The Effect of Plaque Morphology on Cap Stresses in Coronary Arteries

2012 ◽  
Author(s):  
A. C. Akyildiz ◽  
L. Speelman ◽  
H. Nieuwstadt ◽  
R. Virmani ◽  
J. Wentzel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Sudden Death ◽  
Coronary Arteries ◽  
Atherosclerotic Plaque ◽  
Vessel Wall ◽  
Thrombus Formation ◽  
Plaque Formation ◽  
Plaque Morphology

Atherosclerosis is a cardiovascular disease characterized by plaque formation in the vessel wall. The region of an atherosclerotic plaque separating its pathological content from the lumen is called cap. Cap rupture initiates thrombus formation and may lead to myocardial infarction and sudden death [1].

Inflammatory cell recruitment in cardiovascular disease: murine models and potential clinical applications

2010 ◽  
Vol 118 (11) ◽  
pp. 641-655 ◽  
Author(s):  
Eileen McNeill ◽  
Keith M. Channon ◽  
David R. Greaves
Keyword(s):  
Cardiovascular Disease ◽  
Atherosclerotic Plaque ◽  
Critical Role ◽  
Disease Process ◽  
Pathological Process ◽  
Plaque Formation ◽  
Murine Models ◽  
Subsequent Transformation ◽  
Inflammatory Monocytes ◽  
Atherosclerotic Plaque Formation

Atherosclerosis is the pathological process that underlies the development of cardiovascular disease, a leading cause of mortality. Atherosclerotic plaque formation is driven by the recruitment of inflammatory monocytes into the artery wall, their differentiation into macrophages and the subsequent transformation of macrophages into cholesterol-laden foam cells. Models of hypercholesterolaemia such as the ApoE (apolipoprotein E)−/− mouse and the application of transgenic technologies have allowed us to undertake a thorough dissection of the cellular and molecular biology of the atherosclerotic disease process. Murine models have emphasized the central role of inflammation in atherogenesis and have been instrumental in the identification of adhesion molecules that support monocyte recruitment, scavenger receptors that facilitate cholesterol uptake by macrophages and other macrophage activation receptors. The study of mice deficient in multiple members of the chemokine family, and their receptors, has shown that chemokines play a critical role in promoting atherosclerotic plaque formation. In the present review, we will discuss novel therapeutic avenues for the treatment of cardiovascular disease that derive directly from our current understanding of atherogenesis gained in experimental animal models.

scholarly journals TCT-359 Atherosclerotic Plaque Formation Relates to Myocardial Bridging in Left Anterior Descending Coronary Arteries

2014 ◽  
Vol 64 (11) ◽  
pp. B104
Author(s):  
Shigemitsu Tanaka ◽  
Yuhei Kobayashi ◽  
Jennifer A. Tremmel ◽  
Ingela Schnittger ◽  
Paul Yock ◽  
...  
Keyword(s):  
Coronary Arteries ◽  
Atherosclerotic Plaque ◽  
Plaque Formation ◽  
Myocardial Bridging ◽  
Atherosclerotic Plaque Formation

Myocardial infarction associated with thrombus formation in non-culprit coronary arteries

2006 ◽  
Vol 23 (1) ◽  
pp. 73-75 ◽  
Author(s):  
Bilal Boztosun ◽  
Emre Gurel ◽  
Yilmaz Gunes ◽  
Ayhan Olcay
Keyword(s):  
Myocardial Infarction ◽  
Coronary Arteries ◽  
Thrombus Formation

scholarly journals Cardiac and coronary artery study on sudden death cases in Hospital Canselor Tuanku Muhriz

2021 ◽  
Vol 5 (10) ◽  
Author(s):  
Shih Sheng Soo ◽  
Siti Balkis Budin ◽  
Ismarulyusda Ishak ◽  
Faridah Mohd Nor ◽  
Nur Najmi Mohamad Anuar
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Sudden Death ◽  
Thrombus Formation ◽  
Arterial Occlusion ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Common Presentation ◽  
Acute Mi

