Materiały źródłowe

• #1 Myocardial Infarction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537076/

  Myocardial infarction (MI), colloquially known as „heart attack,” is caused by decreased or complete cessation of blood flow to a portion of the myocardium. […] Most myocardial infarctions are due to underlying coronary artery disease, the leading cause of death in the United States. With coronary artery occlusion, the myocardium is deprived of oxygen. Prolonged deprivation of oxygen supply to the myocardium can lead to myocardial cell death and necrosis. […] The acute occlusion of one or multiple large epicardial coronary arteries for more than 20 to 40 minutes can lead to acute myocardial infarction. The occlusion is usually thrombotic and due to the rupture of a plaque formed in the coronary arteries. The occlusion leads to a lack of oxygen in the myocardium, which results in sarcolemmal disruption and myofibril relaxation.

• #2 Myocardial Infarction: Practice Essentials, Background, Definitions

  https://emedicine.medscape.com/article/155919-overview

  Myocardial infarction (MI) (ie, heart attack) is the irreversible death (necrosis) of heart muscle secondary to prolonged lack of oxygen supply (ischemia). […] Myocardial infarction (MI) usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in an epicardial coronary artery, resulting in an acute reduction of blood supply to a portion of the myocardium. […] The process of acute coronary thrombosis leading to ACS involves the pathogenic mechanism of plaque rupture, and less frequently plaque erosion. […] Atherosclerosis is the disease primarily responsible for most acute coronary syndrome (ACS) cases. Approximately 90% of myocardial infarctions (MIs) result from an acute thrombus that obstructs an atherosclerotic coronary artery.

• #3 Ischemic heart disease – McMaster Pathophysiology Review

  https://www.pathophys.org/acs/

  Ischemic heart disease: a condition in which imbalance between myocardial oxygen supply and demand, most often caused by atherosclerosis of the coronary arteries, results in myocardial hypoxia and accumulation of waste metabolites. […] Myocardial ischemia is a consequence of reduced blood flow in coronary arteries, due to a combination of fixed vessel narrowing and abnormal vascular tone as a result of atherosclerosis and endothelial dysfunction. This leads to an imbalance between myocardial oxygen supply and demand. […] In atherosclerotic arteries, however, endothelial dysfunction contributes to myocardial ischemia in the following ways: Inappropriate vasoconstriction of coronary arteries. […] Resulting impairment in blood flow causes a marked imbalance between myocardial oxygen supply and demand.

• #4 What is a Heart Attack? | American Heart Association

  https://www.heart.org/en/health-topics/heart-attack/about-heart-attacks

  A heart attack occurs when blood flow to the heart muscle is reduced or blocked. […] A heart attack occurs when the blood flow that brings oxygen to the heart is reduced or cut off. If blood flow is reduced or stopped for too long, the heart muscle begins to die. […] This happens when coronary arteries that supply the heart muscle with blood flow become narrowed from plaque — a buildup of fat, cholesterol and other substances. This slow process is known as atherosclerosis. […] When a heart attack occurs, the heart muscle that has lost blood supply begins to suffer injury. It begins to die if blood supply is not restored. The amount of damage to the heart muscle depends on the size of the area supplied by the blocked artery and the time between injury and treatment. […] Heart muscle damaged by a heart attack heals by forming scar tissue. It usually takes several weeks for your heart muscle to heal.

• #4 What is a Heart Attack? | American Heart Association

  https://www.heart.org/en/health-topics/heart-attack/about-heart-attacks

  The amount of damage to the heart muscle can affect how well the heart pumps blood. […] Sometimes a coronary artery temporarily contracts or spasms. When this happens, the artery narrows, and blood flow to part of the heart muscle decreases or stops. […] A heart attack is when blood flow to the heart is blocked. It’s a circulation problem.

• #5 Myocardial ischemia – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/myocardial-ischemia/symptoms-causes/syc-20375417

  Myocardial ischemia occurs when blood flow to your heart is reduced, preventing the heart muscle from receiving enough oxygen. The reduced blood flow is usually the result of a partial or complete blockage of your heart’s arteries (coronary arteries). […] Myocardial ischemia occurs when blood flow to the heart muscle (myocardium) is obstructed by a partial or complete blockage of a coronary artery by a buildup of plaques (atherosclerosis). If the plaques rupture, you can have a heart attack (myocardial infarction). […] A sudden, severe blockage of one of the heart’s artery can lead to a heart attack. […] Myocardial ischemia occurs when the blood flow through one or more of your coronary arteries is decreased. The low blood flow decreases the amount of oxygen your heart muscle receives.

