To the Editor:
Percutaneous transluminal angioplasty (PTA) and stenting are increasingly used as an alternative to carotid endarterectomy (CEA) for patients with carotid stenosis. Cerebral hyperperfusion syndrome following CEA has been widely reported in the surgical literature. It is timely that interventionists increase their awareness of such a syndrome, as it can also happen after PTA. In the case reported by McCabe et al.,1 however, there was really no objective documentation of hyperperfusion. Moreover, the case was not heralded by or associated with any of the typical symptoms of hyperperfusion syndrome, such as unilateral headache or seizures.2
The Doppler findings of increased peak systolic and end-diastolic velocity over the stented internal carotid artery (ICA) are even more puzzling. The authors postulated that hyperperfusion may manifest as increased flow velocity in the ICA. Instead of increased blood flow, we suspect that the turbulence is caused by a sharp bend of the right ICA immediately above the stent (see Figure 3 of McCabe et al), significant residual stenosis, or spasm. It would help if the authors could state the Doppler findings of the left and right ICA before the stenting procedure. Even if the flow volume to the middle cerebral artery (MCA) is increased, it is hard to translate this into elevated flow velocity in the ICA, which is a large-caliber vessel at least 6 mm in diameter (3 to 4 times larger than the MCA in diameter and 9 to 16 times greater in cross-sectional area). In patients with the hyperperfusion syndrome, flow velocity in the MCA is increased by 2 to 3 times compared with that during baseline transcranial Doppler studies.3 4 Even if the MCA flow is increased 3 times, the flow in the ICA is only increased by a factor of 2/9 (Figure⇓). No studies on hyperperfusion syndrome, post-CEA seizures, or post-CEA intracranial hemorrhage had documented elevated flow velocity in the ICA.
In McCabe’s case, the patient was taking aspirin 300 mg daily and dipyridamole 200 mg twice daily. In addition, he was given 5000 U heparin injection during the procedure, followed by 1000 U/h as an infusion for 7 hours. In the context of a major CVA only 5 months previously and potentially further silent embolic events from the carotid lesion, it is possible that the intracranial hemorrhage was a spontaneous episode as a result of the aggressive anticoagulation and antiplatelet therapy. In addition, the normal activated partial thromboplastin time (APTT) at the time of neurological deterioration was unusual despite continuous IV heparin. We would like to know the activated clotting time or APTT results between stenting procedure and the acute deterioration to see whether there was any period of over-anticoagulation or the anticoagulation was inadequate throughout the procedure.
All in all, we think it was an interesting case report, but the title may more appropriately reflect the case if the word “reperfusion” is deleted.
- Copyright © 2000 by American Heart Association
McCabe DJH, Brown MM, Clifton A. Fatal cerebral reperfusion hemorrhage after carotid stenting. Stroke.. 1999;30:2483–2486.
Reigel MM, Hollier LH, Sundt TM Jr, Piepgras DG, Sharbrough FW, Cherry KJ. Cerebral hyperperfusion syndrome: a cause of neurologic dysfunction after carotid endarterectomy. Eur J Vasc Surg.. 1987;5:628–634.
Jorgensen LG, Schroeder TV. Defective cerebrovascular autoregulation after carotid endarterectomy. Eur J Vasc Surg.. 1993;7:370–379.
Jansen C, Sprengers AM, Moll FL, Vermeulen FE, Hamerlijnck RP, van Gijn J, Ackerstaff RG. Prediction of intracerebral haemorrhage after carotid endarterectomy by clinical criteria and intraoperative transcranial Doppler monitoring. Eur J Vasc Surg.. 1994;3:303–308.
We thank Drs Ho and Cheung for their interest in our case report. We disagree about the lack of objective evidence for hyperperfusion, since we documented an increase in velocity of flow on color Doppler ultrasound in the treated internal carotid artery, without significant stenosis or spasm. The fact that the intracerebral hemorrhage in our case was not heralded by or associated with any of the typical symptoms of the hyperperfusion syndrome emphasizes the importance of considering the diagnosis even if these features are not present. Ho and Cheung have suggested that the increased peak systolic and end-diastolic velocities in the ICA were caused by a sharp bend, stenosis, or spasm of the ICA immediately above the stent. These alternative explanations for the increased velocities were excluded by additional angiographic views of the left ICA taken at the time of the procedure, which were not published in the case report.R1 We regret that we cannot provide Ho and Cheung with the Doppler findings before treatment; this was not performed because the patient was referred to our center with the results of a digital subtraction angiogram. The calculations by Ho and Cheung of the relationship between flow in the ICA and the MCA are very interesting, but they assume that the diameter of the MCA remains unchanged, which is probably not correct. More importantly, they have assumed that all of the ICA flow is distributed to the ipsilateral MCA only. In fact, flow will be distributed between the MCA and the other branches of the circle of Willis, particularly if there is an abnormal increase in ipsilateral cerebral perfusion pressure. Using their own model, we have calculated that a doubling of the velocity of flow in the ICA, as recorded in our patient, distributed evenly between the MCA, anterior cerebral artery, and the anterior communicating artery would result in approximately a 3-fold increase in velocity in the MCA. This is entirely consistent with the figures recorded by transcranial Doppler in patients with the hyperperfusion syndrome.R2 We agree that antiplatelet and anticoagulant therapies could have contributed to the cerebral hemorrhage in our patient, but we discussed in our article the reasons that we favored hyperperfusion as the primary cause. The patient was not treated with an aggressive anticoagulant regimen, as suggested by Ho and Cheung, and the activated clotting time was not measured. In conclusion, we do not agree that “reperfusion” should be deleted from our title. However, further studies of carotid and transcranial Doppler ultrasound after carotid stenting are clearly warranted to improve our understanding of the mechanism of hyperperfusion injury in these patients.