Background: Sudden death (SD) is defined as an unexpected natural death within an hour onset of symptoms or unwitnessed death that occurs within 24 hours, which accounts for most cardiovascular deaths in Malaysia. This study aimed to evaluate the extent of histopathological changes in the heart and to study the demographic trend in SD cases in Kuala Lumpur, Malaysia. Methods: Specimens from all SD cases were received from 2017 to 2018 by the Forensic Unit, Hospital Canselor Tuanku Mukhriz (HCTM) were studied. The specimens were the left ventricular myocardium and left anterior descending artery (LAD), which were fixed in 10% formalin with haematoxylin and eosin staining. The tissues were graded histologically based on changes such as arterial occlusion, myocardial infarction, and/or thrombus formation. Results: Out of 545 medicolegal deaths, only 25 cases (4.6%) had samples available for analysis. Among these 25 patients, 24 (96%) were male patients and only one (4%) was a female patient. The available samples were from patients aged between 30 to 79 years old. In terms of ethinicity, Malays (40%) were the most numerous, followed by patients of Chinese and Indian ethnicities.The majority of the SD cases had a body mass index (BMI) that ranged between underweight (56%) and obese (40%). Besides, there were 10 (40%) cases of coronary artery with atheroma and 15 (60%) cases of myocardial infarction. The most common presentation of atherosclerosis was grade III and IV, and acute MI was the most common presentation at death, followed by healed infarcts and old infarcts. Discussion and Conclusion: Our findings reflect worsening risk factor levels in cardiovascular diseases, compounded by demographic trends. Further studies on biomarkers specific for cardiac diseases are warranted to understand imminent sudden cardiac death.

scholarly journals GPVI inhibition by glenzocimab synergistically inhibits atherosclerotic plaque-induced platelet activation when combined with conventional dual antiplatelet therapy

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
F O Alenazy ◽  
M H Harbi ◽  
D P Kavanagh ◽  
J Price ◽  
P Brady ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Animal Model ◽  
Platelet Aggregation ◽  
Platelet Activation ◽  
Atherosclerotic Plaque ◽  
Ex Vivo ◽  
Thrombus Formation ◽  
Microvascular Thrombosis ◽  
Antithrombotic Effects ◽  
St Elevation

Abstract Introduction Aspirin and a potent platelet P2Y12 inhibitor, such as prasugrel or ticagrelor, are not always sufficient to prevent thrombus formation in patients with ST-elevation MI (STEMI), leading to “slow flow” or “no reflow” effects after stenting. GPIIb/IIIa inhibitors, such as eptifibatide, may help in this setting, but are not used routinely due to their bleeding risk. GPVI has critical roles in thrombosis and a minimal role in haemostasis. Here we tested whether depletion of GPVI has effects on thrombus formation after MI in an animal model and investigated the effects of a novel platelet GPVI inhibitor, glenzocimab (a Fab fragment of a monoclonal antibody), on platelet activation and thrombus formation when combined with aspirin and ticagrelor. Methods We used intravital microscopy in a murine model of ST-elevation myocardial infarction and ischaemia-reperfusion injury to investigate microvascular thrombosis. We investigated the antithrombotic effects of adding glenzocimab (previously known as ACT017) to blood from healthy donors and 20 patients with ACS treated with aspirin and ticagrelor. We compared the effect of glenzocimab with the GPIIb/IIIa inhibitor eptifibatide ex-vivo. We stimulated platelets with collagen and atherosclerotic plaque material that was sourced from patients undergoing carotid endarterectomy. We investigated effects on platelet aggregation, spreading, signalling, adhesion, thrombin generation, thrombus formation and clot stability ex vivo. Results Genetic depletion of GPVI in an animal model of myocardial infarction reduced microvascular thrombosis. Ex vivo, aspirin and ticagrelor partially inhibited atherosclerotic plaque-induced platelet aggregation (assessed by multiple electrode aggregometry) by 48% compared to control (34±3 vs. 65±4 U; P<0.001; Figure 1). Atherosclerotic plaque-induced platelet aggregation, adhesion, secretion and activation were critically dependent on platelet GPVI activation and were potently inhibited by glenzocimab. Glenzocimab alone reduced atherosclerotic plaque-induced platelet aggregation by 75% compared to control (16±4 vs. 65±4 U; P<0.001; Figure 1) and by over 95% when combined with aspirin and ticagrelor (3±1 vs 65±4 U; P<0.001; Figure 1). Furthermore, glenzocimab provided multiple synergistic antithrombotic effects when added to the blood of aspirin and ticagrelor-treated patients with ACS ex vivo. Glenzocimab and the GPIIb/IIIa inhibitor, eptifibatide, had many similar antithrombotic effects but glenzocimab had less effect on mechanisms of general haemostasis compared to eptifibatide, as assessed by ROTEM (Figure 2). Conclusions The addition of glenzocimab to aspirin and ticagrelor provides synergistic inhibition of multiple critical mechanisms of atherothrombosis. Glenzocimab and the GPIIb/IIIa inhibitor, eptifibatide, share many similar antithrombotic effects, although glenzocimab has less impact on mechanisms involved in haemostasis compared to eptifibatide. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Academy of Medical Sciences UK Clinical Lecturer Starter GrantRoyal Embassy of Saudi Arabia

