Morphological and biomechanical aspects of vulnerable coronary plaque.
Vulnerable plaque morphology has been described by gross pathology and intravascular ultrasound, but morphological criteria cannot fully explain vulnerability, which involves four distinct factors: 1) inflammatory and biological processes; 2) geometry; 3) composition; and 4) hemodynamic stress. These last three aspects underlie the biomechanical study of vulnerable plaque. By virtue of the nature of their evolution, atherosclerotic plaques tend to be excentric, and this is a crucial morphological feature, causing circumferential stress to peak in very specific juxta-luminal locations, where it can exceed the rupture threshold of collagen, the basic constituent of arterial architecture. The lipido-necrotic core covered by a fibrous cap, formed in young plaques, is another morphological feature, which, can also increase and concentrate circumference stress in the juxta-luminal fibrous cap. The larger the lipid core, the thinner the fibrous cap and the greater is the stress. There are also inflammatory processes in such areas, which tend to reduce cap thickness. Ruptures occur when this thickness falls below 65 microns. Heart rate, blood pressure and pulse pressure are all biomechanical factors affecting vulnerable arterial walls, increasing circumferential stress and material fatigue. Vulnerable plaques are almost always associated with positive arterial remodeling. Numerical simulation has shown such so-called compensatory remodeling to be exclusively due to the healthy arc stretching in vulnerable plaques. Positive remodeling is optimal when the healthy arc is around 170 degrees, which keeps the lumen area relatively stable as long as the plaque does not exceed 40% to 50%. This mechanism does not apply to concentric plaques. In conclusion, the mechanism of vulnerable plaque rupture is highly complex and multifactorial. This complexity more or less precludes prediction in individual cases: we are in the realms of chaos theory and acute sensitivity to initial conditions. The greatest caution is therefore required in any attempt to predict rupture from diagnostic imagery, which provides only morphological data on plaque's nature.
Finet
G
G
Department of Hemodynamics and Interventional Cardiology, Hospices Civils de Lyon and Claude Bernard University, Lyon 1; INSERM Unit E886, 69394 Lyon, France. gerard.finet@creatis.univ-lyon1.fr
Ohayon
J
J
Rioufol
G
G
Lefloch
S
S
Tracqui
P
P
Dubreuil
O
O
Tabib
A
A
D001696:Biomechanical Phenomena; D001794:Blood Pressure / Q000502:physiology; D003324:Coronary Artery Disease / Q000473:pathology* / Q000503:physiopathology; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology; D005355:Fibrosis; D005544:Forecasting; D006339:Heart Rate / Q000502:physiology; D018056:Hemorheology; D006801:Humans; D007249:Inflammation; D008055:Lipids / Q000737:chemistry; D008955:Models, Cardiovascular; D009336:Necrosis; D017711:Nonlinear Dynamics; D011673:Pulsatile Flow / Q000502:physiology; D012422:Rupture, Spontaneous; D013314:Stress, Mechanical
D008055:Lipids