Materiały źródłowe

• #1 Acute Coronary Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK459157/

  Acute coronary syndrome (ACS) refers to a group of conditions that include ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina. […] ACS is a manifestation of CHD (coronary heart disease) and usually a result of plaque disruption in coronary arteries (atherosclerosis). […] The underlying pathophysiology in ACS is decreased blood flow to part of heart musculature which is usually secondary to plaque rupture and formation of thrombus. […] Sometimes ACS can be secondary to vasospasm with or without underlying atherosclerosis. The result is decreased blood flow to a part of heart musculature resulting first in ischemia and then infarction of that part of the heart.

• #2 New Concepts on the Pathophysiology of Acute Coronary Syndrome

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404112

  Acute coronary syndrome (ACS) is the most severe form of ischemic heart disease. […] Although it is caused by atherosclerotic plaque thrombosis or nonatherosclerotic causes, its pathophysiological mechanism of ACS is not fully understood, and its concept is constantly updated and developed. […] At present, the main pathophysiological mechanisms include plaque rupture, plaque erosion, calcified nodules (CN) and non-atherosclerotic causes such as coronary vasospasm and myocardial bridging (MB). […] These mechanisms may overlap and coexist in some ACS patients. […] Therefore, the pathophysiological mechanism of ACS is complex, and is of great significance for the diagnosis and treatment of ACS. […] This review will discuss the pathophysiological mechanisms of ACS to provide new thoughts on the pathogenesis, diagnosis and treatment of ACS.

• #3 Pathophysiology of Acute Coronary Syndromes—Diagnostic and Treatment Considerations

  https://pmc.ncbi.nlm.nih.gov/articles/PMC10381786/

  Coronary artery disease and acute coronary syndromes are accountable for significant morbidity and mortality, despite the preventive measures and technological advancements in their management. Thus, it is mandatory to further explore the pathophysiology in order to provide tailored and more effective therapies, since acute coronary syndrome pathogenesis is more varied than previously assumed. It consists of plaque rupture, plaque erosion, and calcified nodules. […] The main pathophysiologic mechanisms underlying the development of ACS involve plaque rupture, erosion, and calcified nodules. […] When it comes to acute coronary syndrome management, the presence of ruptured plaques almost always necessitates emergent reperfusion, whereas the presence of plaque erosions may indicate the possibility of conservative management with potent antiplatelet and anti-atherosclerotic medications.

• #4 Pathophysiology of Acute Coronary Syndromes—Diagnostic and Treatment Considerations

  https://www.mdpi.com/2075-1729/13/7/1543

  Coronary artery disease and acute coronary syndromes are accountable for significant morbidity and mortality, despite the preventive measures and technological advancements in their management. […] Thus, it is mandatory to further explore the pathophysiology in order to provide tailored and more effective therapies, since acute coronary syndrome pathogenesis is more varied than previously assumed. It consists of plaque rupture, plaque erosion, and calcified nodules. […] The main pathophysiologic mechanisms underlying the development of ACS involve plaque rupture, erosion, and calcified nodules. […] The rupture of the fibrous cap exposes the lipid-rich core to the bloodstream, resulting in a chain reaction of events. […] Inflammation is important in both the beginning and development of plaque rupture.

• #5 Mechanisms of acute coronary syndromes related to atherosclerosis – UpToDate

  https://www.uptodate.com/contents/mechanisms-of-acute-coronary-syndromes-related-to-atherosclerosis

  Mechanisms of acute coronary syndromes related to atherosclerosis […] Acute coronary syndromes (ACS) represent a clinical spectrum of acute coronary artery disease that includes unstable angina, acute myocardial infarction (MI), and sudden coronary death. In most cases, the underlying mechanism is obstruction of coronary artery blood flow by a thrombus that develops as a result of rupture or erosion of an underlying atherosclerotic plaque. […] This topic focuses on the mechanisms of ACS related to destabilization of atherosclerotic plaques.

• #6 Acute Coronary Syndrome: Practice Essentials, Background, Etiology

  https://emedicine.medscape.com/article/1910735-overview

  Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those for ST-segment elevation myocardial infarction (STEMI) to presentations found in nonST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. It is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery. […] Atherosclerosis is the primary cause of ACS, with most cases occurring from the disruption of a previously nonsevere lesion. […] In terms of pathology, ACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery. […] The major trigger for coronary thrombosis is considered to be plaque rupture caused by the dissolution of the fibrous cap, the dissolution itself being the result of the release of metalloproteinases (collagenases) from activated inflammatory cells. This event is followed by platelet activation and aggregation, activation of the coagulation pathway, and vasoconstriction. This process culminates in coronary intraluminal thrombosis and variable degrees of vascular occlusion.

