Materiały źródłowe

• #1 Aortic Dissection – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441963/

  Aortic dissection occurs when a tear in the intimal layer of the aortic wall allows blood to enter the space between the intima and media, creating a false lumen. […] Chronic exposure to high pulsatile pressure and shear stress, especially in susceptible individuals, weakens these layers, leading to the initial intimal tear. […] The blood then flows into the space between the intima and media, expanding the false lumen. […] In most cases, the dissection propagates either anterograde (distally) or retrograde (proximally). […] The direction of propagation dictates the complications that arise: distal propagation can obstruct blood flow to the major branches of the aorta, leading to ischemia in affected territories such as the coronary, cerebral, spinal, or visceral arteries. […] Proximal propagation, as seen in type A dissections, often causes life-threatening complications like acute aortic regurgitation, cardiac tamponade, or even rupture.

• #2 Aortic dissection – Wikipedia

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

  Aortic dissection (AD) occurs when an injury to the innermost layer of the aorta allows blood to flow between the layers of the aortic wall, forcing the layers apart. […] The initiating event in aortic dissection is a tear in the intimal lining of the aorta. Due to the high pressures in the aorta, blood enters the media at the point of the tear. The force of the blood entering the media causes the tear to extend. It may extend proximally (closer to the heart) or distally (away from the heart) or both. […] In an aortic dissection, blood penetrates the intima and enters the media layer. The high pressure rips the tissue of the media apart along the laminated plane splitting the inner two-thirds and the outer one-third of the media apart. […] While it is not always clear why an intimal tear may occur, quite often it involves degeneration of the collagen and elastin that make up the media. This is known as cystic medial necrosis and is most commonly associated with Marfan syndrome and is also associated with Ehlers-Danlos syndrome. […] In about 13% of aortic dissections, no evidence of an intimal tear is found. In these cases, the inciting event is thought to be an intramural hematoma (caused by bleeding within the media).

• #3 Acute Aortic Dissection: Overview, Pathophysiology & Risk Factors, Prehospital Care

  https://emedicine.medscape.com/article/756835-overview

  Aortic dissection essentially features a tear in the intimal layer, followed by the formation and propagation of a subintimal hematoma. The dissecting hematoma commonly occupies up to 50% and, occasionally, 100% of the aortic circumference, leading to the development of a false lumen or double-barreled aorta. This can reduce the flow of blood to any of the major arteries arising from the aorta. If the dissection involves the pericardial space, cardiac tamponade can result. […] The normal aorta contains collagen, elastin, and smooth muscle cells, which help contribute to the layers of the aorta, the intima, the media, and the adventitia. Degenerative changes associated with aging lead to the breakdown of the collagen, elastin, and smooth muscle, as well as to an increase in basophilic ground substance. This is termed cystic medial necrosis, the hallmark histologic change associated with dissection and with Marfan syndrome.

• #4 Aortic dissection | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/aortic-dissection?lang=us

  Aortic dissection is the prototype and most common form of acute aortic syndromes and a type of arterial dissection. It occurs when blood enters the medial layer of the aortic wall through a tear or penetrating ulcer in the intima and tracks longitudinally along with the media, forming a second blood-filled channel (false lumen) within the vessel wall. […] The normal lumen lined by intima is called the true lumen and the blood-filled channel in the media is termed the false lumen. In most cases the vessel wall is abnormal. Causes include: hypertension (pathogenesis: medial degeneration) […] inherited connective tissue disorders (pathogenesis: medial degeneration) […] atherosclerosis (pathogenesis: penetrating ulcer) […] vasculitis (pathogenesis: inflammation) […] pregnancy (pathogenesis: unknown) […] iatrogenic: aortic catheterization, intra-aortic balloon pump. […] The false lumen typically has higher and less pulsatile pressure, thought to be due to reduced distal outflow. The true lumen is often smaller due to compression by the false lumen.

• #5 Acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection – Patel- Annals of Cardiothoracic Surgery

  https://www.annalscts.com/article/view/4185/html

  The aorta, similar to other arteries, is composed of three layers from deep to superficial: intima, media, and adventitia. The intima, being in direct contact with blood, is a thin layer primarily composed of endothelial cells on a basement membrane. The media is the largest layer and is composed of muscle and connective tissue, while the adventitia is a thin layer of connective tissue. There are two primary hypotheses that have been proposed to explain acute aortic dissection. The first theory holds that an initial tear in the intima leads to blood from the aortic lumen surging into the media and separating the intima from the aorta and creating a true and false lumen. In contrast, the second theory holds that the vasa vasorum in the more outer portions of the media hemorrhage first, and then secondarily cause intimal rupture. In both theories, it is thought that the pressure of pulsatile blood flow extends the dissection, typically in an anterograde fashion. In 10-20% of acute aortic dissection cases, a variant such as an aortic intramural hematoma or penetrating atherosclerotic ulcer occurs.

• #6 Aortic Dissection – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/diseases-of-the-aorta-and-its-branches/aortic-dissection

  Aortic dissection is the surging of blood through a tear in the aortic intima with separation of the intima and media and creation of a false lumen (channel). The intimal tear may be a primary event or secondary to hemorrhage within the media. […] Aortic dissections often occur in patients with preexisting degeneration of the aortic media. Causes and risk factors include connective tissue disorders, atherosclerotic disease, systemic rheumatic diseases, and injury. Atherosclerotic risk factors, notably hypertension, contribute in more than two-thirds of patients. After rupture of the intima, which is a primary event in some patients and secondary to hemorrhage within the media in others, blood flows into the media, creating a false channel that extends distally or, less commonly, proximally along the artery.

• #7 Acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection – Patel- Annals of Cardiothoracic Surgery

  https://www.annalscts.com/article/view/4185/html

  The aorta, similar to other arteries, is composed of three layers from deep to superficial: intima, media, and adventitia. The intima, being in direct contact with blood, is a thin layer primarily composed of endothelial cells on a basement membrane. The media is the largest layer and is composed of muscle and connective tissue, while the adventitia is a thin layer of connective tissue. There are two primary hypotheses that have been proposed to explain acute aortic dissection. The first theory holds that an initial tear in the intima leads to blood from the aortic lumen surging into the media and separating the intima from the aorta and creating a true and false lumen. In contrast, the second theory holds that the vasa vasorum in the more outer portions of the media hemorrhage first, and then secondarily cause intimal rupture. In both theories, it is thought that the pressure of pulsatile blood flow extends the dissection, typically in an anterograde fashion. In 10-20% of acute aortic dissection cases, a variant such as an aortic intramural hematoma or penetrating atherosclerotic ulcer occurs.

• #8 Acute Aortic Dissection • LITFL • CCC Cardiology

  https://litfl.com/acute-aortic-dissection/

  aortic dissection is a type of acute aortic syndrome (AAS) characterized by blood entering the medial layer of the wall with the creation of a false lumen. […] There are 3 possibilities as to how the blood enters the media: Atherosclerotic ulcer leading to intimal tear, Disruption of vasa vasorum causing intramural haematoma, De novo intimal tear. […] Following dissection, blood flow into the media may cause: extension up or down, rupture, vessel branch occlusion, aortic regurgitation, pericardial effusion / tamponade.

• #9 Aortic dissection – Wikipedia

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

  Aortic dissection (AD) occurs when an injury to the innermost layer of the aorta allows blood to flow between the layers of the aortic wall, forcing the layers apart. […] The initiating event in aortic dissection is a tear in the intimal lining of the aorta. Due to the high pressures in the aorta, blood enters the media at the point of the tear. The force of the blood entering the media causes the tear to extend. It may extend proximally (closer to the heart) or distally (away from the heart) or both. […] In an aortic dissection, blood penetrates the intima and enters the media layer. The high pressure rips the tissue of the media apart along the laminated plane splitting the inner two-thirds and the outer one-third of the media apart. […] While it is not always clear why an intimal tear may occur, quite often it involves degeneration of the collagen and elastin that make up the media. This is known as cystic medial necrosis and is most commonly associated with Marfan syndrome and is also associated with Ehlers-Danlos syndrome. […] In about 13% of aortic dissections, no evidence of an intimal tear is found. In these cases, the inciting event is thought to be an intramural hematoma (caused by bleeding within the media).

• #10 Aortic Dissection: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/2062452-overview

  Most classic aortic dissections begin at one of the following three distinct anatomic locations: Approximately 2.2 cm above the aortic root, distal to the left subclavian artery, and the aortic arch. […] The most common site of dissection is the first few centimeters of the ascending aorta, with 90% occurring within 10 cm of the aortic valve. […] Between 5% and 10% of dissections do not have an obvious intimal tear. These often are attributed to rupture of the aortic vasa vasorum as first described by Krukenberg in 1920. […] Ascending aortic involvement may result in death from wall rupture, hemopericardium and tamponade, occlusion of the coronary ostia with myocardial infarction, or severe aortic insufficiency. The nervi vascularis (ie, bundles of nerve fibers found in the aortic adventitia) are involved in the production of pain.

• #11 Aortic Dissection – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441963/

  As the false lumen develops, it typically becomes larger than the true lumen, increasing the risk of aneurysm formation and eventual rupture if left untreated. […] The 3 most common sites for acute aortic dissection include: The area approximately 2 to 2.5 cm above the aortic root (the most frequent site), Just distal to the origin of the left subclavian artery, Within the aortic arch. […] These dissections are highly lethal if not recognized and treated promptly, often leading to death due to aortic rupture or tamponade.

• #12 Acute Aortic Dissection: Overview, Pathophysiology & Risk Factors, Prehospital Care

  https://emedicine.medscape.com/article/756835-overview

  Any disease that weakens the strength of the aortic wall will predispose one to aortic dissection. Shearing forces give rise to the separation of the layers in the media of the aorta. Intimal rupture occurs at points of fixation along the aorta where the hydraulic stress is maximal. The most common site is the first few centimeters of the ascending aorta, with 90% found within 10 cm of the aortic valve. The second most common site is just distal to the left subclavian artery.

• #13 Aortic Dissection: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/2062452-overview

  Most classic aortic dissections begin at one of the following three distinct anatomic locations: Approximately 2.2 cm above the aortic root, distal to the left subclavian artery, and the aortic arch. […] The most common site of dissection is the first few centimeters of the ascending aorta, with 90% occurring within 10 cm of the aortic valve. […] Between 5% and 10% of dissections do not have an obvious intimal tear. These often are attributed to rupture of the aortic vasa vasorum as first described by Krukenberg in 1920. […] Ascending aortic involvement may result in death from wall rupture, hemopericardium and tamponade, occlusion of the coronary ostia with myocardial infarction, or severe aortic insufficiency. The nervi vascularis (ie, bundles of nerve fibers found in the aortic adventitia) are involved in the production of pain.

• #14 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  Aortic dissection arises from a tear in the aortic intima exposing the medial layer to the pulsatile blood flow. The intimal tear is frequently found in segments exposed to the greatest shear stress, namely the right lateral wall (opposite the main pulmonary artery) of the ascending aorta or in the proximal segment of the descending aorta. The progressive separation of the aortic wall layers results in the formation of a false lumen and its subsequent propagation can be followed either by aortic rupture in the case of adventitial disruption, or by re-entry back into the true lumen through another intimal tear. Aortic rupture quickly leads to exsanguination and death. In the event of blood redirection into the true lumen, creating natural fenestration, the patient can present as relatively stable with adequate perfusion. The false lumen may also end blindly in a cul-de-sac, creating a blood clot. Rarely, when thrombosis occurs very early in the event, the thrombosed false lumen is smaller than the true lumen. When thrombosis occurs late, the false lumen is usually larger than the true one. Moreover, the false lumen grows during blood clotting and further compresses the true lumen, leading to decreased systemic perfusion. The dissection can also extend into aortic branches and increase mortality risk, especially if coronary arteries are involved.