• #6

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

  Myocardial cell death occurs within as little as 20 minutes as a result of prolonged ischaemia. Absolute necrosis may occur within 2-4 hours. […] Heart failure (HF) is a debilitating condition that is characterised by shortness of breath, fatigue and exercise intolerance. HF is a clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood at rest or during physical activity. […] The cycle commences with insult to the myocardium. Neurohormonal compensatory activities are triggered when cardiac output declines. […] Heart failure with reduced left ventricular systolic function resulting in poor cardiac output activates neurohormonal responses that over the long term can be either maladaptive or ineffectual.

• #7 Ischemic heart disease – McMaster Pathophysiology Review

  https://www.pathophys.org/acs/

  Myocyte necrosis as a result of prolonged myocardial ischemia. […] The amount of tissue that succumbs to infarction depends on: Mass of myocardim perfused by the occluded vessel, Magnitude and duration of impaired coronary blood flow, Oxygen demand of the affected region, Adequacy of collateral vessels that provide blood supply from neighbouring nonoccluded coronary vessels, Degree of tissue response to the ischemic process. […] Common initiating pathophysiologic mechanism: Disruption of an atherosclerotic plaque (i.e. plaque rupture) with subsequent platelet aggregation and formation of an intracoronary thrombus. […] Resulting impairment in blood flow causes a marked imbalance between myocardial oxygen supply and demand. […] Early changes in infarction (minutes to days): Drop in tissue oxygen levels, Rapid conversion from aerobic to anaerobic metabolism, Impaired glycolysis and ATP production impaired contractile protein function, Systolic dysfunction loss of synchroneous myocyte contraction compromised cardiac output, Diastolic dysfunction reduced ventricular compliance (i.e. impaired relaxation) and elevation of ventricular filling pressures.

• #8 Myocardial Infarction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537076/

  These changes are one of the first ultrastructural changes in the process of MI, which are followed by mitochondrial alterations. The prolonged ischemia ultimately results in liquefactive necrosis of myocardial tissue. The necrosis spreads from sub-endocardium to sub-epicardium. […] Depending on the territory affected by the infarction, the cardiac function is compromised. Due to the negligible regeneration capacity of the myocardium, the infarcted area heals by scar formation, and often, the heart is remodeled characterized by dilation, segmental hypertrophy of remaining viable tissue, and cardiac dysfunction.

• #9 Heart attack | Heart and Stroke Foundation

  https://www.heartandstroke.ca/heart-disease/conditions/heart-attack

  A heart attack occurs when blood flow to a section of the heart becomes blocked and the heart muscle cant get oxygen. If the blood flow isnt restored quickly, that section of the heart begins to die. Depending on how long the blood supply is cut off, the damage can be mild, severe or cause lifelong problems. In some cases a heart attack can be fatal. […] Most commonly, a heart attack happens when blood flow through one or more of the coronary arteries is blocked. This stops oxygen from reaching parts of the heart. […] The most common cause of blocked blood flow is narrowing and hardening of the arteries (atherosclerosis). […] Atherosclerosis is the buildup of cholesterol plaque on the inside wall of an artery. […] The buildup of plaque causes the arteries to harden. […] Over time, the artery can narrow or become blocked.

• #9 Heart attack | Heart and Stroke Foundation

  https://www.heartandstroke.ca/heart-disease/conditions/heart-attack

  A plaque can also burst open, causing surrounding blood to clot around it. […] Blood clots can become so large that they can also block blood flow through the artery to the heart, causing a heart attack. […] Heart attacks can also be caused by a coronary artery spasm. […] A spasm causes a temporary tightening of a coronary artery. […] The tightening can stop blood flow through the artery. […] Some recreational drugs can cause a life-threatening spasm. […] Often, the causes of spasms are not known.