• #7 New Concepts on the Pathophysiology of Acute Coronary Syndrome

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404112/htm

  Acute coronary syndrome (ACS) is the most severe form of ischemic heart disease. Although it is caused by atherosclerotic plaque thrombosis or nonatherosclerotic causes, its pathophysiological mechanism of ACS is not fully understood, and its concept is constantly updated and developed. At present, the main pathophysiological mechanisms include plaque rupture, plaque erosion, calcified nodules (CN) and non-atherosclerotic causes such as coronary vasospasm and myocardial bridging (MB). These mechanisms may overlap and coexist in some ACS patients. Therefore, the pathophysiological mechanism of ACS is complex, and is of great significance for the diagnosis and treatment of ACS. This review will discuss the pathophysiological mechanisms of ACS to provide new thoughts on the pathogenesis, diagnosis and treatment of ACS.

• #8 Acute coronary syndrome – Wikipedia

  https://en.wikipedia.org/wiki/Acute_coronary_syndrome

  Acute coronary syndrome (ACS) is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. […] In those who have ACS, atheroma rupture is most commonly found 60% when compared to atheroma erosion (30%), thus causes the formation of thrombus which block the coronary arteries. Plaque rupture is responsible for 60% in ST elevated myocardial infarction (STEMI) while plaque erosion is responsible for 30% of the STEMI and vice versa for Non ST elevated myocardial infarction (NSTEMI). […] After the coronary arteries are unblocked, there is a risk of reperfusion injury due spreading inflammatory mediators throughout the body.

• #9 Insight into Pathogenesis of Acute Coronary Syndrome | Radiology Key

  https://radiologykey.com/insight-into-pathogenesis-of-acute-coronary-syndrome/

  Insight into Pathogenesis of Acute Coronary Syndrome […] Ruptured plaques are thin fibrous cap atheromas with luminal thrombi. These lesions usually have an extensive necrotic core containing large numbers of cholesterol crystals and a thin fibrous cap infiltrated by foamy macrophages and a paucity of T lymphocytes. The fibrous cap is thinnest at the site of rupture and consists of a few collagen bundles and rare smooth muscle cells. The luminal thrombus is in communication with the lipid-rich necrotic core. […] The perception of rupture of an advanced atherosclerotic lesion as the primary mechanism responsible for ACS was widely accepted. However, this paradigm was challenged by inconsistent findings in two pathological studies, which showed that coronary thrombi could arise without rupture. […] To better understand the underlying mechanism of ACS, Virmani et al. proposed another plaque morphological classification scheme based on their comprehensive autopsy observation. Their categories included intimal xanthoma, intimal thickening, pathological intimal thickening, fibrous cap atheroma, thin fibrous cap atheroma, calcified nodule, and fibrocalcific plaque. The accumulation of lipid in relation to the formation of fibrous cap which changes over time, as well as thrombosis was taken into account in the classification. More importantly, their classification highlighted the importance of plaque erosion in thrombotic events. […] In a consensus statement, ruptured plaque was defined as plaque with a structural defect or gap in the fibrous cap that separates the lipid-rich necrotic core of a plaque from the flowing blood, thereby exposing the thrombogenic core of the plaque. […] The incidence of plaque rupture as an underlying pathology of ACS ranged from 50 to 75 % in autopsy studies depends on the population: 75 % in patients with acute myocardial infarction (AMI), 55-65 % in sudden coronary death (SCD), and 36 % in unstable angina (UA). […] Plaque rupture was found to be responsible for the culprit lesion in 44 % of patients, while 31 % had plaque erosion. Plaque rupture was more frequently observed in patients with STEMI (72 %) than in those with NSTEACS (32 %).

• #10 New Concepts on the Pathophysiology of Acute Coronary Syndrome

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404112/htm

  The first is plaque rupture, mainly involving atherosclerotic plaques rich in lipids and thin fibrous caps. Metalloproteinases (MMP) degrade the fibrous cap resulting in rupture and necrosis of the core exposed to the vascular lumen, leading to platelet activation and thrombosis. In a small proportion of cases, plaque rupture occurs at the site of calcified nodules (CN). Plaque rupture may occur with or without systemic inflammation. […] The second is plaque erosion, where thrombus formation occurs mainly in the area of endothelial desquamation adjacent to the atherosclerotic plaque, without destroying the fibrous cap covering the plaque tissue. […] The third mechanism is caused by non-atherosclerotic causes in the absence of obvious thrombosis, such as coronary vasospasm and myocardial bridging (MB).

• #11 Pathogenesis of Stable and Acute Coronary Syndromes | Thoracic Key

  https://thoracickey.com/pathogenesis-of-stable-and-acute-coronary-syndromes/

  Unstable angina and acute MI are almost always caused by a luminal thrombus superimposed on an atherosclerotic plaque with or without concomitant vasospasm. […] The most frequent cause of coronary thrombi is plaque rupture. In plaque rupture, a structural defect in the fibrous cap exposes the highly thrombogenic core to the blood. […] By definition, when no plaque rupture is identified, despite a thorough search, the term plaque erosion is used. […] This worldwide survey shows that plaque rupture is the major cause of coronary thrombosis, responsible for approximately 75% of cases.

