Materiały źródłowe

• #1 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Coronary artery disease (CAD) is characterized by the development of atherosclerosis in the coronary arteries, which can sometimes be asymptomatic. […] CAD is marked by an inadequate supply of blood and oxygen to the myocardium. The condition arises from occlusion of the coronary arteries and results in a demand-supply mismatch of oxygen. CAD typically involves the formation of plaques in the lumen of coronary arteries that impede blood flow. […] The hallmark of the pathophysiology of CAD is atherosclerotic plaque formation. Plaque is a buildup of fatty material that narrows the arterial lumen and impedes blood flow. The first step in the process is the formation of a „fatty streak” by subendothelial deposition of lipid-laden macrophages, also called „foam cells.” When a vascular insult occurs, the intima layer breaks, and monocytes migrate into the subendothelial space, where they become macrophages. These macrophages take up oxidized LDL particles, leading to foam cell formation. T cells get activated, and cytokines are released to aid in the inflammatory process. Growth factors activate smooth muscles, which also take up oxidized LDL particles and collagen, deposit along with activated macrophages, and increase the population of foam cells. Subendothelial plaque subsequently develops.

• #1 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  The vascular endothelium is the layer of cells lying under the epithelium lining the inside of the vessel and the muscular layer, which is a boundary between the circulating blood and the vascular wall. Its cells are specialized in maintaining vascular homeostasis, which is crucial for the proper functioning of organs, especially the heart. […] Inflammation in diseases such as polyarteritis nodosa and cryoglobulinemia is driven by IC deposition (antibody-mediated IC formation, microaneurysms). […] In recent years, there has been substantial research showing correlations between genetic factors and endothelial function and dysfunction, which in turn are associated with an increased risk of developing CAD.

• #1 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Coronary artery disease is usually caused by a build up cholesterol rich deposits or plaques on the lining inside the artery. These plaques are also called atheromatous plaques or simply atheromas and they cause a thickening of the arterial wall and a narrowing of the arterial space through which blood flows to reach the heart. […] An atheroma usually starts to develop as a result of damage or injury to the inner lining of the artery called the endothelium. Once the endothelium is damaged, cholesterol, fats, lipoproteins and other debris start to accumulate at the site of injury in the wall or intima of the artery. […] High concentrations of low density lipoprotein (LDL) penetrate the damaged endothelium and undergo a chemical process called oxidation. This altered LDL acts as a beacon that attracts white blood cells or leukocytes to migrate towards the vessel wall. As macrophages appear, they engulf the lipoproteins and become foam cells. These foam cells give rise to the earliest visible form of an atheromatous lesion called the fatty streak.

• #1 Coronary Artery Atherosclerosis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/153647-overview

  The mechanisms of atherogenesis remain uncertain, but the response-to-injury hypothesis is the most widely accepted proposal. […] Endothelial dysfunction is the initial step that allows diffusion of lipids and inflammatory cells (ie, monocytes, T lymphocytes) into the endothelial and subendothelial spaces. […] Oxidative stress has therefore been recognized as the most significant contributor to atherosclerosis by causing LDL oxidation and increasing nitric oxide breakdown. […] The presence of risk factors accelerates the rate of development of atherosclerosis.

• #1 Coronary Artery Atherosclerosis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/153647-overview

  Atherosclerosis is the principal cause of coronary artery disease (CAD), in which atherosclerotic changes are present within the walls of the coronary arteries. […] Atherosclerosis is a disease of large and medium-sized muscular arteries and is characterized by the following: endothelial dysfunction, vascular inflammation, buildup of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall. […] Atherosclerotic buildup results in the following: plaque formation, vascular remodeling, acute and chronic luminal obstruction, abnormalities of blood flow, diminished oxygen supply to target organs. […] By impairing or obstructing normal blood flow, atherosclerotic buildup causes myocardial ischemia. […] The earliest pathologic lesion of atherosclerosis is the fatty streak, which is observed in the aorta and coronary arteries of most individuals by age 20 years.

• #1 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Once the fatty streak is formed, it then attracts the smooth muscle cells to the site, where they multiply and start to produce extracellular matrix comprising of collagen and proteoglycan. It is this extracellular matrix that forms a large portion of the atherosclerotic plaque. This turns the fatty streak into a fibrous plaque. The lesion then starts to bulge into the inner wall of the blood vessel causing a significant narrowing of the luminal space. […] Next, the fibrous plaque starts to support itself. It develops its own small vessels to provide it with a supply of blood in a process called angiogenesis. Thereafter, the plaques begin to calcify as calcium starts to deposit. The final plaque is made up of a cap of fibrous tissue covering a core that is rich in lipids as well as necrotic or dead cells. The edge of this cap is key in acute coronary disease. This region is prone to rupture, which exposes the underlying core of lipids and necrotic material to thrombogenic factors in the blood. This can cause the aggregation of platelets that form a clot across the plaque and further narrow the artery.

• #1 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  The plaque could grow or become stable over time if no further endothelial insult occurs. A fibrous cap forms if the plaque becomes stable and the lesion calcifies over time. The lesion can become hemodynamically significant as time passes. Myocardial tissue perfusion can become insufficient, triggering angina symptoms during times of increased demand (eg, exercise) if the lumen has at least 70% obstruction. […] Key stages involved in atherosclerotic plaque formation include the following: During atherosclerosis, vascular smooth muscle cells (SMCs) proliferate and migrate, forming a fibrous cap that stabilizes the plaque. These SMCs can undergo transdifferentiation, giving rise to various cell types within the plaque core, including osteoblast-like, myofibroblast-like, foam-like, and mesenchymal-stem-like cells.

• #1 Coronary artery disease – Wikipedia

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

  Coronary artery disease (CAD), also called coronary heart disease (CHD), or ischemic heart disease (IHD), is a type of heart disease involving the reduction of blood flow to the cardiac muscle due to a build-up of atheromatous plaque in the arteries of the heart. […] CAD can cause stable angina, unstable angina, myocardial ischemia, and myocardial infarction. […] Atherosclerosis is a type of arteriosclerosis which is the chronic inflammation of the arteries which causes them to harden and accumulate cholesterol plaques (atheromatous plaques) on the artery walls. […] Coronary artery disease is characterized by heart problems that result from atherosclerosis. […] The narrowing of coronary arteries reduces the supply of oxygen-rich blood flowing to the heart, which becomes more pronounced during strenuous activities during which the heart beats faster and has an increased oxygen demand.

• #1 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Atherosclerosis is the main etiopathogenic process that causes CAD, and its progression is related to an interplay between environmental and genetic factors, with the latter exerting their effects either directly or via cardiovascular risk factors. […] Briefly, atherosclerosis is a silent progressive chronic process characterized by accumulation of lipids, fibrous elements, and inflammatory molecules in the walls of the large arteries. This process begins with the efflux of low-density lipoprotein (LDL) cholesterol to the subendothelial space, which can then be modified and oxidized by various agents. […] The final result of this process is formation of the first typical atherosclerotic lesion, ie, the fatty streak, in which foam cells are present in the subendothelial space. […] The thickness of the fibrous cap is key for maintaining the integrity of the atherosclerotic plaque, and two types of plaque can be defined depending on the balance between formation and degradation of this fibrous cap, ie, stable and unstable or vulnerable.

• #1 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Plaque stability is intimately linked with the type of calcification present. Stable plaques are often characterized by macrocalcifications and a thick, collagen-rich extracellular matrix within the fibrous cap, providing structural stability. In contrast, unstable plaques tend to have microcalcifications and a thin fibrous cap, heightening the risk of plaque rupture.

• #1 Coronary Artery Disease – Stable Angina Topic Review

  https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/coronary-artery-disease-stable-angina

  The primary symptoms of occlusive CAD include chronic stable angina pectoris. […] Patients may describe angina as a tightness, discomfort, not pain, squeezing, indigestion, heaviness, or an elephant sitting on my chest, and often describe the sensations of squeezing and tightness by placing a fist in the center of the chest (Levines sign). […] Treatment of chronic stable angina is aimed at increasing myocardial oxygen supply and reducing myocardial oxygen demand, as discussed in Pathophysiology. […] Nitroglycerin is metabolized to form the vasoactive free radical nitric oxide. […] Statins play a pivotal role in reducing CV events and mortality; see HMG-CoA Reductase Inhibitors Topic Review. […] Myocardial stunning occurs when transient ischemia resulting from total or subtotal coronary occlusion, such as during an ACS, results in segmental myocardial dysfunction.

• #1 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Vulnerable plaques have a thin fibrous cap made mostly of type I collagen and few or no smooth muscle cells, but abundant macrophages and proinflammatory and prothrombotic molecules. These plaques are prone to erosion or rupture, exposing the core of the plaque to circulating coagulation proteins, causing thrombosis, sudden occlusion of the artery lumen, and usually an acute coronary syndrome. […] The heritability of some phenotypes associated with arteriosclerosis has already been determined, and generally ranges from 40% to 55%. […] The second step is to study the genetic architecture of the disease, ie, identify the loci, and within these loci, the genetic variants that modulate disease susceptibility. […] In the case of CAD, notable successes include the identification of variants in ALOX5AP as being associated with coronary and cerebrovascular diseases, in MEF2A as being associated with CAD, and in PCSK9 as a gene for which variation is relevant in the metabolism of cholesterol.

• #1 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

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

  Coronary artery disease is due to […] Coronary artery atherosclerosis: Subintimal deposition of atheromas in large and medium-sized coronary arteries. […] Vascular endothelial dysfunction can promote atherosclerosis and contribute to coronary artery spasm. Endothelial dysfunction is also recognized as a cause of angina in the absence of epicardial coronary artery stenosis or spasm. […] Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing angina pectoris). The degree of stenosis required to cause ischemia varies with oxygen demand. […] Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.

• #1 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

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

  The consequences of acute ischemia, collectively referred to as acute coronary syndromes (ACS), depend on the location and degree of obstruction and range from unstable angina, nonST-segment elevation myocardial infarction (NSTEMI), to ST-segment elevation myocardial infarction (STEMI), which can result in transmural infarction, and other complications including malignant ventricular arrhythmias, conduction defects, heart failure, and sudden death. […] Coronary artery spasm is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia (vasospastic angina) may result. […] In arteries with atheroma, the atheroma causes endothelial dysfunction, possibly resulting in local hypercontractility. Proposed mechanisms include loss of sensitivity to intrinsic vasodilators (eg, acetylcholine) and increased production of vasoconstrictors (eg, angiotensin II, endothelin, leukotrienes, serotonin, thromboxane) in the area of the atheroma.

• #1 Coronary artery disease in rheumatoid arthritis: Pathogenesis, risk factors, clinical manifestations, and diagnostic implications – UpToDate

  https://www.uptodate.com/contents/coronary-artery-disease-in-rheumatoid-arthritis-pathogenesis-risk-factors-clinical-manifestations-and-diagnostic-implications

  Coronary artery disease in rheumatoid arthritis: Pathogenesis, risk factors, clinical manifestations, and diagnostic implications […] The prevalence of atherosclerotic coronary artery disease (CAD) is increased in patients with chronic inflammatory diseases such as rheumatoid arthritis (RA) or systemic lupus erythematosus. […] The epidemiologic evidence, possible pathogenetic mechanisms, and clinical relevance of CAD in RA will be reviewed here. […] Many of the underlying mechanisms of pathogenesis of atherosclerosis are shared in patients with and without rheumatoid arthritis (RA). […] Among the general population, it is increasingly clear that inflammation has a significant role in the development of coronary artery disease (CAD) and that the innate and adaptive immune systems play an important role in the initiation and progression of atherosclerosis.

