Elevated Admission Blood Pressure and Acute Ischemic Lesions in Spontaneous Intracerebral Hemorrhage

Author(s):  
Ethem Murat Arsava ◽  
Ozlem Kayim-Yildiz ◽  
Kader K. Oguz ◽  
Erhan Akpinar ◽  
Mehmet Akif Topcuoglu
Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Jill Slater ◽  
Holly Morhaim ◽  
Steven Rudolph

Background: Current American Heart Association guidelines for targeted blood pressure management in spontaneous intracerebral hemorrhage (ICH), published in 2010, suggest a target mean arterial pressure of less than 110 or a blood pressure of less than 160/90 in patients without elevated intracranial pressure. These guidelines acknowledge that these recommendations have been based on incomplete efficacy evidence. A lower level recommendation was given for reducing target blood pressure to a systolic of 140, based on the INTERACT trial published in 2008. The INTERACT2 trial, published in May 2013, has been interpreted to establish the safety of rapid blood pressure lowering to 140 systolic. Purpose: To determine the current level of adoption by stroke centers of lower targets for blood pressure in patients with spontaneous intracerebral hemorrhage, and whether these targets have changed in 2013. Methods: We developed a web-based survey that was distributed via email and professional groups to stroke advanced practice nurses and stroke program coordinators. The survey asked specific questions regarding changes in clinical practice and stroke center policies on blood pressure management in spontaneous ICH. The survey was anonymous, and the survey software was able to exclude multiple entries from the same computer. Results: Responses were obtained from academic medical centers, community teaching hospitals, and community non-teaching hospitals. Awareness of the results of INTERACT2 was known by 65%, 50%, and 31% of stroke nurses at these hospitals, respectively. Targets for systolic blood pressure were changed in 2013 at 46%, 44%, and 11% of hospitals by group. A time target to lower blood pressure of less than one hour was adopted by 57%, 46%, and 28% respectively. Conclusion: Stroke centers have rapidly adopted changes in blood pressure management in intracerebral hemorrhage in advance of guideline revisions. Non-teaching hospitals were less likely to adopt these changes.


1999 ◽  
Vol 27 (3) ◽  
pp. 480-485 ◽  
Author(s):  
Adnan I. Qureshi ◽  
Donald L. Bliwise ◽  
Nancy G. Bliwise ◽  
M. Sohail Akbar ◽  
Guven Uzen ◽  
...  

Stroke ◽  
2019 ◽  
Vol 50 (8) ◽  
pp. 2023-2029 ◽  
Author(s):  
Afshin A. Divani ◽  
Xi Liu ◽  
Mario Di Napoli ◽  
Simona Lattanzi ◽  
Wendy Ziai ◽  
...  

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Fabricio Simao ◽  
Jian Guan ◽  
Allen Clermont ◽  
Loc-Duyen Pham ◽  
Tuna Ustunkaya ◽  
...  

Introduction: Hypertension is a leading risk factor for spontaneous intracerebral hemorrhage. Plasma Kallikrein (PKa) has been implicated in contributing to hemorrhage following thrombolytic therapy, however, its role in spontaneous intracerebral hemorrhage is currently not available. This report investigates the role of PKa on hemorrhage and hypertension in stroke-prone spontaneously hypertensive rats (SHRSP). Methods: SHRSP were fed with a high salt containing stroke-prone diet to increase blood pressure and induce spontaneous intracerebral hemorrhage. The roles of PKa on blood pressure, intracerebral hemorrhage, and survival in SHRSP were examined in rats receiving a PKa inhibitor (BPCCB) or plasma prekallikrein antisense oligonucleotide (PK ASO) compared with rats receiving control ASO. Effects on PKa on the proteolytic cleavage of atrial natriuretic peptide (ANP) were analyzed by tandem mass spectrometry. Results: PKa activity in plasma was increased by 29% in SHRSP on high salt diet compared with control rats. Cleaved kininogen, a substrate for PKa, was 2-fold greater in SHRSP plasma during stroke compared with SHRSP without stroke symptoms. Systemic administration of BPCCB or PK ASO to SHRSP reduced intracerebral hemorrhage (Fig. 1A) and blood pressure (Fig. 1B), and improved neurological function and survival when compared with rats receiving control ASO. Since PKa inhibition was associated with reduced blood pressure in hypertensive rats, we investigated the effects of PKa on the cleavage of ANP. Incubation of PKa with ANP resulted in the generation fragment ANP 5-28 , which displayed reduced effects on blood pressure lowering compared with full length ANP. Conclusions: PKa contributes to increased blood pressure in SHRSP, which is associated with intracerebral hemorrhage and reduced survival. PKa-mediated cleavage of ANP reduces its blood pressure lowering effects and thereby may contribute to hypertension-induced intracerebral hemorrhage.


Stroke ◽  
2018 ◽  
Vol 49 (2) ◽  
pp. 348-354 ◽  
Author(s):  
Pil-Wook Chung ◽  
Joon-Tae Kim ◽  
Nerses Sanossian ◽  
Sidney Starkmann ◽  
Scott Hamilton ◽  
...  

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