• #12 Pathophysiology of Acute Coronary Syndrome | IntechOpen

  https://www.intechopen.com/online-first/1215703

  Acute coronary syndrome (ACS) encompasses a spectrum of conditions caused by the sudden, reduced blood flow to the myocardium, leading to myocardial ischemia and, in severe cases, infarction. The primary pathophysiological mechanism involves the rupture of an atherosclerotic plaque within a coronary artery, resulting in thrombus formation. Plaque rupture exposes subendothelial elements, activating platelets and initiating a coagulation cascade that leads to clot development. The extent and stability of the thrombus determine the severity of coronary obstruction, with partial blockage causing unstable angina and complete occlusion leading to myocardial infarction. Other contributory factors include coronary vasospasm, endothelial dysfunction, and inflammation. The ischemic damage caused by ACS disrupts myocardial cell membranes, releasing cardiac biomarkers such as troponin into the bloodstream. Early recognition and intervention are critical in ACS management to restore perfusion and minimize myocardial injury.

• #13 Overview of Acute Coronary Syndromes (ACS) – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-acute-coronary-syndromes-acs

  Acute coronary syndromes result from acute obstruction of a coronary artery. […] The most common cause of acute coronary syndromes is an acute thrombus in an atherosclerotic coronary artery. Atheromatous plaque sometimes becomes unstable or inflamed, causing it to rupture or split, exposing thrombogenic material, which activates platelets and the coagulation cascade and produces an acute thrombus. […] Initial consequences vary with size, location, and duration of obstruction and range from transient ischemia to infarction. Measurement of high sensitivity troponin indicates that some cell necrosis probably occurs even with mild ischemia; thus, ischemic events occur on a continuum, and classification into subgroups, although useful, is somewhat arbitrary. Sequelae of the acute event depend primarily on the mass and type of cardiac tissue infarcted.

• #14 Pathophysiology of Acute Coronary Syndrome | IntechOpen

  https://www.intechopen.com/online-first/1215703

  As atherosclerotic plaques mature, they become more prone to clinical complications. Plaque rupture, ulceration, or erosion exposes highly thrombogenic substances to the bloodstream, leading to partial or complete vascular occlusion and thrombosis. […] Partial or complete thrombosis associated with an unstable plaque is a central factor in acute coronary syndromes. […] These complex interactions highlight the multifactorial nature of plaque destabilization and the potential for acute cardiovascular events.

• #15 New Insights into Pathophysiology and New Risk Factors for ACS

  https://www.mdpi.com/2077-0383/12/8/2883

  A relatively new concept is represented by the superficial erosion of atherosclerotic plaque as the cause of ACS. Historical data suggest a prevalence of 20% of ACS patients characterized by plaque erosion in the culprit lesions, while more recent reports indicate about 40% of ACS patients displaying plaque erosion. […] The majority of ACS has been caused by the rupture of an atherosclerotic plaque with thrombus formation. Studies among patients referred for an ACS have documented the rupture of lipid-rich plaque in two thirds of cases. However, a non-negligible proportion of patients experience ACS due to plaque erosion, calcific nodules, coronary spasm, and spontaneous coronary artery dissection. […] The NLRP3 inflammasome is a key mediator of inflammatory diseases, including atherosclerosis and other vascular diseases. Recent evidence has suggested that IL-1β-mediated inflammation drives atherothrombotic events, indicating that NLRP3 inflammasome is a major contributor to atherosclerosis.

• #16 New Concepts on the Pathophysiology of Acute Coronary Syndrome

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404112/htm

  The lesions of coronary events caused by erosion are in some ways diametrically opposed to the morphological features of TCFA. […] Eroded plaques have intact fibrous caps and high concentrations of ECM molecules. […] This suggests that effective antiplatelet therapy without stents may be effective against ACS caused by plaque erosion, thereby avoiding stent-related complications. […] The EROSION study demonstrated the feasibility and safety of antithrombotic therapy instead of stent placement in ACS patients caused by plaque erosion, and provided a new option for the treatment of patients with plaque erosion. […] In recent decades, the clinical presentation of ACS has shifted and NSTEMI has surpassed STEMI, which may be related to the increasing proportion of patients with plaque erosion.

• #17 Pathophysiology of Acute Coronary Syndromes—Diagnostic and Treatment Considerations

  https://www.mdpi.com/2075-1729/13/7/1543

  The pathogenesis of plaque erosion involves a combination of factors, including endothelial dysfunction, inflammation, and platelet activation. […] The presence of plaque erosion in culprit coronary arteries of patients with an ACS has been increasingly more common over the years. […] The formation of calcified nodules in coronary arteries involves a complex interplay of biological processes, including inflammation, osteogenic transformation, and matrix remodeling. […] Calcified nodules have been implicated in the pathogenesis of ACS, particularly in patients with non-obstructive coronary artery disease. […] The presence of calcified nodules is associated with a higher risk of adverse cardiovascular events, including target vessel revascularization, recurrent ACS, and mortality. […] Acute coronary syndromes have been at the forefront of scientific research due to their presumed healthcare burden. Recent evidence suggests that their pathophysiology is more diverse than previously thought, involving plaque rupture, plaque erosion, and calcified nodules.

