Correction
for
Hiro et al., J Am Coll Cardiol 52 (6) 500.
CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Takafumi Hiro, MD, PhD, FACC*,
Yusaku Fukumoto, MD, PhD,
Takashi Fujii, MD, PhD and
Masunori Matsuzaki, MD, PhD, FACC
* Division of Cardiology, Department of Medicine and Clinical Science, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami Kogushi, Ube, Yamaguchi, 755-8505, Japan (Email: thiro{at}yamaguchi-u.ac.jp).
First of all, we would like to express our deep appreciation for the sincere academic criticism of Dr. Hoeks and colleagues. Key points of their criticism were: 1) our study (1) did not answer the basic question whether local wall shear stress distribution is indeed related to plaque rupture; 2) we did not fully appreciate the influence of local blood pressure within a stenosis; and 3) the combination of high velocities due to lumen narrowing, the vasa vasorum, plaque composition and structure, and pressure wave reflection mainly contribute to plaque rupture. We do not have any critical arguments against their points.
Actually, we also had recognized the importance of such factors before our article was published. We previously reported the importance of in-plaque stress concentration in plaque rupture (2). The major driving force of plaque rupture is related to wall-distending pressure, tensile in-plaque stresses, inward pressure gradients, and inward bleeding. As they pointed out, we showed just a statistical relationship between local elevation of shear stress and future rupture point. However, the research of the direct cause-effect relationship between some local situations and plaque rupture is substantially difficult. The reasons are as follows: - 1 Because the prevalence of plaque rupture is relatively low (approximately 3% per year), a prospective study to clarify the direct trigger or predictor of plaque rupture is quite a long way off.
- 2 According to fracture mechanics, there are several kinds of material fracture. The initiation of some types of fracture, such as fatigue breakdown or time-dependent fracture, does not necessarily require great values of stress, which should overcome the strength of the material.
- 3 As Dr. Hoeks and colleagues suggested, there are quite a few factors that we have to consider as a determinant of plaque rupture. It has been documented that vulnerable plaques can frequently be observed in the nonculprit segments in patients with acute coronary syndrome. It is not yet fully understood in such cases how or why a particular plaque ruptured among many vulnerable plaques. Therefore, it can be speculated that plaque rupture is a rather stochastic phenomenon. If plaque rupture is not a deterministic process, a direct, single cause of plaque rupture might not exist.
Our study was not intended to clarify the main player in plaque rupture but rather to propose that shear stress, the value of which is very small, might not be a negligible factor in the initiation of plaque rupture or in the prediction of its future rupture point. We expect further thorough investigations of the plaque rupture mechanism.
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References
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1. Fukumoto Y, Hiro T, Fujii T, et al. Localized elevation of shear stress is related to coronary plaque rupture: a 3-dimensional intravascular ultrasound study with in-vivo color mapping of shear stress distribution J Am Coll Cardiol 2008;51:645-650.[Abstract/Free Full Text]2. Imoto K, Hiro T, Fujii T, et al. Longitudinal structural determinants of atherosclerotic plaque vulnerability: a computational analysis of stress distribution using vessel models and three-dimensional intravascular ultrasound imaging J Am Coll Cardiol 2005;46:1507-1515.[Abstract/Free Full Text]
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