• #15 Aortic Dissection: A Review of the Pathophysiology, Management and Prospective Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8762162/

  The core physiopathological principle underlying AD is an increase in pressure leading to the separation of the layers of the media which creates a false lumen within the aortic wall. There are two main factors related to its development: structural weakness of the aortic wall, and increased wall tension. Many connective tissue components are implicated as culprits in the pathogenesis of AD, and several connective tissue diseases such as Marfan and Ehler-Danlos syndromes are important predisposing factors. Firstly, damaged interlaminar elastic fibers weaken the structural integrity of the aortic media. Secondly, Fibrillin, a glycoprotein that plays a role in organizing elastic fibers by forming scaffolds around elastin, may also play a role. The degeneration of the aortic media is also facilitated/accelerated by Medin, a fibril protein which forms oligomers that damage the aortic wall, via two mechanisms: Cytotoxicity of smooth muscle cells, and increased induction of matrix metalloproteinases (MMP). The strong association between hypertension and AD highlights the role of wall tension in the pathology of the disease. Hypertension, the most commonly associated condition with AD, illustrates the importance of wall tension; however, most hypertensive patients do not have dissections, thus illustrating the importance of degenerative changes – to which hypertension itself may be a contributor.

• #16 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  An electron microscopy study showed that the extracellular matrix is spare in the interlamellar space of the medial layer at the dissection entry site and adjacent intact tissue, and spirally thickened collagen fibrils are often accompanied by attenuated, fragmented or disrupted elastic lamellae. Moreover, the basement membrane of the smooth muscle cells is usually thin or even lacking. In contrast, the intimal layer does not show any specific changes in the aortic dissection. […] At the molecular level, aortic dissection is the result of remodelling of the aortic wall structure as a result of inflammation and extracellular matrix degradation. Activated macrophages infiltrate the tunica media and release matrix metalloproteinases (MMPs) and pro-inflammatory cytokines. The excessive production of MMP-1, MMP-9 and MMP-12 leads to the accelerated degradation of collagen and elastin fibres. These MMPs also play a role in the pathogenesis of aortic aneurysm and Marfan syndrome. Not only the increased release of MMPs themselves, but also the imbalance between them and their tissue inhibitors (TIMPs) promote the proteolytic dominance in aortic dissection.

• #17 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  An electron microscopy study showed that the extracellular matrix is spare in the interlamellar space of the medial layer at the dissection entry site and adjacent intact tissue, and spirally thickened collagen fibrils are often accompanied by attenuated, fragmented or disrupted elastic lamellae. Moreover, the basement membrane of the smooth muscle cells is usually thin or even lacking. In contrast, the intimal layer does not show any specific changes in the aortic dissection. […] At the molecular level, aortic dissection is the result of remodelling of the aortic wall structure as a result of inflammation and extracellular matrix degradation. Activated macrophages infiltrate the tunica media and release matrix metalloproteinases (MMPs) and pro-inflammatory cytokines. The excessive production of MMP-1, MMP-9 and MMP-12 leads to the accelerated degradation of collagen and elastin fibres. These MMPs also play a role in the pathogenesis of aortic aneurysm and Marfan syndrome. Not only the increased release of MMPs themselves, but also the imbalance between them and their tissue inhibitors (TIMPs) promote the proteolytic dominance in aortic dissection.

• #18 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  An electron microscopy study showed that the extracellular matrix is spare in the interlamellar space of the medial layer at the dissection entry site and adjacent intact tissue, and spirally thickened collagen fibrils are often accompanied by attenuated, fragmented or disrupted elastic lamellae. Moreover, the basement membrane of the smooth muscle cells is usually thin or even lacking. In contrast, the intimal layer does not show any specific changes in the aortic dissection. […] At the molecular level, aortic dissection is the result of remodelling of the aortic wall structure as a result of inflammation and extracellular matrix degradation. Activated macrophages infiltrate the tunica media and release matrix metalloproteinases (MMPs) and pro-inflammatory cytokines. The excessive production of MMP-1, MMP-9 and MMP-12 leads to the accelerated degradation of collagen and elastin fibres. These MMPs also play a role in the pathogenesis of aortic aneurysm and Marfan syndrome. Not only the increased release of MMPs themselves, but also the imbalance between them and their tissue inhibitors (TIMPs) promote the proteolytic dominance in aortic dissection.

• #19 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  An electron microscopy study showed that the extracellular matrix is spare in the interlamellar space of the medial layer at the dissection entry site and adjacent intact tissue, and spirally thickened collagen fibrils are often accompanied by attenuated, fragmented or disrupted elastic lamellae. Moreover, the basement membrane of the smooth muscle cells is usually thin or even lacking. In contrast, the intimal layer does not show any specific changes in the aortic dissection. […] At the molecular level, aortic dissection is the result of remodelling of the aortic wall structure as a result of inflammation and extracellular matrix degradation. Activated macrophages infiltrate the tunica media and release matrix metalloproteinases (MMPs) and pro-inflammatory cytokines. The excessive production of MMP-1, MMP-9 and MMP-12 leads to the accelerated degradation of collagen and elastin fibres. These MMPs also play a role in the pathogenesis of aortic aneurysm and Marfan syndrome. Not only the increased release of MMPs themselves, but also the imbalance between them and their tissue inhibitors (TIMPs) promote the proteolytic dominance in aortic dissection.

• #20

  https://link.springer.com/article/10.1007/s11427-024-2693-5

  Aortic dissection is a critical vascular disease that is characterized by a high mortality rate and inflammation significantly influences its onset and progression. Recent studies highlight the integral role of macrophages, key players in the immune system, in the pathological landscape of aortic dissection. These cells are involved in crucial processes, such as the remodeling of the extracellular matrix, immunocyte infiltration, and phenotypic switching of smooth muscle cells, which are essential for the structural integrity and functional dynamics of the aortic wall. […] Despite these insights, the specific contributions of macrophages to the development and progression of aortic dissection remains unclear. This review explores the pathogenesis of aortic dissection with a focus on macrophages and describes their origins, phenotypic variations, and potential roles based on the most recent research findings.

• #21 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  An electron microscopy study showed that the extracellular matrix is spare in the interlamellar space of the medial layer at the dissection entry site and adjacent intact tissue, and spirally thickened collagen fibrils are often accompanied by attenuated, fragmented or disrupted elastic lamellae. Moreover, the basement membrane of the smooth muscle cells is usually thin or even lacking. In contrast, the intimal layer does not show any specific changes in the aortic dissection. […] At the molecular level, aortic dissection is the result of remodelling of the aortic wall structure as a result of inflammation and extracellular matrix degradation. Activated macrophages infiltrate the tunica media and release matrix metalloproteinases (MMPs) and pro-inflammatory cytokines. The excessive production of MMP-1, MMP-9 and MMP-12 leads to the accelerated degradation of collagen and elastin fibres. These MMPs also play a role in the pathogenesis of aortic aneurysm and Marfan syndrome. Not only the increased release of MMPs themselves, but also the imbalance between them and their tissue inhibitors (TIMPs) promote the proteolytic dominance in aortic dissection.

• #22 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  An electron microscopy study showed that the extracellular matrix is spare in the interlamellar space of the medial layer at the dissection entry site and adjacent intact tissue, and spirally thickened collagen fibrils are often accompanied by attenuated, fragmented or disrupted elastic lamellae. Moreover, the basement membrane of the smooth muscle cells is usually thin or even lacking. In contrast, the intimal layer does not show any specific changes in the aortic dissection. […] At the molecular level, aortic dissection is the result of remodelling of the aortic wall structure as a result of inflammation and extracellular matrix degradation. Activated macrophages infiltrate the tunica media and release matrix metalloproteinases (MMPs) and pro-inflammatory cytokines. The excessive production of MMP-1, MMP-9 and MMP-12 leads to the accelerated degradation of collagen and elastin fibres. These MMPs also play a role in the pathogenesis of aortic aneurysm and Marfan syndrome. Not only the increased release of MMPs themselves, but also the imbalance between them and their tissue inhibitors (TIMPs) promote the proteolytic dominance in aortic dissection.

• #23 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  VEGF-mediated neoangiogenesis may be another process underlying aortic wall remodelling. VEGF (vascular endothelial growth factor) is the growth factor driving angiogenesis and vasculogenesis, but it also exerts proinflammatory actions. The production of VEGF is increased in the neovessels and their surrounding immune-inflammatory infiltrate of the degraded medial layer. […] Arterial hypertension is, as described below, one of the main risk factors for aortic dissection. It can act directly as a parietal stressor and indirectly as a proinflammatory trigger, mainly by inducing macrophage recruitment and activation. The hypertensive patients show elevated concentrations of proinflammatory molecules such as interleukin (IL)-6, VEGF, macrophage chemoattractant protein-1 (MCP-1), MMP-2 and MMP-9, suggesting that hypertension promotes a proinflammatory state, which subsequently leads to the excessive extracellular matrix degeneration and culminates in the aortic dissection.

• #24 Aortic Dissection – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/diseases-of-the-aorta-and-its-branches/aortic-dissection

  The pathophysiologic sequence of aortic dissections involves aortic wall inflammation, apoptosis of vascular smooth muscle cells, degeneration of aortic media, elastin disruption, and vessel dissection. Dissections may communicate back with the true aortic lumen through intimal rupture at a distal site, maintaining systemic blood flow.

• #25 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  BAV is a congenital heart defect in which the aortic valve leaflet changes from tricuspid to bicuspid. The bicuspid leaflets are known to cause hemodynamic dysfunction that leads to enlargement of the aorta, aneurysm, and dissection. […] Hypertension contributes to the deterioration of arterial walls. Approximately 65-75% of AD patients also have hypertension. This is well explained by Dong et al., who performed a study in 838 confirmed acute AD patients, finding that 585 acute AD cases were associated with hypertension. […] Tobacco smoking accelerates atherosclerosis and is a major risk factor for aortic aneurysms and dissections. […] Aortic smooth muscle cells are the main components of the tunica media and are responsible for aortic wall integrity and arterial wall remodeling. Any degradation of this structure can directly alter the aortic wall and lead to CVD. Certain inflammatory diseases that affect the integrity of the blood vessels such as aortitis, giant cell arteritis, Takayasus arteritis, systemic lupus erythematous, syphilitic aortitis, and rheumatoid arthritis can cause AD if not well treated.

• #26 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  VEGF-mediated neoangiogenesis may be another process underlying aortic wall remodelling. VEGF (vascular endothelial growth factor) is the growth factor driving angiogenesis and vasculogenesis, but it also exerts proinflammatory actions. The production of VEGF is increased in the neovessels and their surrounding immune-inflammatory infiltrate of the degraded medial layer. […] Arterial hypertension is, as described below, one of the main risk factors for aortic dissection. It can act directly as a parietal stressor and indirectly as a proinflammatory trigger, mainly by inducing macrophage recruitment and activation. The hypertensive patients show elevated concentrations of proinflammatory molecules such as interleukin (IL)-6, VEGF, macrophage chemoattractant protein-1 (MCP-1), MMP-2 and MMP-9, suggesting that hypertension promotes a proinflammatory state, which subsequently leads to the excessive extracellular matrix degeneration and culminates in the aortic dissection.