• #1 Role of interleukins in the pathogenesis of coronary heart disease: A literature review

  https://www.wjgnet.com/1949-8462/full/v17/i3/103947.htm

  Interleukins (ILs), a subset of cytokines, play a critical role in the pathogenesis of coronary heart disease (CHD) by mediating inflammation. This review article summarizes the role of ILs such as IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, and IL-10 in the pathogenesis of CHD. […] IL-6 helps serve as a reliable biomarker for the degree of CAD, as determined by the Gensini score, and is a key factor in the development of atherosclerosis. […] IL-1 plays a central role in the pathogenesis of CHD by mediating inflammation and contributing to the development and progression of atherosclerosis. […] IL-2 plays a complex and less direct role in the pathogenesis of CHD compared to other ILs like IL-1 or IL-6. […] IL-3 may be involved in the process of vascular remodeling, making individuals with elevated levels of IL-3 especially vulnerable to coronary restenosis.

• #1 Role of interleukins in the pathogenesis of coronary heart disease: A literature review

  https://www.wjgnet.com/1949-8462/full/v17/i3/103947.htm

  The risk prediction model, which combines these serum cytokines (IL-4 and IL-17) with clinical risk factors (sex, smoking, and diabetes) and the protective factor HDL-C, might be able to distinguish between patients with CAD and those who may have CAD but do not have MI. […] IL-5 plays a multifaceted role in CHD pathogenesis, with both pro-atherogenic and anti-atherogenic effects. […] IL-6 is a key factor in the development of atherosclerosis. […] IL-7 contributes to the pathogenesis of CHD by driving vascular inflammation, endothelial dysfunction, and immune cell activation. […] IL-8 plays a part in the progression of CAD occurrences. […] IL-9 may interact with established CAD risk factors to cause CAD. […] IL-10 indicates a proinflammatory state in acute coronary syndrome patients. […] The development of CHD and atherosclerosis is significantly influenced by inflammation. ILs, a subset of cytokines, play a critical role in the pathogenesis of CHD by mediating inflammation, which is a key factor in atherosclerosis and its complications.

• #1 Mechanism of salidroside against coronary artery disease by network pharmacology analysis | BMC Complementary Medicine and Therapies | Full Text

  https://bmccomplementmedtherapies.biomedcentral.com/articles/10.1186/s12906-023-04027-3

  The pathophysiological mechanisms of CAD are complex. It is well known that CAD is a chronic inflammatory disease. Several proinflammatory cytokines, such as IL-6, IL-18, TNF- and C-reactive protein, have been reported to be independently associated with the risk of coronary heart disease. […] The enrichment analysis of salidroside in the treatment of CAD suggests that salidroside can regulate inflammatory biological processes, such as leukocyte apoptotic process, leukocyte migration, and inflammatory response in the treatment of CAD, which is consistent with the pharmacological mechanism of salidroside. […] More intriguingly, many biological processes and signaling pathways related to angiogenesis were enriched in the enrichment analysis. Angiogenesis is the formation of new blood vessels.

• #1 Inflammatory Factors in Coronary Heart Disease: Mechanism, diagnosis and therapy | Frontiers Research Topic

  https://www.frontiersin.org/research-topics/38940/inflammatory-factors-in-coronary-heart-disease-mechanism-diagnosis-and-therapy/magazine

  Coronary Heart Disease (CHD), a group of clinical syndromes caused by the development of coronary atherosclerosis, has become the main cause of death in human. […] Recent studies have shown that CHD, including coronary atherosclerosis, myocardial infarction, myocardial ischemia-reperfusion injury, are defined as a kind of inflammatory diseases. Inflammatory factors, cytokines involved in inflammatory response, have gradually become an important biomarker of CHD and effective target for treatment, including anti-inflammatory factors and pro-inflammatory factors. […] In recent years, the Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS) has found that IL-1 Antibody could significantly improve the long-term prognosis of patients with coronary heart disease, screening by high CRP, indicating a milestone in the anti-inflammatory treatment of CHD.

• #1 Pathophysiology of Coronary Heart Disease: A Brief Review

  https://www.degruyter.com/document/doi/10.7556/jaoa.2004.20022/html?lang=en

  An accumulating body of evidence suggests that atherosclerotic progression results from microinflammation mediated by proinflammatory cytokines. […] Chronic low-level inflammation increases atherosclerotic plaque deposition in animal models. […] Newer information reveals that CRP is a modulator of inflammation and may have both proinflammatory and antiinflammatory actions, which may directly contribute to endothelial dysfunction by inducing cytokine release and surface expression of adhesion molecules. […] Therefore, the term vulnerable patient may be more appropriate and is proposed now for the identification of subjects with high likelihood of having cardiac events develop in the near future. […] According to Naghavi et al, markers suggesting the presence of vulnerable blood include increased levels of CRP and circulating interleukin-6 levels, which are elevated in patients with acute coronary syndromes.

• #1

  https://crimsonpublishers.com/ojchd/fulltext/OJCHD.000545.php

  Coronary artery diseases (CAD) known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease (CHD), or ischemic heart disease (IHD). CAD is the largest contributor of cardiovascular diseases (CVDs) and mortality rate is due in prevalence to atherosclerosis, a chronic inflammatory condition of the arterial wall. Atherosclerosis is a pathological process that affects large- and medium-sized arteries and causes coronary artery disease (angina pectoris and myocardial infarction), cerebrovascular disease (ischemic stroke and vascular dementia) and peripheral vascular disease (intermittent claudication and gangrene). Atherosclerosis is a chronic cumulative disease progressing over years. It is characterized by atherosclerotic plaques formed in the wall of the vessels, consisting of necrotic cores, calcified regions, accumulated modified lipids, and inflamed smooth muscle cells (SMCs), endothelial cells, leukocytes, and foam cells. Lesions begin early as fatty streaks and progress into pathologic lesions under the influence of both genetic and lifestyle insults. The pathologist Felix Marchand first introduced the term atherosclerosis in 1904, describing the association of fatty degeneration and vessel stiffening. This process affects medium and large-sized arteries and is characterized by patchy intramural thickening of the sub-intima that encroaches on the arterial lumen. The earliest visible lesion of atherosclerosis is the fatty streak, which is due to an accumulation of lipid-laden foam cells in the intimal layer of the artery. With time; the fatty streak evolves into a fibrous plaque, the hallmark of established atherosclerosis. Ultimately the lesion may evolve to contain large amounts of lipid; if it becomes unstable, denudation of overlying endothelium, or plaque rupture, may result in thrombotic occlusion of the overlying artery. Atherosclerotic lesions (atheromata) are composed of three major components. The first is the cellular component comprised predominately of smooth muscle cells and macrophages. The second component is the connective tissue matrix and extracellular lipid. The third component is intracellular lipid that accumulates within macrophages, thereby converting them into foam cells. Atherosclerotic lesions develop as a result of inflammatory stimuli, subsequent release of various cytokines, proliferation of smooth muscle cells, synthesis of connective tissue matrix, and accumulation of macrophages and lipid. Excess generation of (ROS) represents an important pathological process in atherogenesis. Each component of the atherosclerotic blood vessel has been demonstrated to increase production of ROS, primarily superoxide anion. Important sources of ROS are vascular smooth muscle cells, endothelial cells, fibroblasts, and infiltrating leukocytes. Production of ROS affects gene transcription, damages DNA, and increases production of inflammatory transcription factors. The two best-characterized effects include oxidation of LDL and scavenging of endothelium-derived NO. The progression of atherosclerotic disease has been described as moving from an early lesion (phase1) to a more advanced fibro-lipid lesion (phase 2). The formation of thrombus or hematoma can advance into an acute phase (phase 3 and 4) or even to total occlusion (phase 5).

• #1 Pathogenesis, Assessment, and Treatment of Coronary Microcirculation Dysfunction – ABC Cardiol

  https://abccardiol.org/en/article/pathogenesis-assessment-and-treatment-of-coronary-microcirculation-dysfunction/

  Cardiovascular disease is the predominant cause of mortality on a global scale. […] Coronary microvascular dysfunction, characterized by impaired coronary flow reserve resulting from functional and/or structural abnormalities in the microcirculation, is linked to adverse cardiovascular outcomes. […] This review aims to explore the prevalence, underlying mechanisms, diagnostic approaches, and therapeutic interventions for coronary microvascular dysfunction.

• #1 Coronary Artery Disease – Stable Angina Topic Review

  https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/coronary-artery-disease-stable-angina

  In the setting of chronic ischemia, collateral circulation may develop to compensate for the reduced blood flow. […] With sudden increases in arterial tone, coronary vasospasm can occur and result in angina. […] Myocardial bridging occurs when a segment of a coronary vessel does not run along the epicardial surface of the heart, but within the myocardium. […] A coronary arterial wall weakened by disease may dilate and form a coronary artery aneurysm. […] Many types of congenital variations of the coronary arteries exist.

• #1 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

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

  Coronary artery dissection is a rare, non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction. […] Treatment generally aims to reduce cardiac workload by decreasing oxygen demand and improving coronary artery blood flow, and, over the long term, to halt and reverse the atherosclerotic process. […] Antiplatelet agents and statins improve short-term and long-term outcomes, probably by improving atheromatous plaque stability and endothelial function. […] Beta-blockers reduce symptoms of angina by reducing heart rate and contractility and decreasing myocardial oxygen demand. […] Aspirin prolongs vein graft patency. Continued smoking has a profound adverse effect on patency. […] Modification of serum lipid levels (particularly with statins) may slow or even partially reverse the progression of CAD.

• #1 Coronary Artery Atherosclerosis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/153647-overview

  The fatty streak is the result of focal accumulation of serum lipoproteins within the intima of the vessel wall. […] The SMCs are responsible for the deposition of extracellular connective tissue matrix and form a fibrous cap that overlies a core of lipid-laden foam cells, extracellular lipid, and necrotic cellular debris. […] Growth of the fibrous plaque results in vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, and compromised oxygen supply to the target organ. […] As endothelial injury and inflammation progress, fibroatheromas grow and form the plaque. […] Denudation of the overlying endothelium or rupture of the protective fibrous cap may result in exposure of the thrombogenic contents of the core of the plaque to the circulating blood. […] Most plaque ruptures occur because of disruption of the fibrous cap, which allows contact between the highly thrombogenic lipid core and the blood.

• #1 Circular RNAs in coronary heart disease: From molecular mechanism to promising clinical application (Review)

  https://www.spandidos-publications.com/10.3892/ijmm.2024.5452

  Coronary heart disease (CHD) remains a leading cause of morbidity and mortality worldwide, posing a substantial public health burden. […] The underlying mechanisms of CHD are multifactorial, involving dyslipidemia, endothelial dysfunction, oxidative stress and chronic inflammation. […] Currently, circular RNAs (circRNAs) have emerged as a pivotal class of non-coding RNAs, attracting substantial attention in the field of cardiovascular research. […] In CHD, emerging evidence suggests that circRNAs play critical roles in the regulation of vascular function, myocardial injury and inflammation. […] This review aims to provide a comprehensive overview of the current understanding of circRNAs in CHD. It summarizes the molecular mechanisms by which circRNAs influence the pathophysiology of CHD, including their roles in cardiomyocyte death, endothelial injury, vascular dysfunction and inflammation.

• #1 Circular RNAs in coronary heart disease: From molecular mechanism to promising clinical application (Review)

  https://www.spandidos-publications.com/10.3892/ijmm.2024.5452

  CircRNAs have emerged as crucial players in the pathogenesis of CHD. […] Research has identified numerous circRNAs that are differentially expressed in patients with CHD compared to healthy controls, suggesting their crucial role in disease progression. […] CircRNAs participate in regulating endothelial cell function in CHD through complex molecular mechanisms involving the sponging of miRNAs and subsequent modulation of mRNA targets. […] VSMC apoptosis is involved in the development and progression of CHD by affecting vascular remodeling, plaque stability and inflammatory responses. […] The inflammatory response is a complex biological process initiated by the immune system to protect the body against harmful stimuli such as pathogens, damaged cells or irritants. […] CircRNAs have a vital role in the inflammatory response associated with the development of CHD. […] Overall, the growing body of evidence highlights the multifaceted roles of circRNAs in CHD, from their involvement in cell proliferation and apoptosis to inflammation, providing new avenues for the diagnosis and treatment of this disease.

