Author + information
- John Folts, PhD⁎ ()
- ↵⁎Department of Medicine, University of Wisconsin Medical School, H6/379 CSC Bx3248, 600 Highland Avenue, Madison, Wisconsin 53792.
We read with interest the paper by Doyle and Caplice in the May 29, 2007, issue of the Journal(1). They describe the importance of neovascularization in vulnerable plaque. We have a theory as to a mechanical mechanism for rupture of a vulnerable plaque (Fig. 1).With normal blood pressure and normal velocity through an artery (A) and normal lateral blood pressure in the vasa vasorum (B), the pressure in the vasa vasorum is equal to the lateral pressure in the artery (A). However, with a 30% to 40% narrowing due to plaque formation (B), the velocity (C) through the narrowed lumen (D) is increased. According to Bernouli’s Theorem, this increased velocity of blood produces a lower lateral blood pressure acting on the plaque (E). The pressure in the neovascularization in the plaque will be near that of the vasa vasorum and systemic pressure, thus a pressure gradient build up is created across the plaque that could rupture the plaque (E). Any increase in systemic pressure or increase in the narrowing of the lumen would further increase the velocity through the narrowed lumen (C). The pressure differential across the plaque would become even greater and be more likely to “blow the top” of the plaque. This plaque rupture mechanism would be another reason for actively trying to prevent transient increases in arterial blood pressure in patients with some coronary artery disease.
Many patients are known to have transient increases in arterial blood pressure caused by physical activity, anxiety, emotional excitement, and stress. A decrease in the arterial lumen can occur from vasospasm or intraplaque hemorrhage. Thus, there might be a variety of mechanisms that increase the velocity through the narrowed lumen leading to an increased pressure gradient across the plaque.
- American College of Cardiology Foundation