scholarly journals PROFIL PENYAKIT JANTUNG KORONER DI IRINA F JANTUNG RSUP PROF. Dr. R. D. KANDOU MANADO

e-CliniC ◽  
2013 ◽  
Vol 1 (1) ◽  
Author(s):  
Andi Eka Dharma Putra Syukri
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Coronary Arteries ◽  
Communicable Disease ◽  
Cardiovascular Disorder ◽  
Industrial Country ◽  
Unhealthy Lifestyle ◽  
Old Myocardial Infarction

Abstract: Heart and Blood Vessels Disease is the leading cause of cardiovascular disorder that mostly happened in developed or industrial country, related to new communicable disease or “infection” caused by imitation of unhealthy lifestyle.1 The cardiovascular disease divided into several type of heart disease such as; coronary heart disease (CHD) that caused by narrowing of of the coronary arteries due to deposition of fat gathering in and around the cells lining the walls of the coronary arteries and blocking of the blood flow. This research aimed to know the  CHD Profile in Irina F Jantung of RSUP Prof.Dr. R.D Kandou Manado in period of January-December 2010. This was retrospective-descriptive study that used medical records in Irina F Jantung of RSUP. Prof. Dr. R.D Kandou Manado. During this period of this research reported 230 cases of CHD; 69 cases (30%) byage groups 61-70 years old, 159 cases (69,13%) by gender and 86 cases were accompanied disease with the greatest proportion of Hypertension 52 cases (55,32%), and Old Myocardial Infarction (OMI) 71 cases (30,87%) as being the most clinical symptom. The frequency of Cardiovascular disease will be increasing every year if there’s no change of diet and unhealthy lifestyle by people in both urban and rural environments and other degenerative diseases are caused. Key words: Heart Disease, Coronary Heart Disease, Old Myocardial Infarction   ABSTRAK : Penyakit Jantung dan Pembuluh Darah (PJPD) adalah penyakit yang mengakibatkan gangguan jantung dan pembuluh darah, paling sering terjadi di negara maju atau negara industri akibat ‘penularan’ yang disebabkan peniruan gaya hidup kurang sehat.1 Penyakit Jantung ini terbagi dalam beberapa jenis penyakit jantung lainnya diantaranya adalah Penyakit Jantung Koroner (PJK) penyakit jantung yang disebabkan oleh penyempitan arteri koroner akibat dari berkumpulnya endapan lemak di dalam dan sekitar sel yang melapisi dinding arteri koroner sehingga menyumbat aliran darah. Tujuan penelitian ini adalah untuk mengetahui Profil PJK di Irina F Jantung Rsup Prof. Dr. R. D Kandou Manado Periode Januari 2010 - Desember 2010. Penelitian ini bersifat deskriptif dengan metoderetrospektif menggunakan buku register di Irina F Jantung RSUP. Prof. Dr. R.D Kandou Manado periode Januari 2010 sampai Desember 2010. Selama periode Januari 2010 sampai Desember 2010 di Irina F Jantung Rsup Prof. Dr. R. D Kandou Manado tercatat 230 kasus PJK. Berdasarkan kelompok Umur 61-70 tahun sebanyak 69 kasus (30%), Jenis Kelamin sebanyak 159 kasus (69,13%), 86 kasus disertai penyakit penyerta yang terbanyak diantaranya Hipertensi 52 kasus (55,32%), dan manifestasi klinis yang didapat adalah Old Myocardial Infarction (OMI) sebanyak 71 kasus (30,87%). Setiap tahun frekuensi penyakit ini akan terus meningkat jika tidak di atur pola makan atau gaya hidup masyarakat yang kurang sehat, baik di lingkungan urban maupun rural dan disebabkan penyakit degeneratif lainnya. Kata kunci: Penyakit Jantung, Jantung Koroner, Old infark miokard