• #1 A network pharmacology approach to reveal the protective mechanism of Salvia miltiorrhiza-Dalbergia odorifera coupled-herbs on coronary heart disease | Scientific Reports

  https://www.nature.com/articles/s41598-019-56050-5

  According to the aetiologies of CHD, these biological processes can be divided into three functional modules, including vascular endothelial function regulation, inflammatory response, and lipid metabolism. […] Through GO and KEGG pathway enrichment analysis of common-target and PPI networks, 10 significant signaling pathways were screened as key action mechanisms of SMDOCH on CHD, and these pathways can be divided into three functional modules: vascular endothelial function regulation, inflammatory response, and lipid metabolism. […] The Vascular endothelial function regulation model showed that SMDOCH may influence vascular endothelial function by regulating hormone (renin, angiotensin, oestrogen) activity and three key upstream pathways: KEGG:04933, KEGG:05418, and KEGG:04066. […] The Inflammatory response model showed that SMDOCH may influence inflammation response through three key signaling pathways: KEGG:04668, KEGG:04064, and KEGG:04620.

• #1 A network pharmacology approach to reveal the protective mechanism of Salvia miltiorrhiza-Dalbergia odorifera coupled-herbs on coronary heart disease | Scientific Reports

  https://www.nature.com/articles/s41598-019-56050-5

  The Lipid metabolism model showed that SMDOCH may influence lipid metabolism by regulating KEGG:04920. […] In conclusion, the cardioprotective effect of the bioactive components of SMDOCH, such as tanshinone IIA from SM as well as formononetin and butin from DO, can be explained, at least in part, by the biological processes vascular endothelial function regulation, inflammatory response, and lipid metabolism through the core targets TP53, ESR1, AKT1, STAT3, and MAPK1.

• #1 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  Cardiovascular diseases (CVDs) are disorders associated with the heart and circulatory system. Atherosclerosis is its major underlying cause. […] This review summarizes the available information on the pathophysiological implications of CVDs, focusing on coronary artery disease along with atherosclerosis as its major cause and arterial hypertension. We discuss the endothelium dysfunction, inflammatory factors, and oxidation associated with atherosclerosis. Mechanisms such as dysfunction of the endothelium and inflammation, which have been identified as critical pathways for development of coronary artery disease, have become easier to diagnose in recent years. […] Atherosclerosis is the main cause of cardiovascular-related death worldwide. It is a thickening and hardening of the arterial wall, accompanies aging, and is related to major adverse impact on the cardiovascular system and various other diseases. Elevated plasma cholesterol level (>150 mg/dL) is a major cause of the development of atherosclerosis.

• #1 Coronary artery disease – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/coronary-artery-disease/symptoms-causes/syc-20350613

  Coronary artery disease (CAD) is a common type of heart disease. It affects the main blood vessels that supply blood to the heart, called the coronary arteries. In CAD, there is reduced blood flow to the heart muscle. A buildup of fats, cholesterol and other substances in and on the artery walls, a condition called atherosclerosis, usually causes coronary artery disease. The buildup, called plaque, makes the arteries narrow. […] Coronary artery disease is caused by the buildup of fats, cholesterol and other substances in and on the walls of the heart arteries. This condition is called atherosclerosis. The buildup is called plaque. Plaque can cause the arteries to narrow, blocking blood flow. The plaque also can burst, causing a blood clot. […] Some causes of atherosclerosis and coronary artery disease are: Diabetes or insulin resistance, High blood pressure, Lack of exercise, Smoking or tobacco use.

• #1 Cardiovascular disease

  https://www.nhs.uk/conditions/cardiovascular-disease/

  Coronary heart disease occurs when the flow of oxygen-rich blood to the heart muscle is blocked or reduced. […] This puts an increased strain on the heart, and can lead to: angina chest pain caused by restricted blood flow to the heart muscle, heart attacks where the blood flow to the heart muscle is suddenly blocked, heart failure where the heart is unable to pump blood around the body properly. […] High blood pressure (hypertension) is one of the most important risk factors for CVD. If your blood pressure is too high, it can damage your blood vessels. […] Smoking and other tobacco use is also a significant risk factor for CVD. The harmful substances in tobacco can damage and narrow your blood vessels. […] Cholesterol is a fatty substance found in the blood. If you have high cholesterol, it can cause your blood vessels to narrow and increase your risk of developing a blood clot.

• #1 Cardiovascular disease

  https://www.nhs.uk/conditions/cardiovascular-disease/

  High blood sugar levels can damage the blood vessels, making them more likely to become narrowed. […] Chronic kidney disease (CKD) is a long-term condition where the kidneys do not work as well as they should. People with chronic kidney disease have an increased risk of developing other serious problems, including CVD. […] If you don’t exercise regularly, it’s more likely that you’ll have high blood pressure, high cholesterol levels and be overweight. All of these are risk factors for CVD. […] Being overweight or obese increases your risk of developing diabetes and high blood pressure, both of which are risk factors for CVD. […] If you have a family history of CVD, your risk of developing it is also increased. […] In the UK people of south Asian and Black African or African Caribbean background have an increased risk of getting CVD. […] A healthy lifestyle can lower your risk of CVD. If you already have CVD, staying as healthy as possible can reduce the chances of it getting worse.

• #1 Relationship between time-varying achieved HbA1c and risk of coronary artery disease events among common haptoglobin phenotype groups with type 2 diabetes: the ADVANCE study | BMJ Open Diabetes Research & Care

  https://drc.bmj.com/content/13/3/e004713

  When compared with HbA1c of 7.0%7.9%, having HbA1c 8.0% was associated with a greater CAD risk among participants with the Hp2-2 phenotype (HR 1.53, 95% CI 1.01 to 2.33), but was not associated with CAD risk among participants without the Hp2-2 phenotype (1.27, 0.90 to 1.79, p-interaction=0.71) […] The current study does not provide evidence to support an HbA1c target of 7.0% when compared with 7.0%7.9% for CAD prevention in either Hp phenotype group. […] Our findings for the CAD outcome among participants with the Hp2-2 phenotype are in line with the existing literatures suggested biological mechanism linking HbA1c and Hp type to CAD. […] Therefore, based on the existing mechanistic literature, preventing high HbA1c may be particularly important for CAD prevention among people with the Hp2-2 phenotype to help reduce Hp2:HbA1c-mediated oxidative damage.

• #1

  https://eurekaselect.com/public/chapter/21850

  Overwhelming evidence suggests that regular physical activity (30 min/day), cessation of cigarette smoking, and consumption of antioxidant nutraceuticals rich in flavonoids and retinoids, fresh vegetables and fruits, omega-3 PUFA, culinary spices, probiotics, Mediterranean-type diet, and DASH DIET lower the risk of atherogenesis and cardiovascular diseases. […] New preventative measures and alternative therapies, including dietary interventions and plant-based foods may be the most cost-effective ways to manage atherosclerosis and cardiovascular illnesses.

• #1 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Coronary artery disease (CAD) is the leading cause of death and disability worldwide, and its prevalence is expected to increase in the coming years. CAD events are caused by the interplay of genetic and environmental factors, the effects of which are mainly mediated through cardiovascular risk factors. […] CAD is a complex chronic inflammatory disease, characterized by remodeling and narrowing of the coronary arteries supplying oxygen to the heart. It can have various clinical manifestations, including stable angina, acute coronary syndrome, and sudden cardiac death. It has a complex etiopathogenesis and a multifactorial origin related to environmental factors, such as diet, smoking, and physical activity, and genetic factors that modulate risk of the disease both individually and through interaction.

• #1 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Our understanding of the genetic architecture of CAD has improved considerably since 2007 when the first GWAS of this disease were published. […] At the beginning of 2013, a meta-analysis of several GWAS identified a final set of about 40 genetic variants associated with CAD that explains approximately 6% of the heritability of CAD. […] Some of these variants are related to lipid metabolism, blood pressure, and inflammation, which confirms the importance of these pathways in the pathogenesis of CAD. […] Genetic studies can shed light on new metabolic pathways associated with the development and progression of atherosclerosis, and provide clues for identifying new pharmacologic targets. […] The genetic variants associated with CAD at the 9p21 locus, which has been the top hit in all CAD GWAS since 2007, lie in an intergenic region close to a cluster of cell-cycle regulating tumor suppressor genes (CDKN2A and CDKN2B) that overlap with a nonprotein coding RNA (CDKN2BAS or ANRIL). […] The identification of genetic variants associated with disease has allowed us to improve our understanding of its pathogenesis, and ultimately to reduce the burden of disease at both the individual and population levels.

• #2 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Coronary artery disease (CAD) is the leading cause of death and disability worldwide, and its prevalence is expected to increase in the coming years. CAD events are caused by the interplay of genetic and environmental factors, the effects of which are mainly mediated through cardiovascular risk factors. […] CAD is a complex chronic inflammatory disease, characterized by remodeling and narrowing of the coronary arteries supplying oxygen to the heart. It can have various clinical manifestations, including stable angina, acute coronary syndrome, and sudden cardiac death. It has a complex etiopathogenesis and a multifactorial origin related to environmental factors, such as diet, smoking, and physical activity, and genetic factors that modulate risk of the disease both individually and through interaction.

• #2

  https://crimsonpublishers.com/ojchd/fulltext/OJCHD.000545.php

  Coronary artery diseases (CAD) known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease (CHD), or ischemic heart disease (IHD). CAD is the largest contributor of cardiovascular diseases (CVDs) and mortality rate is due in prevalence to atherosclerosis, a chronic inflammatory condition of the arterial wall. Atherosclerosis is a pathological process that affects large- and medium-sized arteries and causes coronary artery disease (angina pectoris and myocardial infarction), cerebrovascular disease (ischemic stroke and vascular dementia) and peripheral vascular disease (intermittent claudication and gangrene). Atherosclerosis is a chronic cumulative disease progressing over years. It is characterized by atherosclerotic plaques formed in the wall of the vessels, consisting of necrotic cores, calcified regions, accumulated modified lipids, and inflamed smooth muscle cells (SMCs), endothelial cells, leukocytes, and foam cells. Lesions begin early as fatty streaks and progress into pathologic lesions under the influence of both genetic and lifestyle insults. The pathologist Felix Marchand first introduced the term atherosclerosis in 1904, describing the association of fatty degeneration and vessel stiffening. This process affects medium and large-sized arteries and is characterized by patchy intramural thickening of the sub-intima that encroaches on the arterial lumen. The earliest visible lesion of atherosclerosis is the fatty streak, which is due to an accumulation of lipid-laden foam cells in the intimal layer of the artery. With time; the fatty streak evolves into a fibrous plaque, the hallmark of established atherosclerosis. Ultimately the lesion may evolve to contain large amounts of lipid; if it becomes unstable, denudation of overlying endothelium, or plaque rupture, may result in thrombotic occlusion of the overlying artery. Atherosclerotic lesions (atheromata) are composed of three major components. The first is the cellular component comprised predominately of smooth muscle cells and macrophages. The second component is the connective tissue matrix and extracellular lipid. The third component is intracellular lipid that accumulates within macrophages, thereby converting them into foam cells. Atherosclerotic lesions develop as a result of inflammatory stimuli, subsequent release of various cytokines, proliferation of smooth muscle cells, synthesis of connective tissue matrix, and accumulation of macrophages and lipid. Excess generation of (ROS) represents an important pathological process in atherogenesis. Each component of the atherosclerotic blood vessel has been demonstrated to increase production of ROS, primarily superoxide anion. Important sources of ROS are vascular smooth muscle cells, endothelial cells, fibroblasts, and infiltrating leukocytes. Production of ROS affects gene transcription, damages DNA, and increases production of inflammatory transcription factors. The two best-characterized effects include oxidation of LDL and scavenging of endothelium-derived NO. The progression of atherosclerotic disease has been described as moving from an early lesion (phase1) to a more advanced fibro-lipid lesion (phase 2). The formation of thrombus or hematoma can advance into an acute phase (phase 3 and 4) or even to total occlusion (phase 5).