• #18 Pathophysiology of Acute Coronary Syndromes—Diagnostic and Treatment Considerations

  https://pmc.ncbi.nlm.nih.gov/articles/PMC10381786/

  The pathogenesis of plaque erosion involves a combination of factors, including endothelial dysfunction, inflammation, and platelet activation. Endothelial dysfunction, characterized by impaired nitric oxide bioavailability and the increased expression of adhesion molecules, leads to a pro-thrombotic state. […] The presence of calcified nodules is associated with a higher risk of adverse cardiovascular events, including target vessel revascularization, recurrent ACS, and mortality. […] Recent evidence suggests that their pathophysiology is more diverse than previously thought, involving plaque rupture, plaque erosion, and calcified nodules.

• #19 New Concepts on the Pathophysiology of Acute Coronary Syndrome

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404112/htm

  The death and desquamation of intimal endothelial cells (ECs) plays an important role in plaque erosion thrombosis. […] The typical feature of plaque rupture under OCT is the discontinuity of the plaque fibrous cap. […] The identification of CMD is of great significance for the diagnosis, treatment and prognosis of ACS. […] In summary, some ACS are due to thrombosis caused by atherosclerotic plaques, and others are due to non-atherosclerotic causes. Several pathophysiological mechanisms of ACS described in this paper are shown in Fig. 1. […] The causes of thrombosis in ACS include plaque rupture, plaque erosion and CN. Their pathophysiological mechanisms are quite different, and it is particularly important to distinguish them and carry out targeted treatment. […] Recent studies have found that plasma Trimethylamine N-Oxide (TMAO) is independently associated with plaque rupture in patients with STEMI, and may be a useful biomarker for plaque rupture, especially in differentiating plaque rupture from plaque erosion. […] In conclusion, the pathophysiological mechanism of ACS is complex and diverse and will require further investigation to determine new therapeutic options.

• #20 New Concepts on the Pathophysiology of Acute Coronary Syndrome

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404112/htm

  Under the background of effective and intensive control of risk factors such as hyperlipidemia and hypertension, the pathophysiology of human AS has also changed. […] Lipid-lowering reduces the lipid core, reduces lesion size, plaque lipid accumulation and inflammatory cell reduction, and even promotes plaque regression and healing. […] However, with the use of statins and other drugs with significant low-density lipoprotein (LDL) lowering effects, ACS events still frequently occur. This suggests that mechanisms that are less responsive to the control of risk factors may be important for ACS today, and has spurred interest in mechanisms other than plaque rupture that may trigger ACS. […] Reconsideration of the concept of the “vulnerable plaque” has led to interest in an alternative mechanism of ACS, namely plaque erosion.

• #21 Heart attack – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/heart-attack/symptoms-causes/syc-20373106

  An acute complete blockage of a medium or large heart artery usually means you’ve had an ST elevation myocardial infarction (STEMI). […] A partial blockage often means you’ve had a non-ST elevation myocardial infarction (NSTEMI). However, some people with non-ST elevation myocardial infarction (NSTEMI) have a total blockage. […] Not all heart attacks are caused by blocked arteries. Other causes include: […] Coronary artery spasm. This is a severe squeezing of a blood vessel that’s not blocked. […] Certain infections. COVID-19 and other viral infections may cause damage to the heart muscle. […] Spontaneous coronary artery dissection (SCAD). This life-threatening condition is caused by a tear inside a heart artery.

• #22 COVID-19 and acute coronary syndrome: emphasis on ACS without atherothrombosis

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-21/covid-19-and-acute-coronary-syndrome-emphasis-on-acs-without-atherothrombosis

  Classic acute myocardial injury in COVID-19 patients has multiple mechanisms, including direct damage to angiotensin-converting enzyme receptors on myocytes, resulting in damage to angiotensin-converting enzyme 2 (ACE2) signalling pathways. […] Another possible mechanism is myocardial ischaemia caused by systemic hypoxia. In the setting of severe COVID-19 infection with acute respiratory distress syndrome (ARDS), multiple microthrombosis, coronary spasm, systemic inflammatory response due to cytokine storm and vasculitis-like vessel damage can be likely triggers, which in severe cases of COVID-19 leads to rupture of the atherosclerotic plaque. […] Systemic inflammation changes coronary blood flow, leading to the activation and rupture of pre-existing atherosclerotic plaques and causes type 1 myocardial infarction. In addition, the degree of microvascular resistance in patients with coronary syndrome X increases. Thus, in COVID-19, ACS without atherothrombosis also occurs.

• #23 Inflammation in Acute Coronary Syndromes: Mechanisms and Clinical Implications – Revista Española de Cardiología (English Edition)

  https://www.revespcardiol.org/en-inflammation-in-acute-coronary-syndromes-articulo-13061146

  Inflammation plays a pivotal role in the pathogenesis of atherosclerosis and its complications. In particular, atherosclerosis is an active process and the inflammatory component appears to be particularly correlated with the development of acute coronary syndromes (ACS). […] Accumulating data demonstrate that in ACS, elevated levels of circulating inflammatory markers, such as C-reactive protein, predict an unfavorable cardiovascular outcome. A better knowledge of the molecular and cellular mechanisms of inflammation might not only further improve prognostic stratification but also allow us to identify novel therapeutic targets. […] The present review summarizes the mechanisms of the inflammatory response in ACS, its clinical implications, and the potential treatment strategies to contrast this phenomenon.

