Logan Steele
Myocardial necrosis, or heart muscle necrosis, is a form of cell injury resulting in the premature death of myocardial tissue. It is caused by factors external to the cell or tissue, such as infection, physical or chemical trauma, hypoxia, or injury. In the context of the cardiac muscle, necrosis is often the result of cardiac arrhythmias following diffuse central nervous system injury. It can also be caused by toxic effects of certain chemicals and drugs, which may lead to acute toxic myocarditis or chronic drug-induced cardiomyopathy. Additionally, necrosis can occur due to ischemia, infarction, and reperfusion, which are common in cardiovascular diseases. The extent of necrosis is influenced by the duration of ischemia and the size of the affected area. Myocardial necrosis is characterised by distinct morphological changes, including cell swelling, plasma membrane damage, and inflammatory responses, ultimately leading to cardiac dysfunction and potential early death.
| Characteristics | Values |
|---|---|
| Definition | The degeneration and death of myocardial tissue |
| Cause | Factors external to the cell or tissue, such as infection, or trauma |
| Types | Fibrinoid necrosis, caseous necrosis, liquefactive necrosis, coagulative necrosis, fat necrosis, gangrene, gummatous necrosis, hemorrhagic necrosis |
| Symptoms | Chest pain, dyspnea, cardiac arrhythmias, progressive heart chamber dilation, ventricular wall thinning, loss of cardiac function |
| Detection | Serologic markers such as troponin I and troponin T, creatine kinase MB isoform 1, electrocardiogram, cardiac magnetic resonance imaging |
| Treatment | Pharmacological and genetic inhibition of necrosis, use of necrostatin-1, stem cell therapy |
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What You'll Learn
Drug toxicity
Cardiotoxicity may be caused by chemotherapy (a usual example is the class of anthracyclines) and/or radiotherapy; complications from anorexia nervosa; adverse effects of heavy metal intake; the long-term abuse of or ingestion at high doses of certain strong stimulants such as cocaine; or an incorrectly administered drug such as bupivacaine. Many mechanisms have been used to explain cardiotoxicity, and it generally depends on the agent inducing cardiac damage. For example, the primary mechanism is thought to be oxidative stress on cardiac myocytes. It is thought that reactive oxygen species (ROS) overwhelm the antioxidant defences of cardiac cells, causing direct cellular damage. This oxidative damage can disrupt mitochondrial function, disrupting energy production in the heart muscle itself, leading to energy depletion and promoting cell death through apoptosis or necrosis.
Chemicals can also cause myocardial injury by direct toxic effects, which result in cell damage and cell death. This type of drug toxicity is dose-related and may present as acute toxic myocarditis or a more chronic drug-induced cardiomyopathy. Acute toxic myocarditis displays interstitial edema, multifocal areas of cardiac muscle cell necrosis with contraction bands, and an inflammatory cell infiltrate consisting of lymphocytes, plasma cells, and polymorphonuclear leukocytes.
Grossly evident myocardial infarction may occur in drug-induced coronary arteritis (as from amphetamines), fibromuscular intimai proliferation (estrogen- and/or progesterone-containing oral contraceptives), or embolization from infective endocarditis (associated with intravenous drug abuse). Large infarct-like areas of necrosis, not related to obstruction of large extramural coronary arteries, have been produced in experimental animals by the administration of large toxic doses of isoproterenol.
The progression of necrosis with contraction bands to myocytolysis is mediated through the lysis of the myofilaments, resulting in an empty appearance of the cells. Various subcellular organelles of cardiac muscle cells are subject to specific damage by toxic agents, including mitochondria. Compounds that interfere with mitochondrial enzymes (cyanide, thyroid hormone), uncouple oxidative phosphorylation (dinitrophenol, cobalt, lead, mercury), bind to mitochondrial DNA (acriflavin), produce mitochondrial mineralization (dehydrotachysterol, sodium phosphate), or produce selective mitochondrial damage by undetermined mechanisms (ionophores).
Cardiotoxicity is one of the most common adverse drug effects, and numerous drugs have been shown to induce lethal arrhythmias by affecting cardiac electrophysiology. Drugs that cause neurotoxicity may also result in cardiotoxicity, although neurotoxicity is typically exhibited at lower doses. The most cardiotoxic and neurotoxic local anesthetic is cocaine.
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Hypoxia
During hypoxia, the cardiac myocytes experience oxidative phosphorylation disruption, leading to a rapid decline in ATP and an increased AMP/ATP ratio. To compensate, autophagy is activated as a pro-survival mechanism to replenish energy under these stressful conditions. However, if the ischemia persists, the autophagic response becomes dysfunctional, leading to impaired autolysosomes.
Prolonged hypoxia can induce the expression and accumulation of BNIP3 mRNA and protein in cardiac myocytes, which, in conjunction with acidosis, can activate a necrosis-like pathway. This pathway includes the early loss of plasma membrane integrity, leading to cardiac myocyte death.