• #27 Aortic Dissection: Symptoms, Types A and B, Treatment

  https://patient.info/heart-health/abdominal-aortic-aneurysm/aortic-dissection

  An aortic dissection occurs in a weakened area of the wall of the aorta. An aortic dissection is a serious condition of sudden onset in which the inner layer of the aorta tears. Blood then surges through the tear, causing the inner and middle layers of the aorta to separate (dissect). […] Certain conditions make a tear in the wall of the aorta more likely. High blood pressure over a long period of time may weaken the wall of the aorta, making it more likely to tear. People who already have an enlarged aorta (aortic aneurysm) are also at increased risk of aortic dissection. […] Aortic dissection is often fatal if the blood-filled channel within the wall of the aorta ruptures through to the outside aortic wall (this is called aortic rupture). However, early diagnosis and treatment of aortic dissection can greatly improve survival.

• #28 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  VEGF-mediated neoangiogenesis may be another process underlying aortic wall remodelling. VEGF (vascular endothelial growth factor) is the growth factor driving angiogenesis and vasculogenesis, but it also exerts proinflammatory actions. The production of VEGF is increased in the neovessels and their surrounding immune-inflammatory infiltrate of the degraded medial layer. […] Arterial hypertension is, as described below, one of the main risk factors for aortic dissection. It can act directly as a parietal stressor and indirectly as a proinflammatory trigger, mainly by inducing macrophage recruitment and activation. The hypertensive patients show elevated concentrations of proinflammatory molecules such as interleukin (IL)-6, VEGF, macrophage chemoattractant protein-1 (MCP-1), MMP-2 and MMP-9, suggesting that hypertension promotes a proinflammatory state, which subsequently leads to the excessive extracellular matrix degeneration and culminates in the aortic dissection.

• #29 Aortic Dissection – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441963/

  Aortic dissection occurs when a tear in the intimal layer of the aortic wall allows blood to enter the space between the intima and media, creating a false lumen. […] Chronic exposure to high pulsatile pressure and shear stress, especially in susceptible individuals, weakens these layers, leading to the initial intimal tear. […] The blood then flows into the space between the intima and media, expanding the false lumen. […] In most cases, the dissection propagates either anterograde (distally) or retrograde (proximally). […] The direction of propagation dictates the complications that arise: distal propagation can obstruct blood flow to the major branches of the aorta, leading to ischemia in affected territories such as the coronary, cerebral, spinal, or visceral arteries. […] Proximal propagation, as seen in type A dissections, often causes life-threatening complications like acute aortic regurgitation, cardiac tamponade, or even rupture.

• #30 Aortic dissection – Wikipedia

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

  Aortic dissection (AD) occurs when an injury to the innermost layer of the aorta allows blood to flow between the layers of the aortic wall, forcing the layers apart. […] The initiating event in aortic dissection is a tear in the intimal lining of the aorta. Due to the high pressures in the aorta, blood enters the media at the point of the tear. The force of the blood entering the media causes the tear to extend. It may extend proximally (closer to the heart) or distally (away from the heart) or both. […] In an aortic dissection, blood penetrates the intima and enters the media layer. The high pressure rips the tissue of the media apart along the laminated plane splitting the inner two-thirds and the outer one-third of the media apart. […] While it is not always clear why an intimal tear may occur, quite often it involves degeneration of the collagen and elastin that make up the media. This is known as cystic medial necrosis and is most commonly associated with Marfan syndrome and is also associated with Ehlers-Danlos syndrome. […] In about 13% of aortic dissections, no evidence of an intimal tear is found. In these cases, the inciting event is thought to be an intramural hematoma (caused by bleeding within the media).

• #31 Aortic Dissection – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441963/

  Aortic dissection occurs when a tear in the intimal layer of the aortic wall allows blood to enter the space between the intima and media, creating a false lumen. […] Chronic exposure to high pulsatile pressure and shear stress, especially in susceptible individuals, weakens these layers, leading to the initial intimal tear. […] The blood then flows into the space between the intima and media, expanding the false lumen. […] In most cases, the dissection propagates either anterograde (distally) or retrograde (proximally). […] The direction of propagation dictates the complications that arise: distal propagation can obstruct blood flow to the major branches of the aorta, leading to ischemia in affected territories such as the coronary, cerebral, spinal, or visceral arteries. […] Proximal propagation, as seen in type A dissections, often causes life-threatening complications like acute aortic regurgitation, cardiac tamponade, or even rupture.

• #32 Aortic Dissection – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441963/

  Aortic dissection occurs when a tear in the intimal layer of the aortic wall allows blood to enter the space between the intima and media, creating a false lumen. […] Chronic exposure to high pulsatile pressure and shear stress, especially in susceptible individuals, weakens these layers, leading to the initial intimal tear. […] The blood then flows into the space between the intima and media, expanding the false lumen. […] In most cases, the dissection propagates either anterograde (distally) or retrograde (proximally). […] The direction of propagation dictates the complications that arise: distal propagation can obstruct blood flow to the major branches of the aorta, leading to ischemia in affected territories such as the coronary, cerebral, spinal, or visceral arteries. […] Proximal propagation, as seen in type A dissections, often causes life-threatening complications like acute aortic regurgitation, cardiac tamponade, or even rupture.

• #33 Aortic Dissection – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441963/

  As the false lumen develops, it typically becomes larger than the true lumen, increasing the risk of aneurysm formation and eventual rupture if left untreated. […] The 3 most common sites for acute aortic dissection include: The area approximately 2 to 2.5 cm above the aortic root (the most frequent site), Just distal to the origin of the left subclavian artery, Within the aortic arch. […] These dissections are highly lethal if not recognized and treated promptly, often leading to death due to aortic rupture or tamponade.

• #34 Aortic dissection | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/aortic-dissection?lang=us

  Aortic dissection is the prototype and most common form of acute aortic syndromes and a type of arterial dissection. It occurs when blood enters the medial layer of the aortic wall through a tear or penetrating ulcer in the intima and tracks longitudinally along with the media, forming a second blood-filled channel (false lumen) within the vessel wall. […] The normal lumen lined by intima is called the true lumen and the blood-filled channel in the media is termed the false lumen. In most cases the vessel wall is abnormal. Causes include: hypertension (pathogenesis: medial degeneration) […] inherited connective tissue disorders (pathogenesis: medial degeneration) […] atherosclerosis (pathogenesis: penetrating ulcer) […] vasculitis (pathogenesis: inflammation) […] pregnancy (pathogenesis: unknown) […] iatrogenic: aortic catheterization, intra-aortic balloon pump. […] The false lumen typically has higher and less pulsatile pressure, thought to be due to reduced distal outflow. The true lumen is often smaller due to compression by the false lumen.

• #35 Aortic dissection | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/aortic-dissection?lang=us

  Aortic dissection is the prototype and most common form of acute aortic syndromes and a type of arterial dissection. It occurs when blood enters the medial layer of the aortic wall through a tear or penetrating ulcer in the intima and tracks longitudinally along with the media, forming a second blood-filled channel (false lumen) within the vessel wall. […] The normal lumen lined by intima is called the true lumen and the blood-filled channel in the media is termed the false lumen. In most cases the vessel wall is abnormal. Causes include: hypertension (pathogenesis: medial degeneration) […] inherited connective tissue disorders (pathogenesis: medial degeneration) […] atherosclerosis (pathogenesis: penetrating ulcer) […] vasculitis (pathogenesis: inflammation) […] pregnancy (pathogenesis: unknown) […] iatrogenic: aortic catheterization, intra-aortic balloon pump. […] The false lumen typically has higher and less pulsatile pressure, thought to be due to reduced distal outflow. The true lumen is often smaller due to compression by the false lumen.

• #36 Aortic dissection | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/aortic-dissection?lang=us

  Aortic dissection is the prototype and most common form of acute aortic syndromes and a type of arterial dissection. It occurs when blood enters the medial layer of the aortic wall through a tear or penetrating ulcer in the intima and tracks longitudinally along with the media, forming a second blood-filled channel (false lumen) within the vessel wall. […] The normal lumen lined by intima is called the true lumen and the blood-filled channel in the media is termed the false lumen. In most cases the vessel wall is abnormal. Causes include: hypertension (pathogenesis: medial degeneration) […] inherited connective tissue disorders (pathogenesis: medial degeneration) […] atherosclerosis (pathogenesis: penetrating ulcer) […] vasculitis (pathogenesis: inflammation) […] pregnancy (pathogenesis: unknown) […] iatrogenic: aortic catheterization, intra-aortic balloon pump. […] The false lumen typically has higher and less pulsatile pressure, thought to be due to reduced distal outflow. The true lumen is often smaller due to compression by the false lumen.

• #37 Aortic dissection | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/aortic-dissection?lang=us

  Aortic dissection is the prototype and most common form of acute aortic syndromes and a type of arterial dissection. It occurs when blood enters the medial layer of the aortic wall through a tear or penetrating ulcer in the intima and tracks longitudinally along with the media, forming a second blood-filled channel (false lumen) within the vessel wall. […] The normal lumen lined by intima is called the true lumen and the blood-filled channel in the media is termed the false lumen. In most cases the vessel wall is abnormal. Causes include: hypertension (pathogenesis: medial degeneration) […] inherited connective tissue disorders (pathogenesis: medial degeneration) […] atherosclerosis (pathogenesis: penetrating ulcer) […] vasculitis (pathogenesis: inflammation) […] pregnancy (pathogenesis: unknown) […] iatrogenic: aortic catheterization, intra-aortic balloon pump. […] The false lumen typically has higher and less pulsatile pressure, thought to be due to reduced distal outflow. The true lumen is often smaller due to compression by the false lumen.

• #38 Acute Aortic Dissection: Overview, Pathophysiology & Risk Factors, Prehospital Care

  https://emedicine.medscape.com/article/756835-overview

  Aortic dissection essentially features a tear in the intimal layer, followed by the formation and propagation of a subintimal hematoma. The dissecting hematoma commonly occupies up to 50% and, occasionally, 100% of the aortic circumference, leading to the development of a false lumen or double-barreled aorta. This can reduce the flow of blood to any of the major arteries arising from the aorta. If the dissection involves the pericardial space, cardiac tamponade can result. […] The normal aorta contains collagen, elastin, and smooth muscle cells, which help contribute to the layers of the aorta, the intima, the media, and the adventitia. Degenerative changes associated with aging lead to the breakdown of the collagen, elastin, and smooth muscle, as well as to an increase in basophilic ground substance. This is termed cystic medial necrosis, the hallmark histologic change associated with dissection and with Marfan syndrome.

• #39 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  Aortic dissection arises from a tear in the aortic intima exposing the medial layer to the pulsatile blood flow. The intimal tear is frequently found in segments exposed to the greatest shear stress, namely the right lateral wall (opposite the main pulmonary artery) of the ascending aorta or in the proximal segment of the descending aorta. The progressive separation of the aortic wall layers results in the formation of a false lumen and its subsequent propagation can be followed either by aortic rupture in the case of adventitial disruption, or by re-entry back into the true lumen through another intimal tear. Aortic rupture quickly leads to exsanguination and death. In the event of blood redirection into the true lumen, creating natural fenestration, the patient can present as relatively stable with adequate perfusion. The false lumen may also end blindly in a cul-de-sac, creating a blood clot. Rarely, when thrombosis occurs very early in the event, the thrombosed false lumen is smaller than the true lumen. When thrombosis occurs late, the false lumen is usually larger than the true one. Moreover, the false lumen grows during blood clotting and further compresses the true lumen, leading to decreased systemic perfusion. The dissection can also extend into aortic branches and increase mortality risk, especially if coronary arteries are involved.

