Cyclic Bending of Coronary Plaques Leads to Much Higher Stress Variations: A Major Factor Contributing to Plaque Rupture Risk

Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Shunichi Kobayashi ◽  
Gregorio A. Sicard ◽  
...  

Mechanical forces play an important role in the complicated process of atherosclerotic plaque rupture which often leads to serious clinical events such as stroke and heart attack [4]. Factors causing the vulnerable plaque cap to fracture are important clinically [2–7]. It is known that coronary plaques are more likely to rupture compared to carotid plaques under comparable conditions (such as stenosis severity at about 50% by diameter). One possible reason is that coronary arteries are under cyclic bending caused by heart motions and compressions. We hypothesize that cyclic bending of coronary atherosclerotic plaques may be a major contributor to critical stress variations in the plaque leading to increased plaque rupture risk. We have developed MRI-based 3D multi-component models with fluid-structure interactions (FSI) in order to perform flow and stress/strain analysis for atherosclerotic plaques and identify possible mechanical and morphological indices for accurate plaque vulnerability assessment [6–7].

2005 ◽  
Vol 127 (7) ◽  
pp. 1185-1194 ◽  
Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Pamela K. Woodard ◽  
Jeffrey E. Saffitz ◽  
...  

Background: Atherosclerotic plaques may rupture without warning and cause acute cardiovascular syndromes such as heart attack and stroke. Methods to assess plaque vulnerability noninvasively and predict possible plaque rupture are urgently needed. Method: MRI-based three-dimensional unsteady models for human atherosclerotic plaques with multi-component plaque structure and fluid-structure interactions are introduced to perform mechanical analysis for human atherosclerotic plaques. Results: Stress variations on critical sites such as a thin cap in the plaque can be 300% higher than that at other normal sites. Large calcification block considerably changes stress/strain distributions. Stiffness variations of plaque components (50% reduction or 100% increase) may affect maximal stress values by 20–50 %. Plaque cap erosion causes almost no change on maximal stress level at the cap, but leads to 50% increase in maximal strain value. Conclusions: Effects caused by atherosclerotic plaque structure, cap thickness and erosion, material properties, and pulsating pressure conditions on stress/strain distributions in the plaque are quantified by extensive computational case studies and parameter evaluations. Computational mechanical analysis has good potential to improve accuracy of plaque vulnerability assessment.


2006 ◽  
Vol 06 (01) ◽  
pp. 35-38
Author(s):  
FRANCESCO SAIA ◽  
JOHANNES A. SCHAAR ◽  
FRITS MASTIK ◽  
CHRIS L. DE KORTE ◽  
SAMANTHA CORNACCHIA ◽  
...  

Acute coronary syndromes originate from atherosclerotic plaque rupture and subsequent developement of coronary thrombosis. Available screening and diagnostic methods are insufficient to identify the atherosclerotic plaques that will rupture and precipitate the coronary event. We developed a new intracoronary diagnostic method based on intravascular ultrasound (IVUS) examination to evaluate the local mechanical properties of atherosclerotic plaques namely IVUS-elastography/palpography. The relationships between local strain, histological features of vulnerability, clinical presentation, and clinical markers of instability were assessed.


2004 ◽  
Vol 126 (3) ◽  
pp. 363-370 ◽  
Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Shunichi Kobayashi ◽  
David N. Ku

Nonlinear 3-D models with fluid-structure interactions (FSI) based on in vitro experiments are introduced and solved by ADINA to perform flow and stress/strain analysis for stenotic arteries with lipid cores. Navier-Stokes equations are used as the governing equations for the fluid. Hyperelastic Mooney-Rivlin models are used for both the arteries and lipid cores. Our results indicate that critical plaque stress/strain conditions are affected considerably by stenosis severity, eccentricity, lipid pool size, shape and position, plaque cap thickness, axial stretch, pressure, and fluid-structure interactions, and may be used for possible plaque rupture predictions.


2021 ◽  
Vol 8 ◽  
Author(s):  
Ching Chee Law ◽  
Rajesh Puranik ◽  
Jingchun Fan ◽  
Jian Fei ◽  
Brett D. Hambly ◽  
...  

Atherosclerosis, which is a primary cause of cardiovascular disease (CVD) deaths around the world, is a chronic inflammatory disease that is characterised by the accumulation of lipid plaques in the arterial wall, triggering inflammation that is regulated by cytokines/chemokines that mediate innate and adaptive immunity. This review focuses on IL-32, -34 and -37 in the stable vs. unstable plaques from atherosclerotic patients. Dysregulation of the novel cytokines IL-32, -34 and -37 has been discovered in atherosclerotic plaques. IL-32 and -34 are pro-atherogenic and associated with an unstable plaque phenotype; whereas IL-37 is anti-atherogenic and maintains plaque stability. It is speculated that these cytokines may contribute to the explanation for the increased occurrence of atherosclerotic plaque rupture seen in patients with COVID-19 infection. Understanding the roles of these cytokines in atherogenesis may provide future therapeutic perspectives, both in the management of unstable plaque and acute coronary syndrome, and may contribute to our understanding of the COVID-19 cytokine storm.


2014 ◽  
Vol 42 (2) ◽  
pp. 443-449 ◽  
Author(s):  
Nordin M.J. Hanssen ◽  
Coen D.A. Stehouwer ◽  
Casper G. Schalkwijk

Cardiovascular disease, caused predominantly by atherosclerotic plaque rupture, remains one of the leading causes of death. However, the mechanism of plaque rupture remains largely unknown. Recent studies have linked high metabolic activity in inflamed atherosclerotic plaques to the development of plaque rupture. AGEs (advanced glycation end-products) are known to be formed as a result of high metabolic activity and are higher in rupture-prone than stable plaques. Furthermore, AGEs seem to be more than mere markers of metabolic activity, as recent studies have elucidated that AGEs and their major precursor, MG (methylglyoxal), may have an important role in the progression of atherosclerosis and plaque rupture. MG can be detoxified by Glo1 (glyoxalase I), thereby preventing the accumulation of MG and MG-derived AGEs. In the present review, data concerning MG, Glo1 and AGEs in the context of plaque phenotype are discussed.


2021 ◽  
Author(s):  
Zhuowen Yang ◽  
Jianting Yao ◽  
Jianxin Wang ◽  
Cong Zhang ◽  
Yang Cao ◽  
...  

Pathological angiogenesis is a critical contributor to atherosclerotic plaque rupture. However, there are few effective theranostic strategies to stabilize plaques by suppressing neovascularization. A polymeric nanosystem using 3 nm manganese...


2019 ◽  
Vol 5 (1 (P)) ◽  
pp. 43
Author(s):  
Erwinanto Erwinanto

Atherosclerotic plaque rupture is closely related to acute coronary syndromes.Stabilization of atherosclerotic plaque which slashes plaque rupture is as importantas regression ofplaque size for reducing cardiovascular events. Dyslipidemia therapy targeting to decrease LDL cholesterol reduces cardiovascular events such as acute myocard infarct, stroke, and death which are suggested to be the result of plaque stabilization. Dyslipidemia therapy also regress atherosclerotic plaque into a smaller volume. Plaque regression improves coronary flow responsible for the reduction of myocardial infarction incidence in patients with coronary heart disease (CHD).This paper consists of two parts. The first part discusses the evidence of cardiovascular event reduction with statin. The second part describes dyslipidemia management based on the 2017 Indonesian Heart Association (PERKI) Guideline on the Management of Dyslipidemia


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