Histology-Based, Lesion-Specific Modeling of Stress Differences Between Plaque Rupture and Plaque Erosion

2011 ◽  
Author(s):  
Ian C. Campbell ◽  
Renu Virmani ◽  
John N. Oshinski ◽  
W. Robert Taylor
Keyword(s):  
Finite Element ◽  
Plaque Rupture ◽  
Solid Wall ◽  
Element Model ◽  
Blood Pool ◽  
Future Studies ◽  
Fibrous Cap ◽  
Plaque Disruption ◽  
Plaque Erosion ◽  
Specific Modeling

Plaque erosion is a cause of thrombosis wherein a thrombus forms over an atherosclerotic plaque without any disruption of the fibrous cap. This is in contrast to plaque rupture, traditionally considered the main cause of atherosclerosis-related thrombosis and frequently studied in biomechanics, wherein the fibrous cap becomes disrupted and exposes the lipid core of the plaque to the blood pool. Also unlike plaque rupture, plaque erosion has been observed to happen most frequently in women [1]. Despite identification, the cause of plaque erosion remains unknown and has been virtually unstudied from a biomechanical perspective. In this study, we employ a unique high-resolution, histology-based finite element model of solid wall stresses to investigate biomechanical differences between plaque rupture and plaque erosion. In future studies, this computed stress distribution can be correlated to expression of biomarkers related to the plaque disruption process in order to investigate the cause of plaque erosion.

Macrophage infiltrates in coronary plaque erosion portend a worse cardiovascular outcome in patients with acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R.A Montone ◽  
V Vetrugno ◽  
M Camilli ◽  
M Russo ◽  
M.G Del Buono ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Vulnerable Plaque ◽  
Cardiac Death ◽  
Cox Regression ◽  
Plaque Rupture ◽  
Culprit Lesion ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Plaque Erosion

Abstract Background Plaque erosion (PE) is responsible for at least one-third of acute coronary syndrome (ACS). Inflammatory activation is considered a key mechanism of plaque instability in patients with plaque rupture through the release of metalloproteinases and the inhibition of collagen synthesis that in turns lead to fibrous cap degradation. However, the clinical relevance of macrophage infiltration has never been investigated in patients with PE. Purpose In our study, we aimed at assessing the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) at the culprit site in ACS patients with PE, evaluating their clinical and OCT correlates, along with their prognostic value. Methods ACS patients undergoing OCT imaging and presenting PE as culprit lesion were retrospectively selected. Presence of MØI at culprit site and in non-culprit segments along the culprit vessel was assessed. The incidence of major adverse cardiac events (MACEs), defined as the composite of cardiac death, recurrent myocardial infarction and target vessel revascularization (TVR), was assessed [follow-up median (interquartile range, IQR) time 2.5 (2.03–2.58) years]. Results We included 153 patients [median age (IQR) 64 (53–75) years, 99 (64.7%) males]. Fifty-one (33.3%) patients presented PE with MØI and 102 (66.7%) PE without MØI. Patients having PE with MØI compared with PE patients without MØI had more vulnerable plaque features both at culprit site and at non-culprit segments. In particular, culprit lesion analysis demonstrated that patients with PE with MØI had a significantly thinner fibrous cap [median (IQR) 100 (60–120) μm vs. 160 (95–190) μm, p<0.001], higher prevalence of thrombus [41 (80.4%) vs. 64 (62.7%), p=0.028], lipid plaque [39 (76.5%) vs. 50 (49.0%), p<0.001], TCFA [20 (39.2%) vs. 14 (13.7%), p=0.001], and a higher maximum lipid arc [median [IQR] 250.0° (177.5°-290.0°) vs. 190.0° (150.0°-260.0°), p=0.018) at the culprit lesion compared with PE without MØI. MACEs were significantly more frequent in PE with MØI patients compared with PE without MØI [11 (21.6%) vs. 6 (5.9%), p=0.008], mainly driven by a higher risk of cardiac death and TVR. At multivariable Cox regression model, PE with MØI [HR=2.95, 95% CI (1.09–8.02), p=0.034] was an independent predictor of MACEs. Conclusion Our study demonstrates that among ACS patients with PE the presence of MØI at culprit lesion is associated with a more aggressive phenotype of coronary atherosclerosis with more vulnerable plaque features, along with a worse prognosis at a long-term follow-up. These findings are of the utmost importance in the era of precision medicine because clearly show that macrophage infiltrates may identify patients with a higher cardiovascular risk requiring more aggressive secondary prevention therapies and a closer clinical follow-up. Prognosis Funding Acknowledgement Type of funding source: None

