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.

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 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.

Development of a Quantitative Mechanical Test of Atherosclerotic Plaque Stability

2010 ◽  
Author(s):  
Ying Wang ◽  
Jinfeng Ning ◽  
Michael A. Sutton ◽  
Susan M. Lessner
Keyword(s):  
Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Mechanical Test ◽  
Coronary Thrombosis ◽  
Plaque Stability ◽  
Fibrous Cap ◽  
Clinical Observations ◽  
Poor Understanding ◽  
Atherosclerotic Plaque Rupture

Atherosclerotic plaque rupture is the main cause of myocardial infarction, coronary thrombosis and stroke. Current clinical observations suggest that an advanced plaque features a thin, collagen-rich fibrous cap infiltrated by macrophages, overlying a large lipid core rich in lipid-laden macrophages. However, due to relatively poor understanding of mechanisms associated with plaque rupture, there is no quantitative standard for plaque stability estimation.

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.

Computed Histological Quantification of Atherosclerotic Plaque Microcalcifications

Angiology ◽  
2020 ◽  
Vol 71 (10) ◽  
pp. 916-919
Author(s):  
John S. H. Danial ◽  
Fabronia Murad ◽  
Ana-J Garcia Saez ◽  
Magdy R. Moawad ◽  
Giovanni S. Urrico ◽  
...  
Keyword(s):  
Spatial Resolution ◽  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Clinical Importance ◽  
Microscopic Analysis ◽  
Fibrous Cap ◽  
Accurate Definition ◽  
Atherosclerotic Plaque Formation ◽  
Definition Of

Inflammation has a central role in atherosclerotic plaque formation and rupture. Intense macrophage inflammatory activity results in microcalcifications which are strongly associated with plaque vulnerability. Microcalcifications with specific critical size between 5 and 65 μ, located in the fibrous cap producing local mechanical stress on the plaque surface and may directly contribute to plaque rupture. Hence, accurate assessment of microcalcifications size and dimension has significant clinical importance. Current invasive and noninvasive plaque imaging has limited spatial resolution which limits accurate definition of microcalcifications in the atherosclerotic plaques. We describe a new imaging technique with high spatial resolution, based on confocal microscopic analysis, using a dedicated software which allows automatic characterization of microcalcifications and quantitative assessment of their extent and localization.

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