• #2 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Coronary artery disease is usually caused by a build up cholesterol rich deposits or plaques on the lining inside the artery. These plaques are also called atheromatous plaques or simply atheromas and they cause a thickening of the arterial wall and a narrowing of the arterial space through which blood flows to reach the heart. […] An atheroma usually starts to develop as a result of damage or injury to the inner lining of the artery called the endothelium. Once the endothelium is damaged, cholesterol, fats, lipoproteins and other debris start to accumulate at the site of injury in the wall or intima of the artery. […] High concentrations of low density lipoprotein (LDL) penetrate the damaged endothelium and undergo a chemical process called oxidation. This altered LDL acts as a beacon that attracts white blood cells or leukocytes to migrate towards the vessel wall. As macrophages appear, they engulf the lipoproteins and become foam cells. These foam cells give rise to the earliest visible form of an atheromatous lesion called the fatty streak.

• #2 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  CAD is caused primarily by plaque formation within the intima of the vessel wall, with plaque being defined as a fatty material growing inside intima along with a severe inflammation, especially if the inflammation is chronic. […] Endothelial dysfunction in modern cardiovascular medicine is described as changes in the production and availability of endothelial-derived NO, prostacyclin, and endothelin, as well as their impact on vascular reactivity. […] The endothelial dysfunction is directly related to a decreased production and sensitivity of cells to NO. As a result, we have an effective disturbance in the functioning of the entire vessel and its homeostasis, which leads to an observation of prothrombotic and proinflammatory phenomena, along with lower susceptibility of the blood vessel wall.

• #2 Coronary Artery Disease: From Mechanism to Clinical Practice | SpringerLink

  https://link.springer.com/chapter/10.1007/978-981-15-2517-9_1

  In most developed countries, coronary artery disease (CAD), mostly caused by atherosclerosis of coronary arteries, is one of the primary causes of death. […] Atherosclerosis contains some highly correlative processes such as lipid disturbances, thrombosis, inflammation, vascular smooth cell activation, remodeling, platelet activation, endothelial dysfunction, oxidative stress, altered matrix metabolism, and genetic factors. […] Risk factors of CAD exist among many individuals of the general population, which includes hypertension, lipids and lipoproteins metabolism disturbances, diabetes mellitus, chronic kidney disease, age, genders, lifestyle, cigarette smoking, diet, obesity, and family history. […] Angina pectoris is caused by myocardial ischemia in the main expression of pain in the chest or adjoining area, which is usually a result of exertion and related to myocardial function disorder.

• #2 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Atherosclerosis is the main etiopathogenic process that causes CAD, and its progression is related to an interplay between environmental and genetic factors, with the latter exerting their effects either directly or via cardiovascular risk factors. […] Briefly, atherosclerosis is a silent progressive chronic process characterized by accumulation of lipids, fibrous elements, and inflammatory molecules in the walls of the large arteries. This process begins with the efflux of low-density lipoprotein (LDL) cholesterol to the subendothelial space, which can then be modified and oxidized by various agents. […] The final result of this process is formation of the first typical atherosclerotic lesion, ie, the fatty streak, in which foam cells are present in the subendothelial space. […] The thickness of the fibrous cap is key for maintaining the integrity of the atherosclerotic plaque, and two types of plaque can be defined depending on the balance between formation and degradation of this fibrous cap, ie, stable and unstable or vulnerable.

• #2 Coronary Artery Atherosclerosis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/153647-overview

  The fatty streak is the result of focal accumulation of serum lipoproteins within the intima of the vessel wall. […] The SMCs are responsible for the deposition of extracellular connective tissue matrix and form a fibrous cap that overlies a core of lipid-laden foam cells, extracellular lipid, and necrotic cellular debris. […] Growth of the fibrous plaque results in vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, and compromised oxygen supply to the target organ. […] As endothelial injury and inflammation progress, fibroatheromas grow and form the plaque. […] Denudation of the overlying endothelium or rupture of the protective fibrous cap may result in exposure of the thrombogenic contents of the core of the plaque to the circulating blood. […] Most plaque ruptures occur because of disruption of the fibrous cap, which allows contact between the highly thrombogenic lipid core and the blood.

• #2 Pathophysiology of Coronary Heart Disease: A Brief Review

  https://www.degruyter.com/document/doi/10.7556/jaoa.2004.20022/html?lang=en

  Coronary heart disease (CHD) remains a persistent public health burden in the United States, and it is the cause of one of every five deaths each year. […] Emerging evidence strongly suggests that coronary heart disease (CHD), once considered the result of vessel-occluding deposition of lipids, is a manifestation of a chronic inflammatory response to injury or infection. […] Evidence suggests that lipid-lowering modes of therapy also reduce inflammation, which may reduce the risk of cardiovascular events, even for individuals with LDL-C levels in the normal range (130 mg/dL) based on the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) guidelines. […] Injury or infection can disrupt normal endothelial function and initiate formation of atherosclerotic lesions known as fatty streaks.

• #2 Pathophysiology of Coronary Heart Disease: A Brief Review

  https://www.degruyter.com/document/doi/10.7556/jaoa.2004.20022/html?lang=en

  Macrophages engulf lipids, becoming activated foam cells that release an array of chemoattractant molecules, cytokines, and growth factors. […] As this cycle is repeated, the plaque develops a fatty core covered by a fibrous matrix that stabilizes the structure. […] Although several types of plaque can result in serious coronary events, retrospective analyses have demonstrated that 70% of all fatal acute myocardial infarctions and sudden coronary deaths are attributable to plaque rupture or plaque erosion. […] Vulnerable plaques are defined as thrombosis-prone or at risk of rapid progression and exhibit some combination of the following: active inflammation, thinning cap with a large lipid core, endothelial denudation with superficial platelet aggregation, fissures, or greater than 90% stenosis.

• #2 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Once the fatty streak is formed, it then attracts the smooth muscle cells to the site, where they multiply and start to produce extracellular matrix comprising of collagen and proteoglycan. It is this extracellular matrix that forms a large portion of the atherosclerotic plaque. This turns the fatty streak into a fibrous plaque. The lesion then starts to bulge into the inner wall of the blood vessel causing a significant narrowing of the luminal space. […] Next, the fibrous plaque starts to support itself. It develops its own small vessels to provide it with a supply of blood in a process called angiogenesis. Thereafter, the plaques begin to calcify as calcium starts to deposit. The final plaque is made up of a cap of fibrous tissue covering a core that is rich in lipids as well as necrotic or dead cells. The edge of this cap is key in acute coronary disease. This region is prone to rupture, which exposes the underlying core of lipids and necrotic material to thrombogenic factors in the blood. This can cause the aggregation of platelets that form a clot across the plaque and further narrow the artery.

• #2 Coronary heart disease (CHD) – Clinic «K+31»

  https://www.k31.ru/en/service/kardiologiya/ishemicheskaya-bolezn-serdca-ibs.html

  According to modern concepts, IHD is based on myocardial damage due to its insufficient blood supply. The imbalance between the real blood supply to the myocardium and its needs for blood supply can occur due to the following circumstances: […] Causes inside the vessel: atherosclerotic narrowing of the lumen of the coronary arteries; thrombosis and thromboembolism of coronary arteries; coronary artery spasm. […] Under the influence of a number of risk factors, atherosclerotic plaque formation occurs. At first, the lumen of the vessel does not change significantly. As lipids accumulate in the plaque, ruptures of its fibrous cover occur, which is accompanied by the deposition of platelets and fibrin, which contribute to local narrowing of the vessel. Along with lipidofibrotic plaques, almost exclusively fibrotic stenosing plaques are formed that undergo calcification.

• #2 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Plaque stability is intimately linked with the type of calcification present. Stable plaques are often characterized by macrocalcifications and a thick, collagen-rich extracellular matrix within the fibrous cap, providing structural stability. In contrast, unstable plaques tend to have microcalcifications and a thin fibrous cap, heightening the risk of plaque rupture.

• #2 Cardiovascular pathology coronary heart disease finale | PPT

  https://www.slideshare.net/slideshow/cardiovascular-pathology-coronary-heart-disease-finale/16814936

  5. Atherosclerosis is a progressive disease involving the development of arterial wall lesions. As they grow, these lesions may narrow or occlude the arterial lumen. Complex lesions may also become unstable and rupture, leading to acute coronary events, such as unstable angina, myocardial infarction, and stroke. […] 6. The acute coronary syndromes are frequently initiated by an unpredictable and abrupt conversion of a stable atherosclerotic plaque to an unstable and potentially life-threatening atherothrombotic lesion through superficial erosion, ulceration, fissuring, rupture, or deep hemorrhage, usually with superimposed thrombosis. […] 7. Sudden cardiac death (SCD) is an unexpected death from cardiac causes within one hour of symptoms. […] 8. Pathogenesis: Severe atherosclerotic coronary artery disease disrupted plaques with or without platelet nonocclusive thrombi. […] 9. Acute myocardial infarction (AMI) is the most common cause of death in adults in the United States. […] 10. Myocardial ischemia occurs when the oxygen supply is insufficient to meet metabolic demands.

• #2 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

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

  The consequences of acute ischemia, collectively referred to as acute coronary syndromes (ACS), depend on the location and degree of obstruction and range from unstable angina, nonST-segment elevation myocardial infarction (NSTEMI), to ST-segment elevation myocardial infarction (STEMI), which can result in transmural infarction, and other complications including malignant ventricular arrhythmias, conduction defects, heart failure, and sudden death. […] Coronary artery spasm is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia (vasospastic angina) may result. […] In arteries with atheroma, the atheroma causes endothelial dysfunction, possibly resulting in local hypercontractility. Proposed mechanisms include loss of sensitivity to intrinsic vasodilators (eg, acetylcholine) and increased production of vasoconstrictors (eg, angiotensin II, endothelin, leukotrienes, serotonin, thromboxane) in the area of the atheroma.

• #2 Inflammatory Factors in Coronary Heart Disease: Mechanism, diagnosis and therapy | Frontiers Research Topic

  https://www.frontiersin.org/research-topics/38940/inflammatory-factors-in-coronary-heart-disease-mechanism-diagnosis-and-therapy/magazine

  Coronary Heart Disease (CHD), a group of clinical syndromes caused by the development of coronary atherosclerosis, has become the main cause of death in human. […] Recent studies have shown that CHD, including coronary atherosclerosis, myocardial infarction, myocardial ischemia-reperfusion injury, are defined as a kind of inflammatory diseases. Inflammatory factors, cytokines involved in inflammatory response, have gradually become an important biomarker of CHD and effective target for treatment, including anti-inflammatory factors and pro-inflammatory factors. […] In recent years, the Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS) has found that IL-1 Antibody could significantly improve the long-term prognosis of patients with coronary heart disease, screening by high CRP, indicating a milestone in the anti-inflammatory treatment of CHD.

• #2 Role of interleukins in the pathogenesis of coronary heart disease: A literature review

  https://www.wjgnet.com/1949-8462/full/v17/i3/103947.htm

  The risk prediction model, which combines these serum cytokines (IL-4 and IL-17) with clinical risk factors (sex, smoking, and diabetes) and the protective factor HDL-C, might be able to distinguish between patients with CAD and those who may have CAD but do not have MI. […] IL-5 plays a multifaceted role in CHD pathogenesis, with both pro-atherogenic and anti-atherogenic effects. […] IL-6 is a key factor in the development of atherosclerosis. […] IL-7 contributes to the pathogenesis of CHD by driving vascular inflammation, endothelial dysfunction, and immune cell activation. […] IL-8 plays a part in the progression of CAD occurrences. […] IL-9 may interact with established CAD risk factors to cause CAD. […] IL-10 indicates a proinflammatory state in acute coronary syndrome patients. […] The development of CHD and atherosclerosis is significantly influenced by inflammation. ILs, a subset of cytokines, play a critical role in the pathogenesis of CHD by mediating inflammation, which is a key factor in atherosclerosis and its complications.