• #10 Coronary artery disease – Wikipedia

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

  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. […] Plaques can be thought of as large „pimples” that protrude into the channel of an artery, causing partial obstruction to blood flow. […] A more severe form is chronic total occlusion (CTO) when a coronary artery is completely obstructed for more than 3 months. […] High levels of cholesterol in the bloodstream lead to atherosclerosis. […] With increased levels of LDL in the bloodstream, LDL particles will form deposits and accumulate within the arterial walls, which will lead to the development of plaques, restricting blood flow. […] 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).

• #11 Myocardial Infarction: Risk Factors, Pathophysiology, Classification, Assessment and Management | Auctores

  https://www.auctoresonline.org/article/myocardial-infarction-risk-factors-pathophysiology-classification-assessment-and-management

  The pathophysiology process can be summarized in the following steps: […] Coronary endothelial dysfunction precedes the lesion formation and increases with progression of CAD. It results from endothelial injury that occurs in response to oxidized LDL, increased levels of blood glucose, hypertension and increased free radicals derived from oxygen. […] Atherosclerosis is the main cause of plaque formation by causing internal inflammation, fibrosis, necrosis and calcification. […] Plaque rupture leads to exposure of blood with the necrotic core that is rich with erythrocytes and highly thrombogenic material leading to clot formation. Plaque rupture represents the most common cause for occurrence of thrombosis (Bentzon et al, 2014).

• #12 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. […] The amount of blood reaching and supplying the heart muscles (myocardium) with oxygen and nutrients can therefore be reduced in the presence of atheromas. […] An atheroma usually starts to develop as a result of damage or injury to the inner lining of the artery called the endothelium. […] High concentrations of low density lipoprotein (LDL) penetrate the damaged endothelium and undergo a chemical process called oxidation. […] This can cause the aggregation of platelets that form a clot across the plaque and further narrow the artery. […] As the deposits on the plaques grow in size and dimension, the blood vessels become further narrowed and there may be obstruction leading to a heart attack or a myocardial infarction.

• #13 Coronary Artery Disease – STEMI Topic Review

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

  Some atherosclerotic plaques have a stable fibrous cap; others, with a thin cap, are considered vulnerable. […] A type 1 MI is caused by atherothrombotic coronary artery disease and usually precipitated by atherosclerotic plaque disruption (rupture or erosion), while a type 2 MI is caused by a mismatch between oxygen supply and demand by a pathophysiological mechanism other than coronary atherothrombosis.

• #13 Coronary Artery Disease – STEMI Topic Review

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

  The most serious form of the acute coronary syndrome, ST segment elevation myocardial infarction, or STEMI, most often results from complete thrombotic occlusion of a major epicardial coronary artery. […] STEMI most often results from coronary thrombosis after plaque rupture rather than fixed obstruction. Unstable angina has a lower incidence of coronary thrombosis compared with non-STEMI or STEMI and is more often associated with fixed atherosclerotic stenosis (with critically low flow). […] The vulnerable plaque responsible for acute coronary syndromes and, ultimately, coronary artery thrombosis, has a thin cap and a necrotic core; see Atherosclerosis Topic Review. […] With plaque rupture or plaque erosion, the thin fibrous cap covering the plaque is disrupted or ulcerated. This exposes the blood flow to tissue factor, activates the clotting cascade and leads to intravascular thrombosis.

• #14 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Notably, the majority of coronary plaques that rupture and cause MI are not the most stenotic but rather possess features that make them more vulnerable such as thin fibrous caps and a high content of activated macrophages. […] The excessive retention or oxidation of LDL in the arterial subendothelial layer provokes monocyte generation from progenitor cells in the BM and their subsequent release into the circulation. […] Inflammatory macrophages release chemokines/cytokines, which promote plaque inflammation. […] As the plaque grows, it becomes unstable and may rupture. […] Due to the inflammatory milieu of the plaque, procoagulant factors are activated and fibrin production increases. […] While efferocytosis prevents inflammation and plaque growth, the impaired efferocytosis of apoptotic/necrotic bodies may lead to further deposition of macrophages/foam cells in the plaque.