scholarly journals Virtual Transcriptomics

2021 ◽  
Author(s):  
Andrew J. Buckler ◽  
Eva Karlöf ◽  
Mariette Lengquist ◽  
T. Christian Gasser ◽  
Lars Maegdefessel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Computed Tomography ◽  
Ischemic Stroke ◽  
Atherosclerotic Plaque ◽  
Computed Tomography Angiography ◽  
Machine Intelligence ◽  
Diagnostic Methods ◽  
Plaque Morphology ◽  
Atherosclerotic Cardiovascular Disease

Objective: Therapeutic advancements in atherosclerotic cardiovascular disease have improved prevention of ischemic stroke and myocardial infarction, but diagnostic methods for atherosclerotic plaque phenotyping to aid individualized therapy are lacking. In this feasibility study, we aimed to elucidate plaque biology by decoding the molecular phenotype of plaques through analysis of computed-tomography angiography images, making a predictive model for plaque biology referred to as virtual transcriptomics. Approach and Results: We employed machine intelligence using paired computed-tomography angiography and transcriptomics from carotid endarterectomies of 40 patients undergoing stroke-preventive surgery for carotid stenosis. Computed tomography angiographies were analyzed with novel software for accurate characterization of plaque morphology and plaque transcriptomes obtained from microarrays, followed by mathematical modeling for prediction of molecular signatures. Four hundred fourteen coding and noncoding RNAs were robustly predicted using supervised models to estimate gene expression based on plaque morphology. Examples of predicted transcripts included ion transporters, cytokine receptors, and a number of microRNAs whereas pathway analyses demonstrated enrichment of several biological processes relevant for the pathophysiology of atherosclerosis and plaque instability. Finally, the ability of the models to predict plaque gene expression was demonstrated using computed tomography angiographies from 4 sequestered patients and comparisons with transcriptomes of corresponding lesions. Conclusions: The results of this pilot study show that atherosclerotic plaque phenotyping by image analysis of conventional computed-tomography angiography can elucidate the molecular signature of atherosclerotic lesions in a multiscale setting. The study holds promise for optimized personalized therapy in the prevention of myocardial infarction and ischemic stroke, which warrants further investigations in larger cohorts.

PATHOGENETIC AND ANGIOGRAPHIC FEATURES IN UNSTABLE ANGINAAND OTHER ACUTE CORONARY SYNDROMES

1987 ◽  
Author(s):  
V Fusler ◽  
L Badimon ◽  
V Turitto ◽  
JJ Badimon ◽  
PC Adams ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Unstable Angina ◽  
Acute Coronary Syndromes ◽  
Vessel Wall ◽  
Plaque Rupture ◽  
Thrombus Formation ◽  
Arterial Injury ◽  
Coronary Syndromes ◽  
Wall Interaction ◽  
Q Wave