• #2 Role of interleukins in the pathogenesis of coronary heart disease: A literature review

  https://www.wjgnet.com/1949-8462/tables/v17/i3/103947.htm

  IL-1 has been shown that chronic administration of IL-1 to the myocardial and coronary arteries causes cardiac dysfunction and coronary arteriosclerosis. Pericardial IL-1 concentrations could indicate the degree of ischemic heart disease, and high levels of IL-1 in pericardial fluid might also directly encourage the development of coronary atherosclerosis. […] IL-6 helps serve as a reliable biomarker for the degree of CAD as determined by the Gensini score and it is a key factor in the development of atherosclerosis. […] One important factor contributing to the elevated IL-7 levels in angina patients seems to be increased release from activated platelets. […] The expression of IL-8 mRNA or plasma IL-8 showed a strong negative connection with the development of CHD. […] IL-10 indicates a proinflammatory state in acute coronary syndrome patients. As a result, IL-10 is a biomarker as useful as other systemic inflammation markers for predicting the risk of future cardiovascular events.

• #2 Pathophysiology of Coronary Heart Disease: A Brief Review

  https://www.degruyter.com/document/doi/10.7556/jaoa.2004.20022/html?lang=en

  An accumulating body of evidence suggests that atherosclerotic progression results from microinflammation mediated by proinflammatory cytokines. […] Chronic low-level inflammation increases atherosclerotic plaque deposition in animal models. […] Newer information reveals that CRP is a modulator of inflammation and may have both proinflammatory and antiinflammatory actions, which may directly contribute to endothelial dysfunction by inducing cytokine release and surface expression of adhesion molecules. […] Therefore, the term vulnerable patient may be more appropriate and is proposed now for the identification of subjects with high likelihood of having cardiac events develop in the near future. […] According to Naghavi et al, markers suggesting the presence of vulnerable blood include increased levels of CRP and circulating interleukin-6 levels, which are elevated in patients with acute coronary syndromes.

• #2 Coronary Artery Atherosclerosis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/153647-overview

  The mechanisms of atherogenesis remain uncertain, but the response-to-injury hypothesis is the most widely accepted proposal. […] Endothelial dysfunction is the initial step that allows diffusion of lipids and inflammatory cells (ie, monocytes, T lymphocytes) into the endothelial and subendothelial spaces. […] Oxidative stress has therefore been recognized as the most significant contributor to atherosclerosis by causing LDL oxidation and increasing nitric oxide breakdown. […] The presence of risk factors accelerates the rate of development of atherosclerosis.

• #2 Coronary Artery Disease – Stable Angina Topic Review

  https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/coronary-artery-disease-stable-angina

  In the setting of chronic ischemia, collateral circulation may develop to compensate for the reduced blood flow. […] With sudden increases in arterial tone, coronary vasospasm can occur and result in angina. […] Myocardial bridging occurs when a segment of a coronary vessel does not run along the epicardial surface of the heart, but within the myocardium. […] A coronary arterial wall weakened by disease may dilate and form a coronary artery aneurysm. […] Many types of congenital variations of the coronary arteries exist.

• #2 Coronary endothelial dysfunction: from pathogenesis to clinical implications | Open Heart

  https://openheart.bmj.com/content/9/2/e002200

  Endothelial dysfunction (ED) has a substantial role in the pathogenesis of atherosclerosis and other vascular diseases. […] In endothelial dysfunction (ED), the small arterioles lose their ability to dilate when needed, and this is a principal determinant of myocardial ischaemia. […] In addition, in the large epicardial coronary arteries, ED is the earliest measurable deterioration of the vessel wall in atherogenesis and precedes the development of morphological changes. […] Altered vascular function alters coronary blood flow and contributes to atherosclerosis lesion development and progression. […] Thus, ED not only affects epicardial and microvascular coronary blood flow but also plays an important role in the development of atherosclerosis. […] Both epicardial and microvascular coronary ED are predictors of CV events, irrespective of the presence or absence of angiographically detectable lesions.

• #2 The pathogenesis of coronary artery disease

  https://www.pulsus.com/scholarly-articles/the-pathogenesis-of-coronary-artery-disease-8934.html

  Coronary Artery Disease (CAD) is caused by plaque build-up in the wall of the arteries that supply blood to the heart. […] Atherosclerosis is the build-up of plaque inside our arteries. Plaque consists of fatty substances, waste products, calcium and the clot-making substance fibrin. As plaque continues to collect on our artery walls, our arteries narrow and stiffen. Plaques damage our arteries, which stops blood flow to our heart muscle. If our heart does not get enough blood, it can’t get the oxygen and nutrients it needs to work properly and this is called ischemia. Not getting enough blood supply to our heart muscle can lead to chest discomfort or chest pain and it is also called angina and it may leads to heart attack. […] Interventional procedures are nonsurgical treatments to get rid of plaque build-up in the arteries and prevent blockages. Common procedures are balloon angioplasty and stenting. Coronary artery bypass graft surgery involves creating a new path for blood to flow when there is a blockage in the coronary arteries.

• #2 Coronary heart disease (CHD) – Clinic «K+31»

  https://www.k31.ru/en/service/kardiologiya/ishemicheskaya-bolezn-serdca-ibs.html

  As each plaque develops and increases, the number of plaques increases, so does the degree of stenosis of the lumen of the coronary arteries, which largely (although not necessarily) determines the severity of the clinical manifestations and the course of IHD. Narrowing the lumen of the artery to 50% is often asymptomatic. Typically, clear clinical manifestations of the disease occur when the lumen is narrowed by 70% or more. The closer the stenosis is located to the beginning of the vessel, the greater the mass of the myocardium undergoes ischemia in accordance with the zone of blood supply. The most severe manifestations of myocardial ischemia are observed with stenosis of the main trunk or the mouth of the left coronary artery.

• #2 Mechanism of salidroside against coronary artery disease by network pharmacology analysis | BMC Complementary Medicine and Therapies | Full Text

  https://bmccomplementmedtherapies.biomedcentral.com/articles/10.1186/s12906-023-04027-3

  Salidroside has been shown to promote angiogenesis significantly. It has been reported that salidroside can increase the expression of VEGF and NO, thus promoting the angiogenesis mediated by bone marrow-derived endothelial progenitor cells. […] Our molecular docking results showed that salidroside bound to several angiogenic-related factors, among which VEGF, HIF1A and KDR were correlated with coronary artery collateral circulation. In addition, cell experiments also confirmed that salidroside can promote the proliferation and migration of HUVECs. […] In conclusion, we believe that salidroside plays an important role in angiogenesis and collateral circulation in CAD.

• #2 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Our understanding of the genetic architecture of CAD has improved considerably since 2007 when the first GWAS of this disease were published. […] At the beginning of 2013, a meta-analysis of several GWAS identified a final set of about 40 genetic variants associated with CAD that explains approximately 6% of the heritability of CAD. […] Some of these variants are related to lipid metabolism, blood pressure, and inflammation, which confirms the importance of these pathways in the pathogenesis of CAD. […] Genetic studies can shed light on new metabolic pathways associated with the development and progression of atherosclerosis, and provide clues for identifying new pharmacologic targets. […] The genetic variants associated with CAD at the 9p21 locus, which has been the top hit in all CAD GWAS since 2007, lie in an intergenic region close to a cluster of cell-cycle regulating tumor suppressor genes (CDKN2A and CDKN2B) that overlap with a nonprotein coding RNA (CDKN2BAS or ANRIL). […] The identification of genetic variants associated with disease has allowed us to improve our understanding of its pathogenesis, and ultimately to reduce the burden of disease at both the individual and population levels.

• #2 Circular RNAs in coronary heart disease: From molecular mechanism to promising clinical application (Review)

  https://www.spandidos-publications.com/10.3892/ijmm.2024.5452

  CircRNAs have emerged as crucial players in the pathogenesis of CHD. […] Research has identified numerous circRNAs that are differentially expressed in patients with CHD compared to healthy controls, suggesting their crucial role in disease progression. […] CircRNAs participate in regulating endothelial cell function in CHD through complex molecular mechanisms involving the sponging of miRNAs and subsequent modulation of mRNA targets. […] VSMC apoptosis is involved in the development and progression of CHD by affecting vascular remodeling, plaque stability and inflammatory responses. […] The inflammatory response is a complex biological process initiated by the immune system to protect the body against harmful stimuli such as pathogens, damaged cells or irritants. […] CircRNAs have a vital role in the inflammatory response associated with the development of CHD. […] Overall, the growing body of evidence highlights the multifaceted roles of circRNAs in CHD, from their involvement in cell proliferation and apoptosis to inflammation, providing new avenues for the diagnosis and treatment of this disease.

• #2 A network pharmacology approach to reveal the protective mechanism of Salvia miltiorrhiza-Dalbergia odorifera coupled-herbs on coronary heart disease | Scientific Reports

  https://www.nature.com/articles/s41598-019-56050-5

  According to the aetiologies of CHD, these biological processes can be divided into three functional modules, including vascular endothelial function regulation, inflammatory response, and lipid metabolism. […] Through GO and KEGG pathway enrichment analysis of common-target and PPI networks, 10 significant signaling pathways were screened as key action mechanisms of SMDOCH on CHD, and these pathways can be divided into three functional modules: vascular endothelial function regulation, inflammatory response, and lipid metabolism. […] The Vascular endothelial function regulation model showed that SMDOCH may influence vascular endothelial function by regulating hormone (renin, angiotensin, oestrogen) activity and three key upstream pathways: KEGG:04933, KEGG:05418, and KEGG:04066. […] The Inflammatory response model showed that SMDOCH may influence inflammation response through three key signaling pathways: KEGG:04668, KEGG:04064, and KEGG:04620.

• #2 Coronary artery disease – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/coronary-artery-disease/symptoms-causes/syc-20350613

  Coronary artery disease (CAD) is a common type of heart disease. It affects the main blood vessels that supply blood to the heart, called the coronary arteries. In CAD, there is reduced blood flow to the heart muscle. A buildup of fats, cholesterol and other substances in and on the artery walls, a condition called atherosclerosis, usually causes coronary artery disease. The buildup, called plaque, makes the arteries narrow. […] Coronary artery disease is caused by the buildup of fats, cholesterol and other substances in and on the walls of the heart arteries. This condition is called atherosclerosis. The buildup is called plaque. Plaque can cause the arteries to narrow, blocking blood flow. The plaque also can burst, causing a blood clot. […] Some causes of atherosclerosis and coronary artery disease are: Diabetes or insulin resistance, High blood pressure, Lack of exercise, Smoking or tobacco use.

• #2 Cardiovascular disease

  https://www.nhs.uk/conditions/cardiovascular-disease/

  Coronary heart disease occurs when the flow of oxygen-rich blood to the heart muscle is blocked or reduced. […] This puts an increased strain on the heart, and can lead to: angina chest pain caused by restricted blood flow to the heart muscle, heart attacks where the blood flow to the heart muscle is suddenly blocked, heart failure where the heart is unable to pump blood around the body properly. […] High blood pressure (hypertension) is one of the most important risk factors for CVD. If your blood pressure is too high, it can damage your blood vessels. […] Smoking and other tobacco use is also a significant risk factor for CVD. The harmful substances in tobacco can damage and narrow your blood vessels. […] Cholesterol is a fatty substance found in the blood. If you have high cholesterol, it can cause your blood vessels to narrow and increase your risk of developing a blood clot.

• #2

  https://consensus.app/questions/pathology-of-cardiovascular-disease/

  Mitochondrial dysfunction plays a crucial role in cardiovascular disease pathogenesis, leading to decreased ATP production and enhanced reactive oxygen species formation. […] Mitochondrial dysfunction is a critical factor in the pathogenesis of CVD. Proper mitochondrial function is essential for high-energy-demand tissues like the heart. In CVD, impaired mitochondrial adaptation leads to abnormalities in the respiratory chain and ATP synthesis, increased oxidative stress, and structural damage to mitochondria. This dysfunction results in extensive cell damage and apoptosis of cardiomyocytes. […] Atherosclerosis is a major underlying cause of CVD, characterized by endothelial dysfunction, inflammation, and oxidative stress. Recent studies have highlighted the role of molecular and cellular elements such as matrix metalloproteinases and immune system components in the pathophysiology of arterial hypertension and coronary artery disease.

