Effect of Baseline Antihypertensive Treatments on Stroke Severity and Outcomes in the BP TARGET Trial

Author:

Maïer Benjamin1234ORCID,Gory Benjamin56ORCID,Lapergue Bertrand7ORCID,Sibon Igor8ORCID,Richard Sebastien9ORCID,Kyheng Maeva10,Labreuche Julien10ORCID,Desilles Jean-Philippe12311ORCID,Blanc Raphael1311ORCID,Piotin Michel1311ORCID,Mazighi Mikael12311ORCID,Halimi Jean-Michel412ORCID,Redjem Hocine,Escalard Simon,Smajda Stanislas,Delvoye François,Hebert Solène,Obadia Michael,Sabben Candice,Obadia Alexandre,Raynouard Igor,Morvan Erwan,Boursin Perrine,Ben Maacha Malek,Consoli Arturo,Wang Adrien,Mione Gioia,Humbertjean Lisa,Bonnerot Matthieu,Lacour Jean-Christophe,Anxionnat René,Tonnelet Romain,Bracard Serge,Barreau Xavier,Marnat Gaultier,Berge Jérôme,Lucas Ludovic,Renou Pauline,Debruxelles Sabrina,Poli Mathilde,Sagnier Sharmila

Affiliation:

1. Interventional Neuroradiology Department, Hôpital Fondation Ophtalmologique Adolphe de Rothschild, Paris, France (B.M., J.-P.D., R.B., M.P., M.M.).

2. Université de Paris, France (B.M., J.-P.D., M.M.).

3. FHU NeuroVasc, Paris, France (B.M., J.-P.D., R.B., M.P., M.M.).

4. EA4245-Transplantation, Immunology and Inflammation, University of Tours, France (B.M., J.-M.H.).

5. Department of Diagnostic and Therapeutic Neuroradiology (B.G.), Université de Lorraine, France.

6. CHRU-Nancy and IADI, INSERM U1254 (B.G.), Université de Lorraine, France.

7. Division of Neurology, Department of Neurology, Stroke Centre, Foch Hospital, University Versailles Saint-Quentin en Yvelines, Suresnes, France (B.L.).

8. Stroke Unit, CHU Bordeaux, Université de Bordeaux, France (I.S.).

9. Department of Neurology (S.R.)), Université de Lorraine, France.

10. CHU Lille, EA 2694 - Santé publique: épidémiologie et qualité des soins, University of Lille, France (M.L., J.L.).

11. Laboratory of Vascular Translational Science, INSERM U1148, Paris, France (J.-P.D., R.B., M.P., M.M.).

12. Nephrology Department, Tours Hospital, France (J.-M.H.). Université de Tours, France (J.M.H.).

Abstract

Background: Acute ischemic stroke (AIS) patients with a history of hypertension experience worse outcomes, which may be explained by a deleterious impact of the renin-angiotensin system (RAS) overactivation. We sought to investigate whether prestroke antihypertensive treatments (AHT) influenced baseline stroke severity and neurological outcomes, in patients with AIS successfully treated by endovascular therapy. Methods: We performed a post hoc analysis of the BP TARGET trial (Blood Pressure Target in Acute Stroke to Reduce Hemorrhage After Endovascular Therapy) and included hypertensive patients with available data regarding AHT at admission, categorized as RAS inhibitors (ACE [angiotensin-converting enzyme] inhibitors, ARBs [angiotensin 2 receptor blockers], and β-blockers) and non-RAS inhibitors (calcium channel blockers and diuretics). Associations of each AHT with National Institutes of Health Stroke Scale (NIHSS) score at baseline were investigated in linear mixed model adjusted for the number of treatments and center. Associations of each AHT with 24-hour NIHSS change, intracranial hemorrhage were performed using linear mixed model adjusted for baseline NIHSS, the number of treatments, center, age, and sex and adjusted for age, sex, diabetes, and current smoking for favorable outcome. All analyses were performed on cases-available data regarding the low number of missing data. Results: Overall, 203 patients with at least one AHT were included. Patients under non-RAS inhibitor treatments had a higher NIHSS score at baseline (adjusted mean difference=3.28 [95% CI, 1.33–5.22]; P =0.001). Conversely, patients under RAS inhibitor treatments had a lower baseline NIHSS score (adjusted mean difference=−2.81 [95% CI, −5.37 to −0.25]; P =0.031). Intracranial hemorrhage occurrence was significantly more frequent in patients under non-RAS inhibitor treatments (adjusted odds ratio of 2.48 [95% CI, 1.12–5.47]; P =0.025). Conversely, the use of RAS inhibitor treatments before AIS was not associated with higher odds of radiographic intracranial hemorrhage. Patients with non-RAS inhibitor treatments had less improvement of NIHSS at 24 hours compared with patients without (adjusted mean difference, 2.83 [95% CI, −0.16 to 5.81]; P =0.063). Baseline RAS inhibitor or noninhibitor treatments were not associated with favorable outcome. Conclusions: We showed an opposite effect of baseline AHT, based on their effect on the RAS. Patients treated with RAS inhibitor agents before AIS exhibited less severe AIS compared with patients under non-RAS inhibitor treatments, developed less intracranial hemorrhage at 24 hours and had a trend toward better NIHSS score at 24 hours. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03160677.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Advanced and Specialized Nursing,Cardiology and Cardiovascular Medicine,Neurology (clinical)

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