Quality of Life and Healthcare Resource Use Associated With Angiographic Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Macdonald, R. Loch; Hunsche, Elke; Schüler, R.; Wlodarczyk, John; Mayer, Stephan A.

doi:10.1161/strokeaha.111.634071

Cited by 33 publications

(47 citation statements)

References 33 publications

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“…This association supports the notion that vasospasm and cerebral ischemia are significant contributors to early and late SAH-related morbidity. 18,22,26,28,29,31,42,43 It also suggests that maneuvers to avoid cerebral ischemia during hospitalization are critical in optimizing the capacity for continued long-term clinical improvement.…”

Section: Figmentioning

confidence: 99%

“…The pathogenesis of cerebral injury due to SAH is multifactorial and complex. Cerebral vasospasm, 18,31,42 hydrocephalus, 40 cortical spreading ischemia, 39 elevated intracranial pressure, 40 and cerebral metabolic dysfunction 34 have all been implicated in cerebral injury following aneurysm rupture. Our results suggest that in select patients, particularly younger patients with no radiographic evidence of large or eloquent stroke, the potential for delayed improvement is greatest.…”

Section: Figmentioning

confidence: 99%

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Time course of recovery following poor-grade SAH: the incidence of delayed improvement and implications for SAH outcome study design

Wilson¹,

Nakaji²,

Albuquerque³

et al. 2013

JNS

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Object Data regarding the time course of recovery after poor-grade subarachnoid hemorrhage (SAH) is lacking. Most SAH studies assess outcome at a single time point, often as early as 3 or 6 months following SAH. The authors hypothesized that recovery following poor-grade SAH is a dynamic process and that early outcomes may not always approximate long-term outcomes. To test this hypothesis, they analyzed long-term outcome data from a cohort of patients with poor-grade aneurysmal SAH to determine the incidence and predictors of early and delayed neurological improvement. Methods The authors reviewed outcome data from 88 poor-grade SAH patients enrolled in a prospective SAH treatment trial (the Barrow Ruptured Aneurysm Trial). They assessed modified Rankin Scale (mRS) scores at discharge, 6 months, 12 months, and 36 months after treatment to determine the incidence and predictors of neurological improvement during each interval. Results The mean aggregate mRS scores at 6 months (3.31 ± 2.1), 12 months (3.28 ± 2.2), and 36 months (3.17 ± 2.3) improved significantly compared with the mean score at hospital discharge (4.33 ± 1.3, p < 0.001), but they did not differ significantly among themselves. Between discharge and 6 months, 61% of patients improved on the mRS. The incidence of improvement between 6–12 months and 12–36 months was 18% and 19%, respectively. Hunt and Hess Grade IV versus V (OR 6.20, 95% CI 2.11–18.25, p < 0.001) and the absence of large (> 4 cm) (OR 2.76, 95% CI 1.02–7.55, p = 0.05) or eloquent (OR 5.17, 95% CI 1.89–14.10, p < 0.01) stroke were associated with improvement up to 6 months. Age ≤ 65 years (OR 5.56, 95% CI 1.17–26.42, p = 0.02), Hunt and Hess Grade IV versus V (OR 4.17, 95% CI 1.10–15.85, p = 0.03), and absence of a large (OR 8.97, 95% CI 2.65–30.40, p < 0.001) or eloquent (OR 4.54, 95% CI 1.46–14.08, p = 0.01) stroke were associated with improvement beyond 6 months. Improvement beyond 1 year was most strongly predicted by the absence of a large stroke (OR 7.62, 95% CI 1.55–37.30, p < 0.01). Conclusions A substantial minority of poor-grade SAH patients will experience delayed recovery beyond the point at which most studies assess outcome. Younger patients, those presenting in better clinical condition, and those without CT evidence of large or eloquent stroke demonstrated the highest capacity for delayed recovery.

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Section: Figmentioning

confidence: 99%

Section: Figmentioning

confidence: 99%

Time course of recovery following poor-grade SAH: the incidence of delayed improvement and implications for SAH outcome study design

Wilson¹,

Nakaji²,

Albuquerque³

et al. 2013

JNS

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“…20,25 Cerebral vasospasm is noted on angiography in as many as 70% of patients following aSAH and is predicted by high mean flow velocities (MFVs) on transcranial Doppler (TCD) ultrasonography. 19,24,26,35 Vasospasm is strongly associated with delayed cerebral ischemia (DCI) 12 and cerebral infarction, 11,39,49 although poor outcomes can still occur in its absence.…”

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confidence: 99%

Vasospasm on transcranial Doppler is predictive of delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis

Kumar¹,

Shahripour²,

Harrigan

2016

JNS

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100

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C erebral vasospasm is a major cause of poor outcomes in aneurysmal subarachnoid hemorrhage (aSAH), resulting in cerebral ischemia, infarction, disability, and death. 20,25 Cerebral vasospasm is noted on angiography in as many as 70% of patients following aSAH and is predicted by high mean flow velocities (MFVs) on transcranial Doppler (TCD) ultrasonography. 19,24,26,35 Vasospasm is strongly associated with delayed cerebral ischemia (DCI) 12 and cerebral infarction, 11,39,49 although poor outcomes can still occur in its absence. Of the current techniques available for diagnosing cerebral vasospasm, catheter angiography and CT angiography are invasive, and require contrast-dye injection and radiation exposure, and therefore do not allow dynamic monitoring of vasospasm. 31The radiation exposure and invasive nature of angiography implies that it is not useful for identifying subclinical vasospasm prior to the onset of the condition, and that its use is frequently restricted to confirm prevalent vasospasm abbreviatioNs aSAH = aneurysmal subarachnoid hemorrhage; CI = confidence interval; DCI = delayed cerebral ischemia; df = degrees of freedom; MFV = mean flow velocity; MWE = mean weighted estimate; NPV = negative predictive value; PPV = positive predictive value; TCD = transcranial Doppler. obJective The impact of transcranial Doppler (TCD) ultrasonography evidence of vasospasm on patient-centered clinical outcomes following aneurysmal subarachnoid hemorrhage (aSAH) is unknown. Vasospasm is known to lead to delayed cerebral ischemia (DCI) and poor outcomes. This systematic review and meta-analysis evaluates the predictive value of vasospasm on DCI, as diagnosed on TCD. methods MEDLINE, Scopus, the Cochrane trial register, and clinicaltrials.gov were searched through September 2014 using key words and the terms "subarachnoid hemorrhage," "aneurysm," "aneurysmal," "cerebral vasospasm," "vasospasm," "transcranial Doppler," and "TCD." Sensitivities, specificities, and positive and negative predictive values were pooled by a DerSimonian and Laird random-effects model. results Seventeen studies (n = 2870 patients) met inclusion criteria. The amount of variance attributable to heterogeneity was significant (I 2 > 50%) for all syntheses. No studies reported the impact of TCD evidence of vasospasm on functional outcome or mortality. TCD evidence of vasospasm was found to be highly predictive of DCI. Pooled estimates for TCD diagnosis of vasospasm (for DCI) were sensitivity 90% (95% confidence interval [CI] 77%-96%), specificity 71% (95% CI 51%-84%), positive predictive value 57% (95% CI 38%-71%), and negative predictive value 92% (95% CI 83%-96%). coNclusioNs TCD evidence of vasospasm is predictive of DCI with high accuracy. Although high sensitivity and negative predictive value make TCD an ideal monitoring device, it is not a mandated standard of care in aSAH due to the paucity of evidence on clinically relevant outcomes, despite recommendation by national guidelines. High-quality randomized trials evaluating the impact ...

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“…8,38 Additionally, the severity of the initial hemorrhage was a powerful factor affecting clinical outcomes, presumably due to brain injury with nonischemic mechanisms. 6,31 Macdonald et al 29 showed that clazosentan reduced mortality and vasospasm-related morbidity in subgroup analyses in patients with a poor WFNS grade (≥ III) and diffuse thick SAH. However, the majority of eligible patients in pooled analysis had a WFNS grade of I or II, and it is possible that the effect of clazosentan may be more pronounced in patients with more serious SAH.…”

Section: 30mentioning

confidence: 99%

“…18,50 Specifically, clazosentan is an endothelin receptor antagonist under investigation for the prevention of vasospasm and vasospasm-related morbidity. 3,4,8,24,[27][28][29][30]37,40,42,43,[45][46][47] Recently, a series of well-designed clinical trials was performed using clazosentan in patients with SAH. In a Phase IIa trial, clazosentan reduced moderate or severe angiographic vasospasm by 55% relative to placebo (p = 0.008).…”

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confidence: 99%

Dissociation of vasospasm-related morbidity and outcomes in patients with aneurysmal subarachnoid hemorrhage treated with clazosentan: a meta-analysis of randomized controlled trials

Shen¹,

Pan²,

Fan³

et al. 2013

JNS

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Object Clazosentan therapy after aneurysmal subarachnoid hemorrhage (SAH) has been found to be effective in reducing the incidence of vasospasm in randomized controlled trials. However, while vasospasm-related morbidity, including delayed ischemic neurological deficits (DINDs) and delayed cerebral infarctions, was consistently decreased, statistical significance was not demonstrated and outcomes were not affected by clazosentan treatment. The objective of this meta-analysis was to determine whether clazosentan treatment after aneurysmal SAH significantly reduced the incidence of DINDs and delayed cerebral infarctions and improved outcomes. Methods All randomized controlled trials investigating the effect of clazosentan were retrieved via searches with sensitive and specific terms. Six variables were abstracted after the assessment of the methodological quality of the trials. Analyses were performed following the method guidelines of the Cochrane Back Review Group. Results Four randomized, placebo-controlled trials met eligibility criteria, enrolling a total of 2181 patients. The meta-analysis demonstrated a significant decrease in the incidence of DINDs (relative risk [RR] 0.76 [95% CI 0.62–0.92]) and delayed cerebral infarction (RR 0.79 [95% CI 0.63–1.00]) in patients treated with clazosentan after aneurysmal SAH. However, this treatment regimen was not shown to outcomes including functional outcomes measured by Glasgow Outcome Scale-Extended (RR 1.12 [95% CI 0.96–1.30]) or mortality (RR 1.02 [95%CI 0.70–1.49]). Adverse events, including pulmonary complications, anemia, and hypotension, were all significantly increased in patients who received clazosentan therapy. Conclusions The results of the present meta-analysis show that treatment with clazosentan after aneurysmal SAH significantly reduced the incidence of the vasospasm-related DINDs and delayed cerebral infarctions, but did not improve poor neurological outcomes in patients with aneurysmal SAH. Further study is required to elucidate the dissociation between vasospasm-related morbidity and outcomes.

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Quality of Life and Healthcare Resource Use Associated With Angiographic Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Cited by 33 publications

References 33 publications

Time course of recovery following poor-grade SAH: the incidence of delayed improvement and implications for SAH outcome study design

Time course of recovery following poor-grade SAH: the incidence of delayed improvement and implications for SAH outcome study design

Vasospasm on transcranial Doppler is predictive of delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis

Dissociation of vasospasm-related morbidity and outcomes in patients with aneurysmal subarachnoid hemorrhage treated with clazosentan: a meta-analysis of randomized controlled trials

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