• #40 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  Aortic dissection arises from a tear in the aortic intima exposing the medial layer to the pulsatile blood flow. The intimal tear is frequently found in segments exposed to the greatest shear stress, namely the right lateral wall (opposite the main pulmonary artery) of the ascending aorta or in the proximal segment of the descending aorta. The progressive separation of the aortic wall layers results in the formation of a false lumen and its subsequent propagation can be followed either by aortic rupture in the case of adventitial disruption, or by re-entry back into the true lumen through another intimal tear. Aortic rupture quickly leads to exsanguination and death. In the event of blood redirection into the true lumen, creating natural fenestration, the patient can present as relatively stable with adequate perfusion. The false lumen may also end blindly in a cul-de-sac, creating a blood clot. Rarely, when thrombosis occurs very early in the event, the thrombosed false lumen is smaller than the true lumen. When thrombosis occurs late, the false lumen is usually larger than the true one. Moreover, the false lumen grows during blood clotting and further compresses the true lumen, leading to decreased systemic perfusion. The dissection can also extend into aortic branches and increase mortality risk, especially if coronary arteries are involved.

• #41 Acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection – Patel- Annals of Cardiothoracic Surgery

  https://www.annalscts.com/article/view/4185/html

  The complexities of management of type B acute dissection continue to remain a challenge. The classic understanding has been that type A and complicated type B acute aortic dissections require surgical resection while uncomplicated type B acute aortic dissection can be treated medically. More recently, emerging evidence from IRAD has begun to elucidate the risk stratification and management of such patients. While no uniform criteria exist to differentiate complicated versus uncomplicated type B acute dissection, a recent interdisciplinary consensus document has suggested the following definition of complicated type B acute aortic dissection: malperfusion indicated by impending organ failure, hypertension when associated with malperfusion or persisting with high levels despite full medical therapy, or increases in periaortic hematoma and hemorrhagic pleural effusion in two subsequent CT examinations suggestive of impending rupture. Per this definition, malperfusion is typically evidenced by clinical signs and/or laboratory markers. Typical clinical features may include: malperfusion of spinal arteries leading to paresis, and paraplegia or malperfusion of visceral arteries leading to abdominal pain. However, for those instances where malperfusion may remain too subtle to evoke clinical symptomology, laboratory markers provide a sensitive method of detection. Elevations in hepatic or pancreatic enzymes may similarly signify mesenteric or celiac malperfusion, while increased creatinine would signify renal malperfusion. Additionally, refractory pain may be a clinical symptom indicative of malperfusion as well. Indeed in IRAD, refractory pain has been noted to be a predictor of mortality increasing the risk of in-hospital mortality by over twenty-fold.

• #42 Aortic Dissection | Thoracic Key

  https://thoracickey.com/aortic-dissection-5/

  Aortic dissection is the main cause of death in acute aortic diseases, more frequent than ruptured abdominal aortic aneurysms and traumas. It carries high mortality reaching 22.7 % within 6 h, 50 % within 24 h, and 68 % within the first week. Therefore, timing to take measures is critical for patient survival. The false lumen enlarges suddenly and can lead to complete or partial compression of the true lumen; therefore, affecting the emergence of the major aortic branches leading to reduce blood supply to brain, abdominal organs (bowels, kidneys, and/or liver) and/or limbs, which is known as malperfusion syndrome. The two mechanisms of ostial obstruction to blood flow are: (1) dynamic obstruction and (2) static obstruction. Dynamic obstruction is characterized by prolapse of the false lumens flap toward the ostium of a major branch during cardiac systole. When the flap touches the ostium, the blood flow for the aortic branch occludes temporally, causing blood flow restriction to the organ. This mechanism is responsible for about 80 % of the total malperfusion syndromes. Static obstruction occurs when the flap occludes continuously and completely the ostium of the aortic branch, leading to the formation of secondary thrombus inside the branch and distal ischemia. Other complication of aortic dissection is the weakening of the arterial wall that can form an aneurysm. In the worst case scenario, disruption of the arterial wall can occur leading to bleeding. It can occur in the pericardial, thoracic, or abdominal cavities. In cases of excessive or persistent bleeding, cardiac tamponade or hemorrhagic shock and death are the final outcomes. Hypertension is a major risk factor and plays a crucial role in both increasing the stress on the aortic wall and the subsequent intimal rupture. Abnormalities of the aortic wall: Diseases such as aortic coarctation (congenital narrowing of aortic segments), aneurysms, and hereditary conditions such as Marfan syndrome and EhlerDanlos syndrome and chromosomal abnormalities, like Turner and Noonan syndrome predispose the aortic wall to intima rupture. Bicuspid aortic valve is a risk factor for acute type A dissection, due to turbulence from the left ventricle blood jet which stresses against the wall of the ascending aorta. Atherosclerosis is not a significant risk factor, present in only 31 % of people affected by acute aortic dissection. The impairment of the blood flow to the ostia of the major branches of the abdominal aorta can lead to visceral and lower limbs ischemia, occurring in 31 % of patients.

• #43 Acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection – Patel- Annals of Cardiothoracic Surgery

  https://www.annalscts.com/article/view/4185/html

  The complexities of management of type B acute dissection continue to remain a challenge. The classic understanding has been that type A and complicated type B acute aortic dissections require surgical resection while uncomplicated type B acute aortic dissection can be treated medically. More recently, emerging evidence from IRAD has begun to elucidate the risk stratification and management of such patients. While no uniform criteria exist to differentiate complicated versus uncomplicated type B acute dissection, a recent interdisciplinary consensus document has suggested the following definition of complicated type B acute aortic dissection: malperfusion indicated by impending organ failure, hypertension when associated with malperfusion or persisting with high levels despite full medical therapy, or increases in periaortic hematoma and hemorrhagic pleural effusion in two subsequent CT examinations suggestive of impending rupture. Per this definition, malperfusion is typically evidenced by clinical signs and/or laboratory markers. Typical clinical features may include: malperfusion of spinal arteries leading to paresis, and paraplegia or malperfusion of visceral arteries leading to abdominal pain. However, for those instances where malperfusion may remain too subtle to evoke clinical symptomology, laboratory markers provide a sensitive method of detection. Elevations in hepatic or pancreatic enzymes may similarly signify mesenteric or celiac malperfusion, while increased creatinine would signify renal malperfusion. Additionally, refractory pain may be a clinical symptom indicative of malperfusion as well. Indeed in IRAD, refractory pain has been noted to be a predictor of mortality increasing the risk of in-hospital mortality by over twenty-fold.

• #44 Aortic Dissection | Thoracic Key

  https://thoracickey.com/aortic-dissection-5/

  Aortic dissection is the main cause of death in acute aortic diseases, more frequent than ruptured abdominal aortic aneurysms and traumas. It carries high mortality reaching 22.7 % within 6 h, 50 % within 24 h, and 68 % within the first week. Therefore, timing to take measures is critical for patient survival. The false lumen enlarges suddenly and can lead to complete or partial compression of the true lumen; therefore, affecting the emergence of the major aortic branches leading to reduce blood supply to brain, abdominal organs (bowels, kidneys, and/or liver) and/or limbs, which is known as malperfusion syndrome. The two mechanisms of ostial obstruction to blood flow are: (1) dynamic obstruction and (2) static obstruction. Dynamic obstruction is characterized by prolapse of the false lumens flap toward the ostium of a major branch during cardiac systole. When the flap touches the ostium, the blood flow for the aortic branch occludes temporally, causing blood flow restriction to the organ. This mechanism is responsible for about 80 % of the total malperfusion syndromes. Static obstruction occurs when the flap occludes continuously and completely the ostium of the aortic branch, leading to the formation of secondary thrombus inside the branch and distal ischemia. Other complication of aortic dissection is the weakening of the arterial wall that can form an aneurysm. In the worst case scenario, disruption of the arterial wall can occur leading to bleeding. It can occur in the pericardial, thoracic, or abdominal cavities. In cases of excessive or persistent bleeding, cardiac tamponade or hemorrhagic shock and death are the final outcomes. Hypertension is a major risk factor and plays a crucial role in both increasing the stress on the aortic wall and the subsequent intimal rupture. Abnormalities of the aortic wall: Diseases such as aortic coarctation (congenital narrowing of aortic segments), aneurysms, and hereditary conditions such as Marfan syndrome and EhlerDanlos syndrome and chromosomal abnormalities, like Turner and Noonan syndrome predispose the aortic wall to intima rupture. Bicuspid aortic valve is a risk factor for acute type A dissection, due to turbulence from the left ventricle blood jet which stresses against the wall of the ascending aorta. Atherosclerosis is not a significant risk factor, present in only 31 % of people affected by acute aortic dissection. The impairment of the blood flow to the ostia of the major branches of the abdominal aorta can lead to visceral and lower limbs ischemia, occurring in 31 % of patients.

• #45 Acute Aortic Syndromes | RECAPEM

  https://recapem.com/acute-aortic-syndromes/

  The presence of blood within the aortic wall layer can cause localized inflammation. This inflammatory response not only weakens the aortic wall, which leads to rupture, pseudoaneurysm, fistula formation with adjacent structures, but also may provoke an inflammatory reaction within adjacent anatomic structures, such as in pleura (causing pleural effusion), the pericardium (causing pericarditis). […] The mortality of acute aortic syndromes is a consequence of its complications. Aortic dissection, as the prototype of this syndrome, can give rise to a variety of organ dysfunction either by rupture or via malperfusion. The latter may be dynamic, static, or mixed. Dynamic malperfusion is the most common and results from the overpressurized false lumen pushing the septum toward the true lumen, leading to collapse of the true lumen and obstruction of branch vessels. Static malperfusion results from stenosis or occlusion of a branch artery caused by the dissection flap, hematoma, embolism, or thrombosis. […] The risk of rupture is greater than aortic dissection as the outer adventitia is thinner.

• #46 Cardiac tamponade due to aortic dissection: clinical picture and treatment with focus on pericardiocentesis

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Cardiac-tamponade-due-to-aortic-dissection-clinical-picture-and-treatment-with-focus-on-pericardiocentesis

  Cardiac tamponade associated with aortic rupture has been identified as a major risk factor for perioperative mortality in patients with acute type A aortic dissection. […] The presence of cardiac tamponade should prompt urgent aortic repair. […] Tamponade-induced hypotension associated with aortic rupture has been identified as a major risk factor for perioperative mortality in patients with AADA. […] The presence of cardiac tamponade should prompt urgent aortic repair. […] Cardiac tamponade is one of the important risk factors in poor outcomes. […] Prolonged hypotension from admission to the operating room is associated with fatal outcomes in more than 40% of patients. […] In-hospital mortality from AADA with cardiac tamponade was 54%, which was more than twice the mortality rate without cardiac tamponade.

• #47 Acute Aortic Dissection: Overview, Pathophysiology & Risk Factors, Prehospital Care

  https://emedicine.medscape.com/article/756835-overview

  Aortic dissection essentially features a tear in the intimal layer, followed by the formation and propagation of a subintimal hematoma. The dissecting hematoma commonly occupies up to 50% and, occasionally, 100% of the aortic circumference, leading to the development of a false lumen or double-barreled aorta. This can reduce the flow of blood to any of the major arteries arising from the aorta. If the dissection involves the pericardial space, cardiac tamponade can result. […] The normal aorta contains collagen, elastin, and smooth muscle cells, which help contribute to the layers of the aorta, the intima, the media, and the adventitia. Degenerative changes associated with aging lead to the breakdown of the collagen, elastin, and smooth muscle, as well as to an increase in basophilic ground substance. This is termed cystic medial necrosis, the hallmark histologic change associated with dissection and with Marfan syndrome.

