Postcarotid Endarterectomy Hyperfusion or Reperfusion Syndrome
To the Editor:
I read with great interest the study by Karapanayiotides et al.1 This study highlighted several important features of the hyperperfusion syndrome and raises several questions.
It is not entirely surprising that the middle cerebral artery mean flow velocities do not reliably predict the occurrence of the hyperperfusion syndrome. The relationship between velocity and volumetric flow is complex and not always predictable. As suggested, it is likely that volumetric flow may contribute to microvascular trauma. Furthermore, the relationship between the release of free radicals and metabolic products after reperfusion and their contribution to intracerebral endothelial dysfunction has not been studied adequately in this setting.
In addition, did the authors find any correlation between the degree of contralateral internal carotid artery stenosis and the risk of hyperperfusion syndrome? It would be interesting to determine whether the precarotid endarterectomy relative interhemispheric difference of cerebral blood flow predicted the hyperperfusion syndrome postcarotid endarterectomy.
Finally, in light of this complex process, the suggestion that “reperfusion syndrome” rather than “hyperperfusion syndrome” be used to describe this process may be appropriate.
Karapanayiotides T, Meuli R, Devuyst G, Piechowski-Jozwiak B, Dewarrat A, Ruchat P, Von Segesser L, Bogousslavsky J. Postcarotid endarterectomy hyperperfusion or reperfusion syndrome. Stroke. 2005; 36: 21–26.
We deeply appreciate Dr Dieter’s interest in our study. We agree with Dr Dieter’s statement that the relationship between velocity and volumetric flow is complex. However, in the case of patients undergoing carotid endarterectomy, this complexity has been elegantly demonstrated only once before.1 The authors concluded that for all pairs of measurement at a regional cerebral blood flow (CBF) of >20 mL/100 g per minute, there was little relationship between regional CBF and middle cerebral artery (MCA) mean flow velocity. Furthermore, postischemic hyperemia after the release of clamping was evident in measurements of mean velocity but not of regional CBF. Accordingly, in a case report studied with single-photon emission computed tomography,2 equally increased MCA mean flow velocities were found in the hyperperfused and the contralateral hemisphere. We believe that our data offer the stimulus for further research on the relationship between transcranial Doppler ultrasonography and other techniques of CBF measurement.
We also agree that the hemodynamic modifications observed after endarterectomy are coupled tightly to delicate neuroeffector mechanisms triggered after reperfusion,3 which amply merits investigation.
In our study, we cannot document any relationship between the degree of contralateral internal carotid artery stenosis and the risk of hyperperfusion syndrome because of the small number of patients. Among the patients who developed symptoms of hyperperfusion, only 1 had bilateral internal carotid artery stenosis >90%. This patient had initially undergone an uncomplicated right endarterectomy, and 1 week later, she underwent a left endarterectomy that was followed 5 days later by a massive intracerebral hemorrhage. This was the only patient who had abnormally increased MCA mean flow velocities ipsilateral to the endarterectomy site (and interestingly, contralateral to it), but most unfortunately, this patient was not studied with perfusion- or diffusion-weighted MRI. We also compared the mean relative interhemispheric difference of the MCA mean flow velocity between patients who developed hyperperfusion syndrome and those who did not and found no difference (27±11 versus 24±10; P=0.3; Mann–Whitney test). However, this analysis has limited value because of the small number of patients and the aforementioned limitations of transcranial Doppler ultrasonography to assess interhemispheric CBF differences over the cortical convexity.