Histology-Based, Lesion-Specific Modeling of Relative Stress Distributions Indicates Plaque Rupture Unlikely in Mice

2012 ◽  
Author(s):  
Ian C. Campbell ◽  
Daiana Weiss ◽  
Renu Virmani ◽  
Raymond P. Vito ◽  
John N. Oshinski ◽  
...  
Keyword(s):  
Finite Element ◽  
Spatial Distribution ◽  
Finite Element Modeling ◽  
Plaque Rupture ◽  
Modern World ◽  
Stress Distributions ◽  
Mechanical Environment ◽  
Relative Stress ◽  
Specific Modeling ◽  
Distribution Of Stresses

Despite decades of research, atherosclerosis remains one of the leading killers in the modern world. Consequently, the atherosclerosis-prone mouse is frequently employed to study the pathophysiology of atherogenesis. To date, no investigator has conclusively observed natural plaque rupture in these commonly-studied strains. A likely explanation for the lack of observation of plaque rupture is that mouse plaques are morphologically different than human plaques and that the consequence of this difference is a solid mechanical environment in the mouse that is unlike that of humans. To investigate this possibility, we used finite element modeling based on histology specimens of mouse and human plaques to examine the spatial distribution of stresses within the walls of plaques in each organism.

Strain Measurement in Coronary Arteries Using Intravascular Ultrasound and Deformable Images

2002 ◽  
Vol 124 (6) ◽  
pp. 734-741 ◽  
Author(s):  
Alexander I. Veress ◽  
Jeffrey A. Weiss ◽  
Grant T. Gullberg ◽  
D. Geoffrey Vince ◽  
Richard D. Rabbitt
Keyword(s):  
Finite Element ◽  
Intravascular Ultrasound ◽  
Coronary Arteries ◽  
Strain Distribution ◽  
Plaque Rupture ◽  
Element Model ◽  
Cross Sectional ◽  
Image Pairs

Atherosclerotic plaque rupture is responsible for the majority of myocardial infarctions and acute coronary syndromes. Rupture is initiated by mechanical failure of the plaque cap, and thus study of the deformation of the plaque in the artery can elucidate the events that lead to myocardial infarction. Intravascular ultrasound (IVUS) provides high resolution in vitro and in vivo cross-sectional images of blood vessels. To extract the deformation field from sequences of IVUS images, a registration process must be performed to correlate material points between image pairs. The objective of this study was to determine the efficacy of an image registration technique termed Warping to determine strains in plaques and coronary arteries from paired IVUS images representing two different states of deformation. The Warping technique uses pointwise differences in pixel intensities between image pairs to generate a distributed body force that acts to deform a finite element model. The strain distribution estimated by image-based Warping showed excellent agreement with a known forward finite element solution, representing the gold standard, from which the displaced image was created. The Warping technique had a low sensitivity to changes in material parameters or material model and had a low dependency on the noise present in the images. The Warping analysis was also able to produce accurate strain distributions when the constitutive model used for the Warping analysis and the forward analysis was different. The results of this study demonstrate that Warping in conjunction with in vivo IVUS imaging will determine the change in the strain distribution resulting from physiological loading and may be useful as a diagnostic tool for predicting the likelihood of plaque rupture through the determination of the relative stiffness of the plaque constituents.

scholarly journals 363 Old but fashioned: IVUS and chromaflo guidance for definition of thrombosis mechanism

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Gabriele Venturi ◽  
Roberto Scarsini ◽  
Gabriele Pesarini ◽  
Michele Pighi ◽  
Flavio Ribichini
Keyword(s):  
Plaque Rupture ◽  
Coronary Thrombosis ◽  
Daily Practice ◽  
Diagnostic Tools ◽  
High Definition ◽  
First Line ◽  
Fibrous Cap ◽  
Plaque Erosion ◽  
Definition Of ◽  
The Cost

Abstract Aims Plaque rupture and plaque erosion are the main causes of coronary thrombosis. While the first one involves fibrous cap disruption, the second one is caused by loss of endothelial continuity. In selected cases with evidence of plaque erosion, antithrombotic therapy without stenting has been suggested as a possible option. OCT is considered the gold standard for definition of thrombosis mechanism and has recently been included in algorithms for evaluation and management of patients with ACS. Also, high definition IVUS was compared with OCT in defining plaque erosion showing promising results. However, the cost and the large amount of contrast medium needed for OCT performance make these diagnostic tools of scarce applicability in daily practice. Methods and results We herein describe the case of a young man acceding to the Cath Lab with the diagnosis of NSTEMI. After baseline angiography and IVUS confirmed presence of Thrombus (Figure 1A and B), thromboaspiration was successfully performed (Figure 1D). The definition of thrombosis mechanism, revealing plaque rupture, was then performed with IVUS and ChromaFlo devices (Figure 1C and E). Also, IVUS was used to optimize stent implantation. Conclusions Although requiring further confirmations, we believe that in selected cases IVUS and ChromaFlo could provide a more applicable first-line diagnostic tool to define thrombosis mechanism. 363 Figure 1Baseline angiographic and IVUS evaluation confirming presence of coronary thrombus (A, B). After successful performance of thromboaspiration (D), plaque rupture was revealed by IVUS and ChromaFlo (C).