• #24 Inflammation in Acute Coronary Syndromes: Mechanisms and Clinical Implications – Revista Española de Cardiología (English Edition)

  https://www.revespcardiol.org/en-inflammation-in-acute-coronary-syndromes-articulo-13061146

  In the last years a growing body of evidence has demonstrated that inflammation plays a pivotal role in the pathogenesis of atherosclerosis and its complications and nowadays atherosclerosis is considered at all effects „an inflammatory disease.” […] Accumulating data demonstrate that elevated levels of circulating inflammatory markers predict an unfavorable cardiovascular outcome in asymptomatic subjects, in patients with stable ischemic heart disease and in patients with acute coronary syndromes (ACS). […] Improved knowledge of the molecular and cellular mechanisms of inflammation might not only further improve prognostic stratification but also allow us to identify novel therapeutic targets. […] The inflammatory response not only promotes initiation of the atherosclerotic process, but also contributes to the subsequent growth of atheroma and the precipitation of acute thrombotic events.

• #25 Pathophysiology of Acute Coronary Syndrome | IntechOpen

  https://www.intechopen.com/online-first/1215703

  The majority of acute coronary syndromes (ACS) result from coronary thrombosis due to rupture or erosion of atherosclerotic lesions. […] ACS typically occurs as a consequence of fibrous cap rupture, superficial erosion, or, in rare cases, vasospasm or disruption of calcified nodules within coronary atherosclerotic plaques. […] Atherosclerosis is a key underlying factor in the pathogenesis of coronary, cerebral, and peripheral vascular diseases. […] Although many hypotheses have been proposed for the pathogenesis of atherosclerosis, the most widely accepted model attributes it to a chronic inflammatory process in response to endothelial injury in the arterial wall. […] Endothelial injury is considered the cornerstone of the response-to-injury hypothesis. […] Chronic inflammation plays a pivotal role in initiating and progressing atherosclerotic lesion formation.

• #26 Inflammation in Acute Coronary Syndromes: Mechanisms and Clinical Implications – Revista Española de Cardiología (English Edition)

  https://www.revespcardiol.org/en-inflammation-in-acute-coronary-syndromes-articulo-13061146

  In summary, atherosclerosis is a chronic process with an important active and ongoing inflammatory component. Inflammation plays an important role not only in „triggering” the atherosclerotic process, but also in promoting atherosclerotic plaque development and complications. […] Individuals with a greater inflammatory response to atherogenic stimuli have a higher risk of developing clinical manifestations of atherosclerosis. […] Indeed, systemic markers of inflammation, such as C-reactive protein (CRP), are associated with a higher long-term risk of acute myocardial infarction, stroke or severe peripheral vascular disease. […] The inflammatory outburst associated with acute coronary syndromes is the expression of activated inflammatory cells some of which are likely to be located in the culprit atherosclerotic plaque where they can determine severe detrimental effects through a variety of different mechanisms.

• #27

  https://www.alliedacademies.org/articles/inflammatory-biomarkers-in-the-pathogenesis-and-prognosis-of-acute-coronary-syndrome-26647.html

  Acute Coronary Syndrome (ACS) is a critical cardiovascular condition that encompasses a spectrum of ischemic heart diseases, including unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Inflammation plays a crucial role in the initiation, progression, and prognosis of ACS. This article aims to provide a comprehensive overview of the role of inflammatory biomarkers in the pathogenesis and prognosis of ACS, highlighting their potential as diagnostic tools and therapeutic targets. […] Inflammatory biomarkers, such as C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-), and various cellular adhesion molecules, have emerged as valuable indicators of the underlying inflammatory processes in ACS. This article explores the mechanistic insights into how these biomarkers contribute to the pathogenesis and prognosis of ACS. The initiation of ACS involves atherosclerotic plaque destabilization, leading to plaque rupture or erosion and subsequent thrombus formation. Inflammation plays a pivotal role in each stage of this process. Inflammatory biomarkers, such as CRP and IL-6, reflect the presence and intensity of systemic inflammation and are associated with endothelial dysfunction, plaque vulnerability, and thrombus formation. Moreover, activated immune cells release cytokines and chemokines that further perpetuate the inflammatory response, contributing to the progression of ACS.

• #28 Inflammation in Acute Coronary Syndromes: Mechanisms and Clinical Implications – Revista Española de Cardiología (English Edition)

  https://www.revespcardiol.org/en-inflammation-in-acute-coronary-syndromes-articulo-13061146

  The cytokines secreted by activated inflammatory cells have the potential to activate the endothelium transforming its antiadhesive and anticoagulant properties into adhesive and procoagulant properties. […] In summary, plaque inflammation has the potential to enhance plaque fissuring by reducing the concentration of proteins contained in extra cellular matrix. […] Inflammation associated with ACS is widespread and not restricted to the culprit stenosis. […] The triggers of the widespread coronary inflammation associated with ACS are still unknown. […] Systemic evidence of inflammation, probably an antigen-driven immune response, is present in about two thirds of patients with ACS. […] Coronary instability associated with raised levels of CRP, a non specific marker of inflammation, is characterized by a worse outcome. […] New treatments which target the triggers of inflammation or modulate the detrimental component of the inflammatory response are urgently required to further improve the outcome of this complex syndrome.

