Use of Quantitative Magnetic Resonance Angiography to Stratify Stroke Risk in Symptomatic Vertebrobasilar Disease
To the Editor:
The recent article by Amin-Hanjani and coworkers1 was interesting, but we believe that there are several flaws in their algorithmic approach. The authors erroneously conclude that distal blood flow reduction, especially in the basilar artery as demonstrated by phase contrast-quantified MRA (QMRA) and surrogate marker presence of distal atherosclerotic stenosis >50%, effectively allows stratification of patients with symptomatic vertebral basilar disease (VBD) into surgical and nonsurgical groups. We believe this is erroneous for several reasons.
Weintraub and Khoury2,3 previously reported that neck angulation, ie, hyperextension and rotational movements, induced mechanical compression of the proximal vertebral artery producing significant hemodynamic changes. By using QMRA, low flow, occlusion, and reversed flow were identified in a significant number of patients. Additionally, hypoplastic vertebral arteries were noted in 25% of the cohort, which was also statistically associated with higher incidence of posterior circulation stroke. Thus, symptomatic VBD can be significantly induced by neck positioning, yet this issue was never addressed in their algorithm. Of particular interest is that basilar artery flow reduction occurred in one third (33%) of the hypoplastic vertebral artery cohort compared with less than 20% of the nonhypoplastic vertebral artery cohort. The issue of hypoplastic vertebral arteries was not addressed by the authors. Sturzenegger and Newell4 feel that even a reversal of flow in the basilar artery is “irrelevant” provided that the perfusion pressure is sufficient.
It is also well known that atherosclerotic plaques by themselves may be an epiphenomena, and thus using this as a surrogate marker may be potentially erroneous.
There are many common causes leading to symptomatic VBD not addressed by the authors that would be of particular interest. It would be informative to know how many patients were female, how many had beauty parlor shampooing in the hyperextended position previous to diagnosis,5 as well as other significant factors of recent infection, performance of yoga, or neck exercises or chiropractic, and so on.
These comments are meant to be instructive in developing an effective flow algorithm of the entire vertebral basilar system. Risk stratification needs to be accurate and hopefully safe. The authors noted that 2 patients experienced stroke in the surgical cohort.
Amin-Hanjani S, Du X, Zhao M, Walsh R, Malisch TW, Charbel FT. Use of quantitative magnetic resonance angiography to stratify stroke risk in symptomatic vertebrobasilar disease. Stroke. 2005; 36: 1140–1145.
Weintraub MI, Khoury A. Critical neck positions as an independent risk factor for posterior circulation stroke: MR angiographic analysis. J Neurol Imaging. 1995; 5: 16–22.
Weintraub MI, Khoury A. Cerebral hemodynamic changes induced by simulated tracheal intubation: a possible role in perioperative stroke? Magnetic resonance angiography and flow analysis in 160 cases. Stroke. 1998; 29: 1644–1649.
We thank Drs Weintraub and Khoury for their interest and comments on our recent publication. To clarify, distal blood flow was the basis for our management algorithm. The presence of >50% stenocclusive symptomatic vertebrobasilar disease (VBD) was not a surrogate marker for stratification within this algorithm as the authors imply, but merely a description of the patient cohort studied with this algorithm. We examined this particular cohort of patients because they represent the population demonstrated to be at high risk of stroke1–3 and also most often referred and considered for intervention.
In regard to the hemodynamic changes that may occur with changes in neck position, we certainly agree, and it is well documented, that there are patients who develop vertebrobasilar insufficiency (VBI) as a result of mechanical compression.4 However, this population is not the patient cohort that formed the basis for the application of our algorithm. We do feel that the use of our algorithm may well extend to such patients, although we have not tested this in the appropriate population of patients with VBI induced by neck rotation or angulation. Measuring distal flow with the head positioned in the posture that tends to aggravate symptoms would certainly be a worthwhile prospective application of the algorithm. Documentation that low distal flow develops under those circumstances would be compelling evidence of mechanical compression as the underlying etiology.
The authors’ comment that the issue of hypoplastic vertebral arteries is not addressed is incorrect and reflects a misunderstanding of the underlying premise of our algorithm. Distal flow reflects the status of the proximal vessels. As such, the presence or absence of a hypoplastic artery and its consequences will be reflected in the distal flow measurement.
In regard to the comment that “there are many common causes to symptomatic VBD,” we would point out that this should more accurately read “there are many common causes to VBI”; symptomatic VBD in our publication is defined as symptoms in the setting of >50% atherosclerotic stenoocclusive disease and therefore does not have “many common causes.” As noted here, our article sought to address risk stratification in symptomatic VBD. We believe that risk stratification for patients with other causes of VBI will also be attainable with a flow-based algorithm and are hopeful that future work by ourselves and others will expand the use of flow-based clinical decision-making.
Prognosis of patients with symptomatic vertebral or basilar artery stenosis. The Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) study group. Stroke. 1998; 29: 1389–1392.
Qureshi AI, Ziai WC, Yahia AM, Mohammad Y, Sen S, Agarwal P, Zaidat OO, Suarez JI, Wityk RJ. Stroke-free survival and its determinants in patients with symptomatic vertebrobasilar stenosis: a multicenter study. Neurosurgery. 2003; 52: 1033–1039; discussion 1039–1040.
Moufarrij NA, Little JR, Furlan AJ, Leatherman JR, Williams GW. Basilar and distal vertebral artery stenosis: long-term follow-up. Stroke. 1986; 17: 938–942.
Kuether TA, Nesbit GM, Clark WM, Barnwell SL. Rotational vertebral artery occlusion: a mechanism of vertebrobasilar insufficiency. Neurosurgery. 1997; 41: 427–432; discussion 432–423.