• #15 Myocardial infarction – Wikipedia

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

  A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, causing catastrophic thrombus formation, totally occluding the artery and preventing blood flow downstream to the heart muscle. […] The complete blockage of a coronary artery caused by a rupture of an atherosclerotic plaque is usually the underlying mechanism of an MI. […] The most common cause of a myocardial infarction is the rupture of an atherosclerotic plaque on an artery supplying heart muscle. […] Atherosclerotic plaques are often present for decades before they result in symptoms. […] The gradual buildup of cholesterol and fibrous tissue in plaques in the wall of the coronary arteries or other arteries, typically over decades, is termed atherosclerosis.

• #15 Myocardial infarction – Wikipedia

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

  If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the blocked coronary artery die (infarction), chiefly through necrosis, and do not grow back. […] Injury to the myocardium also occurs during re-perfusion. This might manifest as ventricular arrhythmia.

• #16 Acute Myocardial Infarction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK459269/

  Acute myocardial infarction occurs due to decreased coronary blood flow, leading to insufficient oxygen supply to the heart and cardiac ischemia. Decreased coronary blood flow is multifactorial. Atherosclerotic plaques classically rupture and lead to thrombosis, contributing to acutely decreased blood flow in the coronary. Other etiologies of myocardial ischemia include coronary artery embolism, which accounts for 2.9% of patients, cocaine-induced ischemia, coronary dissection, and coronary vasospasm.[4][5] […] The rupture of an atherosclerotic plaque initiates an inflammatory response of monocytes and macrophages, leading to thrombus formation and platelet aggregation. This process decreases oxygen delivery through the coronary artery, resulting in inadequate oxygenation of the myocardium (see Image. Specimen Showing MI). The subsequent inability to produce ATP in the mitochondria triggers an ischemic cascade, ultimately leading to apoptosis (cell death) of the endocardium or myocardial infarction.

• #17 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 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. 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.

• #17 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 spasm is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia (vasospastic angina) may result. Marked narrowing can trigger thrombus formation, causing infarction or life-threatening arrhythmia. Spasm can occur in arteries with or without atheroma. […] 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. Recurrent spasm may damage the intima, leading to atheroma formation. […] 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. Dissection may occur in atherosclerotic or non-atherosclerotic coronary arteries. Non-atherosclerotic dissection is more likely in pregnant or postpartum females and/or patients with fibromuscular dysplasia or other connective tissue disorders.

• #18 Heart Attack | Myocardial Infarction | MedlinePlus

  https://medlineplus.gov/heartattack.html

  Each year almost 800,000 Americans have a heart attack. A heart attack happens when blood flow to the heart suddenly becomes blocked. Without the blood coming in, the heart can’t get oxygen. If not treated quickly, the heart muscle begins to die. […] The most common cause of heart attacks is coronary artery disease (CAD). With CAD, there is a buildup of cholesterol and other material, called plaque, on their inner walls or the arteries. This is atherosclerosis. It can build up for years. Eventually an area of plaque can rupture (break open). A blood clot can form around the plaque and block the artery. […] A less common cause of heart attack is a severe spasm (tightening) of a coronary artery. The spasm cuts off blood flow through the artery.

• #19 Myocardial Infarction

  https://webpath.med.utah.edu/TUTORIAL/MYOCARD/MYOCARD.html

  Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is most often related to progressive atherosclerosis with increasing occlusion of coronary arteries. […] The pathogenesis can include: Occlusive intracoronary thrombus – a thrombus overlying an atheromatous plaque is estimated to cause 75% of myocardial infarctions, with superficial plaque erosion present in the remaining 25%. […] The molecular events during MI relate to the initial ischemic event, reperfusion, and subsequent inflammatory response. Up to 6 hours following the initial ischemic event, most myocardial cell loss occurs via apoptosis. After that, necrosis predominates. Ischemic endothelial cells express adhesion molecules that attract neutrophils that subsequently migrate into damaged myocardium.

• #20 Ischemic Heart Disease Pathophysiology Paradigms Overview: From Plaque Activation to Microvascular Dysfunction

  https://www.mdpi.com/1422-0067/21/21/8118

  In the last decades, some authors suggested that the course of atherosclerosis is supported by inflammation, from its beginning to thrombotic complications. In fact, it has been hypothesized that inflammation stimulates atherosclerosis initiation and evolution. It also contributes to the acute thrombotic complications of atherosclerotic plaque. However, inflammation represents a response to myocardial ischemia, which involves myocardium initially becoming systemic later. […] Acute myocardial infarction (AMI) produces a significant local inflammatory response, which starts in the myocardium and propagates systemically through the blood stream. Lots of inflammatory cytokines, such as tumor necrosis factor alpha (TNFα) and various chemokines that are weakly represented in healthy hearts, reach high levels during myocardial infarction. Elevation of acute phase reactants such as CRP and increased peripheral white blood cell count, especially neutrophils, are common during ACS.