• #29 Anticoagulant Therapy for Acute Coronary Syndromes | ICR Journal

  https://www.icrjournal.com/articles/anticoagulant-therapy-acute-coronary-syndromes?language_content_entity=en

  Anticoagulation in conjunction with antiplatelet therapy is central to the management of acute coronary syndromes (ACS). When used effectively it is associated with a reduction in recurrent ischaemic events including myocardial infarction and stent thrombosis as well as a reduction in death. […] The central process underlying ACS is the development of a thrombus overlying a ruptured or eroded plaque, leading to various degrees of acute vessel occlusion and myocardial ischaemia. […] A thrombus that originates following plaque rupture consists largely of platelets; in addition, coagulation pathways are also triggered by plaque rupture and platelet aggregation. […] Acute coronary syndromes are characterised by vascular inflammation, subsequent endothelial dysfunction and platelet activation, followed by thrombus formation.

• #30 Best Practices in Pharmacotherapy for Acute Coronary Syndromes | USC Journal

  https://www.uscjournal.com/articles/best-practices-pharmacotherapy-acute-coronary-syndromes?language_content_entity=en

  ACS occur when a lipid-rich thin atherosclerotic plaque ruptures. This exposes the endothelium to thrombogenic substances, such as platelets and clotting factors, which leads to thrombus formation, limiting blood flow through the coronary vasculature. Platelets bind to the exposed endothelial surface while also activating other platelets via thrombin, thromboxane A2, adenosine diphosphate (ADP), epinephrine, and other mediators. Platelet binding occurs via glycoprotein (GP) IIb/IIIa receptors expressed on platelet membranes, cross-linking activated platelets to other platelets via fibrinogen. Activated monocytes release metalloproteinases and tissue factor, which interact with the vulnerable plaque. Activation of these different pathways results in platelet aggregation and activation of the clotting cascade, leading to thrombus formation. If the vessel is partially occluded, UA or NSTEMI may occur, whereas complete occlusion may lead to STEMI. The degree of obstruction and the timing of presentation influence the degree of myocardial damage.

• #31 Anticoagulant Therapy for Acute Coronary Syndromes | ICR Journal

  https://www.icrjournal.com/articles/anticoagulant-therapy-acute-coronary-syndromes?language_content_entity=en

  Activation of coagulation pathways is crucial for thrombus formation. Fibroblasts and smooth muscle cells express the membrane protein tissue factor, which is also present in blood. At sites of vascular damage, platelets express disulphide isomerase, which cleaves tissue factor into its active form. Activated tissue factor can then bind factor VIIa and the resulting complex activates factors VII, IX and X. Factors Xa and V complex together promoting thrombin generation. […] The presence of thrombin activates factors V and VII promoting prothrombin conversion to thrombin by the more active complex XaVa. Fibrin generation from fibrinogen is triggered early in the coagulation cascade resulting in thrombus formation.

• #32 Overview of Acute Coronary Syndromes (ACS) – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-acute-coronary-syndromes-acs

  Ischemic (but not infarcted) tissue has impaired contractility and relaxation, resulting in hypokinetic or akinetic segments; these segments may expand or bulge during systole (called paradoxical motion). The size of the affected area determines effects, which range from minimal to mild heart failure to cardiogenic shock; usually, large parts of myocardium must be ischemic to cause significant myocardial dysfunction. […] Myocardial infarction is myocardial necrosis resulting from abrupt reduction in coronary blood flow to part of the myocardium. Infarcted tissue is permanently dysfunctional; however, there is a zone of potentially reversible ischemia adjacent to infarcted tissue. […] Electrical dysfunction can be significant in any form of acute coronary syndrome. Ischemic and necrotic cells are incapable of normal electrical activity, resulting in various ECG changes (predominantly ST-T abnormalities), arrhythmias, and conduction disturbances.

• #33

  https://www.heartonline.org.au/articles/pathophysiology/pathophysiology-of-acute-coronary-syndrome-and-heart-failure

  The course of plaque development and progression is extremely complex and involves the interplay of multiple pathological processes. […] Management targets rapid reperfusion to prevent avoidable cell death, and thereby maintaining myocardial function as best as possible. […] The choice of treatment is governed by multiple factors including the underlying pathology, location of the blockage, number of vessels involved, and residual cardiac function. […] Myocardial cell death occurs within as little as 20 minutes as a result of prolonged ischaemia. Absolute necrosis may occur within 2-4 hours.

