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.

scholarly journals Applicability of Recent Dyslipidemia Guidelines in Clinical Practice

2019 ◽  
Vol 5 (1 (P)) ◽  
pp. 43
Author(s):  
Erwinanto Erwinanto
Keyword(s):  
Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Coronary Flow ◽  
Cardiovascular Events ◽  
Ldl Cholesterol ◽  
Plaque Rupture ◽  
Heart Association ◽  
Plaque Stabilization ◽  
Plaque Regression ◽  
Atherosclerotic Plaque Rupture

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

scholarly journals Cocaine-Associated Myocardial Infarction: Should They All Be Stented?

2011 ◽  
Vol 2011 ◽  
pp. 1-2 ◽  
Author(s):  
Sazzli Kasim ◽  
Ronan O'Donabhain ◽  
Eugene Mcfadden
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Platelet Activation ◽  
Atherosclerotic Plaque ◽  
Acute Coronary Syndromes ◽  
Plaque Rupture ◽  
Coronary Syndromes ◽  
Atherosclerotic Plaque Rupture ◽  
Catheterization Procedure

Cocaine use is a known cause of chest pain and acute myocardial infarction and frequently leads to cardiac catheterization procedure. The treatment of cocaine-related acute coronary syndromes presents unique challenges because a variety of mechanisms including atherosclerotic plaque rupture, platelet activation, and coronary vasospasm may contribute to the pathogenesis. Our case highlights important considerations taken in dealing with this acute scenario

Abstract 128: Serum Anti-MAA Antibody Titers are Associated with Acute Myocardial Infarction and MMP-9

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Faisal Ahmed ◽  
Michael J Duryee ◽  
Scott W Shurmur ◽  
Michael D Johnston ◽  
Carlos D Hunter ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Inflammatory Responses ◽  
Plaque Rupture ◽  
Protein Antigens ◽  
Serum Samples ◽  
Antibody Isotypes ◽  
Antibody Titers ◽  
Atherosclerotic Plaque Rupture

Introduction Atherosclerotic plaque rupture is the leading cause of acute myocardial infarction (AMI). Malondialdehyde acetaldehyde (MAA) modified proteins have recently been implicated in this process by their ability to initiate inflammatory responses. Matrix metalloproteinase 9 (MMP-9) is increased following AMI and has been associated with the disease due to its ability to degrade the fibrotic cap that forms on some plaques. Objective The purpose of this study was to evaluate the relationship between MMP-9 and anti-MAA antibody isotypes in patients experiencing acute myocardial infarction (AMI). Methods Serum samples from AMI patients (n=10) were collected and tested for the presence of anti-MAA antibody isotypes, peak CK, peak troponin, and MMP-9 levels. Samples were collected at the time of AMI, 24 and 48 hours post event. Data was correlated to determine relationships with antibody isotypes directed against MAA protein antigens. Results MMP-9 increased significantly from the initial presentation at 24 hours post-AMI (p=0.006) and 48 hours post-AMI (p= 0.044). Anti-MAA IgM decreased significantly (p= 0.021) between initial and 24 hours post AMI. A similar significant decrease was observed for anti-MAA IgG (p= 0.006). Anti-MAA IgA levels did not change significantly post-AMI. Significant correlations were demonstrated between peak CK and anti-MAA IgG 24 hours post AMI (r= -0.819, p= 0.013), between peak troponin and anti-MAA IgG 24 hours post AMI (r= -0.860, p= 0.006) and between MMP-9 levels 24 hours post AMI and anti-MAA IgM levels 24 hours post MI ( r= 0.0712, p=0.021). Conclusions The negative correlation of anti-MAA IgG to cardiac enzymes is suggestive that myocardial infarction and tissue necrosis results in the release of the MAA antigen from infarcted myocardium and clearance of anti-MAA antibodies. Additionally, anti-MAA IgM and MMP-9 are positively correlated with each other 24 hours post-AMI, suggesting that anti-MAA IgM titers may correlate to the severity of the AMI and thus CAD. Implications Anti-MAA antibodies might serve as important biomarkers of impending atherosclerotic plaque rupture and subsequent AMI and warrants further investigation in a larger cohort of patients.

