» Articles » PMID: 39069917

Premorbid Blood Pressure Control Modifies Risk of DWI Lesions With Acute Blood Pressure Reduction in Intracerebral Hemorrhage

Overview
Journal Hypertension
Date 2024 Jul 29
PMID 39069917
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Hypoperfusion due to blood pressure (BP) reduction is a potential mechanism of cerebral ischemia after intracerebral hemorrhage. However, prior evaluations of the relationship between BP reduction and ischemia have been conflicting. Untreated chronic hypertension is common in intracerebral hemorrhage and alters cerebral autoregulation. We hypothesized that the risk of diffusion-weighted imaging (DWI) hyperintensities from acute BP reduction is modified by premorbid BP control.

Methods: Individuals enrolled in the ERICH study (Ethnic/Racial Variations of Intracerebral Hemorrhage) from 2010 to 2015 were categorized as untreated, treated, or nonhypertensive based on preintracerebral hemorrhage diagnosis and antihypertensive medication use. The percent reduction of systolic BP (SBP) was calculated between presentation and 24 hours from admission. The primary outcome was the presence of DWI lesions. Using logistic regression, we tested the association between chronic hypertension status, SBP reduction, and their interaction with DWI lesion presence.

Results: From 3000 participants, 877 with available magnetic resonance imaging met inclusion (mean age, 60.5±13.3 years; 42.5% women). DWI lesions were detected in 25.9%. Untreated, treated, and no hypertension accounted for 32.6%, 47.9%, and 19.5% of cases, respectively. SBP reduction was not directly associated with DWI lesions; however, an interaction effect was observed between SBP reduction and chronic hypertension status (=0.036). Nonhypertensive subjects demonstrated a linear risk of DWI lesion presence with greater SBP reduction, whereas untreated hypertension demonstrated a stable risk across a wide range of SBP reduction (=0.023).

Conclusions: Premorbid BP control, especially untreated hypertension, may influence the relationship between DWI lesions and acute BP reduction after intracerebral hemorrhage.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01202864.

Citing Articles

Antihypertensive Medication Class and Functional Outcomes After Nonlobar Intracerebral Hemorrhage.

Ridha M, Burke J, Sekar P, Woo D, Hannawi Y JAMA Netw Open. 2025; 8(2):e2457770.

PMID: 39899295 PMC: 11791703. DOI: 10.1001/jamanetworkopen.2024.57770.

References
1.
Kidwell C, Rosand J, Norato G, Dixon S, Worrall B, James M . Ischemic lesions, blood pressure dysregulation, and poor outcomes in intracerebral hemorrhage. Neurology. 2017; 88(8):782-788. PMC: 5344081. DOI: 10.1212/WNL.0000000000003630. View

2.
Petersen N, Silverman A, Strander S, Kodali S, Wang A, Sansing L . Fixed Compared With Autoregulation-Oriented Blood Pressure Thresholds After Mechanical Thrombectomy for Ischemic Stroke. Stroke. 2020; 51(3):914-921. PMC: 7050651. DOI: 10.1161/STROKEAHA.119.026596. View

3.
Gioia L, Klahr A, Kate M, Buck B, Dowlatshahi D, Jeerakathil T . The intracerebral hemorrhage acutely decreasing arterial pressure trial II (ICH ADAPT II) protocol. BMC Neurol. 2017; 17(1):100. PMC: 5437568. DOI: 10.1186/s12883-017-0884-4. View

4.
Greenberg S, Ziai W, Cordonnier C, Dowlatshahi D, Francis B, Goldstein J . 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2022; 53(7):e282-e361. DOI: 10.1161/STR.0000000000000407. View

5.
Ridha M, Megjhani M, Nametz D, Kwon S, Velazquez A, Ghoshal S . Suboptimal Cerebral Perfusion is Associated with Ischemia After Intracerebral Hemorrhage. Neurocrit Care. 2023; 40(3):996-1005. PMC: 11089072. DOI: 10.1007/s12028-023-01863-6. View