Cognitive and Functional Outcome After Out of Hospital Cardiac Arrest

Alexander, Michael P.; Lafleche, Ginette; Schnyer, David M.; Lim, Chun Soo; Verfaellie, Mieke

doi:10.1017/s1355617710001633

Cited by 63 publications

(70 citation statements)

References 21 publications

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“…Previous diabetes mellitus 41 (12) 59 (18) 19 (11) 25 (15) 16 (11) 23 (16) 17 (14) Bystander defibrillation, n (%) 34 (10) 34 (10) 24 (14) 23 (14) 17 (12) 19 (14 found, and further post hoc analyses showed a statistical significant difference between all patients with cardiac arrest and STEMI control subjects in Italy (Italy: 33°C/STEMI control subjects, P=0.01; 36°C/STEMI control subjects, P=0.003) but no statistical significant difference between the 2 temperature groups (Italy: 33°C/36°C, P=0.59). There were no significant differences found between any of the 3 groups in the other countries (P>0.30).…”

Section: Resultsmentioning

confidence: 99%

“…9,10 In a recent review, 30% to 50% of survivors after cardiac arrest were reported to suffer from cognitive impairment. 11 The generalizability of previous studies is poor because of small sample sizes, [12][13][14] missing data, 13,14 and patient selection, that is, the exclusion of those with a poor outcome, 14 inclusion of only patients with severe symptoms, 12 or absence of a nonarrest control group. 11 Optimally, OHCA survivors should be evaluated for the cognitive functions known to be most affected: memory, attention, and executive functions.…”

Section: Clinical Perspective On P 1349mentioning

confidence: 99%

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Cognitive Function in Survivors of Out-of-Hospital Cardiac Arrest After Target Temperature Management at 33°C Versus 36°C

et al. 2015

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Background— Target temperature management is recommended as a neuroprotective strategy after out-of-hospital cardiac arrest. Potential effects of different target temperatures on cognitive impairment commonly described in survivors have not been investigated sufficiently. The primary aim of this study was to evaluate whether a target temperature of 33°C compared with 36°C was favorable for cognitive function; the secondary aim was to describe cognitive impairment in cardiac arrest survivors in general. Methods and Results— Study sites included 652 cardiac arrest survivors originally randomized and stratified for site to temperature control at 33°C or 36°C within the Target Temperature Management trial. Survival until 180 days after the arrest was 52% (33°C, n=178/328; 36°C, n=164/324). Survivors were invited to a face-to-face follow-up, and 287 cardiac arrest survivors (33°C, n=148/36°C, n=139) were assessed with tests for memory (Rivermead Behavioural Memory Test), executive functions (Frontal Assessment Battery), and attention/mental speed (Symbol Digit Modalities Test). A control group of 119 matched patients hospitalized for acute ST-segment–elevation myocardial infarction without cardiac arrest performed the same assessments. Half of the cardiac arrest survivors had cognitive impairment, which was mostly mild. Cognitive outcome did not differ ( P >0.30) between the 2 temperature groups (33°C/36°C). Compared with control subjects with ST-segment–elevation myocardial infarction, attention/mental speed was more affected among cardiac arrest patients, but results for memory and executive functioning were similar. Conclusions— Cognitive function was comparable in survivors of out-of-hospital cardiac arrest when a temperature of 33°C and 36°C was targeted. Cognitive impairment detected in cardiac arrest survivors was also common in matched control subjects with ST-segment–elevation myocardial infarction not having had a cardiac arrest. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01946932.

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Section: Resultsmentioning

confidence: 99%

Section: Clinical Perspective On P 1349mentioning

confidence: 99%

Cognitive Function in Survivors of Out-of-Hospital Cardiac Arrest After Target Temperature Management at 33°C Versus 36°C

et al. 2015

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“…A third study illustrated cognitive differences between a control subject group and a patient group following outof-hospital arrest. Two-thirds of the patients showed mild deficits in memory and one-third showed more severe impairments in memory, psychomotor function, and other cognitive domains (Alexander et al, 2011). Newer studies have also explored novel tests that are not as specific and timeconsuming as a complete neurocognitive battery; these have been shown to be more sensitive than the MMSE or the CPC.…”

Section: Cognitive Function In Cardiac Arrest Survivorsmentioning

confidence: 99%

“…In recent practice, the two most common measures of cognitive function for resuscitated cardiac arrest patients have been the cerebral performance category (CPC) score and the mini-mental state examination (MMSE) (Moulaert et al, 2009;Alexander et al, 2011). Both tests provide healthcare providers with rapid yet nongranular diagnostic tools for potentially differentiating a spectrum of cognitive impairments.…”

Section: Introductionmentioning

confidence: 99%

Feasibility of Cognitive Functional Assessment in Cardiac Arrest Survivors Using an Abbreviated Laptop-Based Neurocognitive Battery