• #48 Mechanism of diffuse alveolar hemorrhage formation in aortic dissection – Turkish Journal of Thoracic and Cardiovascular Surgery

  https://tgkdc.dergisi.org/text.php?id=2806

  Mechanism of diffuse alveolar hemorrhage formation in aortic dissection […] In Type A aortic dissections, aneurysm is opened in the pericardium in case of anterior ruptures and pericardial tamponade occurs. In case of posterior or left lateral wall ruptures, extravasated blood directly enters to the media and adventitia of the left pulmonary or main pulmonary arteries, advancing toward the pulmonary interstitium or alveoli. […] Extravasated blood from the aorta passes into the pulmonary interstitium through high pressure, leading to intrapulmonary hemorrhage or hemoptysis. […] Nonetheless, relevant data regarding the relationship between diffuse alveolar hemorrhage and aortic dissection or its underlying mechanism are not available in the aforementioned study. To the best of our knowledge, the mechanism of hemoptysis is as mentioned above.

• #49 Diagnosis and clinical management of aortic dissection | RRCC

  https://www.dovepress.com/diagnosis-and-clinical-management-of-aortic-dissection-peer-reviewed-fulltext-article-RRCC

  Aortic branches may become occluded by the dissecting intima and media, dissect off the true lumen to be perfused only by the false lumen, or remain uninvolved. […] This variable pattern of dissection accounts for the wide variety of clinical presentations of aortic dissection. […] If acute aortic rupture does not occur, the false lumen may enlarge over time and become aneurysmal in nature, eventually leading to thrombosis or rupture into the pericardium, the pleural space (usually left), or less commonly the abdomen.

• #50 Diagnosis and clinical management of aortic dissection | RRCC

  https://www.dovepress.com/diagnosis-and-clinical-management-of-aortic-dissection-peer-reviewed-fulltext-article-RRCC

  Aortic branches may become occluded by the dissecting intima and media, dissect off the true lumen to be perfused only by the false lumen, or remain uninvolved. […] This variable pattern of dissection accounts for the wide variety of clinical presentations of aortic dissection. […] If acute aortic rupture does not occur, the false lumen may enlarge over time and become aneurysmal in nature, eventually leading to thrombosis or rupture into the pericardium, the pleural space (usually left), or less commonly the abdomen.

• #51

  https://link.springer.com/article/10.1007/s12630-010-9370-9

  Acute aortic dissection of the ascending aorta is potentially a highly lethal condition requiring rapid diagnosis and urgent surgical treatment. […] Transesophageal echocardiography has now become a critical monitoring tool in the assessment of hemodynamic instability in aortic dissection. Hemodynamic instability in aortic dissection can result from numerous factors, which are summarized in Table 2. The mechanism of hemodynamic instability can be approached using Guytons concept of venous return combined with bedside echography. […] First, Pms can fall from massive hemorrhage, and vasodilatory shock can result if the shock state is prolonged. Right atrial pressure can increase if coronary artery perfusion is compromised from ostial dissection. This condition can lead to either left or right ventricular systolic or diastolic dysfunction with or without mitral regurgitation. Acute aortic insufficiency from aortic dilation of leaflet disruption, will also lead to an increase in Pra as a result of several mechanisms.

• #52 Aortic Dissection: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/2062452-overview

  Most classic aortic dissections begin at one of the following three distinct anatomic locations: Approximately 2.2 cm above the aortic root, distal to the left subclavian artery, and the aortic arch. […] The most common site of dissection is the first few centimeters of the ascending aorta, with 90% occurring within 10 cm of the aortic valve. […] Between 5% and 10% of dissections do not have an obvious intimal tear. These often are attributed to rupture of the aortic vasa vasorum as first described by Krukenberg in 1920. […] Ascending aortic involvement may result in death from wall rupture, hemopericardium and tamponade, occlusion of the coronary ostia with myocardial infarction, or severe aortic insufficiency. The nervi vascularis (ie, bundles of nerve fibers found in the aortic adventitia) are involved in the production of pain.

• #53 Acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection – Patel- Annals of Cardiothoracic Surgery

  https://www.annalscts.com/article/view/4185/html

  The complexities of management of type B acute dissection continue to remain a challenge. The classic understanding has been that type A and complicated type B acute aortic dissections require surgical resection while uncomplicated type B acute aortic dissection can be treated medically. More recently, emerging evidence from IRAD has begun to elucidate the risk stratification and management of such patients. While no uniform criteria exist to differentiate complicated versus uncomplicated type B acute dissection, a recent interdisciplinary consensus document has suggested the following definition of complicated type B acute aortic dissection: malperfusion indicated by impending organ failure, hypertension when associated with malperfusion or persisting with high levels despite full medical therapy, or increases in periaortic hematoma and hemorrhagic pleural effusion in two subsequent CT examinations suggestive of impending rupture. Per this definition, malperfusion is typically evidenced by clinical signs and/or laboratory markers. Typical clinical features may include: malperfusion of spinal arteries leading to paresis, and paraplegia or malperfusion of visceral arteries leading to abdominal pain. However, for those instances where malperfusion may remain too subtle to evoke clinical symptomology, laboratory markers provide a sensitive method of detection. Elevations in hepatic or pancreatic enzymes may similarly signify mesenteric or celiac malperfusion, while increased creatinine would signify renal malperfusion. Additionally, refractory pain may be a clinical symptom indicative of malperfusion as well. Indeed in IRAD, refractory pain has been noted to be a predictor of mortality increasing the risk of in-hospital mortality by over twenty-fold.

• #54 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  BAV is a congenital heart defect in which the aortic valve leaflet changes from tricuspid to bicuspid. The bicuspid leaflets are known to cause hemodynamic dysfunction that leads to enlargement of the aorta, aneurysm, and dissection. […] Hypertension contributes to the deterioration of arterial walls. Approximately 65-75% of AD patients also have hypertension. This is well explained by Dong et al., who performed a study in 838 confirmed acute AD patients, finding that 585 acute AD cases were associated with hypertension. […] Tobacco smoking accelerates atherosclerosis and is a major risk factor for aortic aneurysms and dissections. […] Aortic smooth muscle cells are the main components of the tunica media and are responsible for aortic wall integrity and arterial wall remodeling. Any degradation of this structure can directly alter the aortic wall and lead to CVD. Certain inflammatory diseases that affect the integrity of the blood vessels such as aortitis, giant cell arteritis, Takayasus arteritis, systemic lupus erythematous, syphilitic aortitis, and rheumatoid arthritis can cause AD if not well treated.

• #55 Aortic Dissection – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/diseases-of-the-aorta-and-its-branches/aortic-dissection

  Aortic dissection is the surging of blood through a tear in the aortic intima with separation of the intima and media and creation of a false lumen (channel). The intimal tear may be a primary event or secondary to hemorrhage within the media. […] Aortic dissections often occur in patients with preexisting degeneration of the aortic media. Causes and risk factors include connective tissue disorders, atherosclerotic disease, systemic rheumatic diseases, and injury. Atherosclerotic risk factors, notably hypertension, contribute in more than two-thirds of patients. After rupture of the intima, which is a primary event in some patients and secondary to hemorrhage within the media in others, blood flows into the media, creating a false channel that extends distally or, less commonly, proximally along the artery.

• #56 Aortic dissection: MedlinePlus Medical EncyclopediaLock

  https://medlineplus.gov/ency/article/000181.htm

  Other risk factors and conditions linked to aortic dissection include: Bicuspid aortic valve, Coarctation (narrowing) of the aorta, Connective tissue disorders (such as Marfan syndrome and Ehlers-Danlos syndrome) and rare genetic disorders, Heart surgery or procedures, Pregnancy, Swelling of the blood vessels due to conditions such as arteritis and syphilis. […] Aortic dissection occurs in about 2 out of every 10,000 people. It can affect anyone, but is most often seen in men ages 40 to 70.

• #57 Aortic dissection: MedlinePlus Medical EncyclopediaLock

  https://medlineplus.gov/ency/article/000181.htm

  Other risk factors and conditions linked to aortic dissection include: Bicuspid aortic valve, Coarctation (narrowing) of the aorta, Connective tissue disorders (such as Marfan syndrome and Ehlers-Danlos syndrome) and rare genetic disorders, Heart surgery or procedures, Pregnancy, Swelling of the blood vessels due to conditions such as arteritis and syphilis. […] Aortic dissection occurs in about 2 out of every 10,000 people. It can affect anyone, but is most often seen in men ages 40 to 70.

• #58 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  BAV is a congenital heart defect in which the aortic valve leaflet changes from tricuspid to bicuspid. The bicuspid leaflets are known to cause hemodynamic dysfunction that leads to enlargement of the aorta, aneurysm, and dissection. […] Hypertension contributes to the deterioration of arterial walls. Approximately 65-75% of AD patients also have hypertension. This is well explained by Dong et al., who performed a study in 838 confirmed acute AD patients, finding that 585 acute AD cases were associated with hypertension. […] Tobacco smoking accelerates atherosclerosis and is a major risk factor for aortic aneurysms and dissections. […] Aortic smooth muscle cells are the main components of the tunica media and are responsible for aortic wall integrity and arterial wall remodeling. Any degradation of this structure can directly alter the aortic wall and lead to CVD. Certain inflammatory diseases that affect the integrity of the blood vessels such as aortitis, giant cell arteritis, Takayasus arteritis, systemic lupus erythematous, syphilitic aortitis, and rheumatoid arthritis can cause AD if not well treated.

• #59 Aortic Dissection: Symptoms, Types A and B, Treatment

  https://patient.info/heart-health/abdominal-aortic-aneurysm/aortic-dissection

  An aortic dissection occurs in a weakened area of the wall of the aorta. An aortic dissection is a serious condition of sudden onset in which the inner layer of the aorta tears. Blood then surges through the tear, causing the inner and middle layers of the aorta to separate (dissect). […] Certain conditions make a tear in the wall of the aorta more likely. High blood pressure over a long period of time may weaken the wall of the aorta, making it more likely to tear. People who already have an enlarged aorta (aortic aneurysm) are also at increased risk of aortic dissection. […] Aortic dissection is often fatal if the blood-filled channel within the wall of the aorta ruptures through to the outside aortic wall (this is called aortic rupture). However, early diagnosis and treatment of aortic dissection can greatly improve survival.

• #60 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  Aneurysm is characterized by artery dilation of at least 1.5 times the normal size. It is associated with aging, smoking, and atherosclerotic disease. Thoracic AA is the most dangerous type of AA, not only because of the location (the aortic root), but also because it can evolve into dissection. It is strongly inherited; to date, 11 genes have been found to contribute to thoracic AA pathogenesis. […] CTDs are a group of congenital disorders responsible for the malformation of blood vessels, leading to their weakness. When present, CTDs are responsible for early AD and aneurysm, explaining why these risk factors are mostly seen in young patients with AD. The common factor among these inherited disorders is that they all contribute in some way to the abnormal formation of the structure of blood vessels, especially the aorta.

• #61 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  Compared with healthy people, those with obesity are more predisposed to develop acute AD, with even more respiratory complications, such as acute lung injury. […] There is a risk of AD developing during or immediately following pregnancy. This is closely related to genetic predisposition, such as MFS, LDS, vEDS, BAV, and TS, but in rare situations it can occur in the absence of these risk factors. […] Iatrogenic AD (IAD) is the presence of AD as a complication of a cardiac procedure. It is a rare and potentially fatal condition that can occur during or after the procedure. […] AD is an uncommon life-threatening condition characterized by a tear in the tunica intima of the aorta. The risk factors described in this review play a key role in AD occurrence and development. Understanding the risk factors for AD may contribute to the slowing down of progression, limiting complications of the disease, and improving patient prognosis.