• #34 Seasonal Variations in the Pathogenesis of Acute Coronary Syndromes

  https://lirias.kuleuven.be/3078326

  Seasonal variations in acute coronary syndromes (ACS) have been reported, with incidence and mortality peaking in the winter. […] However, the underlying pathophysiology for these variations remain speculative. […] The prevalence of the 3 most common pathologies (plaque rupture, plaque erosion, and calcified plaque) were compared between the 4 seasons. […] After adjusting for age, sex, and other coronary risk factors, winter was significantly associated with increased risk of plaque rupture (odds ratio [OR], 1.652; 95% CI, 1.157-2.359; P=0.006) and decreased risk of plaque erosion (OR, 0.623; 95% CI, 0.429-0.905; P=0.013), compared with summer as a reference. […] Seasonal variations in the incidence of ACS reflect differences in the underlying pathobiology. […] A different approach may be needed for the prevention and treatment of ACS depending on the season of its occurrence.

• #35 Genetics of the acute coronary syndrome

  https://atm.amegroups.org/article/view/9572/html

  Acute coronary syndrome is the most important example of a complex, or multifactorial, disease. […] Significant advances have been made in identifying chromosomal loci linked to or genetic variations that confer susceptibility to CAD using microarray-based or high-throughput RNA sequencing methods. […] Genome wide association studies have definitely elucidated that such disease is the result of the interaction of common genetic variants, mostly implicated in the lipid metabolism, cell proliferation and inflammation. […] CAD is a complex multifactorial disease which has, however, an important genetic component.

• #36 Acute Psychological Stress as a Precipitant of Acute Coronary Syndromes in Patients With Undiagnosed Ischemic Heart Disease: A Case Report and Literature Review

  https://www.psychiatrist.com/pcc/acute-psychological-stress-precipitant-acute-coronary/

  Acute psychological stress causes a number of physiologic responses that can trigger acute coronary syndromes in individuals with silent coronary artery disease. […] Acute coronary syndrome is thought to be the end result of a complex mechanism involving platelet activation and endothelial dysfunction. Several studies have shown that acute mental stress leads to enhanced platelet activation and endothelial dysfunction. The mechanism behind this involves both the autonomic nervous system and the neuroendocrine response. […] Acute psychological stress may lead to acute coronary syndromes in patients with previously silent disease.

• #37

  https://www.alliedacademies.org/articles/inflammatory-biomarkers-in-the-pathogenesis-and-prognosis-of-acute-coronary-syndrome-26647.html

  Inflammatory biomarkers not only provide insights into the pathogenesis of ACS but also serve as important prognostic indicators. Elevated levels of CRP, IL-6, and TNF- have been associated with adverse outcomes, including recurrent myocardial infarction, cardiovascular death, and heart failure in ACS patients. These biomarkers not only reflect the extent of myocardial injury but also indicate the ongoing inflammatory response, which can promote adverse remodeling, ventricular dysfunction, and subsequent cardiovascular events. The use of inflammatory biomarkers in clinical practice has shown promise in the diagnosis, risk stratification, and therapeutic management of ACS. High-sensitivity CRP has been incorporated into risk assessment algorithms, such as the Framingham Risk Score, to improve risk prediction. Additionally, targeted anti-inflammatory therapies, such as monoclonal antibodies against IL-1 and IL-6 receptors, have demonstrated potential in reducing cardiovascular events in ACS patients.

• #38 Acute Coronary Syndrome: Practice Essentials, Background, Etiology

  https://emedicine.medscape.com/article/1910735-overview

  Attention to the underlying mechanisms of ischemia is important when managing ACS. A simple predictor of demand is rate-pressure product, which can be lowered by beta blockers (eg, metoprolol or atenolol) and pain/stress relievers (eg, morphine), while supply may be improved by oxygen, adequate hematocrit, blood thinners (eg, heparin, IIb/IIIa agents such as abciximab, eptifibatide, tirofiban, or thrombolytics), and/or vasodilators (eg, nitrates, amlodipine).

• #39 Acute Coronary Syndrome (ACS): Causes, Symptoms & Treatment

  https://my.clevelandclinic.org/health/diseases/22910-acute-coronary-syndrome

  There’s no cure for acute coronary syndrome, but early diagnosis and prompt treatment can protect your heart from further damage and help it work as well as possible. […] Acute coronary syndrome treatment focuses on relieving pain and improving blood flow so your heart can work as well as possible, as quickly as possible. Your healthcare provider recommends treatment based on the specific condition you have. Treatment typically involves a combination of medication and procedures to open your arteries and restore heart function. […] Surgical treatments for acute coronary syndrome involve reopening your artery to restore regular blood flow. Your healthcare provider may recommend: Angioplasty with stent (small metal mesh tube) to open the blocked area of your artery. Coronary artery bypass surgery (coronary artery bypass grafting, or CABG) to create a new pathway for blood flow. Percutaneous coronary intervention (PCI) to open a blocked artery. […] The outlook for acute coronary syndrome depends on the specific condition and its severity, including the extent of heart muscle damage. Timely diagnosis and treatment, along with lifestyle changes, can help give you the best chance for a healthy life.