Iannacone

Leary²,

Esposito³

et al. 2014

Therapeutic Hypothermia and Temperature Management

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Cardiac arrest survivors exhibit varying degrees of neurological recovery even in the setting of targeted temperature management (TTM) use, ranging from severe impairments to making a seemingly full return to neurologic baseline function. We sought to explore the feasibility of utilizing a laptop-based neurocognitive battery to identify more subtle cognitive deficits in this population. In a convenience sample of cardiac arrest survivors discharged with a cerebral performance category (CPC) of 1, we evaluated the use of a computerized neurocognitive battery (CNB) in this group compared to a healthy control normative population. The CNB was designed to test 11 specific neurocognitive domains, including such areas as working memory and spatial processing. Testing was scored for both accuracy and speed. In a feasibility convenience sample of 29 cardiac arrest survivors, the mean age was 52.9 -16.7 years; 12 patients received postarrest TTM and 17 did not receive TTM. Patients tolerated the battery well and performed at normative levels for both accuracy and speed on most of the 11 domains, but showed reduced accuracy of working memory and speed of spatial memory with large magnitudes (>1 SD), even among those receiving TTM. Across all domains, including those using speed and accuracy, 7 of the 29 subjects (24%) achieved statistically significant scores lower from the normative population in two or more domains. In this population of CPC 1 cardiac arrest survivors, a sensitive neurocognitive battery was feasible and suggests that specific cognitive deficits can be detected compared to a normative population, despite CPC 1 designation. Such testing might allow improved measurement of outcomes following TTM interventions in future trials.

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“…1 Owing to the overall decrease in CBF after ischemia, neuronal cell death 1 can occur in major regions of the brain responsible for learning, memory, and cognitive function. 2 It is thought that during global ischemia, PKCd (a novel PKC) levels are elevated causing PKCd to translocate to the nucleus (activation) resulting in cellular damage. In the normal brain, PKCd levels are nominal whereas global ischemia can cause activation/translocation of PKCd.…”

Section: Introductionmentioning

confidence: 99%

Protein Kinase C Delta Modulates Endothelial Nitric Oxide Synthase after Cardiac Arrest

Lin

Gresia

Stradecki

et al. 2014

J Cereb Blood Flow Metab

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We previously showed that inhibition of protein kinase C delta (PKCd) improves brain perfusion 24 hours after asphyxial cardiac arrest (ACA) and confers neuroprotection in the cortex and CA1 region of the hippocampus 7 days after arrest. Therefore, in this study, we investigate the mechanism of action of PKCd-mediated hypoperfusion after ACA in the rat by using the two-photon laser scanning microscopy (TPLSM) to observe cortical cerebral blood flow (CBF) and laser Doppler flowmetry (LDF) detecting regional CBF in the presence/absence of dV1-1 (specific PKCd inhibitor), nitric oxide synthase (NOS) substrate (L-arginine, L-arg) and inhibitor (N o -Nitro-L-arginine, NLA), and nitric oxide (NO) donor (sodium nitroprusside, SNP). There was an increase in regional LDF and local (TPLSM) CBF in the presence of dV1-1 þ L-arg, but only an increase in regional CBF under dV1-1 þ SNP treatments. Systemic blood nitrite levels were measured 15 minutes and 24 hours after ACA. Nitrite levels were enhanced by pretreatment with dV1-1 30 minutes before ACA possibly attributable to enhanced endothelial NOS protein levels. Our results suggest that PKCd can modulate NO machinery in cerebral vasculature. Protein kinase C delta can depress endothelial NOS blunting CBF resulting in hypoperfusion, but can be reversed with dV1-1 improving brain perfusion, thus providing subsequent neuroprotection after ACA. Keywords: asphyxial cardiac arrest; middle cerebral artery occlusion; neuroprotection; palmitic acid methyl ester; stearic acid methyl ester INTRODUCTIONWe previously showed that inhibition of protein kinase C delta (PKCd) via dV1-1 can increase perfusion 24 hours after asphyxial cardiac arrest (ACA). Global cerebral ischemia (via ACA) causes derangement of cerebral blood flow (CBF) responsible for neuronal cell death in the CA1 region of the hippocampus as well as the cortex.1 Owing to the overall decrease in CBF after ischemia, neuronal cell death 1 can occur in major regions of the brain responsible for learning, memory, and cognitive function.2 It is thought that during global ischemia, PKCd (a novel PKC) levels are elevated causing PKCd to translocate to the nucleus (activation) resulting in cellular damage. In the normal brain, PKCd levels are nominal whereas global ischemia can cause activation/translocation of PKCd.3 Inhibition of PKCd (via specific inhibitor of PKCd, dV1-1) can cause a revival of CBF 24 hours after ischemia to counteract hypoperfusion or low CBF found to be suppressed after cardiac arrest from 38% to 65%. 1,4 We previously showed that pretreatment of dV1-1 before ACA can enhance perfusion 24 hours after ischemia, resulting in improved neuronal survival in the hippocampal CA1 and cortex regions in our rat model of ACA.1 Here, we sought out to define the specific mechanism(s) of how inhibition of PKCd can alleviate these pathologies. The possible endothelium and endothelial-mediated nitric oxide synthase (eNOS) involvement as a target for PKCd relating to general circulation was first reported by Monti et al.

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Cognitive and Functional Outcome After Out of Hospital Cardiac Arrest

Cited by 63 publications

References 21 publications

Cognitive Function in Survivors of Out-of-Hospital Cardiac Arrest After Target Temperature Management at 33°C Versus 36°C

Cognitive Function in Survivors of Out-of-Hospital Cardiac Arrest After Target Temperature Management at 33°C Versus 36°C

Feasibility of Cognitive Functional Assessment in Cardiac Arrest Survivors Using an Abbreviated Laptop-Based Neurocognitive Battery

Protein Kinase C Delta Modulates Endothelial Nitric Oxide Synthase after Cardiac Arrest

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