Numerous triggers to atherosclerotic plaque rupture have been proposed in recent studies (Loree, Kamm et al. 1992). These include mechanisms such as shear stress injury, transient collapse of the stenosis, and rupture of the vasa vasorum, turbulent plaque injury and internal mechanical stress. Yet, the exact biomechanical mechanism of plaque rupture is not fully understood and requires an insight into the individual factors of plaque stability. It has been shown that morphological characteristics of the lesion and biomechanical stresses within the fibrous cap play an important role in determining plaque stability. the correlation between the degree of mechanical strain and the composition of an atherosclerotic plaque has not been fully explained [Rodriguez-Granillo et al. 2006, Huang, Virmani et al. 2001, Loree, Kamm et al. 1992].
This study is focus on the inflammatory activities, geometrical properties and biomechanical behavior of a vulnerable plaque in order to distinguish between stable and unstable lesions and thus improve the patient's risk assessment.
The primary endpoint is to develop a scientific model for the vulnerable plaque and a clinical methodology to characterize the stresses acting on a vulnerable thin-cap atheroma. The secondary endpoint is to develop a diagnostic tool for quantitative risk assessment, based on various geometric and biomechanical parameters and cytokine levels.
A better understanding of the pathophysiology of plaque vulnerability along with analysis of the biomechanical stresses might eventually lead to early detection of plaque rupture. The ability to identify plaque stability would add significant information and would allow better prediction of the risk for plaque rupture, which may be translated to medical actions and interventional therapeutic steps.
Virtual histology assessment is performed before catheterization with a commercially available system (VH-IVUS imaging system, Volcano Corp). A 20-MHz, 2.9F, mechanically rotating IVUS catheter will be advanced 10 mm distal to the culprit lesion under fluoroscopic guidance. Then, the IVUS catheter will withdraw, using an automated transducer pullback (0.5mm/sec), 10 mm proximal to the lesion. The IVUS gated acquisitions are recorded during transducer pullback and stored for offline analysis.
So far, we have analyzed ~50 native coronary segments with intermediate severity stenosis (50-70%) obtained from 30 patients.
In this study we analyze the tissue characterization and develop a diagnostic tool with the potential to detect unstable lesions before plaque rupture. This will possibly improve the definition of high-risk category. The geometrical analysis stage is intended to look at the geometrical properties of the lesion from different perspectives than those described in the literature so far. It consists of the definition of geometrical distribution of tissues in the plaque as well as the definition of new structural indices in the lesion.
Furthermore, we perform a three-dimensional reconstruction of a culprit lesion which provides a better comprehension of the plaque structure and tissue distribution along the diseased segment. In addition, it offers a superior basis for the stress distribution analysis within the lesion.
