scholarly journals Induced Hypertension for Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Stroke ◽  
2018 ◽  
Vol 49 (1) ◽  
pp. 76-83 ◽  
Author(s):  
Celine S. Gathier ◽  
Walter M. van den Bergh ◽  
Mathieu van der Jagt ◽  
Bon H. Verweij ◽  
Jan Willem Dankbaar ◽  
...  
Stroke ◽  
2015 ◽  
Vol 46 (11) ◽  
pp. 3277-3281 ◽  
Author(s):  
Celine S. Gathier ◽  
Jan Willem Dankbaar ◽  
Mathieu van der Jagt ◽  
Bon H. Verweij ◽  
Annemarie W. Oldenbeuving ◽  
...  

2017 ◽  
Vol 43 (5-6) ◽  
pp. 266-271 ◽  
Author(s):  
Bhaskar Roy ◽  
Louise D. McCullough ◽  
Rajat Dhar ◽  
James Grady ◽  
Yu-Bo Wang ◽  
...  

Background: The main reason for morbidity after aneurysmal subarachnoid hemorrhage (aSAH) is delayed cerebral ischemia (DCI). The mainstay of medical therapy for treating DCI is induced hypertension with vasopressors to restore cerebral perfusion. Both phenylephrine (PE) and norepinephrine (NE) are commonly used for induced hypertension, but the impact of the initial choice of vasopressor on the efficacy, adverse effects, or outcome after hemodynamic therapy for DCI is unknown. Methods: Sixty-three patients with aSAH between January 2012 and October 2014, who developed DCI (defined as new focal deficit or decline in Glasgow Coma Score) and in which PE (n = 45) or NE (n = 18) treatment was initiated were evaluated in this retrospective study. Baseline characteristics, adverse effects, the need to change or add vasopressors, the response to therapy, the need for endovascular therapy, new infarct development, discharge disposition, and 3 months modified Rankin score were all compared between pressor groups. Results: Baseline characteristics (e.g., Hunt Hess and Fisher grades) were similar. There were no differences in the overall rate of complications including arrhythmia, pulmonary edema, or kidney injury. However, those initiated on PE were more likely to be changed to an alternate vasopressor (64 vs. 33%, p = 0.016), mostly for bradycardia or failure to reach therapeutic targets. Patients initially treated with PE were less likely to respond neurologically (71 vs. 94%, p = 0.01) or to be discharged to home or acute rehabilitation facilities (73 vs. 94%, p = 0.02) and were more likely to have a delayed infarct on imaging (62 vs. 33%, p = 0.04). Conclusions: Our study suggests that patients with DCI after aSAH initiated on PE are more likely to require treatment change to another vasopressor and are at greater risk for poor clinical outcomes compared to patients started on NE. Larger comparative studies are warranted.


Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 820
Author(s):  
Keshav Jayaraman ◽  
Meizi Liu ◽  
Gregory J. Zipfel ◽  
Umeshkumar Athiraman

Numerous studies have demonstrated the ability of isoflurane conditioning to provide multifaceted protection against aneurysmal subarachnoid hemorrhage (SAH)-associated delayed cerebral ischemia (DCI); however, preclinical studies have not yet examined whether other commonly used inhalational anesthetics in neurological patients such as sevoflurane or desflurane are also protective against SAH-induced neurovascular deficits. We therefore sought to identify the potential for sevoflurane and desflurane conditioning to protect against DCI in an endovascular perforation mouse model of SAH. Neurological function was assessed daily via neuroscore. Large artery vasospasm and microvessel thrombosis were assessed three days after SAH or sham surgery. Four groups were examined: Sham, SAH + room air, SAH + 2% Sevoflurane, and SAH + 6% Desflurane. For the SAH groups, one hour after surgery, mice received 2% sevoflurane, 6% desflurane, or room air for one hour. We found that conditioning with sevoflurane or desflurane attenuated large artery vasospasm, reduced microvessel thrombosis, and improved neurologic function. Given their frequent clinical use and strong safety profile in patients (including those with SAH), these data strongly support further studies to validate these findings in preclinical and clinical studies and to elucidate the mechanisms by which these agents might be acting.