Adhesive Strength of Atherosclerotic Plaques Depends on Collagen Content

2012 ◽  
Author(s):  
Ying Wang ◽  
John A. Johnson ◽  
Abigail Fulp ◽  
Michael A. Sutton ◽  
Susan M. Lessner
Keyword(s):  
Energy Release Rate ◽  
Energy Release ◽  
Atherosclerotic Plaque ◽  
Release Rate ◽  
Adhesive Strength ◽  
Plaque Rupture ◽  
Mechanical Test ◽  
Coronary Thrombosis ◽  
Local Energy ◽  
Plaque Composition

Atherosclerotic plaque rupture is a major cause of myocardial infarction, coronary thrombosis and stroke. In a previous study, we proposed a new plaque rupture mechanism, plaque separation at the shoulder, and developed a novel quantitative mechanical test to measure the adhesive strength between the atherosclerotic plaque and the underlying vascular wall in mouse models using the local energy release rate, G, as a quantifiable metric for direct comparison of plaque separation strengths (1). We have now investigated structure-function relationships between the local energy release rate and local plaque composition. We hypothesize that adhesive strength varies with plaque composition in mice of different genotypes, and that it correlates with collagen deposition and macrophage content in lesions. Mice which are genetically deficient in matrix metalloproteinase 12 (MMP12), have previously been shown to demonstrate altered lesion composition (2). Therefore, we used apoE knockout (KO) and apoE MMP-12 double knockout (DKO) mice for our experiments and expected to see a difference in local energy release rates between strains.

Abstract 16294: A Case of Paradoxical Coronary Embolism in a Patient With Undiagnosed Malignancy

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Anh Do ◽  
Lindsey Aurora ◽  
MOHAMMAD ZAIDAN
Keyword(s):  
Myocardial Infarction ◽  
Lower Extremity ◽  
Atherosclerotic Plaque ◽  
Residual Disease ◽  
Plaque Rupture ◽  
Epigastric Pain ◽  
Case Reports ◽  
History Of ◽  
Coronary Embolism ◽  
Atherosclerotic Plaque Rupture

Introduction: Coronary embolism is a rare cause of acute myocardial infarction (AMI) in comparison with atherosclerotic plaque rupture. We present a case of an inferior ST elevation myocardial infarction caused by coronary embolism. The source was thought to be from the combination of deep vein thrombosis (DVT) and patent foramen ovale (PFO), accounting for a unique presentation and pathophysiology. Case: An 86-year-old female with a history of hypertension, non-small cell lung cancer status post resection with no residual disease, presented with a three-day history of epigastric discomfort, dyspnea on exertion and confusion. On presentation, she was afebrile with normal vital signs. Physical exam revealed epigastric pain on palpation. Initial labs were significant for high sensitivity troponin elevation to 9591 ng/L. ECG showed ST elevations in leads II, III, aVF. Coronary angiogram showed distal left anterior descending artery 71% stenosis and left posterior descending artery 99% stenosis. Given multiple distal locations concerning for coronary emboli, coronary angioplasty was done without stenting given no evidence of plaque rupture. After the angiogram, patient was found to have slurred speech and left sided facial droop. CT head showed multiple embolic infarcts. A transesophageal echocardiogram revealed a small PFO but no valvular vegetation/calcification or left atrial appendage thrombus. Lower extremity dopplers demonstrated lower extremity DVT. CT abdomen showed a pancreatic mass with hepatic metastasis, concerning for metastatic pancreatic adenocarcinoma. Patient was started on atorvastatin and aspirin only as AMI was due to a suspected embolic event. She received an IVC filter due to contraindication of anticoagulation in acute stroke and discharged to follow up with Oncology outpatient. Conclusions: In comparison to atherosclerotic plaque rupture, AMI as a result of an embolic coronary phenomena is rare. In fact, less than 1% of AMIs are caused by paradoxical embolism due to a PFO. There are many case reports about embolic AMI due to valvular vegetation or calcification. However, paradoxical coronary embolism due to PFO should be considered in patients with risk factors for a hypercoagulable state such as malignancy or DVT.

Ferrite-encapsulated nanoparticles with stable photothermal performance for multimodal imaging-guided atherosclerotic plaque neovascularization therapy

2021 ◽  
Author(s):  
Zhuowen Yang ◽  
Jianting Yao ◽  
Jianxin Wang ◽  
Cong Zhang ◽  
Yang Cao ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Multimodal Imaging ◽  
Plaque Rupture ◽  
Pathological Angiogenesis ◽  
Atherosclerotic Plaque Rupture ◽  
Encapsulated Nanoparticles

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...

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