Plaque Rupture and Plaque Erosion

1999 ◽  
Vol 82 (S 01) ◽  
pp. 1-3 ◽  
Author(s):  
Allen P. Burke ◽  
Andrew Farb ◽  
Renu Virmani
Keyword(s):  
Risk Factors ◽  
Plaque Rupture ◽  
Coronary Thrombosis ◽  
Premenopausal Women ◽  
Matrix Degradation ◽  
Multiple Substrates ◽  
Fibrous Cap ◽  
Plaque Erosion ◽  
Elevated Cholesterol ◽  
Common Substrate

SummaryThere are multiple substrates for coronary thrombosis overlying an atherosclerotic plaque. The most common, plaque rupture, consists of an interruption of a thin fibrous cap overlying a lipid rich core. Plaque rupture is a result of macrophage infiltration and matrix degradation, is often seen in calcified plaques, and is highly associated with hypercholesterolemia. A less common substrate, plaque erosion, is not associated with elevated cholesterol and is the prime cause of coronary thrombosis in premenopausal women. The characteristic histologic features are abundant surface smooth muscle cells and proteoglycans, and a small or absent lipid rich core. The mechanisms of plaque erosion are unclear, and there are no consistent risk factors, although patients are often smokers.

scholarly journals Coronary plaque composition influences biomechanical stress and predicts plaque rupture in a morpho-mechanic OCT analysis

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Andrea Milzi ◽  
Enrico Domenico Lemma ◽  
Rosalia Dettori ◽  
Kathrin Burgmaier ◽  
Nikolaus Marx ◽  
...  
Keyword(s):  
Finite Element Analysis ◽  
Finite Element ◽  
Vessel Wall ◽  
Plaque Rupture ◽  
Area Under The Curve ◽  
Stress Concentrations ◽  
Element Analysis ◽  
Biomechanical Stress ◽  
Fibrous Cap ◽  
Maximal Stress

Plaque rupture occurs if stress within coronary lesions exceeds the protection exerted by the fibrous cap overlying the necrotic lipid core. However, very little is known about the biomechanical stress exerting this disrupting force. Employing optical coherence tomography (OCT), we generated plaque models and performed finite-element analysis to simulate stress distributions within the vessel wall in 10 ruptured and 10 non-ruptured lesions. In ruptured lesions, maximal stress within fibrous cap (peak cap stress [PCS]: 174 ± 67 vs. 52 ± 42 kPa, p<0.001) and vessel wall (maximal plaque stress [MPS]: 399 ± 233 vs. 90 ± 95 kPa, p=0.001) were significantly higher compared to non-ruptured plaques. Ruptures arose in the immediate proximity of maximal stress concentrations (angular distances: 21.8 ± 30.3° for PCS vs. 20.7 ± 23.7° for MPS); stress concentrations excellently predicted plaque rupture (area under the curve: 0.940 for PCS, 0.950 for MPS). This prediction of plaque rupture was superior to established vulnerability features such as fibrous cap thickness or macrophage infiltration. In conclusion, OCT-based finite-element analysis effectively assesses plaque biomechanics, which in turn predicts plaque rupture in patients. This highlights the importance of morpho-mechanic analysis assessing the disrupting effects of plaque stress.

scholarly journals Finite element head model for the crew injury assessment in a light armoured vehicle

2020 ◽  
Vol 22 (2) ◽  
Author(s):  
Michał Burkacki ◽  
Wojciech Wolański ◽  
Sławomir Suchoń ◽  
Kamil Joszko ◽  
Bożena Gzik-Zroska ◽  
...  
Keyword(s):  
Finite Element ◽  
Head Injury ◽  
Human Head ◽  
Element Model ◽  
Head Model ◽  
Dynamic Effects ◽  
Vehicle Model ◽  
Future Studies ◽  
Injury Assessment

Purpose: The aim of this paper was the development of a finite element model of the soldier’s head to assess injuries suffered by soldiers during blast under a light armoured vehicle. Methods: The application of a multibody wheeled armoured vehicle model, including the crew and their equipment, aenabled the researchers to analyse the most dangerous scenarios of the head injury. These scenarios have been selected for a detailed analysis using the finite element head model which allowed for the examination of dynamic effects on individual head structures. In this paper, the authors described stages of the development of the anatomical finite element head model. Results: The results of the simulations made it possible to assess parameters determining the head injury of the soldier during the IED explosion. The developed model allows the determination of the parameters of stress, strain and pressure acting on the structures of the human head. Conclusion: In future studies, the model will be used to carry out simulations which will improve the construction of the headgear in order to minimize the possibility of the head injury.