Author(s):  
Claudia Ditz ◽  
Björn Machner ◽  
Hannes Schacht ◽  
Alexander Neumann ◽  
Peter Schramm ◽  
...  

AbstractPlatelet activation has been postulated to be involved in the pathogenesis of delayed cerebral ischemia (DCI) and cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage (aSAH). The aim of this study was to investigate potentially beneficial effects of antiplatelet therapy (APT) on angiographic CVS, DCI-related infarction and functional outcome in endovascularly treated aSAH patients. Retrospective single-center analysis of aSAH patients treated by endovascular aneurysm obliteration. Based on the post-interventional medical regime, patients were assigned to either an APT group or a control group not receiving APT. A subgroup analysis separately investigated those APT patients with aspirin monotherapy (MAPT) and those receiving dual treatment (aspirin plus clopidogrel, DAPT). Clinical and radiological characteristics were compared between groups. Possible predictors for angiographic CVS, DCI-related infarction, and an unfavorable functional outcome (modified Rankin scale ≥ 3) were analyzed. Of 160 patients, 85 (53%) had received APT (n = 29 MAPT, n = 56 DAPT). APT was independently associated with a lower incidence of an unfavorable functional outcome (OR 0.40 [0.19–0.87], P = 0.021) after 3 months. APT did not reduce the incidence of angiographic CVS or DCI-related infarction. The pattern of angiographic CVS or DCI-related infarction as well as the rate of intracranial hemorrhage did not differ between groups. However, the lesion volume of DCI-related infarctions was significantly reduced in the DAPT subgroup (P = 0.011). Post-interventional APT in endovascularly treated aSAH patients is associated with better functional outcome at 3 months. The beneficial effect of APT might be mediated by reduction of the size of DCI-related infarctions.


2012 ◽  
Vol 34 (2) ◽  
pp. 292-298 ◽  
Author(s):  
P.C. Sanelli ◽  
N. Anumula ◽  
C.E. Johnson ◽  
J.P. Comunale ◽  
A.J. Tsiouris ◽  
...  

2018 ◽  
Vol 128 (5) ◽  
pp. 1311-1317 ◽  
Author(s):  
Christoph J. Griessenauer ◽  
Robert M. Starke ◽  
Paul M. Foreman ◽  
Philipp Hendrix ◽  
Mark R. Harrigan ◽  
...  

OBJECTIVEEndothelin-1, a potent vasoconstrictor, and its receptors may be involved in the pathogenesis of aneurysmal subarachnoid hemorrhage (aSAH), clinical vasospasm, delayed cerebral ischemia (DCI), and functional outcome following aSAH. In the present study, common endothelin single nucleotide polymorphisms (SNPs) and their relation to aSAH were evaluated.METHODSBlood samples from all patients enrolled in the Cerebral Aneurysm Renin Angiotensin System (CARAS) study were used for genetic evaluation. The CARAS study prospectively enrolled patients with aSAH at 2 academic institutions in the US from 2012 to 2015. Common endothelin SNPs were detected using 5′ exonnuclease (TaqMan) genotyping assays. Analysis of associations between endothelin SNPs and aSAH and its clinical sequelae was performed.RESULTSSamples from 149 patients with aSAH and 50 controls were available for analysis. In multivariate logistic regression analysis, the TG (odds ratio [OR] 2.102, 95% confidence interval [CI] 1.048–4.218, p = 0.036) and TT genotypes (OR 7.884, 95% CI 1.003–61.995, p = 0.05) of the endothelin-1 T/G SNP (rs1800541) were significantly associated with aSAH. There was a dominant effect of the G allele (CG/GG genotypes; OR 4.617, 95% CI 1.311–16.262, p = 0.017) of the endothelin receptor A G/C SNP (rs5335) on clinical vasospasm. Endothelin SNPs were not associated with DCI or functional outcome.CONCLUSIONSCommon endothelin SNPs were found to be associated with presentation with aSAH and clinical vasospasm. Further studies are required to elucidate the relevant pathophysiology and its potential implications in the treatment of patients with aSAH.


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