• #2 Cardiovascular disease

  https://www.nhs.uk/conditions/cardiovascular-disease/

  High blood sugar levels can damage the blood vessels, making them more likely to become narrowed. […] Chronic kidney disease (CKD) is a long-term condition where the kidneys do not work as well as they should. People with chronic kidney disease have an increased risk of developing other serious problems, including CVD. […] If you don’t exercise regularly, it’s more likely that you’ll have high blood pressure, high cholesterol levels and be overweight. All of these are risk factors for CVD. […] Being overweight or obese increases your risk of developing diabetes and high blood pressure, both of which are risk factors for CVD. […] If you have a family history of CVD, your risk of developing it is also increased. […] In the UK people of south Asian and Black African or African Caribbean background have an increased risk of getting CVD. […] A healthy lifestyle can lower your risk of CVD. If you already have CVD, staying as healthy as possible can reduce the chances of it getting worse.

• #2 Relationship between time-varying achieved HbA1c and risk of coronary artery disease events among common haptoglobin phenotype groups with type 2 diabetes: the ADVANCE study | BMJ Open Diabetes Research & Care

  https://drc.bmj.com/content/13/3/e004713

  The present study suggests that (1) glycemic control is particularly important in the Hp2-2 phenotype for CAD prevention and that (2) our previous findings that the ACCORD and ADVANCE intensive glucose-lowering therapies only decreased CAD risk in the Hp2-2 phenotype could have been due to avoiding high HbA1c (eg, 8.0%) in participants with the Hp2-2 phenotype, rather than achieving especially strict glycemic control (eg, HbA1c 6.5% or 6.0%).

• #2 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Coronary artery disease (CAD) is characterized by the development of atherosclerosis in the coronary arteries, which can sometimes be asymptomatic. […] CAD is marked by an inadequate supply of blood and oxygen to the myocardium. The condition arises from occlusion of the coronary arteries and results in a demand-supply mismatch of oxygen. CAD typically involves the formation of plaques in the lumen of coronary arteries that impede blood flow. […] The hallmark of the pathophysiology of CAD is atherosclerotic plaque formation. Plaque is a buildup of fatty material that narrows the arterial lumen and impedes blood flow. The first step in the process is the formation of a „fatty streak” by subendothelial deposition of lipid-laden macrophages, also called „foam cells.” When a vascular insult occurs, the intima layer breaks, and monocytes migrate into the subendothelial space, where they become macrophages. These macrophages take up oxidized LDL particles, leading to foam cell formation. T cells get activated, and cytokines are released to aid in the inflammatory process. Growth factors activate smooth muscles, which also take up oxidized LDL particles and collagen, deposit along with activated macrophages, and increase the population of foam cells. Subendothelial plaque subsequently develops.

• #3 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  CAD is caused primarily by plaque formation within the intima of the vessel wall, with plaque being defined as a fatty material growing inside intima along with a severe inflammation, especially if the inflammation is chronic. […] Endothelial dysfunction in modern cardiovascular medicine is described as changes in the production and availability of endothelial-derived NO, prostacyclin, and endothelin, as well as their impact on vascular reactivity. […] The endothelial dysfunction is directly related to a decreased production and sensitivity of cells to NO. As a result, we have an effective disturbance in the functioning of the entire vessel and its homeostasis, which leads to an observation of prothrombotic and proinflammatory phenomena, along with lower susceptibility of the blood vessel wall.

• #3 Pathophysiology of Coronary Heart Disease: A Brief Review

  https://www.degruyter.com/document/doi/10.7556/jaoa.2004.20022/html?lang=en

  An accumulating body of evidence suggests that atherosclerotic progression results from microinflammation mediated by proinflammatory cytokines. […] Chronic low-level inflammation increases atherosclerotic plaque deposition in animal models. […] Newer information reveals that CRP is a modulator of inflammation and may have both proinflammatory and antiinflammatory actions, which may directly contribute to endothelial dysfunction by inducing cytokine release and surface expression of adhesion molecules. […] Therefore, the term vulnerable patient may be more appropriate and is proposed now for the identification of subjects with high likelihood of having cardiac events develop in the near future. […] According to Naghavi et al, markers suggesting the presence of vulnerable blood include increased levels of CRP and circulating interleukin-6 levels, which are elevated in patients with acute coronary syndromes.

• #3 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Coronary artery disease is usually caused by a build up cholesterol rich deposits or plaques on the lining inside the artery. These plaques are also called atheromatous plaques or simply atheromas and they cause a thickening of the arterial wall and a narrowing of the arterial space through which blood flows to reach the heart. […] An atheroma usually starts to develop as a result of damage or injury to the inner lining of the artery called the endothelium. Once the endothelium is damaged, cholesterol, fats, lipoproteins and other debris start to accumulate at the site of injury in the wall or intima of the artery. […] High concentrations of low density lipoprotein (LDL) penetrate the damaged endothelium and undergo a chemical process called oxidation. This altered LDL acts as a beacon that attracts white blood cells or leukocytes to migrate towards the vessel wall. As macrophages appear, they engulf the lipoproteins and become foam cells. These foam cells give rise to the earliest visible form of an atheromatous lesion called the fatty streak.

• #3 Coronary Artery Atherosclerosis: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/153647-overview

  The fatty streak is the result of focal accumulation of serum lipoproteins within the intima of the vessel wall. […] The SMCs are responsible for the deposition of extracellular connective tissue matrix and form a fibrous cap that overlies a core of lipid-laden foam cells, extracellular lipid, and necrotic cellular debris. […] Growth of the fibrous plaque results in vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, and compromised oxygen supply to the target organ. […] As endothelial injury and inflammation progress, fibroatheromas grow and form the plaque. […] Denudation of the overlying endothelium or rupture of the protective fibrous cap may result in exposure of the thrombogenic contents of the core of the plaque to the circulating blood. […] Most plaque ruptures occur because of disruption of the fibrous cap, which allows contact between the highly thrombogenic lipid core and the blood.

• #3 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Plaque stability is intimately linked with the type of calcification present. Stable plaques are often characterized by macrocalcifications and a thick, collagen-rich extracellular matrix within the fibrous cap, providing structural stability. In contrast, unstable plaques tend to have microcalcifications and a thin fibrous cap, heightening the risk of plaque rupture.

• #3 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

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

  The consequences of acute ischemia, collectively referred to as acute coronary syndromes (ACS), depend on the location and degree of obstruction and range from unstable angina, nonST-segment elevation myocardial infarction (NSTEMI), to ST-segment elevation myocardial infarction (STEMI), which can result in transmural infarction, and other complications including malignant ventricular arrhythmias, conduction defects, heart failure, and sudden death. […] Coronary artery spasm is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia (vasospastic angina) may result. […] In arteries with atheroma, the atheroma causes endothelial dysfunction, possibly resulting in local hypercontractility. Proposed mechanisms include loss of sensitivity to intrinsic vasodilators (eg, acetylcholine) and increased production of vasoconstrictors (eg, angiotensin II, endothelin, leukotrienes, serotonin, thromboxane) in the area of the atheroma.

• #3

  https://eurekaselect.com/public/chapter/21850

  Atherosclerosis is characterized by hardening/narrowing of arteries and reduction of blood flow to vital organs. Animal models and human research show that endothelial dysfunction and plaque development precede the pathogenesis of atherosclerosis, and related coronary heart disease, neurological, and renal disorders. […] Biomarkers like C-reactive protein, IL-6, IL-8, phospholipase A2, cardiac troponin, MicroRNA, miR-21, and other endothelial inflammation biomarkers are novel targets for monitoring atherosclerosis-related cardiovascular disorders. Anti-platelet and anti-cholesterol drugs are used in the treatment of atherogenesis and blood vessel clots. […] Thus, safe and cost-effective non-pharmacological anti-atherogenic and anticoagulant therapies are urgently needed. Nutraceuticals, functional foods, plant-derived therapies, antioxidant/anti-inflammation, foods/fruits/vegetables, and lifestyle changes (e.g., physical activity, less alcohol, smoking cessation) reduce atherogenesis, diabetes mellitus, obesity, hypertension, LDL, and C-reactive protein in all age groups, especially younger people.

• #3

  https://crimsonpublishers.com/ojchd/fulltext/OJCHD.000545.php

  Coronary artery diseases (CAD) known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease (CHD), or ischemic heart disease (IHD). CAD is the largest contributor of cardiovascular diseases (CVDs) and mortality rate is due in prevalence to atherosclerosis, a chronic inflammatory condition of the arterial wall. Atherosclerosis is a pathological process that affects large- and medium-sized arteries and causes coronary artery disease (angina pectoris and myocardial infarction), cerebrovascular disease (ischemic stroke and vascular dementia) and peripheral vascular disease (intermittent claudication and gangrene). Atherosclerosis is a chronic cumulative disease progressing over years. It is characterized by atherosclerotic plaques formed in the wall of the vessels, consisting of necrotic cores, calcified regions, accumulated modified lipids, and inflamed smooth muscle cells (SMCs), endothelial cells, leukocytes, and foam cells. Lesions begin early as fatty streaks and progress into pathologic lesions under the influence of both genetic and lifestyle insults. The pathologist Felix Marchand first introduced the term atherosclerosis in 1904, describing the association of fatty degeneration and vessel stiffening. This process affects medium and large-sized arteries and is characterized by patchy intramural thickening of the sub-intima that encroaches on the arterial lumen. The earliest visible lesion of atherosclerosis is the fatty streak, which is due to an accumulation of lipid-laden foam cells in the intimal layer of the artery. With time; the fatty streak evolves into a fibrous plaque, the hallmark of established atherosclerosis. Ultimately the lesion may evolve to contain large amounts of lipid; if it becomes unstable, denudation of overlying endothelium, or plaque rupture, may result in thrombotic occlusion of the overlying artery. Atherosclerotic lesions (atheromata) are composed of three major components. The first is the cellular component comprised predominately of smooth muscle cells and macrophages. The second component is the connective tissue matrix and extracellular lipid. The third component is intracellular lipid that accumulates within macrophages, thereby converting them into foam cells. Atherosclerotic lesions develop as a result of inflammatory stimuli, subsequent release of various cytokines, proliferation of smooth muscle cells, synthesis of connective tissue matrix, and accumulation of macrophages and lipid. Excess generation of (ROS) represents an important pathological process in atherogenesis. Each component of the atherosclerotic blood vessel has been demonstrated to increase production of ROS, primarily superoxide anion. Important sources of ROS are vascular smooth muscle cells, endothelial cells, fibroblasts, and infiltrating leukocytes. Production of ROS affects gene transcription, damages DNA, and increases production of inflammatory transcription factors. The two best-characterized effects include oxidation of LDL and scavenging of endothelium-derived NO. The progression of atherosclerotic disease has been described as moving from an early lesion (phase1) to a more advanced fibro-lipid lesion (phase 2). The formation of thrombus or hematoma can advance into an acute phase (phase 3 and 4) or even to total occlusion (phase 5).

• #3 Pathogenesis, Assessment, and Treatment of Coronary Microcirculation Dysfunction – ABC Cardiol

  https://abccardiol.org/en/article/pathogenesis-assessment-and-treatment-of-coronary-microcirculation-dysfunction/

  Cardiovascular disease is the predominant cause of mortality on a global scale. […] Coronary microvascular dysfunction, characterized by impaired coronary flow reserve resulting from functional and/or structural abnormalities in the microcirculation, is linked to adverse cardiovascular outcomes. […] This review aims to explore the prevalence, underlying mechanisms, diagnostic approaches, and therapeutic interventions for coronary microvascular dysfunction.