Microcalcification Acts as a Stress and Stretch Amplifier in the Coronary Atherosclerotic Plaque Affecting Its Vulnerability: An IVUS-Based Finite Element Study

2012 ◽  
Author(s):  
Yuan Huang ◽  
Wenkai Wang ◽  
Zhongzhao Teng ◽  
Daniel R. Obaid ◽  
Jing He ◽  
...  
Keyword(s):  
Finite Element ◽  
Plaque Rupture ◽  
High Stress ◽  
Material Strength ◽  
Stress Concentrations ◽  
Mortality And Morbidity ◽  
High Stress Concentration ◽  
Fibrous Cap ◽  
High Stress Level ◽  
Rupture Site

Atherosclerotic disease remains a leading cause of mortality and morbidity worldwide despite significant advances in its management (1). Atherosclerosis, characterized by plaque consisting a lipid-rich necrotic core encapsulated in a fibrous cap, may result in plaque rupture and subsequently cause acute ischaemic events such as myocardial infarction and stroke. Under physiological conditions, plaque is subjected to mechanical loading due to blood pressure and flow and rupture possibly occurs if these extra loadings exceed the material strength of the fibrous cap (2–4). This hypothesis has been indirectly validated by the combination of histological examination and finite element simulations that the rupture site often bears a high stress concentration either in carotid (3, 5, 6) or coronary (2) plaques. It has been noted that most rupture sites are located at the shoulder region (2), where the curvature is locally large (4) leading to a high stress level (7). However, the rupture site does not always coincide with the site where high stress concentrations appear and about thirty to forty percent of ruptures occur in the middle region where the calculated stress is relatively low (2, 8). This demonstrates the limitations of current approaches.

Abstract 12442: Hypercholesterolemia and Angiotensin II Induces Spontaneous Atherothrombotic Occlusion of balloon-injured Rabbit Iliac Arteries; Effects of Lipid-Lowering Therapies

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Katsuya Honda
Keyword(s):  
Animal Model ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Plaque Rupture ◽  
Oral Treatment ◽  
Lipid Lowering ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Plaque Erosion ◽  
First Time

Background: Atherothrombotic occlusion of a coronary artery with an intact fibrous cap is a major cause of acute coronary syndrome that is attributed to plaque erosion. We developed an animal model of spontaneous atherothrombotic occlusion of fibrous cap-intact arteries in rabbits. Methods and Results: We performed balloon injury in bilateral iliofemoral arteries in male Japanese white rabbits fed with high (2 %) cholesterol diet and infused with angiotensin II (50 ng/kg/min). Animals were divided into 3 groups; 1. no treatment, 2. Ezetimibe 0.6 mg/kg/day, and 3. Rosuvastatin 1.0 mg/kg/day. We examined the occurrence of atherothrombosis by high-resolution ultrasonograpy (Vevo2100) 3 times/week. (Fig. A) After the occurrence of acute thrombotic occlusion, the presence of thrombosis was confirmed by angiographic and histopathologic examination. Histochemical analysis in the atherothrombotic sites revealed; 1) no severe stenosis (% stenosis: 49±7), 2) no plaque rupture or lipid core, and 3) no PECAM1-positive endothelial layer. Interestingly, there were smooth muscle-like cells (αSMA+/SM1, SM2, SMemb and calponin-) with tissue factor expression at the neointima-thrombus interface. Oral treatment with Ezetimibe but not Rosuvastatin significantly reduced the incidence of atherothrombotic occlusion (Fig. B). Serum from the model rabbits induced TF in cultured rat smooth muscle cells. TF induction by serum from Ezetimibe-treated rabbits was significantly less compared with those from animals without treatment or with Rosuvastatin treatment (Fig. C). Conclusions: We established for the first time an appropriate animal model of spontaneous atherothromobotic occlusion in rabbits, which mimicked the pathological features of plaque erosion observed in human coronary arteries. This model may provide a clue to a mechanistic understanding and potential therapeutic approaches for plaque erosion.

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