• #40 PCSK9 Inhibitors

  https://www.hcplive.com/view/pcsk9-inhibitors

  PCSK9i are a class of monoclonal antibodies that effectively lower LDL-C levels and are particularly useful for patients with high cardiovascular risk, including those with acute coronary syndrome (ACS) or familial hypercholesterolemia. […] Both medications have demonstrated significant efficacy in lowering LDL-C levels and improving cardiovascular outcomes in high-risk patients, particularly those who do not achieve adequate LDL-C level reduction with statin therapy alone. […] In conclusion, alirocumab and evolocumab are the 2 PCSK9i currently available, offering valuable options for intensive LDL-C level lowering in high-risk patients, especially those with statin resistance or intolerance.

• #41 New Insights into Pathophysiology and New Risk Factors for ACS

  https://www.mdpi.com/2077-0383/12/8/2883

  The significant advances achieved in recent years have contributed to a finer comprehension of atherosclerosis pathophysiology. The paradigm of ruptured culprit lesions as the only cause of ACS has shifted to a more complex series of mechanisms that probably deserve different approaches from the interventional and non-interventional points of view.

• #42 New Concepts on the Pathophysiology of Acute Coronary Syndrome

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404112/htm

  The concept of ACS is also developing. For example, plaque erosion gradually dominates in the era of intensive lipid lowering, and the concept of the “vulnerable patient” also leads to new in the management of ACS patients. […] The “Vulnerable plaque” was initially studied at autopsy. Therefore, these studies have a limited number of patients with TCFA morphology who did not rupture or even triggered ACS resulting in death. […] The development of several emerging technologies, including endovascular imaging, has added new insight in the role of TCFA in the pathophysiology of ACS. […] The occurrence of plaque rupture usually occurs in asymptomatic ACS patients, which makes it difficult to predict. […] The management of coronary heart disease should not be regarded as a disease, but as a spectrum of disease.

• #43 Treatment options for acute coronary syndromeAccessibility ToolsIncrease TextDecrease TextGrayscaleHigh ContrastNegative ContrastLight BackgroundLinks UnderlineReadable FontReset

  https://heartresearch.org.uk/treatment-options-for-acute-coronary-syndrome-that-harness-the-bodys-natural-clot-busting-mechanism/

  Summary: Acute coronary syndrome (ACS), a sudden reduction in the blood flow to the heart, is the cause of thousands of deaths and hospitalisations in the UK each year. […] This study aims to explore novel therapeutic combinations that may harness the body’s natural clot busting mechanism, known as fibrinolysis. […] Our work has shown that individuals with ACS have impairment in this natural system and that those with the slowest rates of so-called “spontaneous” fibrinolysis are more likely to have a future cardiovascular event. […] In this project, Professor Mutch and her team will investigate new treatment strategies that could help promote spontaneous fibrinolysis in patients and may reduce repeated cardiovascular events. […] This work will develop a solid understanding of how to harness the body’s natural clot busting system, using both existing and novel treatment options in ACS.

• #44 Slow Coronary Blood Flow: Pathogenesis and Clinical Implications | ECR Journal

  https://www.ecrjournal.com/articles/slow-coronary-blood-flow-pathogenesis-and-clinical-implications?language_content_entity=en

  Coronary slow flow (CSF) phenomenon, also known as cardiac syndrome Y, is defined as the delayed opacification of the coronary vasculature at the distal level. […] Different hypotheses and theories have been postulated about its substrate and mechanism, such as microvascular and endothelial dysfunction. […] Researchers have been trying to characterise this phenomenon and understand its pathophysiological mechanisms. Myocardial biopsy studies have demonstrated the presence of microvascular disease and an increased resting coronary vasomotor tone. […] The normal coronary vasculature consists of epicardial vessels with little resistance to blood flow; and the microvasculature is the main source for regulation of myocardial flow. Coronary vascular tone is regulated via the endothelium and reflects the balance of opposite factors such as endothelin, the most potent vasoconstrictor agent, and vasodilators agents such as NO, which seems to be the most important contributor to acute regulation of vascular tone.

• #45 Slow Coronary Blood Flow: Pathogenesis and Clinical Implications | ECR Journal

  https://www.ecrjournal.com/articles/slow-coronary-blood-flow-pathogenesis-and-clinical-implications?language_content_entity=en

  Beltrame et al. reported the presence of an increased resting coronary vasomotor tone in coronary resistance vessels in patients with CSF, suggesting the presence of microvascular spasm. […] Other authors have theorised that high homocysteine levels are responsible for endothelial dysfunction in CSF. […] Pekdemir et al. demonstrated that the decreased fractional flow reserve in patients with CSF was attributed to increased resistance in the epicardial coronary arteries due to diffuse atherosclerotic disease. […] This supports the theory that CSF caused by the deterioration of endothelial function could be considered a precursor of atherosclerosis. […] However, other theories have emerged that challenge the hypothesis of endothelial dysfunction in the pathogenesis of CSF. […] They found that endothelial function was not impaired in patients with CSF and concluded that abnormalities in endothelial function and the endothelial NO pathway do not play a major role in the pathogenesis of CSF suggesting that further investigations are needed to elucidate the importance of other biological factors, such as platelet activation or the role of endothelin.

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