Artikel
Alteration of the cerebral blood flow and volume of cerebrovascular territories in correlation with the angiographic vasospasm
Veränderungen des zerebralen Blutflusses und Volumens innerhalb von Gefäßterritorien in Korrelation mit dem angiographischen Vasospasmus
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Veröffentlicht: | 30. Mai 2008 |
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Gliederung
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Objective: A disturbed microcirculation may contribute to delayed ischemic neurological deterioration after subarachnoid hemorrhage (SAH). However, to what content these mechanisms worsen or attenuate the effects of a proximal cerebral vasospasm (CVS), is not well characterized so far. The aim of the present study was, therefore, to investigate the effect of proximal angiographic CVS on the regional cerebral blood flow (rCBF) and volume (rCBV) in patients after SAH.
Methods: 58 patients suffering from aneurysmal SAH were evaluated prospectively. Proximal CVS was determined by the percentage of diameter reduction of proximal vessels in the follow-up angiography (DSA) compared to the baseline DSA. Angiographic CVS was graded into the categories: none (control) (0%), mild (<33%), moderate (34–66%) and severe (>66%). Follow-up DSA was performed on day 7±3 after SAH. MRI including perfusion (PWI) and diffusion weighted imaging (DWI) was carried out within 24 hours of each DSA, respectively. rCBF and rCBV in the territory of the anterior (ACA), the middle cerebral artery (MCA) and the basal ganglia (BG) was determined and compared to the corresponding contralateral territory.
Results: Angiographic CVS was observed in 43 of 58 patients. Mild CVS occurred in 10, moderate in 20 and severe in 13 patients. rCBF was reduced in all 3 vascular territories depending on the degree of proximal CVS. Maximum reduction in severe CVS was observed in the BG (13±7 [ml/100 g/min] vs 42±11 (control, mean ± SD)). The diameter of the ACA was reduced from 32±8 (control) to 18±5 (severe CVS). However, in the MCA territory, a minor reduction in the rCBF from 45±11 (control) to 29±6 was seen. Therefore the rCBV in the MCA territory compared to the contralateral side increased to 124%, indicating a compensatory microvascular vasodilatation. In the ACA territory, the rCBV decreased to 75% and was unchanged in the BG (99% compared to the contralateral side).
Conclusions: The present data indicate unequal compensatory possibilities for the decrease in reduced CBF due to proximal CVS in different vascular territories. The results are further comparable with a, at lest in parts, conserved autoregulation in the MCA territory during proximal CVS, which may attenuate the vulnerability of this area compared to the ACA- and BG territory.