Arteriovenous Malformations (AVM) are a rare but potentially deadly tangle of blood vessels that can form in the brain.  Their cause is not completely understood but for some time now, scientists have suspected that there is a link between these formations and a specific protein called Vascular Endothelial Growth Factor (VEGF).   Dr. Robert Solomon, Head of the Department of Neurological Surgery, Dr. E. Sander Connolly, from the Cerebrovascular Center, and colleagues recently looked at levels of this protein in the blood of 13 patients treated for AVM and found a surprising trend.

AVMs are unpredictable and usually aren’t found until they become symptomatic.  Unfortunately this is often after they hemorrhage and require emergency brain surgery.   Researchers continue to look for clues that will lead to earlier detection and cure, among these is the possible link to VEGF.

VEGF is known to stimulate the formation of new blood vessels (angiogenesis) and under normal conditions this can be a good thing:  It helps our wounds heal,  increases blood supply to muscles when we exercise, and can bypass a blocked blood vessel.

VEGF can be triggered under abnormal conditions too and this is not so good, most notably when a tumor becomes metastatic.  A number of studies have also shown increased levels of the protein associated with AVMs.

Based on these studies Dr. Solomon, Dr. Connolly, and their team hypothesized that levels of VEGF would be higher in the blood of their patients with AVMs and that those levels would decrease after treatment.

They took samples from thirteen patients treated at Columbia University Medical Center right before surgery, 24 hours after, and then 30 days later.  They compared these results to a control group of 29 back surgery patients (without AVMs) who were treated at the same hospital.

The surprising result was that the patients with the AVM had lower levels of VEGF than the control group to begin with.  After surgery the level dropped even further and then over the course of the next 30 days the level of VEGF rose and became equal to that of the control group.

One hyposthesis for this confounding result is that the AVM itself acts as a VEGF “sink”, re-routing the circulating VEGF out of the blood stream and focusing it locally at the site of the AVM.  This is confirmed by a number of other studies that show higher local levels of the protein in  AVM tissue.

In any case, the researchers demonstrated that, though complicated, a relationship does exist between circulating levels of VEGF and the presence of AVM.  The exact cause and cure for AVM remains unsolved but this certainly offers an important clue.

To learn more see the authors’ study, Plasma Levels of Vascular Endothelial Growth Factor After Treatment for Cerebral Arteriovenous Malformations in the American Heart Association’s journal, Stroke