• #62 Aortic Dissection – Acute Aortic Syndrome – Aortic Diseases – Vascular Diseases, Peripheral – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.2.23.

  Aortic dissection is caused by a tear of the intima with blood penetrating into the media. This results in the separation of the intima from the media and adventitia and creates a false lumen of the aorta. […] Risk factors for aortic dissection include hypertension (usually poorly controlled), bicuspid aortic valve and coarctation of the aorta (including patients after surgical correction of these malformations), history of aortic disease (eg, aortic aneurysm) or aortic valve disease, positive family history of aortic disease, congenital connective tissue diseases (Marfan syndrome, Ehlers-Danlos syndrome), cystic medial degeneration (in patients 50 years of age), aortitis, trauma (traffic accidents, iatrogenic), hemodynamic and hormonal factors during pregnancy (50% of aortic dissections in patients aged 40 years occur in pregnant women), Turner syndrome, cardiovascular surgery, professional weightlifting, tobacco smoking, and IV use of cocaine or amphetamines.

• #63 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  Compared with healthy people, those with obesity are more predisposed to develop acute AD, with even more respiratory complications, such as acute lung injury. […] There is a risk of AD developing during or immediately following pregnancy. This is closely related to genetic predisposition, such as MFS, LDS, vEDS, BAV, and TS, but in rare situations it can occur in the absence of these risk factors. […] Iatrogenic AD (IAD) is the presence of AD as a complication of a cardiac procedure. It is a rare and potentially fatal condition that can occur during or after the procedure. […] AD is an uncommon life-threatening condition characterized by a tear in the tunica intima of the aorta. The risk factors described in this review play a key role in AD occurrence and development. Understanding the risk factors for AD may contribute to the slowing down of progression, limiting complications of the disease, and improving patient prognosis.

• #64 Acute aortic dissection developed after cardiopulmonary resuscitation: transesophageal echocardiographic observations and proposed mechanism of injury

  https://www.accjournal.org/journal/view.php?doi=10.4266/acc.2015.00633

  There has been no report about aortic dissection due to cardiopulmonary resuscitation (CPR). […] We present here a case of acute aortic dissection as a rare complication of CPR and propose the potential mechanism of injury on the basis of transesophageal echocardiographic observations. […] External chest compression during cardiopulmonary resuscitation (CPR) may be traumatic. […] The aorta is considered to be safe from traumatic injury because it is located deep in the chest and surrounded by bony structures. […] Here we report a case of aortic dissection that developed after CPR, which was observed by TEE, and describe possible mechanisms of aortic injury on the basis of transesophageal echocardiographic observation of the aorta during CPR in this case. […] We identified a direct relationship between resuscitation and aortic injury because aortic dissection, not seen on the first TEE, was observed on the second TEE after ROSC.

• #65 Aortic dissection: MedlinePlus Medical EncyclopediaLock

  https://medlineplus.gov/ency/article/000181.htm

  Aortic dissection is a serious condition in which there is a tear in the wall of the major artery carrying blood out of the heart (aorta). As the tear extends along the wall of the aorta, blood can flow in between the layers of the blood vessel wall (dissection). This can lead to aortic rupture or decreased blood flow (ischemia) to organs. […] Aortic dissection most often happens because of a tear or damage to the inner wall of the aorta. This very often occurs in the chest (thoracic) part of the artery, but it may also occur in the abdominal aorta. […] When a tear occurs, it creates 2 channels: One in which blood continues to travel; Another where blood stays still. […] An aortic dissection may also cause abnormal widening or ballooning of the aorta (aneurysm). […] The exact cause is unknown, but more common risks include: Aging, Atherosclerosis, Blunt trauma to the chest, such as hitting the steering wheel of a car during an accident, High blood pressure.

• #66 Aortic Dissection – Acute Aortic Syndrome – Aortic Diseases – Vascular Diseases, Peripheral – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.2.23.

  Aortic dissection is caused by a tear of the intima with blood penetrating into the media. This results in the separation of the intima from the media and adventitia and creates a false lumen of the aorta. […] Risk factors for aortic dissection include hypertension (usually poorly controlled), bicuspid aortic valve and coarctation of the aorta (including patients after surgical correction of these malformations), history of aortic disease (eg, aortic aneurysm) or aortic valve disease, positive family history of aortic disease, congenital connective tissue diseases (Marfan syndrome, Ehlers-Danlos syndrome), cystic medial degeneration (in patients 50 years of age), aortitis, trauma (traffic accidents, iatrogenic), hemodynamic and hormonal factors during pregnancy (50% of aortic dissections in patients aged 40 years occur in pregnant women), Turner syndrome, cardiovascular surgery, professional weightlifting, tobacco smoking, and IV use of cocaine or amphetamines.

• #67 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  Aortic dissection (AD) is a life-threatening condition characterized by a split between the tunica intima and tunica media of the aorta. The aim of this review is to describe the patient characteristics, drugs, and medical procedures that may contribute to an increased risk of AD, raising awareness of this life-threatening condition. Understanding the risk factors for AD is important for disease management. […] AD has been described as occurring in the area where the pressure that is applied on the aorta is greater than its strength. The incidence of AD is higher in older patients than in younger patients. In young patients, AD is typically associated with connective tissue disorders (CTDs), such as Marfan syndrome (MFS), Ehlers-Danlos syndrome (EDS), and Loeys-Dietz syndrome (LDS). In older patients, it is most often associated with underlying cardiovascular diseases (CVDs), such as atherosclerosis and hypertension, and aneurysms.

• #68 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  The risk of developing acute AD is amplified with MFS. FBN1 encodes fibrillin-1, which forms microfibrils. Any FBN1 gene mutation that occurs on chromosome 15q21.1 reduces the amount of fibrillin 1. Structural alterations or fibrillin instability lead to structural changes in vascular smooth muscle cells, and vascular tissue weakness exposes the patient to AD. […] In vEDS, mutations in the COL3A1 gene, which encodes collagen type III, are responsible for lower collagen levels. Collagen fibers are one of the most important components of connective tissue, and a mutation that induces the reduction of collagen fiber may cause vascular smooth muscle weakness, with thinning of the intima and media, which leads to aneurysm and, potentially, AD. […] LDS is a rare CTD caused by the mutations in genes affecting the TGF- (TGFBR1, TGFBR2, SMAD3, TGFB2, and TGFB3) pathway. These mutations induce the alteration of signaling in the TGF- family, which can interfere with the collagen production responsible for connective tissue formation. The direct cardiovascular consequence is the weakness of the blood vessels leading to aneurysm and AD.

• #69 Aortic dissection in patients with Marfan syndrome based on the IRAD data – de Beaufort- Annals of Cardiothoracic Surgery

  https://www.annalscts.com/article/view/16411/16584

  Marfan syndrome is a heritable disorder of the fibrillin 1 (FBN1) gene, which encodes the connective tissue protein fibrillin-1. In most patients, the connective tissue disorder leads to abnormalities of the aortic wall, causing progressive aortic dilatation, thus increasing the risk of acute aortic dissection. Aortic root dilatation/dissection is in fact one of the cardinal features of Marfan syndrome, according to the revised Ghent criteria. […] We noted significantly larger diameters of the aortic annulus and root in the Marfan syndrome cohort, but not larger diameters more distally. This supports that aortic dilatation in Marfan syndrome involves the annulus and root predominantly. The increased diameter of the aortic annulus is associated with a higher incidence of aortic valve insufficiency.

• #70 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  The risk of developing acute AD is amplified with MFS. FBN1 encodes fibrillin-1, which forms microfibrils. Any FBN1 gene mutation that occurs on chromosome 15q21.1 reduces the amount of fibrillin 1. Structural alterations or fibrillin instability lead to structural changes in vascular smooth muscle cells, and vascular tissue weakness exposes the patient to AD. […] In vEDS, mutations in the COL3A1 gene, which encodes collagen type III, are responsible for lower collagen levels. Collagen fibers are one of the most important components of connective tissue, and a mutation that induces the reduction of collagen fiber may cause vascular smooth muscle weakness, with thinning of the intima and media, which leads to aneurysm and, potentially, AD. […] LDS is a rare CTD caused by the mutations in genes affecting the TGF- (TGFBR1, TGFBR2, SMAD3, TGFB2, and TGFB3) pathway. These mutations induce the alteration of signaling in the TGF- family, which can interfere with the collagen production responsible for connective tissue formation. The direct cardiovascular consequence is the weakness of the blood vessels leading to aneurysm and AD.

• #71 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  The risk of developing acute AD is amplified with MFS. FBN1 encodes fibrillin-1, which forms microfibrils. Any FBN1 gene mutation that occurs on chromosome 15q21.1 reduces the amount of fibrillin 1. Structural alterations or fibrillin instability lead to structural changes in vascular smooth muscle cells, and vascular tissue weakness exposes the patient to AD. […] In vEDS, mutations in the COL3A1 gene, which encodes collagen type III, are responsible for lower collagen levels. Collagen fibers are one of the most important components of connective tissue, and a mutation that induces the reduction of collagen fiber may cause vascular smooth muscle weakness, with thinning of the intima and media, which leads to aneurysm and, potentially, AD. […] LDS is a rare CTD caused by the mutations in genes affecting the TGF- (TGFBR1, TGFBR2, SMAD3, TGFB2, and TGFB3) pathway. These mutations induce the alteration of signaling in the TGF- family, which can interfere with the collagen production responsible for connective tissue formation. The direct cardiovascular consequence is the weakness of the blood vessels leading to aneurysm and AD.

• #72 Risk Factors for Aortic Dissection | USC Journal

  https://www.uscjournal.com/articles/risk-factors-aortic-dissection?language_content_entity=en

  BAV is a congenital heart defect in which the aortic valve leaflet changes from tricuspid to bicuspid. The bicuspid leaflets are known to cause hemodynamic dysfunction that leads to enlargement of the aorta, aneurysm, and dissection. […] Hypertension contributes to the deterioration of arterial walls. Approximately 65-75% of AD patients also have hypertension. This is well explained by Dong et al., who performed a study in 838 confirmed acute AD patients, finding that 585 acute AD cases were associated with hypertension. […] Tobacco smoking accelerates atherosclerosis and is a major risk factor for aortic aneurysms and dissections. […] Aortic smooth muscle cells are the main components of the tunica media and are responsible for aortic wall integrity and arterial wall remodeling. Any degradation of this structure can directly alter the aortic wall and lead to CVD. Certain inflammatory diseases that affect the integrity of the blood vessels such as aortitis, giant cell arteritis, Takayasus arteritis, systemic lupus erythematous, syphilitic aortitis, and rheumatoid arthritis can cause AD if not well treated.

• #73 Aortic Dissection – Acute Aortic Syndrome – Aortic Diseases – Vascular Diseases, Peripheral – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.2.23.

  Aortic dissection is caused by a tear of the intima with blood penetrating into the media. This results in the separation of the intima from the media and adventitia and creates a false lumen of the aorta. […] Risk factors for aortic dissection include hypertension (usually poorly controlled), bicuspid aortic valve and coarctation of the aorta (including patients after surgical correction of these malformations), history of aortic disease (eg, aortic aneurysm) or aortic valve disease, positive family history of aortic disease, congenital connective tissue diseases (Marfan syndrome, Ehlers-Danlos syndrome), cystic medial degeneration (in patients 50 years of age), aortitis, trauma (traffic accidents, iatrogenic), hemodynamic and hormonal factors during pregnancy (50% of aortic dissections in patients aged 40 years occur in pregnant women), Turner syndrome, cardiovascular surgery, professional weightlifting, tobacco smoking, and IV use of cocaine or amphetamines.

