Prognostic Value and Determinants of Ultraearly Angiographic Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Qureshi, Adnan I.; Sung, Gene; Suri, M A; Straw, Robert N.; Guterman, Lee R.; Hopkins, L N

doi:10.1097/00006123-199905000-00017

Cited by 69 publications

(47 citation statements)

References 33 publications

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“…The frequency of elevated MCA mBFV (38%) was substantially higher than that of admission angiographic vasospasm found in our study (7.5%) and in the literature (10–13%) [5, 6]. This discrepancy is most likely due to the fact that a MCA mBFV above the normal range (90 cm/s) was regarded as abnormal in our study, whereas higher cutoffs (ranging from 120 to 200 cm/s) have been shown to have the most precise correlation with large-vessel angiographic vasospasm [4, 8, 9].…”

Section: Discussioncontrasting

confidence: 62%

“…Whereas younger age and elevated WBC count were associated with acute-phase mBFV elevations in our study, poor clinical grade is the only consistently identified predictor of acute angiographic vasospasm [5, 6]. In one of these studies, angiographic vasospasm predicted subsequent symptomatic vasospasm [6].…”

Section: Discussionmentioning

confidence: 58%

“…Angiographic evidence of vasospasm detected within 48 h of aneurysm rupture occurs in 10–13% [5, 6] of the SAH patients. This acute angiographic vasospasm has been associated with symptomatic vasospasm, cerebral infarction and poor outcome [5, 6].…”

Section: Introductionmentioning

confidence: 99%

“…This acute angiographic vasospasm has been associated with symptomatic vasospasm, cerebral infarction and poor outcome [5, 6]. …”

Section: Introductionmentioning

confidence: 99%

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Transcranial Doppler Ultrasound in the Acute Phase of Aneurysmal Subarachnoid Hemorrhage

et al. 2009

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Background: Angiographic studies suggest that acute vasospasm within 48 h of aneurysmal subarachnoid hemorrhage (SAH) predicts symptomatic vasospasm. However, the value of transcranial Doppler within 48 h of SAH is unknown. Methods: We analyzed 199 patients who had at least 1 middle cerebral artery (MCA) transcranial Doppler examination within 48 h of SAH onset. Abnormal MCA mean blood flow velocity (mBFV) was defined as >90 cm/s. Delayed cerebral ischemia (DCI) was defined as clinical deterioration or radiological evidence of infarction due to vasospasm. Results: Seventy-six patients (38%) had an elevation of MCA mBFV >90 cm/s within 48 h of SAH onset. The predictors of elevated mBFV included younger age (OR = 0.97 per year of age, p = 0.002), admission angiographic vasospasm (OR = 5.4, p = 0.009) and elevated white blood cell count (OR = 1.1 per 1,000 white blood cells, p = 0.003). Patients with elevated mBFV were more likely to experience a 10 cm/s fall in velocity at the first follow-up than those with normal baseline velocities (24 vs. 10%, p < 0.01), suggestive of resolving spasm. DCI developed in 19% of the patients. An elevated admission mBFV >90 cm/s during the first 48 h (adjusted OR = 2.7, p = 0.007) and a poor clinical grade (Hunt-Hess score 4 or 5, OR = 3.2, p = 0.002) were associated with a significant increase in the risk of DCI. Conclusion: Early elevations of mBFV correlate with acute angiographic vasospasm and are associated with a significantly increased risk of DCI. Transcranial Doppler ultrasound may be an early useful tool to identify patients at higher risk to develop DCI after SAH.

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Section: Discussioncontrasting

confidence: 62%

Section: Discussionmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

“…This acute angiographic vasospasm has been associated with symptomatic vasospasm, cerebral infarction and poor outcome [5, 6]. …”

Section: Introductionmentioning

confidence: 99%

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Transcranial Doppler Ultrasound in the Acute Phase of Aneurysmal Subarachnoid Hemorrhage

et al. 2009

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“…It correlates with delayed cerebral infarction [4] and is a major source of morbidity and mortality of SAH patients [5]. Besides this ‘typical' form of cerebral vasospasm, there is also a so-called early angiographic vasospasm (EAVS) that can be visualized on admission angiography in about 1 out of 10 SAH patients [6,7]. …”

Section: Introductionmentioning

confidence: 99%

Early Vasospasm after Aneurysmal Subarachnoid Hemorrhage Predicts the Occurrence and Severity of Symptomatic Vasospasm and Delayed Cerebral Ischemia