• #21 Acute Myocardial Infarction (MI) – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/acute-myocardial-infarction-mi

  Myocardial infarction is defined as myocardial necrosis in a clinical setting consistent with myocardial ischemia. […] MI can be classified into 5 types based on etiology and circumstances: Type 1: Spontaneous MI caused by ischemia due to a primary coronary event (eg, plaque rupture, erosion, or fissuring; coronary dissection). […] NonST-segment elevation myocardial infarction (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by cardiac biomarkers in blood; troponin I or troponin T and CK-MB will be elevated) without acute ST-segment elevation. […] ST-segment elevation myocardial infarction (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by nitroglycerin. […] Myocardial infarction in the absence of obstructive coronary artery disease (MINOCA) is found in about 5 to 6% of patients with acute MI who undergo coronary angiography. […] Patients with MINOCA tend to have myocardial necrosis without significant coronary atherosclerosis.

• #22 What is a STEMI Heart Attack?

  https://my.clevelandclinic.org/health/diseases/22068-stemi-heart-attack

  Among heart attacks, STEMIs are typically more severe. […] STEMI is one of three conditions that fall under acute coronary syndrome, a disease that happens because of limited or no blood flow to a part of your heart. […] The key characteristic that identifies a STEMI is the ST-segment elevation. ST-segment elevation usually indicates a total blockage of the involved coronary artery and that the heart muscle is currently dying. […] Treating a STEMI is time-sensitive. […] PCI is time-sensitive, which is why hospitals set a door-to-balloon time goal for heart attack cases. […] Severe blockages of your heart’s arteries may need coronary artery bypass grafting (CABG, pronounced like „cabbage). […] The outlook after a STEMI depends on several factors. The most important factor is how much damage there is to the heart muscle from the STEMI.

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

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

  If a plaque breaks open, it can cause a blood clot in the heart. […] A heart attack may be caused by a complete or partial blockage of a heart (coronary) artery. One way to classify heart attacks is whether an electrocardiogram (ECG or EKG) shows some specific changes (ST elevation) that require emergency invasive treatment. […] Not all heart attacks are caused by blocked arteries. Other causes include coronary artery spasm, certain infections, and spontaneous coronary artery dissection (SCAD).

• #24 Ischemic Heart Disease Pathophysiology Paradigms Overview: From Plaque Activation to Microvascular Dysfunction

  https://www.mdpi.com/1422-0067/21/21/8118

  Several years ago, it was proposed that myocardial ischemia might be caused by coronary arteries spasms: vasospasm of one of the main coronary arteries are able to cause complete occlusion. In 1959, Prinzmetal described a syndrome of angina with electrocardiographic ST-segment elevation, in absence of coronary obstruction. “Prinzmetal” angina is caused by transient vasospasm with an acute reduction of coronary blood supply, rather than by a myocardial metabolic demand increase. The significance of coronary spasm has been demonstrated in other clinical scenarios with an involvement of the coronary microcirculation. Moreover, it is now recognized that spasm can be initiated by several factors, i.e., vasomotor tone at rest, segmental epicardial coronary hyperactivity, and an organic stenosis.

• #25 Heart Attack: Symptoms & Treatment

  https://my.clevelandclinic.org/health/diseases/16818-heart-attack-myocardial-infarction

  Heart attacks are possible without ruptured plaque, but this is rare and only accounts for about 5% of all heart attacks. […] Treating a heart attack means restoring blood flow to the affected heart muscle as soon as possible. This can happen in a variety of ways, ranging from medication to surgery. […] Providers restore circulation to your affected heart muscle with a procedure called percutaneous coronary intervention (PCI) or angioplasty. […] People who have severe blockages of their coronary arteries may undergo coronary artery bypass grafting (CABG). […] Opening your artery with a catheter is critical in restoring blood flow. The sooner that happens, the better the chance of a good outcome.

