Reasons for exclusion from thrombolytic therapy following acute ischemic stroke

Cocho, Dolores; Belvis, R.; Marti-Fabregas, J.; Molina‐Porcel, Laura; Díaz-Manera, Jordi; Aleu, A.; Pagonabarraga, J.; Garcia-Bargo, D.; Mauri, A.; Marti-Vilalta, J. -L.

doi:10.1212/01.wnl.0000152041.20486.2f

Cited by 113 publications

(88 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1,2 Unfortunately, only a small proportion of acute stroke patients actually receive tPA. [3][4][5][6] Several reasons have been identified for the low rates of thrombolysis, the most common being arrival outside the appropriate time window. 7,8 Up to 50% of all ischemic stroke patients initially present with mild or rapidly improving symptoms, 9 and a large proportion of these patients are not treated with IV tPA, despite presenting within the 4.5-hour time window.…”

mentioning

confidence: 99%

Baseline Predictors of Poor Outcome in Patients Too Good to Treat With Intravenous Thrombolysis

Ali

Siddiqui

et al. 2016

Stroke

View full text Add to dashboard Cite

Background and Purpose-Several studies have reported poor outcomes in patients too good to treat with intravenous thrombolysis because of mild or rapidly improving symptoms. We sought to determine baseline clinical and imaging predictors of poor outcome in these patients. Methods-Among 3950 consecutive stroke admissions (2009)(2010)(2011)(2012)(2013)(2014)(2015) in our local Get With the Guidelines-Stroke database, 632 patients presented ≤4.5 hours and did not receive tissue-type plasminogen activator, with 380 of 632 (60.1%) being too good to treat. Univariate and multivariable analyses explored the clinical and imaging features associated with poor outcome (defined as not being discharged to home) in these 380 cases. Results-Among these 380 cases, only 68% were discharged home; the other 25% to inpatient rehabilitation, 4% to a skilled nursing facility, and 3% expired or were discharged to hospice. Patients with poor outcome were older, were more often Hispanic, had more vascular risk factors, and had higher median National Institutes of Health Stroke Scale. Imaging characteristics associated with poor outcomes included large or multifocal infarction and poor collaterals. In multivariable analysis, only age, initial National Institutes of Health Stroke Scale, and infarct location were independently associated with poor outcome. Conclusions-Approximately one third of patients deemed too good for intravenous tissue-type plasminogen activator are unable to be discharged directly to home. Given the current safety profile of intravenous tissue-type plasminogen activator, our results suggest that the concept of being too good to treat should be re-examined with an emphasis on the features associated with poor outcome identified in our study. If replicated, these findings could be incorporated into tissue-type plasminogen activator decision-making algorithms.

show abstract

mentioning

confidence: 99%

Baseline Predictors of Poor Outcome in Patients Too Good to Treat With Intravenous Thrombolysis

Ali

Siddiqui

et al. 2016

Stroke

View full text Add to dashboard Cite

show abstract

“…Thrombolytic therapy (eg, recombinant tissue plasminogen activator) to achieve early arterial recanalization is the only option currently available to treat ischemic stroke. But this therapy's time-dependent effect (within 3 h after the event) limits its clinical use to only 5% of candidate patients (1), and it carries an increased risk of intracranial hemorrhage, reperfusion injury, and diminishing cerebral artery reactivity (2)(3)(4)(5). Neuronal death and injury after cerebral ischemia involve pathological changes associated with necrosis and delayed apoptosis (6,7).…”

mentioning

confidence: 99%

Poststroke neuronal rescue and synaptogenesis mediated in vivo by protein kinase C in adult brains

Sun

Hongpaisan

Nelson

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

114

103

View full text Add to dashboard Cite

Global cerebral ischemia/hypoxia, as can occur during human stroke, damages brain neural networks and synaptic functions. The recently demonstrated protein kinase C (PKC) activation-induced synaptogenesis in rat hippocampus suggested the potential of PKC-mediated antiapoptosis and synaptogenesis during conditions of neurodegeneration. Consequently, we examined the effects of chronic bryostatin-1, a PKC activator, on the cerebral ischemia/hypoxia-induced impairment of synapses and neurotrophic activity in the hippocampal CA1 area and on hippocampus-dependent spatial learning and memory. Postischemic/hypoxic bryostatin-1 treatment effectively rescued ischemia-induced deficits in synaptogenesis, neurotrophic activity, and spatial learning and memory. These results highlight a neuroprotective signaling pathway, as well as a therapeutic strategy with an extended time window for reducing brain damage due to stroke by activating particular PKC isozymes.bryostatin ͉ ischemia ͉ neuroprotection ͉ protein kinase C ͉ rat T emporary or permanent restriction of cerebral blood flow and oxygen supply results in cerebral ischemia and ischemic stroke, the third-leading cause of death and the most common cause of long-term disability in developed countries. Thrombolytic therapy (eg, recombinant tissue plasminogen activator) to achieve early arterial recanalization is the only option currently available to treat ischemic stroke. But this therapy's time-dependent effect (within 3 h after the event) limits its clinical use to only 5% of candidate patients (1), and it carries an increased risk of intracranial hemorrhage, reperfusion injury, and diminishing cerebral artery reactivity (2-5). Neuronal death and injury after cerebral ischemia involve pathological changes associated with necrosis and delayed apoptosis (6, 7). Neurons in the infarction core of focal, severe stroke are immediately eliminated and cannot be saved once ischemia develops. The ischemic penumbra, (i.e, brain tissues surrounding the core in focal ischemic stroke) and the sensitive neurons/networks in global cerebral ischemia are still sustained by the diminished blood supply, however. Further damage in these ischemic brain tissues occurs in a delayed manner after cerebral ischemia/stroke (8-10), responsible for clinical deterioration. Thus, effective postischemic therapy with an extended time window remains one of the greatest challenges to modern medical practice.A consistent consequence of cerebral ischemia/hypoxia in humans and other mammals is central nervous system dysfunction, the nature of which depends on the location and extent of injury. It has been well established that global cerebral ischemia/hypoxia selectively injures or damages the pyramidal neurons in the dorsal hippocampal CA1 area (11-14), which are essential for episodic memory, providing a sensitive measure for monitoring ischemic damage and recovery functionally. Experimental cerebral ischemia is usually induced focally through, for example, occlusion of the middle cerebral artery, or globally...

show abstract

“…12 Among the estimated 30%-40% of patients who might be receiving IV tPA upon arrival to the treatment center, 16 only a significantly smaller proportion of acute ischemic stroke patients actually get the treatment. The reasons for exclusions among the patients who arrive within 3 hours of symptom onset are frequently avoidable 13,16,20,26 and include in-hospital delays. In our study, 31.3% of patients who presented within 3 hours from last seen well received IV thrombolysis.…”

Section: Resultsmentioning

confidence: 99%

Unsuspected coagulopathy rarely prevents IV thrombolysis in acute ischemic stroke

Rost¹,

Masrur²,

Pervez³

et al. 2009

Neurology

View full text Add to dashboard Cite

show abstract

Reasons for exclusion from thrombolytic therapy following acute ischemic stroke

Cited by 113 publications

References 7 publications

Baseline Predictors of Poor Outcome in Patients Too Good to Treat With Intravenous Thrombolysis

Baseline Predictors of Poor Outcome in Patients Too Good to Treat With Intravenous Thrombolysis

Poststroke neuronal rescue and synaptogenesis mediated in vivo by protein kinase C in adult brains

Unsuspected coagulopathy rarely prevents IV thrombolysis in acute ischemic stroke

Contact Info

Product

Resources

About