Jabbarli¹,

Reinhard²,

Shah³

et al. 2016

Cerebrovasc Dis

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Background: Cerebral vasospasm usually develops several days after subarachnoid hemorrhage (SAH) and is generally acknowledged as a strong outcome predictor. In contrast, much less is known about the nature and eventual consequences of early angiographic vasospasm (EAVS) seen on admission digital subtraction angiography (DSA). Therefore, we aimed at identifying the risk factors and clinical impact of EAVS after SAH. Methods: Five hundred and thirty-one SAH patients with admission DSA performed within 72 h after the bleeding event were selected from a comprehensive database containing all consecutive SAH patients treated at our institution between January 2005 and December 2012. Predictors of EAVS, as well as associations between EAVS and delayed vasospasm-related complications, and unfavorable outcome (defined as modified Rankin scale >3) were evaluated in univariate and multivariate analyses. Results: EAVS was seen on 60 DSAs (11.3%) and was independently correlated with delayed symptomatic vasospasm requiring intra-arterial spasmolysis (OR 5.24, p < 0.0001), angioplasty (OR 2.56, p = 0.015) and repetitive endovascular treatment (OR 4.71, p < 0.0001). EAVS also increased the risk for multiple versus single territorial infarction on the follow-up CT scan(s) (OR 2.04, p = 0.047) and independently predicted unfavorable outcome (OR 2.93, p = 0.008). The presence of radiographic signs suspicious for fibromuscular dysplasia were independently associated with the occurrence of EAVS (OR 2.98, p = 0.026) and the need for repetitive endovascular vasospasm treatment (OR 3.95, p = 0.019). Conclusions: In view of the strong correlation with delayed symptomatic vasospasm and its ischemic complications, EAVS can be considered an alerting signal for severe symptomatic vasospasm. Therefore, more attention should be paid to the presence of EAVS on admission DSA.

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Ischemia triggered by spreading neuronal activation is induced by endothelin‐1 and hemoglobin in the subarachnoid space

Petzold

Einhäupl

Dirnagl

et al. 2003

Annals of Neurology

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Delayed cerebral vasospasm has a major impact on the outcome of subarachnoid hemorrhage. Two important candidates to cause the arterial spasm are the red blood cell product oxyhemoglobin and the vasoconstrictor endothelin-1, although oxyhemoglobin alone is not sufficient to induce cerebral ischemia and endothelin-1 leads to ischemia only at relatively high concentrations. In this study, we demonstrated that the combination of oxyhemoglobin and endothelin-1 triggered spreading neuronal activation in rat cortex in vivo. In contrast with the expected transient increase of regional cerebral blood flow during spreading depression, however, cerebral blood flow decreased profoundly and was long-lasting, paralleled by delayed repolarization of the steady (direct current) potential. These changes are characteristic of cortical spreading ischemia. Replacing oxyhemoglobin for the nitric oxide synthase inhibitor Nomega-nitro-L-arginine mimicked these effects, implicating nitric oxide scavenging functions of oxyhemoglobin. Furthermore, the effect of endothelin-1 was related to a reduction of Na(+)-/K(+)-ATPase activity rather than solely to its vasoconstrictive properties. In conclusion, the threshold concentration of endothelin-1 that induces cerebral ischemia is profoundly reduced via a complex interaction between the neuronal/astroglial network and the cortical microcirculation if nitric oxide availability declines. The results may have implications for the understanding of subarachnoid hemorrhage-related cortical lesions.

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Prognostic Value and Determinants of Ultraearly Angiographic Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Abstract: Our analysis suggests that patients with angiographic evidence of vasospasm at admission are at high risk for both symptomatic vasospasm and poor outcome. We also found that early surgery did not aggravate this risk.

Cited by 69 publications

References 33 publications

Transcranial Doppler Ultrasound in the Acute Phase of Aneurysmal Subarachnoid Hemorrhage

Transcranial Doppler Ultrasound in the Acute Phase of Aneurysmal Subarachnoid Hemorrhage

Early Vasospasm after Aneurysmal Subarachnoid Hemorrhage Predicts the Occurrence and Severity of Symptomatic Vasospasm and Delayed Cerebral Ischemia

Ischemia triggered by spreading neuronal activation is induced by endothelin‐1 and hemoglobin in the subarachnoid space

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