In summary, hypoxia contributes to necrosis of the cardiac muscle by inducing oxidative stress, triggering autophagic responses, and activating necrosis-like pathways in cardiac myocytes, ultimately resulting in reduced oxygen supply and, in severe cases, irreversible damage to the heart muscle.
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Physical or chemical trauma
Necrosis is a form of cell injury that results in the premature death of cells in living tissue by autolysis. It is caused by factors external to the cell or tissue, such as physical or chemical trauma, which result in the unregulated digestion of cell components.
Physical trauma that causes necrosis includes mechanical trauma, which is physical damage to the body that causes cellular breakdown. This can be caused by something as severe as a spider bite or as minor as a skin wound. Electric shock and damage to blood vessels that disrupt the blood supply to the heart can also cause necrosis. Extreme temperatures can also cause necrosis due to cell disruption, especially in bone cells.
Chemical trauma can also cause necrosis. Alkaline and acidic compounds cause liquefactive and coagulative necrosis, respectively. The severity of chemical necrosis depends on multiple factors, including compound concentration, type of tissue affected, and extent of exposure.
In the case of the heart, or cardiac muscle, necrosis can be caused by myocardial injury, which is often the result of direct toxic effects from certain chemicals and drugs. This type of drug toxicity is dose-related and may present as acute toxic myocarditis or chronic drug-induced cardiomyopathy. Acute toxic myocarditis displays interstitial edema, multifocal areas of cardiac muscle cell necrosis with contraction bands, and an inflammatory cell infiltrate consisting of lymphocytes, plasma cells, and polymorphonuclear leukocytes.
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Cardiomyocyte death
There are several types of necrosis that can occur in cardiac muscle cells, including:
- Coagulative necrosis: Characterised by the formation of a gelatinous substance in dead tissues, where the architecture of the tissue is maintained. This type of necrosis is typically seen in hypoxic environments and is caused by severe ischemia.
- Liquefactive necrosis: Characterised by the digestion of dead cells to form a viscous liquid mass. This type of necrosis is typical of bacterial or fungal infections due to their ability to stimulate an inflammatory response.
- Caseous necrosis: Considered a combination of coagulative and liquefactive necrosis, typically caused by mycobacteria, fungi, or foreign substances. The necrotic tissue appears white and friable, and dead cells leave granular particles.
- Fibrinoid necrosis: Usually caused by immune-mediated vascular damage, marked by complexes of antigen and antibodies deposited within arterial walls.
Recent studies have also explored the role of necrostatin-1 in reducing infarct size after I/R injury, suggesting potential clinical applications. Additionally, the discovery of tissue-resident cardiac stem cells and the benefits of exogenously delivered bone marrow-derived stem cells have challenged the belief that cardiomyocyte loss is irreversible.
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Cardiac arrhythmias
Heart muscle necrosis is the degeneration and death of myocardial tissue, often resulting from cardiac arrhythmias following a diffuse central nervous system injury. Cardiac arrhythmias are abnormal heart rhythms that can be caused by a variety of factors, including myocardial infarction, myocardial ischemia, and toxic injuries.
Myocardial infarction (MI) is a common cause of cardiac arrhythmias and occurs when a coronary artery becomes completely blocked, leading to a lack of blood and oxygen to the heart muscle. This can result in irreversible myocardial injury and necrosis of the cardiac muscle. The extent of necrosis after MI is influenced by the duration of ischemia and the size of the affected area. Proximal left anterior descending (LAD) artery occlusions in humans are associated with a greater extent of necrosis and a poorer prognosis.
Myocardial ischemia, also known as cardiac ischemia, is another cause of cardiac arrhythmias. It occurs when blood flow to the heart muscle is partially or completely obstructed by a buildup of plaques (atherosclerosis) or a blood clot. This reduces the heart's ability to pump blood and can lead to arrhythmias and, if sudden and severe, a heart attack. Myocardial ischemia can develop slowly over time as arteries become blocked or quickly due to a sudden blockage.
Additionally, cardiac arrhythmias can be induced by coronary artery spasms, which are temporary tightenings of the muscles in the artery wall that decrease or prevent blood flow to the heart muscle. This can be caused by high cholesterol levels in the blood, leading to the formation of plaques and subsequent artery blockage.
Overall, cardiac arrhythmias resulting from various factors can lead to heart muscle necrosis and potentially fatal outcomes. Understanding the causes of arrhythmias is crucial for early detection, treatment, and prevention to improve patient outcomes and reduce the risk of necrosis and other complications.
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Frequently asked questions
Necrosis is a form of cell injury that results in the premature death of cells in living tissue by autolysis. It is caused by factors external to the cell or tissue, such as infection, or trauma, resulting in the unregulated digestion of cell components.
Myocardial necrosis is caused by acute myocardial cell death or irreversible myocardial injury. It can be caused by diffuse central nervous system injury, resulting in cardiac arrhythmias, or by direct toxic effects of chemicals and drugs.
Cardiac necrosis often leads to symptoms such as chest pain and/or dyspnea. It can be detected through electrocardiograms and biochemical markers such as troponin I and troponin T.
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