• #26 Ischemic Heart Disease Pathophysiology Paradigms Overview: From Plaque Activation to Microvascular Dysfunction

  https://www.mdpi.com/1422-0067/21/21/8118

  In the coronary tree, arterioles with 50–200 μm in diameter represent the microcirculation that reflects approximately 60% of coronary resistance. In the last decades, coronary microcirculation function and structure abnormalities have been described as a relevant IHD pathogenic mechanism. Coronary microvascular dysfunction (CMD) represents a common pathophysiological mechanism of type II myocardial infarction. CMD determines an increase in flow resistance, leading to myocardial ischemia, in response to reduced perfusion pressure. […] IHD pathophysiology is complicated and multifaceted and it is not only attributable to the simplistic obstructive CAD. Atherosclerosis is just one of multiple components playing in a complex pathophysiological process that includes inflammation, thrombosis, CMD and impaired angiogenesis, underlying the “elusive link” between CAD and IHD.

• #27 Epidemiology, Pathophysiology, Diagnosis and Treatment of Heart Failure in Diabetes

  https://www.e-dmj.org/journal/view.php?number=2539

  The coronary flow reserve (CFR) is the ratio between hyperemic and resting coronary flow, and the reduction of CFR has been reported to represent coronary microvascular dysfunction. […] Diabetic cardiomyopathy is defined by the existence of abnormal myocardial structure and performance in the absence of other cardiac risk factors, such as coronary artery disease, hypertension, and significant valvular disease, in individuals with DM. […] Hyperglycemia causes the formation of advanced glycation end products (AGEs), which are glycated proteins or lipids after prolonged exposure to glucose. […] Impairment in mitochondrial bioenergetics results in impaired intracellular calcium handling. […] Oxidative stress, inflammation, impaired mitochondrial energetics, intracellular calcium handling, and increased neurohumoral activation all contribute to the anatomic and functional alteration associated with diabetic cardiomyopathy.

• #28 Myocardial Infarction: Practice Essentials, Background, Definitions

  https://emedicine.medscape.com/article/155919-overview

  Typical MI initially manifests as coagulation necrosis that is ultimately followed by a healing process characterized by formation of myocardial scarring, known as myocardial fibrosis. […] In some occasions, restoration of blood flow to the damaged myocardium triggers further ischemic cellular damage, this paradoxical effect is known as reperfusion injury.

• #29 Radiation-induced heart disease: a review of classification, mechanism and prevention

  https://www.ijbs.com/v15p2128.htm

  Radiation-induced endothelial cell injury is deemed to be the primary and fundamental cause of myocardial injury. […] The above inflammatory factors can not only mediate the production of inflammation, but also promote the proliferation of endothelial cells and fibroblasts, the increase of collagen deposition can cause the thickening of vessel walls and the stenosis of lumen. […] Myocardial ischemia and hypoxia, inflammatory responses, collagen deposition, and proliferation of endothelial cells and fibroblasts lead to tissue remodeling, cardiac fibrosis, and atherosclerosis, and these changes are the primary endpoints of RIHD. […] In normal cell, reactive oxygen species (ROS) are important mediators of cellular processes such as immune response, cell signal transduction, microbial defense, differentiation, cell adhesion and apoptosis.

• #30 Ischemic heart disease – McMaster Pathophysiology Review

  https://www.pathophys.org/acs/

  Acute inflammatory response with infiltration of neutrophils leading to further tissue damage. […] Late changes in infarction (days to weeks): Resorption of irreversibly injured/dead myocytes by macrophages, Fibrous tissue deposition and scarring, Ventricular remodeling. […] Arrhythmias can also be caused by interruption of perfusion to structures of the conduction pathway (i.e. SA node, AV node, bundle branches). […] Can be directly caused by impaired contractility resulting in both systolic and diastolic dysfunction. […] Severely decreased cardiac output and hypotension with inadequate perfusion of peripheral tissues develops when more than 40% of the LV mass is infarcted.

• #31 Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure | Nature Communications

  https://www.nature.com/articles/s41467-019-13690-5

  Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. […] Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. […] Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. […] These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies.

