Author + information
- Michael Koutouzis, MD and
- Zenon S. Kyriakides, MD, PhD⁎ ()
- ↵⁎Director, B Cardiology Department, Red Cross Hospital, 1 Red Cross Str., Athens 115 26, Greece
We have read with great interest the article by Kolodgie et al. (1) focusing on elimination of intraplaque angiogenesis. It seems that neovascularization within the vessel wall plays an important role in plaque destabilization, and it is a determinant of vulnerability.
The beneficial effect of statins in patients with atherosclerotic disease is well established. This effect goes beyond lipid lowering, because statins also have other effects, which is why statins are considered pleiotropic. One of these is its effect on angiogenesis. We recently presented that patients on statin treatment have reduced intraplaque angiogenesis in their carotid endarterectomy specimens when compared with patients not receiving this kind of drug (2). This finding provides a new insight to the statins’ pathophysiologic mechanism of action. The fact that it was a cross-sectional, retrospective study without randomization cannot lead us to any causal conclusions about statins and intraplaque angiogenesis. However, there are strong indications favoring that hypothesis. Vascular endothelial growth factor is a well-recognized and potent angiogenetic factor. It is known that pravastatin, but also fenofibrate, reduces vascular endothelial growth factor plasma levels in humans (3).
These findings raise the question of whether statins are the antiangiogenetic factor for which we are searching. To answer this question, further investigation is needed, and maybe it is time for a randomized trial with standard dose and duration of treatment to test the effect on intraplaque angiogenesis.
- American College of Cardiology Foundation