• #74 Acute Aortic Dissection: Overview, Pathophysiology & Risk Factors, Prehospital Care

  https://emedicine.medscape.com/article/756835-overview

  Aortic dissection essentially features a tear in the intimal layer, followed by the formation and propagation of a subintimal hematoma. The dissecting hematoma commonly occupies up to 50% and, occasionally, 100% of the aortic circumference, leading to the development of a false lumen or double-barreled aorta. This can reduce the flow of blood to any of the major arteries arising from the aorta. If the dissection involves the pericardial space, cardiac tamponade can result. […] The normal aorta contains collagen, elastin, and smooth muscle cells, which help contribute to the layers of the aorta, the intima, the media, and the adventitia. Degenerative changes associated with aging lead to the breakdown of the collagen, elastin, and smooth muscle, as well as to an increase in basophilic ground substance. This is termed cystic medial necrosis, the hallmark histologic change associated with dissection and with Marfan syndrome.

• #75 Acute Aortic Dissection: Overview, Pathophysiology & Risk Factors, Prehospital Care

  https://emedicine.medscape.com/article/756835-overview

  Aortic dissection essentially features a tear in the intimal layer, followed by the formation and propagation of a subintimal hematoma. The dissecting hematoma commonly occupies up to 50% and, occasionally, 100% of the aortic circumference, leading to the development of a false lumen or double-barreled aorta. This can reduce the flow of blood to any of the major arteries arising from the aorta. If the dissection involves the pericardial space, cardiac tamponade can result. […] The normal aorta contains collagen, elastin, and smooth muscle cells, which help contribute to the layers of the aorta, the intima, the media, and the adventitia. Degenerative changes associated with aging lead to the breakdown of the collagen, elastin, and smooth muscle, as well as to an increase in basophilic ground substance. This is termed cystic medial necrosis, the hallmark histologic change associated with dissection and with Marfan syndrome.

• #76

  https://step2.medbullets.com/cardiovascular/120030/aortic-dissection

  Aortic dissection is a condition that results from a tear in the innermost layer of the aorta leading to a hematoma and separation of layers of the aortic wall. […] Patients with hypertension and advanced age are more at risk for dissection. […] An intimal tear of the aorta causes an intramural aortic hemorrhage that separates the intima from the media. […] The resulting hematoma may rupture through the adventitia, leading to a thoracic or abdominal cavity hemorrhage or cardiac tamponade. […] Dissection involves fragility of the media layer of the aorta. […] Formation of extracellular matrix on the media wall with accumulation of mucoid material resulting in cystic degeneration. […] Initial tear in the intima leads to the progression of aortic dissection.

• #77 Aortic Dissection – Acute Aortic Syndrome – Aortic Diseases – Vascular Diseases, Peripheral – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.2.23.

  Aortic dissection is caused by a tear of the intima with blood penetrating into the media. This results in the separation of the intima from the media and adventitia and creates a false lumen of the aorta. […] Risk factors for aortic dissection include hypertension (usually poorly controlled), bicuspid aortic valve and coarctation of the aorta (including patients after surgical correction of these malformations), history of aortic disease (eg, aortic aneurysm) or aortic valve disease, positive family history of aortic disease, congenital connective tissue diseases (Marfan syndrome, Ehlers-Danlos syndrome), cystic medial degeneration (in patients 50 years of age), aortitis, trauma (traffic accidents, iatrogenic), hemodynamic and hormonal factors during pregnancy (50% of aortic dissections in patients aged 40 years occur in pregnant women), Turner syndrome, cardiovascular surgery, professional weightlifting, tobacco smoking, and IV use of cocaine or amphetamines.

• #78 Acute Aortic Dissection: A Rare but Important Cause of Acute Pericarditis

  https://www.acc.org/Latest-in-Cardiology/Articles/2020/09/14/09/08/Acute-Aortic-Dissection

  Slow leakage or exudate stemming from the dissecting hematoma appeared to have caused pericardial inflammation. […] The underlying mechanism of pericardial effusion was not a rupture of AAD because none of our patients experienced gross rupture of the ascending aorta. The amount of pericardial effusion may increase during the course of disease and lead to clinical tamponade. […] Recently, AAD has been known to be closely related to systemic and aortic wall inflammation, manifesting as increased levels of cytokine and inflammatory biomarkers including matrix metallopeptidase-9, granulocyte-colony stimulating factor, interleukin-6 and C-reactive protein, among others. […] It may be valuable to determine whether exudate from the dissected aortic wall, which is rich in inflammatory cytokines, causes pericardial inflammation and results in acute pericarditis.

• #79 Acute Aortic Dissection: A Rare but Important Cause of Acute Pericarditis

  https://www.acc.org/Latest-in-Cardiology/Articles/2020/09/14/09/08/Acute-Aortic-Dissection

  Slow leakage or exudate stemming from the dissecting hematoma appeared to have caused pericardial inflammation. […] The underlying mechanism of pericardial effusion was not a rupture of AAD because none of our patients experienced gross rupture of the ascending aorta. The amount of pericardial effusion may increase during the course of disease and lead to clinical tamponade. […] Recently, AAD has been known to be closely related to systemic and aortic wall inflammation, manifesting as increased levels of cytokine and inflammatory biomarkers including matrix metallopeptidase-9, granulocyte-colony stimulating factor, interleukin-6 and C-reactive protein, among others. […] It may be valuable to determine whether exudate from the dissected aortic wall, which is rich in inflammatory cytokines, causes pericardial inflammation and results in acute pericarditis.

• #80 Immune Response Associated Gene Signatures in Aortic Dissection Compared to Aortic Aneurysm

  https://www.imrpress.com/journal/FBL/29/2/10.31083/j.fbl2902064/htm

  In summary, we identified immune response and immune system related pathways as the most significant affected pathways in TAD; We identified five genes which are mainly involved in immune response processes. […] Our results indicate that immune response and immune related pathways have the highest impact on TAD development, linked to the key genes RNASE2, CXCL8, IL6R, and potentially also CCL2.

• #81 Aortic aneurysms: current pathogenesis and therapeutic targets | Experimental & Molecular Medicine

  https://www.nature.com/articles/s12276-023-01130-w

  Although the TGF- signaling pathway is the primary mechanism for the synthesis of contractile and ECM proteins, the complexity of this signaling means that the intrinsic role of TGF- in the pathophysiology of aortic aneurysms is unclear. […] Mutations in the genes involved in the canonical TGF- signaling pathway, including TGFBR1, TGFBR2, SMAD3, SMAD4, and TGF-2, have been identified as predisposing factors for aortic aneurysms and dissections with Marfanoid features. […] Vascular inflammation is the main initiating factor in aortic aneurysms and substantially influences aortic wall remodeling through the death of aortic wall cells, SMC phenotypic switching, and the secretion of proteases. […] Cytokines are crucial contributors to inflammatory alterations during AAA formation, and altered expression and epigenetic changes in cytokines were present in AAA tissue samples.

• #82

  https://link.springer.com/article/10.1007/s11427-024-2693-5

  Aortic dissection is a critical vascular disease that is characterized by a high mortality rate and inflammation significantly influences its onset and progression. Recent studies highlight the integral role of macrophages, key players in the immune system, in the pathological landscape of aortic dissection. These cells are involved in crucial processes, such as the remodeling of the extracellular matrix, immunocyte infiltration, and phenotypic switching of smooth muscle cells, which are essential for the structural integrity and functional dynamics of the aortic wall. […] Despite these insights, the specific contributions of macrophages to the development and progression of aortic dissection remains unclear. This review explores the pathogenesis of aortic dissection with a focus on macrophages and describes their origins, phenotypic variations, and potential roles based on the most recent research findings.

• #83 Frontiers | Pathogenesis of Aortic Aneurysm and Dissection

  https://www.frontiersin.org/research-topics/53514/pathogenesis-of-aortic-aneurysm-and-dissectionundefined

  Aortic aneurysm and dissection (AAD) is a life-threatening condition due to a tear in the intimal layer of the aorta or bleeding within the aortic wall, resulting in the separation of the different layers of the aortic wall. Medial degeneration is a typical pathological feature of AAD. It is mainly characterized by „excessive loss” of smooth muscle cells (SMCs) and extracellular matrix remodeling. […] As it stands, apoptosis, inflammation and oxidative stress are considered as the main mechanism leading to the reduction of the number of SMCs. The „excessive loss” of SMCs is manifested by the reduction of the total number of SMCs and the number of contractive SMCs. It is believed that M1 type macrophages promote AAD formation mainly through the following mechanisms: inducing apoptosis of SMCs; Increase the secretion of inflammatory factors such as IL-6, IL-8 and IL-11 to recruit inflammatory cells (neutrophils, monocytes and macrophages) to further expand tissue inflammation. Neutrophil activation can promote local inflammation and increase the risk of aortic rupture by increasing the analysis of inflammatory factors such as IL-6. Therefore, inflammation is the mechanism of neutrophils promoting AAD. Oxidative stress is involved in AAD-related pathological processes such as endothelial dysfunction, smooth muscle cell proliferation, apoptosis, phenotypic transformation, and vascular remodeling. […] The relationship between cell death and AAD has also gradually attracted academic attention.

• #84 Frontiers | Pathogenesis of Aortic Aneurysm and Dissection

  https://www.frontiersin.org/research-topics/53514/pathogenesis-of-aortic-aneurysm-and-dissectionundefined

  Aortic aneurysm and dissection (AAD) is a life-threatening condition due to a tear in the intimal layer of the aorta or bleeding within the aortic wall, resulting in the separation of the different layers of the aortic wall. Medial degeneration is a typical pathological feature of AAD. It is mainly characterized by „excessive loss” of smooth muscle cells (SMCs) and extracellular matrix remodeling. […] As it stands, apoptosis, inflammation and oxidative stress are considered as the main mechanism leading to the reduction of the number of SMCs. The „excessive loss” of SMCs is manifested by the reduction of the total number of SMCs and the number of contractive SMCs. It is believed that M1 type macrophages promote AAD formation mainly through the following mechanisms: inducing apoptosis of SMCs; Increase the secretion of inflammatory factors such as IL-6, IL-8 and IL-11 to recruit inflammatory cells (neutrophils, monocytes and macrophages) to further expand tissue inflammation. Neutrophil activation can promote local inflammation and increase the risk of aortic rupture by increasing the analysis of inflammatory factors such as IL-6. Therefore, inflammation is the mechanism of neutrophils promoting AAD. Oxidative stress is involved in AAD-related pathological processes such as endothelial dysfunction, smooth muscle cell proliferation, apoptosis, phenotypic transformation, and vascular remodeling. […] The relationship between cell death and AAD has also gradually attracted academic attention.

• #85 Malperfusion syndromes in acute type A aortic dissection

  https://www.oaepublish.com/articles/2574-1209.2021.108

  Malperfusion syndrome itself results in an inflammatory cascade resulting from end-organ ischemia, increased myeloperoxidase production, and complement consumption. […] The downstream upregulation of TNF-alpha and IL-1 results in a positive feedback loop, which is mediated by leukocyte extravasation and cytokine release, leading to further end-organ injury. […] Thus, the inflammatory cascade brought on by end-organ ischemia significantly impairs clinical outcomes even after successful operative repair of the dissection. […] The pathogenesis of MMP creates an added layer of complexity. Intestinal ischemia disrupts the gut mucosal barrier, which incites endotoxin release to the portal system and mediates reperfusion injury. […] Perhaps the greatest contributor to the high mortality rate in MMP syndrome is the autoregulatory response of the splanchnic vessels to ischemia, which occurs when there is a 75% decrease in blood flow to the celiac and superior mesenteric artery vascular beds.

