scholarly journals Effect of Systolic Blood Pressure Reduction on Hematoma Expansion, Perihematomal Edema, and 3-Month Outcome Among Patients With Intracerebral Hemorrhage

2010 ◽  
Vol 67 (5) ◽  
pp. 570 ◽  
Author(s):  
Adnan I. Qureshi
2017 ◽  
Vol 38 (9) ◽  
pp. 1551-1563 ◽  
Author(s):  
Adnan I Qureshi ◽  
Mushtaq H Qureshi

Acute hypertensive response is a common systemic response to occurrence of intracerebral hemorrhage which has gained unique prominence due to high prevalence and association with hematoma expansion and increased mortality. Presumably, the higher systemic blood pressure predisposes to continued intraparenchymal hemorrhage by transmission of higher pressure to the damaged small arteries and may interact with hemostatic and inflammatory pathways. Therefore, intensive reduction of systolic blood pressure has been evaluated in several clinical trials as a strategy to reduce hematoma expansion and subsequent death and disability. These trials have demonstrated either a small magnitude benefit (second intensive blood pressure reduction in acute cerebral hemorrhage trial and efficacy of nitric oxide in stroke trial) or no benefit (antihypertensive treatment of acute cerebral hemorrhage 2 trial) with intensive systolic blood pressure reduction compared with modest or standard blood pressure reduction. The differences may be explained by the variation in intensity of systolic blood pressure reduction between trials. A treatment threshold of systolic blood pressure of ≥180 mm with the target goal of systolic blood pressure reduction to values between 130 and 150 mm Hg within 6 h of symptom onset may be best supported by current evidence.


Stroke ◽  
2019 ◽  
Vol 50 (8) ◽  
pp. 2016-2022 ◽  
Author(s):  
Audrey C. Leasure ◽  
Adnan I. Qureshi ◽  
Santosh B. Murthy ◽  
Hooman Kamel ◽  
Joshua N. Goldstein ◽  
...  

2012 ◽  
Vol 125 (7) ◽  
pp. 718.e1-718.e6 ◽  
Author(s):  
Adnan I. Qureshi ◽  
Yuko Y. Palesch ◽  
Renee Martin ◽  
Jill Novitzke ◽  
Salvador Cruz Flores ◽  
...  

2015 ◽  
Vol 33 (5) ◽  
pp. 1069-1073 ◽  
Author(s):  
Yuki Sakamoto ◽  
Masatoshi Koga ◽  
Kenichi Todo ◽  
Satoshi Okuda ◽  
Yasushi Okada ◽  
...  

Stroke ◽  
2020 ◽  
Vol 51 (10) ◽  
pp. 3030-3038
Author(s):  
Adnan I. Qureshi ◽  
Wei Huang ◽  
Iryna Lobanova ◽  
Daniel F. Hanley ◽  
Chung Y. Hsu ◽  
...  

Background and Purpose: We determined the rates and predictors of acute kidney injury (AKI) and renal adverse events (AEs), and effects of AKI and renal AEs on death or disability in patients with intracerebral hemorrhage. Methods: We analyzed data from a multicenter trial which randomized 1000 intracerebral hemorrhage patients with initial systolic blood pressure ≥180 mm Hg to intensive (goal 110–139 mm Hg) over standard (goal 140–179 mm Hg) systolic blood pressure reduction within 4.5 hours of symptom onset. AKI was identified by serial assessment of daily serum creatinine for 3 days post randomization. Results: AKI and renal AEs were observed in 149 patients (14.9%) and 65 patients (6.5%) among 1000 patients, respectively. In multivariate analysis, the higher baseline serum creatinine (≥110 μmol/L) was associated with AKI (odds ratio 2.4 [95% CI, 1.2–4.5]) and renal AEs (odds ratio 3.1 [95% CI, 1.2–8.1]). Higher area under the curve for intravenous nicardipine dose was associated with AKI (odds ratio 1.003 [95% CI, 1.001–1.005]) and renal AEs (odds ratio 1.003 [95% CI, 1.001–1.006]). There was a higher risk to death (relative risk 2.6 [95% CI, 1.6–4.2]) and death or disability (relative risk 1.5 [95% CI, 1.3–1.8]) at 90 days in patients with AKI but not in those with renal AEs. Conclusions: Intracerebral hemorrhage patients with higher baseline serum creatinine and those receiving higher doses of nicardipine were at higher risk for AKI and renal AEs. Occurrence of AKI was associated higher rates of death or disability at 3 months. Registration: URL: https://clinicaltrials.gov . Unique identifier: NCT01176565.


Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Tapan Thacker ◽  
Andrew Buletko ◽  
Jason Mathew ◽  
Natalie Organek ◽  
Muhammad Shazam Hussain ◽  
...  

Introduction: Despite studies of aggressive blood pressure reduction in primary intracerebral hemorrhage (ICH), the potential for inducing ischemia remains a concern. The primary objective of this study is to determine the relationship between blood pressure and acute cerebral ischemia following ICH. Methods: We performed a retrospective chart review of patients with primary ICH admitted between January 2013 and December 2014 in whom MRI brain with diffusion-weighted imaging (DWI) was performed within 2 weeks of admission. Acute ischemia was defined as DWI hyperintensity with corresponding apparent diffusion coefficient hypointensity. Lesions adjacent to the ICH or after an invasive procedure were excluded and all MRIs were performed prior to digital subtraction angiography. Serial blood pressure measurements were collected from admission to 72h post ictus. Clinical deterioration was defined as any acute exam change not explained by seizure, hematoma expansion or other medical causes. Results: Among 119 patients with primary ICH (mean age 69.3 years, 58% males, 65% Caucasians), 28 (23.5%) had acute ischemia. Acute ischemia was associated with lower mean 24-hour SBP (132 mmHg in DWI+ versus 141 mmHg in DWI-, p<0.001), greater mean change in SBP from admission to 24 hours (67 mmHg in DWI+ versus -42 mmHg in DWI-, p=0.002), lower mean minimum SBP at 72 hours (104 mmHg in DWI+ versus 111 mmHg in DWI-, p=0.008) and lobar ICH location (35% in DWI+ versus 14% in DWI-, p=0.009). Minimum SBP <120 mmHg during the first 72 hour after ICH has a sensitivity of 96% in predicting DWI lesions in patients with ICH (p=0.014). Overall, patients with DWI+ lesions had a higher incidence of clinical deterioration (32% in DWI+ versus 6% in DWI-, p<0.001) and longer length of stay compared to patients without DWI lesions (13 days in DWI+ versus 8 days in DWI-, p=0.006). Hematoma volume, initial NIH Stroke Scale and admission SBP were not significantly associated with DWI lesions in patients with primary ICH. Conclusions: Aggressive SBP reduction, particularly SBP<120 mmHg within the first 72h of ICH, can be associated with acute cerebral ischemia. A third of acute ischemic lesions are associated with clinical deterioration.


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