostat 2 mg at week 32.

Serious adverse events were reported in 1.9% of patients in the baxdrostat 1 mg group, 3.4% in the baxdrostat 2 mg group and 2.7% in the placebo group during part 1. Hyperkalaemia was the most frequent side effect, leading to discontinuation in 0.8% of patients on baxdrostat 1 mg and 1.5% on baxdrostat 2 mg. Adrenocortical insufficiency never occurred during the trial.

This study confirms the antihypertensive efficacy of this new class of drugs, which are able to selectively block aldosterone biosynthesis at the enzymatic level.

Similar results were obtained in uncontrolled hypertensive patients in the ADVANCE-HTN trial by treatment with lorundrostat.6 The efficacy of baxdrostat, observed in resistant hypertension patients in the BrigHTN study, extends to a broader number of patients with resistant and uncontrolled hypertensives.7

The proportion of patients reaching controlled BP was almost 40%, which may imply significant protection in terms of cardiovascular events and/or chronic kidney disease.

All these recent data underscore the role of aldosterone dysregulation in the development of elevated BP and uncontrolled or resistant hypertension, favouring the progression of hypertension-mediated target organ damage.

Up to now, mineralocorticoid receptor antagonists have been used in patients with hyperaldosteronism to control BP, despite some undesirable side effects, including hyperkalaemia, sexual dysfunction and gynaecomastia.

Aldosterone synthase inhibitors have demonstrated similar antihypertensive efficacy and have a better safety and tolerability profile.

The innovative mechanism of action of this new class of drugs could be beneficial in other aldosterone-driven phenotypes, such as obesity, type 2 diabetes and chronic kidney disease, when renin–angiotensin–aldosterone system activation may be inappropriate.

To further explore the potential use of aldosterone synthase inhibitor, other randomised controlled trials are warranted to identify specific patients most likely to benefit.

References

  1. Benetos A, Gautier S, Freminet A, et al. Reduction of antihypertensive treatment in nursing home residents. N Engl J Med 2025. 
    Crossref | PubMed
  2. Benetos A, Labat C, Rossignol P, et al. Treatment with multiple blood pressure medications, achieved blood pressure, and mortality in older nursing home residents: the PARTAGE Study. JAMA Intern Med 2015;175:989–95. 
    Crossref | PubMed
  3. Sheppard JP, Burt J, Lown M, et al. Effect of antihypertensive medication reduction vs usual care on short-term blood pressure control in patients with hypertension aged 80 years and older: the OPTIMISE randomized clinical trial. JAMA 2020;323:2039–51. 
    Crossref | PubMed
  4. Moonen JEF, Foster-Dingley JC, de Ruijter W, et al. Effect of discontinuation of antihypertensive treatment in elderly people on cognitive functioning – the DANTE study Leiden: a randomized clinical trial. JAMA Intern Med 2015;175:1622–30. 
    Crossref | PubMed
  5. Flack JM, Azizi M, Brown JM, et al. Efficacy and safety of baxdrostat in uncontrolled and resistant hypertension. N Engl J Med 2025. 
    Crossref | PubMed
  6. Laffin LJ, Kopjar B, Melgaard C, et al. Lorundrostat efficacy and safety in patients with uncontrolled hypertension. N Engl J Med 2025;392:1813–23. 
    Crossref | PubMed
  7. Freeman MW, Halvorsen YD, Marshall W, et al. Phase 2 trial of baxdrostat for treatment-resistant hypertension. N Engl J Med 2023;388:395–405. 
    Crossref | PubMed