Empagliflozin for Patients With Presumed Resistant Hypertension: A Post Hoc Analysis of the EMPA-REG OUTCOME Trial.


Journal

American journal of hypertension
ISSN: 1941-7225
Titre abrégé: Am J Hypertens
Pays: United States
ID NLM: 8803676

Informations de publication

Date de publication:
31 12 2020
Historique:
received: 02 02 2020
revised: 13 03 2020
accepted: 29 04 2020
pubmed: 6 5 2020
medline: 9 11 2021
entrez: 6 5 2020
Statut: ppublish

Résumé

Type 2 diabetes (T2D) and resistant hypertension often coexist, greatly increasing risk of target-organ damage and death. We explored the effects of empagliflozin in patients with and without presumed resistant hypertension (prHT) in a post hoc analysis of EMPA-REG OUTCOME (NCT01131676). Overall, 7,020 patients received empagliflozin 10, 25 mg, or placebo with median follow-up of 3.1 years. We defined baseline prHT as ≥3 classes of antihypertensive drugs including a diuretic and uncontrolled blood pressure (BP; systolic blood pressure (SBP) ≥140 and/or diastolic blood pressure ≥90 mm Hg) or ≥4 classes of antihypertensive, including a diuretic, and controlled BP. We explored the effect of empagliflozin on cardiovascular (CV) death, heart failure (HF) hospitalization, 3-point major adverse cardiac events, all-cause death, and incident/worsening nephropathy by Cox regression and BP over time by a mixed-repeated-measures-model analysis. 1,579 (22.5%) patients had prHT. The mean difference in change in SBP from baseline to week 12 vs. placebo was -4.5 (95% confidence interval, -5.9 to -3.1) mm Hg (P < 0.001) in prHT and -3.7 (-4.5, -2.9) mm Hg (P < 0.001) in patients without prHT. SBP was more frequently controlled (<130/80 mm Hg) with empagliflozin than with placebo. Patients with prHT had 1.5- to 2-fold greater risk of HF hospitalization, incident/worsening nephropathy, and CV death compared with those without prHT. Empagliflozin improved all outcomes in patients with and without prHT (interaction P > 0.1 for all outcomes). Empagliflozin induced a clinically relevant reduction in SBP and consistently improved all outcomes regardless of prHT status. Due to these dual effects, empagliflozin should be considered for patients with hypertension and T2D.

Sections du résumé

BACKGROUND
Type 2 diabetes (T2D) and resistant hypertension often coexist, greatly increasing risk of target-organ damage and death. We explored the effects of empagliflozin in patients with and without presumed resistant hypertension (prHT) in a post hoc analysis of EMPA-REG OUTCOME (NCT01131676).
METHODS
Overall, 7,020 patients received empagliflozin 10, 25 mg, or placebo with median follow-up of 3.1 years. We defined baseline prHT as ≥3 classes of antihypertensive drugs including a diuretic and uncontrolled blood pressure (BP; systolic blood pressure (SBP) ≥140 and/or diastolic blood pressure ≥90 mm Hg) or ≥4 classes of antihypertensive, including a diuretic, and controlled BP. We explored the effect of empagliflozin on cardiovascular (CV) death, heart failure (HF) hospitalization, 3-point major adverse cardiac events, all-cause death, and incident/worsening nephropathy by Cox regression and BP over time by a mixed-repeated-measures-model analysis.
RESULTS
1,579 (22.5%) patients had prHT. The mean difference in change in SBP from baseline to week 12 vs. placebo was -4.5 (95% confidence interval, -5.9 to -3.1) mm Hg (P < 0.001) in prHT and -3.7 (-4.5, -2.9) mm Hg (P < 0.001) in patients without prHT. SBP was more frequently controlled (<130/80 mm Hg) with empagliflozin than with placebo. Patients with prHT had 1.5- to 2-fold greater risk of HF hospitalization, incident/worsening nephropathy, and CV death compared with those without prHT. Empagliflozin improved all outcomes in patients with and without prHT (interaction P > 0.1 for all outcomes).
CONCLUSIONS
Empagliflozin induced a clinically relevant reduction in SBP and consistently improved all outcomes regardless of prHT status. Due to these dual effects, empagliflozin should be considered for patients with hypertension and T2D.

Identifiants

pubmed: 32369546
pii: 5830772
doi: 10.1093/ajh/hpaa073
pmc: PMC7814223
doi:

Substances chimiques

Antihypertensive Agents 0
Benzhydryl Compounds 0
Glucosides 0
Sodium-Glucose Transporter 2 Inhibitors 0
empagliflozin HDC1R2M35U

Banques de données

ClinicalTrials.gov
['NCT01131676']

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1092-1101

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of American Journal of Hypertension, Ltd.

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Auteurs

João Pedro Ferreira (JP)

Université de Lorraine, Centre d'Investigations Cliniques Plurithématique Inserm 1433, Nancy, France.
CHRU de Nancy, Inserm U1116, Nancy, France.
FCRIN INI-CRCT, Nancy, France.

David Fitchett (D)

Division of Cardiology, St Michael's Hospital, University of Toronto, Toronto, Ontario, Canada.

Anne Pernille Ofstad (AP)

Boehringer Ingelheim Norway KS, Asker, Norway.

Bettina Johanna Kraus (BJ)

Comprehensive Heart Failure Center, University of Würzburg, Würzburg, Germany.
Department of Internal Medicine I, University Hospital Würzburg, Würzburg, Germany.

Christoph Wanner (C)

Department of Internal Medicine I, University Hospital Würzburg, Würzburg, Germany.

Isabella Zwiener (I)

Boehringer Ingelheim Pharma GmbH & Co. KG, Ingelheim, Germany.

Bernard Zinman (B)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada.

Sabine Lauer (S)

Boehringer Ingelheim Pharma GmbH & Co. KG, Ingelheim, Germany.

Jyothis T George (JT)

Boehringer Ingelheim International GmbH, Ingelheim, Germany.

Patrick Rossignol (P)

Université de Lorraine, Centre d'Investigations Cliniques Plurithématique Inserm 1433, Nancy, France.
CHRU de Nancy, Inserm U1116, Nancy, France.
FCRIN INI-CRCT, Nancy, France.

Faiez Zannad (F)

Université de Lorraine, Centre d'Investigations Cliniques Plurithématique Inserm 1433, Nancy, France.
CHRU de Nancy, Inserm U1116, Nancy, France.
FCRIN INI-CRCT, Nancy, France.

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Classifications MeSH