Angiography in patients with unstable angina or myocardial infarction with subtotal coronary occlusions reveals eccentric stenoses with irregularborders suggesting ruptured atherosclerotic plaques. In addition, the closer the angiogram is to the time of chest pain the higher is the likelihoodof observing a thrombotic filling defect distal to the stenotic region. Thus, we: 1) have investigated the relationship among platelet-vessel wall interaction, rheology, andthrombogenicsubstrate and 2) propose a hypothesisaccounting for thrombosis in the acute coronary syndromes.1) Platelet Vessel Wall Interactions, Rheology and Substrate - We have studied substrate and rheology in both an 'ex vivo' perfusion chamber and 'in vivo'swine model. Qur results, combinedwith those of others, show the following:-Platelet Vessel Wall Interaction and Thrombus Formation - a) In superficial arterial injury plateletsadherevia platelet membrane glycoprotein (GP) lb to the vessel wall to form a monolayer. Von Willebrand Factor (vWF), a high molecular weight glycoprotein found in plasma, platelets, and endothelial cells, binds GPIb and supports platelet adhesion. Platelet derived growth factors(PDGF) from these adherent platelets may contribute to atherogenesis. b) In deep arterial injury, plateletsare stimulated by three pathways -arachidonate, ADP and the "third pathway" -leading to exposure of platelet receptors (GPIIb/IIIa), and subsequent aggregation. Fibrinogenand vWF participate in aggregation bybinding to GPIIb/IIIa. Simultaneously, thrombin stimulates aggregation andthe formation of fibrin that stabilizes platelet aggregates, c) Both a platelet monolayer and aggregation with thrombosis, produce vasoconstriction due to release of platelet products (serotonin, thromboxane A2,and PDGF).- Rheology - a) Stenotic lesions produce a high local shear rate, whichenhances platelet-vessel wall interaction and, in the presence of acute rupture, platelet deposition and subsequent thrombus formation, b) Platelet deposition and thrombosis are particularly favored if the site of rupture includes the stenosis with its high shear rate,while the stasis in the post-stenotic region favors proprogationof thrombus.- Substrate - a) Plaque rupture produces a rough surface and exposes collagen and fat to flowing blood. Thisstimulates mural thrombosis, b) Such thrombus is either fixed or labile depending on the degree of plaque rupture or damage.2) Acute and Subacute Coronary Syndromes - The above observations in the swine model, coupled with recent clinical and pathological observations support the following:-Unstable Angina - Mild or restricted plaque rupture with or without activated mural thrombus, by increasingthe stenosis, explains the increase in exertional angina; subsequent labile thrombosis with platelet-related vasoconstriction explains the resting angina.-Q Wave Myocardial Infarction - The thrombus is occlusive and fixed or persistent because the damage to the vessel wall or to the plaque is more severe or extensive than in unstable angina.-Non-Q Wave Myocardial Infarction -In this syndrome, intermediate between unstable angina and Q wave myocardial infarction, the occlusive thrombus is more transient than in Q wave infarction because of less substrate exposure or damage.

Thrombosis

2019 ◽  
pp. 59-68
Author(s):  
Freek Verheugt
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Acute Myocardial Infarction ◽  
Venous Thromboembolism ◽  
Left Ventricle ◽  
Secondary Prevention ◽  
Thrombus Formation ◽  
Thrombotic Occlusion ◽  
Anticoagulant Drugs ◽  
Prevention Of Cardiovascular Disease

Blood coagulation plays a role in the pathogenesis of acute and chronic vascular disease. Acute myocardial infarction is generally associated with partial or complete thrombotic occlusion of one of the coronary arteries, whereas embolic stroke usually is associated with clot formation in the left atrium, left ventricle, or carotid arteries. Arteries in the lower extremities may get occluded by thrombosis, leading to ischaemia or amputation. Finally, venous thromboembolism is mainly caused by thrombus formation in the veins of the pelvis and/or the legs. This chapter deals with the effectiveness and safety of antiplatelet and anticoagulant drugs in primary and secondary prevention of cardiovascular disease.

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