• #3 Coronary Artery Disease – Stable Angina Topic Review

  https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/coronary-artery-disease-stable-angina

  Atherosclerotic coronary artery disease (CAD) affects the coronary arteries, which deliver blood to the myocardium. […] The term ischemic heart disease implies a physiologically significant myocardial oxygen supply/demand mismatch. The most common cause of this mismatch is flow-limiting atherosclerotic narrowing of the coronary artery, resulting in the potential for inadequate coronary flow. […] Atherosclerosis of the coronary arteries is the most common cause of ischemic heart disease. […] In general, symptoms of stable angina will not develop unless there is flow-limiting stenosis of a major epicardial coronary vessel (left anterior descending, circumflex or right coronary artery). […] Angiographic estimation of the severity of coronary luminal stenosis is subjective and somewhat unreliable.

• #3 Coronary artery disease – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/coronary-artery-disease/

  Coronary artery disease (CAD) is a condition that is most commonly caused by atherosclerosis and the subsequent reduction in blood supply to the myocardium, resulting in a mismatch between myocardial oxygen supply and demand. […] Stable atherosclerotic plaque vascular stenosis increased resistance to blood flow in the coronary arteries decreased myocardial blood flow oxygen supply-demand mismatch myocardial ischemia. […] The extent of coronary stenosis determines the severity of the oxygen supply-demand mismatch and, thus, the severity of myocardial ischemia. […] Severe ischemia results in myocardial infarction. […] Factors reducing oxygen supply include coronary atherosclerosis and sequelae, including rupture of an unstable atherosclerotic plaque, thrombosis, and stenosis. […] Factors increasing oxygen demand include heart rate, afterload, and anemia.

• #3 Coronary Sinus Reduction For Refractory Angina   – Shockwave Medical

  https://shockwavemedical.com/en-eu/disease-states/coronary-sinus-reduction/

  Angina pain is often a symptom of CAD, when plaque buildup occurs in the arteries supplying the oxygen-rich blood to the heart, forcing the heart to work harder. […] Shockwave Reducer is a small, balloon-expandable, hourglass-shaped device that establishes a narrowing in the coronary sinus. The resulting increase in back pressure is hypothesized to redistribute blood into the ischemic myocardium to help reduce angina symptoms. […] While the primary imaging endpoint showed no improvement in transmural myocardial perfusion, it did show improvement in subendocardial perfusion, supporting the theorized mechanism of action of the Shockwave Reducer.

• #3 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Our understanding of the genetic architecture of CAD has improved considerably since 2007 when the first GWAS of this disease were published. […] At the beginning of 2013, a meta-analysis of several GWAS identified a final set of about 40 genetic variants associated with CAD that explains approximately 6% of the heritability of CAD. […] Some of these variants are related to lipid metabolism, blood pressure, and inflammation, which confirms the importance of these pathways in the pathogenesis of CAD. […] Genetic studies can shed light on new metabolic pathways associated with the development and progression of atherosclerosis, and provide clues for identifying new pharmacologic targets. […] The genetic variants associated with CAD at the 9p21 locus, which has been the top hit in all CAD GWAS since 2007, lie in an intergenic region close to a cluster of cell-cycle regulating tumor suppressor genes (CDKN2A and CDKN2B) that overlap with a nonprotein coding RNA (CDKN2BAS or ANRIL). […] The identification of genetic variants associated with disease has allowed us to improve our understanding of its pathogenesis, and ultimately to reduce the burden of disease at both the individual and population levels.

• #3 Role of LncRNAs in the Pathogenesis of Coronary Artery Disease

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404096

  Coronary artery disease (CAD), caused by coronary artery occlusion, is a common cardiovascular disease worldwide. Long non-coding RNAs (lncRNAs) are implicated in the regulation of endothelial cell injury, angiogenesis, plaque formation, and other pathological mechanisms in CAD by acting on different cell types. Some lncRNAs are significantly upregulated in CAD patients; however, other lncRNAs are significantly downregulated. Differential expression of lncRNAs in CAD patients enables them to be exploited as potential biomarkers to evaluate disease progression and diagnosis/prognosis in CAD patients. In this study, we reviewed the role of lncRNAs in the development of different clinical subtypes of CAD.

• #3 Circular RNAs in coronary heart disease: From molecular mechanism to promising clinical application (Review)

  https://www.spandidos-publications.com/10.3892/ijmm.2024.5452

  CircRNAs have emerged as crucial players in the pathogenesis of CHD. […] Research has identified numerous circRNAs that are differentially expressed in patients with CHD compared to healthy controls, suggesting their crucial role in disease progression. […] CircRNAs participate in regulating endothelial cell function in CHD through complex molecular mechanisms involving the sponging of miRNAs and subsequent modulation of mRNA targets. […] VSMC apoptosis is involved in the development and progression of CHD by affecting vascular remodeling, plaque stability and inflammatory responses. […] The inflammatory response is a complex biological process initiated by the immune system to protect the body against harmful stimuli such as pathogens, damaged cells or irritants. […] CircRNAs have a vital role in the inflammatory response associated with the development of CHD. […] Overall, the growing body of evidence highlights the multifaceted roles of circRNAs in CHD, from their involvement in cell proliferation and apoptosis to inflammation, providing new avenues for the diagnosis and treatment of this disease.

• #3 A network pharmacology approach to reveal the protective mechanism of Salvia miltiorrhiza-Dalbergia odorifera coupled-herbs on coronary heart disease | Scientific Reports

  https://www.nature.com/articles/s41598-019-56050-5

  The Lipid metabolism model showed that SMDOCH may influence lipid metabolism by regulating KEGG:04920. […] In conclusion, the cardioprotective effect of the bioactive components of SMDOCH, such as tanshinone IIA from SM as well as formononetin and butin from DO, can be explained, at least in part, by the biological processes vascular endothelial function regulation, inflammatory response, and lipid metabolism through the core targets TP53, ESR1, AKT1, STAT3, and MAPK1.

• #3 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Once the fatty streak is formed, it then attracts the smooth muscle cells to the site, where they multiply and start to produce extracellular matrix comprising of collagen and proteoglycan. It is this extracellular matrix that forms a large portion of the atherosclerotic plaque. This turns the fatty streak into a fibrous plaque. The lesion then starts to bulge into the inner wall of the blood vessel causing a significant narrowing of the luminal space. […] Next, the fibrous plaque starts to support itself. It develops its own small vessels to provide it with a supply of blood in a process called angiogenesis. Thereafter, the plaques begin to calcify as calcium starts to deposit. The final plaque is made up of a cap of fibrous tissue covering a core that is rich in lipids as well as necrotic or dead cells. The edge of this cap is key in acute coronary disease. This region is prone to rupture, which exposes the underlying core of lipids and necrotic material to thrombogenic factors in the blood. This can cause the aggregation of platelets that form a clot across the plaque and further narrow the artery.

• #3 Relationship between time-varying achieved HbA1c and risk of coronary artery disease events among common haptoglobin phenotype groups with type 2 diabetes: the ADVANCE study | BMJ Open Diabetes Research & Care

  https://drc.bmj.com/content/13/3/e004713

  When compared with HbA1c of 7.0%7.9%, having HbA1c 8.0% was associated with a greater CAD risk among participants with the Hp2-2 phenotype (HR 1.53, 95% CI 1.01 to 2.33), but was not associated with CAD risk among participants without the Hp2-2 phenotype (1.27, 0.90 to 1.79, p-interaction=0.71) […] The current study does not provide evidence to support an HbA1c target of 7.0% when compared with 7.0%7.9% for CAD prevention in either Hp phenotype group. […] Our findings for the CAD outcome among participants with the Hp2-2 phenotype are in line with the existing literatures suggested biological mechanism linking HbA1c and Hp type to CAD. […] Therefore, based on the existing mechanistic literature, preventing high HbA1c may be particularly important for CAD prevention among people with the Hp2-2 phenotype to help reduce Hp2:HbA1c-mediated oxidative damage.

• #4 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  CAD is caused primarily by plaque formation within the intima of the vessel wall, with plaque being defined as a fatty material growing inside intima along with a severe inflammation, especially if the inflammation is chronic. […] Endothelial dysfunction in modern cardiovascular medicine is described as changes in the production and availability of endothelial-derived NO, prostacyclin, and endothelin, as well as their impact on vascular reactivity. […] The endothelial dysfunction is directly related to a decreased production and sensitivity of cells to NO. As a result, we have an effective disturbance in the functioning of the entire vessel and its homeostasis, which leads to an observation of prothrombotic and proinflammatory phenomena, along with lower susceptibility of the blood vessel wall.

• #4 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Once the fatty streak is formed, it then attracts the smooth muscle cells to the site, where they multiply and start to produce extracellular matrix comprising of collagen and proteoglycan. It is this extracellular matrix that forms a large portion of the atherosclerotic plaque. This turns the fatty streak into a fibrous plaque. The lesion then starts to bulge into the inner wall of the blood vessel causing a significant narrowing of the luminal space. […] Next, the fibrous plaque starts to support itself. It develops its own small vessels to provide it with a supply of blood in a process called angiogenesis. Thereafter, the plaques begin to calcify as calcium starts to deposit. The final plaque is made up of a cap of fibrous tissue covering a core that is rich in lipids as well as necrotic or dead cells. The edge of this cap is key in acute coronary disease. This region is prone to rupture, which exposes the underlying core of lipids and necrotic material to thrombogenic factors in the blood. This can cause the aggregation of platelets that form a clot across the plaque and further narrow the artery.

• #4 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Vulnerable plaques have a thin fibrous cap made mostly of type I collagen and few or no smooth muscle cells, but abundant macrophages and proinflammatory and prothrombotic molecules. These plaques are prone to erosion or rupture, exposing the core of the plaque to circulating coagulation proteins, causing thrombosis, sudden occlusion of the artery lumen, and usually an acute coronary syndrome. […] The heritability of some phenotypes associated with arteriosclerosis has already been determined, and generally ranges from 40% to 55%. […] The second step is to study the genetic architecture of the disease, ie, identify the loci, and within these loci, the genetic variants that modulate disease susceptibility. […] In the case of CAD, notable successes include the identification of variants in ALOX5AP as being associated with coronary and cerebrovascular diseases, in MEF2A as being associated with CAD, and in PCSK9 as a gene for which variation is relevant in the metabolism of cholesterol.

• #4 Cardiovascular pathology coronary heart disease finale | PPT

  https://www.slideshare.net/slideshow/cardiovascular-pathology-coronary-heart-disease-finale/16814936

  5. Atherosclerosis is a progressive disease involving the development of arterial wall lesions. As they grow, these lesions may narrow or occlude the arterial lumen. Complex lesions may also become unstable and rupture, leading to acute coronary events, such as unstable angina, myocardial infarction, and stroke. […] 6. The acute coronary syndromes are frequently initiated by an unpredictable and abrupt conversion of a stable atherosclerotic plaque to an unstable and potentially life-threatening atherothrombotic lesion through superficial erosion, ulceration, fissuring, rupture, or deep hemorrhage, usually with superimposed thrombosis. […] 7. Sudden cardiac death (SCD) is an unexpected death from cardiac causes within one hour of symptoms. […] 8. Pathogenesis: Severe atherosclerotic coronary artery disease disrupted plaques with or without platelet nonocclusive thrombi. […] 9. Acute myocardial infarction (AMI) is the most common cause of death in adults in the United States. […] 10. Myocardial ischemia occurs when the oxygen supply is insufficient to meet metabolic demands.