• #32 Scientists identify mechanism behind genetic link to heart disease – Queen Mary University of London

  https://www.qmul.ac.uk/media/news/2013/smd/scientists-identify-mechanism-behind-genetic-link-to-heart-disease.html

  In this study the scientists focused on the gene region known as 9p21. This region has been strongly associated with heart disease, but it has been unclear whether it contributes to risk by increasing the build-up of plaque or by making it more likely that the plaque may break down, leading to a heart attack. […] The team analysed genetic data from more than 30,000 individuals drawn from multiple international studies focused on the 9p21 gene region. They found that individuals carrying two versions (homozygous) of the risk variant of the 9p21 gene were 23 per cent more likely to develop a more serious form of the disease, with blockages in more than one of the three coronary arteries carrying blood to the heart. […] The study also showed that individuals carrying the genetic risk variant were no more likely to have a heart attack than individuals with CAD who do not carry the genetic risk variant.

• #33 Scientists identify mechanism behind genetic link to heart disease – Queen Mary University of London

  https://www.qmul.ac.uk/media/news/2013/smd/scientists-identify-mechanism-behind-genetic-link-to-heart-disease.html

  This finding is important as it suggests this genetic variant, carried by around 75 per cent of the population, increases the risk of heart disease by promoting the build-up of deposits within the walls of the arteries. […] Understanding the mechanisms involved means it is now possible to look at developing new therapies and treatments which can potentially reduce this build-up.

• #34 Radiation-induced heart disease: a review of classification, mechanism and prevention

  https://www.ijbs.com/v15p2128.htm

  However, glutathione and other antioxidants are also consumed during their activity, and the cell’s ability to maintain redox balance is ultimately impaired. […] When the amount of endogenous and/or exogenous ROS exceeds the scavenging capacity of antioxidants, ROS begins to dominate and cause damage to cardiac myocytes. […] Cell apoptosis and necrosis occur in various types of cells in the heart after exposure to radiation, among which mitochondrial dysfunction and irreversible damage are the key links of cell apoptosis and necrosis, and the occurrence of mitochondrial dysfunction is closely related to endoplasmic reticulum (ER) stress. […] With the development of research, several studies have indicated that micro-RNAs (miRNAs) play an important role in the occurrence and progression of RIHD.

• #35 Heart Failure Pathogenesis Elucidation and New Treatment Method Development | JMA Journal

  https://www.jmaj.jp/detail.php?id=10.31662%2Fjmaj.2022-0106

  Several primary diseases, such as ischemic heart disease, valvular disease, and hypertension, cause HF, and some disease groups exhibit cardiac hypertrophy in response to stimuli before cardiac dysfunction. […] Cardiac hypertrophy is a compensatory response to increased workload and maintains cardiac function, which, if prolonged, can cause HF. […] The mechanism underlying this limitation of angiogenesis is unknown. […] p53, a known Hif-degrading factor, is activated in failing cardiomyocytes. […] DNA damage is also an important factor in human heart disease. […] Despite several studies outlining the importance of DNA damage in various heart diseases, we have not fully elucidated the specific molecular mechanisms underlying DNA damage involved in HF development and progression. […] HF pathogenesis is primarily associated with genetic and environmental factors.

• #36 Ischemic Heart Disease Pathophysiology Paradigms Overview: From Plaque Activation to Microvascular Dysfunction

  https://www.mdpi.com/1422-0067/21/21/8118

  Ischemic heart disease still represents a large burden on individuals and health care resources worldwide. By conventions, it is equated with atherosclerotic plaque due to flow-limiting obstruction in large–medium sized coronary arteries. However, clinical, angiographic and autoptic findings suggest a multifaceted pathophysiology for ischemic heart disease and just some cases are caused by severe or complicated atherosclerotic plaques. Currently there is no well-defined assessment of ischemic heart disease pathophysiology that satisfies all the observations and sometimes the underlying mechanism to everyday ischemic heart disease ward cases is misleading. […] In order to better examine this complicated disease and to provide future perspectives, it is important to know and analyze the pathophysiological mechanisms that underline it, because ischemic heart disease is not always determined by atherosclerotic plaque complication. Therefore, in order to have a more complete comprehension of ischemic heart disease we propose an overview of the available pathophysiological paradigms, from plaque activation to microvascular dysfunction.

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