• #4

  https://crimsonpublishers.com/ojchd/fulltext/OJCHD.000545.php

  Coronary artery diseases (CAD) known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease (CHD), or ischemic heart disease (IHD). CAD is the largest contributor of cardiovascular diseases (CVDs) and mortality rate is due in prevalence to atherosclerosis, a chronic inflammatory condition of the arterial wall. Atherosclerosis is a pathological process that affects large- and medium-sized arteries and causes coronary artery disease (angina pectoris and myocardial infarction), cerebrovascular disease (ischemic stroke and vascular dementia) and peripheral vascular disease (intermittent claudication and gangrene). Atherosclerosis is a chronic cumulative disease progressing over years. It is characterized by atherosclerotic plaques formed in the wall of the vessels, consisting of necrotic cores, calcified regions, accumulated modified lipids, and inflamed smooth muscle cells (SMCs), endothelial cells, leukocytes, and foam cells. Lesions begin early as fatty streaks and progress into pathologic lesions under the influence of both genetic and lifestyle insults. The pathologist Felix Marchand first introduced the term atherosclerosis in 1904, describing the association of fatty degeneration and vessel stiffening. This process affects medium and large-sized arteries and is characterized by patchy intramural thickening of the sub-intima that encroaches on the arterial lumen. The earliest visible lesion of atherosclerosis is the fatty streak, which is due to an accumulation of lipid-laden foam cells in the intimal layer of the artery. With time; the fatty streak evolves into a fibrous plaque, the hallmark of established atherosclerosis. Ultimately the lesion may evolve to contain large amounts of lipid; if it becomes unstable, denudation of overlying endothelium, or plaque rupture, may result in thrombotic occlusion of the overlying artery. Atherosclerotic lesions (atheromata) are composed of three major components. The first is the cellular component comprised predominately of smooth muscle cells and macrophages. The second component is the connective tissue matrix and extracellular lipid. The third component is intracellular lipid that accumulates within macrophages, thereby converting them into foam cells. Atherosclerotic lesions develop as a result of inflammatory stimuli, subsequent release of various cytokines, proliferation of smooth muscle cells, synthesis of connective tissue matrix, and accumulation of macrophages and lipid. Excess generation of (ROS) represents an important pathological process in atherogenesis. Each component of the atherosclerotic blood vessel has been demonstrated to increase production of ROS, primarily superoxide anion. Important sources of ROS are vascular smooth muscle cells, endothelial cells, fibroblasts, and infiltrating leukocytes. Production of ROS affects gene transcription, damages DNA, and increases production of inflammatory transcription factors. The two best-characterized effects include oxidation of LDL and scavenging of endothelium-derived NO. The progression of atherosclerotic disease has been described as moving from an early lesion (phase1) to a more advanced fibro-lipid lesion (phase 2). The formation of thrombus or hematoma can advance into an acute phase (phase 3 and 4) or even to total occlusion (phase 5).

• #4 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Our understanding of the genetic architecture of CAD has improved considerably since 2007 when the first GWAS of this disease were published. […] At the beginning of 2013, a meta-analysis of several GWAS identified a final set of about 40 genetic variants associated with CAD that explains approximately 6% of the heritability of CAD. […] Some of these variants are related to lipid metabolism, blood pressure, and inflammation, which confirms the importance of these pathways in the pathogenesis of CAD. […] Genetic studies can shed light on new metabolic pathways associated with the development and progression of atherosclerosis, and provide clues for identifying new pharmacologic targets. […] The genetic variants associated with CAD at the 9p21 locus, which has been the top hit in all CAD GWAS since 2007, lie in an intergenic region close to a cluster of cell-cycle regulating tumor suppressor genes (CDKN2A and CDKN2B) that overlap with a nonprotein coding RNA (CDKN2BAS or ANRIL). […] The identification of genetic variants associated with disease has allowed us to improve our understanding of its pathogenesis, and ultimately to reduce the burden of disease at both the individual and population levels.

• #4 Role of LncRNAs in the Pathogenesis of Coronary Artery Disease

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404096

  Coronary artery disease (CAD), caused by coronary artery occlusion, is a common cardiovascular disease worldwide. Long non-coding RNAs (lncRNAs) are implicated in the regulation of endothelial cell injury, angiogenesis, plaque formation, and other pathological mechanisms in CAD by acting on different cell types. Some lncRNAs are significantly upregulated in CAD patients; however, other lncRNAs are significantly downregulated. Differential expression of lncRNAs in CAD patients enables them to be exploited as potential biomarkers to evaluate disease progression and diagnosis/prognosis in CAD patients. In this study, we reviewed the role of lncRNAs in the development of different clinical subtypes of CAD.

• #4 Cardiovascular pathology coronary heart disease finale | PPT

  https://www.slideshare.net/slideshow/cardiovascular-pathology-coronary-heart-disease-finale/16814936

  1. The document discusses coronary heart disease, which is caused by impaired blood flow due to atherosclerosis in most cases. […] 2. The pathogenesis of coronary heart disease involves LDL cholesterol entering the arterial wall and being taken up by scavenger cells, forming fatty streaks and atheromatous plaques that can progress and restrict blood flow. […] 3. Pathogenesis of Coronary Heart Disease HDL (good) cholesterol removes excess cholesterol in the blood stream. LDL (bad) cholesterol enters the arterial wall and is taken up by our bodys scavenger cells. Subsequently, they will turn into fatty streaks which progress into atheromatous plaques. Hence, LDL cholesterol is said to promote atherosclerosis. […] 4. Atherosclerosis is by far the most common cause of CHD, and atherosclerotic plaque disruption the most frequent cause of myocardial infarction and sudden death. More than 90% of persons with CHD have coronary atherosclerosis.

• #4 Cardiovascular disease

  https://www.nhs.uk/conditions/cardiovascular-disease/

  High blood sugar levels can damage the blood vessels, making them more likely to become narrowed. […] Chronic kidney disease (CKD) is a long-term condition where the kidneys do not work as well as they should. People with chronic kidney disease have an increased risk of developing other serious problems, including CVD. […] If you don’t exercise regularly, it’s more likely that you’ll have high blood pressure, high cholesterol levels and be overweight. All of these are risk factors for CVD. […] Being overweight or obese increases your risk of developing diabetes and high blood pressure, both of which are risk factors for CVD. […] If you have a family history of CVD, your risk of developing it is also increased. […] In the UK people of south Asian and Black African or African Caribbean background have an increased risk of getting CVD. […] A healthy lifestyle can lower your risk of CVD. If you already have CVD, staying as healthy as possible can reduce the chances of it getting worse.

• #4 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

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

  Coronary artery dissection is a rare, non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction. […] Treatment generally aims to reduce cardiac workload by decreasing oxygen demand and improving coronary artery blood flow, and, over the long term, to halt and reverse the atherosclerotic process. […] Antiplatelet agents and statins improve short-term and long-term outcomes, probably by improving atheromatous plaque stability and endothelial function. […] Beta-blockers reduce symptoms of angina by reducing heart rate and contractility and decreasing myocardial oxygen demand. […] Aspirin prolongs vein graft patency. Continued smoking has a profound adverse effect on patency. […] Modification of serum lipid levels (particularly with statins) may slow or even partially reverse the progression of CAD.

• #4 Coronary endothelial dysfunction: from pathogenesis to clinical implications | Open Heart

  https://openheart.bmj.com/content/9/2/e002200

  ED in epicardial vessels not only affects coronary blood flow, but a loss of NO bioavailability contributes to the initiation and progression of atherosclerosis through alterations in endothelial permeability, inflammatory activation and increased thrombosis. […] A reduction in NO bioavailability, either by decreased production or increased destruction, results in ED. […] A variety of factors may damage endothelial cells, resulting in ED. […] All of these interacting pathologies contribute to the initiation and progression of atherosclerosis. […] The association of ED with epicardial CAD as well as disease of other large vessels is well documented. […] Coronary ED has been associated with coronary plaque progression, vulnerable plaque features, increased risk of major adverse CV events, cerebrovascular events, thrombotic events and congestive heart failure. […] Overall, the wide breadth of clinical associations indicates the high potential impact of an ED-targeted therapeutic or intervention.

• #4 Coronary heart disease (CHD) – Clinic «K+31»

  https://www.k31.ru/en/service/kardiologiya/ishemicheskaya-bolezn-serdca-ibs.html

  According to modern concepts, IHD is based on myocardial damage due to its insufficient blood supply. The imbalance between the real blood supply to the myocardium and its needs for blood supply can occur due to the following circumstances: […] Causes inside the vessel: atherosclerotic narrowing of the lumen of the coronary arteries; thrombosis and thromboembolism of coronary arteries; coronary artery spasm. […] Under the influence of a number of risk factors, atherosclerotic plaque formation occurs. At first, the lumen of the vessel does not change significantly. As lipids accumulate in the plaque, ruptures of its fibrous cover occur, which is accompanied by the deposition of platelets and fibrin, which contribute to local narrowing of the vessel. Along with lipidofibrotic plaques, almost exclusively fibrotic stenosing plaques are formed that undergo calcification.

• #5 Coronary artery disease – Wikipedia

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

  The resultant reduction in the heart’s blood supply due to atherosclerosis in coronary arteries causes shortness of breath, angina pectoris (chest pains that are usually relieved by rest), and potentially fatal heart attacks (myocardial infarctions). […] Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the heart’s muscle cells. […] Typically, coronary artery disease occurs when part of the smooth, elastic lining inside a coronary artery develops atherosclerosis. […] With atherosclerosis, the artery’s lining becomes hardened, stiffened, and accumulates deposits of calcium, fatty lipids, and abnormal inflammatory cells to form a plaque. […] Calcium phosphate (hydroxyapatite) deposits in the muscular layer of the blood vessels appear to play a significant role in stiffening the arteries and inducing the early phase of coronary arteriosclerosis.

• #5

  https://consensus.app/questions/pathology-of-cardiovascular-disease/

  Mitochondrial dysfunction plays a crucial role in cardiovascular disease pathogenesis, leading to decreased ATP production and enhanced reactive oxygen species formation. […] Mitochondrial dysfunction is a critical factor in the pathogenesis of CVD. Proper mitochondrial function is essential for high-energy-demand tissues like the heart. In CVD, impaired mitochondrial adaptation leads to abnormalities in the respiratory chain and ATP synthesis, increased oxidative stress, and structural damage to mitochondria. This dysfunction results in extensive cell damage and apoptosis of cardiomyocytes. […] Atherosclerosis is a major underlying cause of CVD, characterized by endothelial dysfunction, inflammation, and oxidative stress. Recent studies have highlighted the role of molecular and cellular elements such as matrix metalloproteinases and immune system components in the pathophysiology of arterial hypertension and coronary artery disease.

• #5 Coronary Artery Disease – Coronary Heart Disease | American Heart Association

  https://www.heart.org/en/health-topics/consumer-healthcare/what-is-cardiovascular-disease/coronary-artery-disease

  Coronary heart disease is a common term for the buildup of plaque in the heart’s arteries that could lead to heart attack or ischemic stroke. […] However, coronary heart disease, or CHD, is actually a result of coronary artery disease, or CAD. […] With CAD, plaque first grows within the walls of the coronary arteries until the blood flow to the heart’s muscle is limited, which prevents the heart muscle from receiving enough oxygen. This is also called ischemia. […] The traditional risk factors for coronary artery disease are high LDL cholesterol, low HDL cholesterol, high blood pressure, family history, diabetes, smoking and obesity. […] Research shows that children and youth are increasingly at risk for CAD. […] Living a healthy lifestyle that combines good nutrition, weight management and getting plenty of physical activity can play a big role in avoiding CAD.

• #5 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

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

  Coronary artery dissection is a rare, non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction. […] Treatment generally aims to reduce cardiac workload by decreasing oxygen demand and improving coronary artery blood flow, and, over the long term, to halt and reverse the atherosclerotic process. […] Antiplatelet agents and statins improve short-term and long-term outcomes, probably by improving atheromatous plaque stability and endothelial function. […] Beta-blockers reduce symptoms of angina by reducing heart rate and contractility and decreasing myocardial oxygen demand. […] Aspirin prolongs vein graft patency. Continued smoking has a profound adverse effect on patency. […] Modification of serum lipid levels (particularly with statins) may slow or even partially reverse the progression of CAD.

• #5 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

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

  Coronary artery disease is due to […] Coronary artery atherosclerosis: Subintimal deposition of atheromas in large and medium-sized coronary arteries. […] Vascular endothelial dysfunction can promote atherosclerosis and contribute to coronary artery spasm. Endothelial dysfunction is also recognized as a cause of angina in the absence of epicardial coronary artery stenosis or spasm. […] Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing angina pectoris). The degree of stenosis required to cause ischemia varies with oxygen demand. […] Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.

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