• #86 Malperfusion syndromes in acute type A aortic dissection

  https://www.oaepublish.com/articles/2574-1209.2021.108

  Malperfusion syndrome itself results in an inflammatory cascade resulting from end-organ ischemia, increased myeloperoxidase production, and complement consumption. […] The downstream upregulation of TNF-alpha and IL-1 results in a positive feedback loop, which is mediated by leukocyte extravasation and cytokine release, leading to further end-organ injury. […] Thus, the inflammatory cascade brought on by end-organ ischemia significantly impairs clinical outcomes even after successful operative repair of the dissection. […] The pathogenesis of MMP creates an added layer of complexity. Intestinal ischemia disrupts the gut mucosal barrier, which incites endotoxin release to the portal system and mediates reperfusion injury. […] Perhaps the greatest contributor to the high mortality rate in MMP syndrome is the autoregulatory response of the splanchnic vessels to ischemia, which occurs when there is a 75% decrease in blood flow to the celiac and superior mesenteric artery vascular beds.

• #87 Malperfusion syndromes in acute type A aortic dissection

  https://www.oaepublish.com/articles/2574-1209.2021.108

  This leads to a compensatory arteriolar vasodilatory response that converts to vasoconstriction when the ischemic period is prolonged. […] Both of these mechanisms can be further compounded by aortic surgery and likely account for the high incidence of necrotic bowel and persistent acidosis that may be observed after central aortic repair.

• #88 Aortic Dissection: A Review of the Pathophysiology, Management and Prospective Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8762162/

  The core physiopathological principle underlying AD is an increase in pressure leading to the separation of the layers of the media which creates a false lumen within the aortic wall. There are two main factors related to its development: structural weakness of the aortic wall, and increased wall tension. Many connective tissue components are implicated as culprits in the pathogenesis of AD, and several connective tissue diseases such as Marfan and Ehler-Danlos syndromes are important predisposing factors. Firstly, damaged interlaminar elastic fibers weaken the structural integrity of the aortic media. Secondly, Fibrillin, a glycoprotein that plays a role in organizing elastic fibers by forming scaffolds around elastin, may also play a role. The degeneration of the aortic media is also facilitated/accelerated by Medin, a fibril protein which forms oligomers that damage the aortic wall, via two mechanisms: Cytotoxicity of smooth muscle cells, and increased induction of matrix metalloproteinases (MMP). The strong association between hypertension and AD highlights the role of wall tension in the pathology of the disease. Hypertension, the most commonly associated condition with AD, illustrates the importance of wall tension; however, most hypertensive patients do not have dissections, thus illustrating the importance of degenerative changes – to which hypertension itself may be a contributor.

• #89 Aortic Dissection – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441963/

  Aortic dissection occurs when a tear in the intimal layer of the aortic wall allows blood to enter the space between the intima and media, creating a false lumen. […] Chronic exposure to high pulsatile pressure and shear stress, especially in susceptible individuals, weakens these layers, leading to the initial intimal tear. […] The blood then flows into the space between the intima and media, expanding the false lumen. […] In most cases, the dissection propagates either anterograde (distally) or retrograde (proximally). […] The direction of propagation dictates the complications that arise: distal propagation can obstruct blood flow to the major branches of the aorta, leading to ischemia in affected territories such as the coronary, cerebral, spinal, or visceral arteries. […] Proximal propagation, as seen in type A dissections, often causes life-threatening complications like acute aortic regurgitation, cardiac tamponade, or even rupture.

• #90 Aortic Dissection: A Review of the Pathophysiology, Management and Prospective Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8762162/

  In addition to hypertension, the role of other biomechanical factors must not be overlooked. For instance, the motion of the aortic root during systole can significantly increase the longitudinal stress placed upon the aortic wall, with the point of maximal increase closely corresponding to the most common location of type A dissection. The geometric properties of the wall itself also play an important role in dissection risk. For instance, the diameter of the aorta is positively correlated with dissection risk and has been used as a marker for surgical intervention. Additionally, the thickness of the wall itself may predispose it to dissection, with studies showing a thinner tunica media amongst AD patients. […] It is important to note that it is the complex interaction between the different factors -rather than an individual factor in and of itself- that provides a satisfactory explanation for the onset of AD; for instance, the aortic diameter alone, long used as a marker of dissection risk, may be insufficiently predictive of said risk.

• #91 Aortic Dissection: A Review of the Pathophysiology, Management and Prospective Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8762162/

  In addition to hypertension, the role of other biomechanical factors must not be overlooked. For instance, the motion of the aortic root during systole can significantly increase the longitudinal stress placed upon the aortic wall, with the point of maximal increase closely corresponding to the most common location of type A dissection. The geometric properties of the wall itself also play an important role in dissection risk. For instance, the diameter of the aorta is positively correlated with dissection risk and has been used as a marker for surgical intervention. Additionally, the thickness of the wall itself may predispose it to dissection, with studies showing a thinner tunica media amongst AD patients. […] It is important to note that it is the complex interaction between the different factors -rather than an individual factor in and of itself- that provides a satisfactory explanation for the onset of AD; for instance, the aortic diameter alone, long used as a marker of dissection risk, may be insufficiently predictive of said risk.

• #92 Aortic Dissection: A Review of the Pathophysiology, Management and Prospective Advances

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8762162/

  In addition to hypertension, the role of other biomechanical factors must not be overlooked. For instance, the motion of the aortic root during systole can significantly increase the longitudinal stress placed upon the aortic wall, with the point of maximal increase closely corresponding to the most common location of type A dissection. The geometric properties of the wall itself also play an important role in dissection risk. For instance, the diameter of the aorta is positively correlated with dissection risk and has been used as a marker for surgical intervention. Additionally, the thickness of the wall itself may predispose it to dissection, with studies showing a thinner tunica media amongst AD patients. […] It is important to note that it is the complex interaction between the different factors -rather than an individual factor in and of itself- that provides a satisfactory explanation for the onset of AD; for instance, the aortic diameter alone, long used as a marker of dissection risk, may be insufficiently predictive of said risk.

• #93 Aortic aneurysms: current pathogenesis and therapeutic targets | Experimental & Molecular Medicine

  https://www.nature.com/articles/s12276-023-01130-w

  Cell death and inflammation are closely associated in pathological environments, including aortic aneurysms. […] Progressive SMC loss is a common pathological feature of aortic aneurysm and dissection. […] Damage to the aortic wall by elastic fiber degradation and deleterious spatial structural remodeling induces coagulation and thrombosis, which results in the maldistribution of oxygen and nutrients from the blood to the aortic wall. […] Recent studies revealed that intramural thrombus, which is colocalized with the active sites of inflammation and angiogenesis, is closely associated with aortic aneurysm formation. […] Thrombus-mediated deprivation of oxygen and nutrients in the aortic wall stimulates the proliferation of a network of small blood vessels in the aneurysm wall, inducing the recruitment of inflammatory cells that produce inflammatory mediators and leading to the weakening of the aneurysm wall and aneurysm rupture.

• #94 Aortic aneurysms: current pathogenesis and therapeutic targets | Experimental & Molecular Medicine

  https://www.nature.com/articles/s12276-023-01130-w

  Cell death and inflammation are closely associated in pathological environments, including aortic aneurysms. […] Progressive SMC loss is a common pathological feature of aortic aneurysm and dissection. […] Damage to the aortic wall by elastic fiber degradation and deleterious spatial structural remodeling induces coagulation and thrombosis, which results in the maldistribution of oxygen and nutrients from the blood to the aortic wall. […] Recent studies revealed that intramural thrombus, which is colocalized with the active sites of inflammation and angiogenesis, is closely associated with aortic aneurysm formation. […] Thrombus-mediated deprivation of oxygen and nutrients in the aortic wall stimulates the proliferation of a network of small blood vessels in the aneurysm wall, inducing the recruitment of inflammatory cells that produce inflammatory mediators and leading to the weakening of the aneurysm wall and aneurysm rupture.

• #95 Aortic aneurysms: current pathogenesis and therapeutic targets | Experimental & Molecular Medicine

  https://www.nature.com/articles/s12276-023-01130-w

  Cell death and inflammation are closely associated in pathological environments, including aortic aneurysms. […] Progressive SMC loss is a common pathological feature of aortic aneurysm and dissection. […] Damage to the aortic wall by elastic fiber degradation and deleterious spatial structural remodeling induces coagulation and thrombosis, which results in the maldistribution of oxygen and nutrients from the blood to the aortic wall. […] Recent studies revealed that intramural thrombus, which is colocalized with the active sites of inflammation and angiogenesis, is closely associated with aortic aneurysm formation. […] Thrombus-mediated deprivation of oxygen and nutrients in the aortic wall stimulates the proliferation of a network of small blood vessels in the aneurysm wall, inducing the recruitment of inflammatory cells that produce inflammatory mediators and leading to the weakening of the aneurysm wall and aneurysm rupture.

• #96 Acute aortic dissection: pathogenesis, risk factors and diagnosis

  https://smw.ch/index.php/smw/article/download/2356/3595?inline=1

  VEGF-mediated neoangiogenesis may be another process underlying aortic wall remodelling. VEGF (vascular endothelial growth factor) is the growth factor driving angiogenesis and vasculogenesis, but it also exerts proinflammatory actions. The production of VEGF is increased in the neovessels and their surrounding immune-inflammatory infiltrate of the degraded medial layer. […] Arterial hypertension is, as described below, one of the main risk factors for aortic dissection. It can act directly as a parietal stressor and indirectly as a proinflammatory trigger, mainly by inducing macrophage recruitment and activation. The hypertensive patients show elevated concentrations of proinflammatory molecules such as interleukin (IL)-6, VEGF, macrophage chemoattractant protein-1 (MCP-1), MMP-2 and MMP-9, suggesting that hypertension promotes a proinflammatory state, which subsequently leads to the excessive extracellular matrix degeneration and culminates in the aortic dissection.

• #97 Frontiers | Pathogenesis of Aortic Aneurysm and Dissection

  https://www.frontiersin.org/research-topics/53514/pathogenesis-of-aortic-aneurysm-and-dissectionundefined

  Aortic aneurysm and dissection (AAD) is a life-threatening condition due to a tear in the intimal layer of the aorta or bleeding within the aortic wall, resulting in the separation of the different layers of the aortic wall. Medial degeneration is a typical pathological feature of AAD. It is mainly characterized by „excessive loss” of smooth muscle cells (SMCs) and extracellular matrix remodeling. […] As it stands, apoptosis, inflammation and oxidative stress are considered as the main mechanism leading to the reduction of the number of SMCs. The „excessive loss” of SMCs is manifested by the reduction of the total number of SMCs and the number of contractive SMCs. It is believed that M1 type macrophages promote AAD formation mainly through the following mechanisms: inducing apoptosis of SMCs; Increase the secretion of inflammatory factors such as IL-6, IL-8 and IL-11 to recruit inflammatory cells (neutrophils, monocytes and macrophages) to further expand tissue inflammation. Neutrophil activation can promote local inflammation and increase the risk of aortic rupture by increasing the analysis of inflammatory factors such as IL-6. Therefore, inflammation is the mechanism of neutrophils promoting AAD. Oxidative stress is involved in AAD-related pathological processes such as endothelial dysfunction, smooth muscle cell proliferation, apoptosis, phenotypic transformation, and vascular remodeling. […] The relationship between cell death and AAD has also gradually attracted academic attention.

• #98 Synthesis of multidimensional pathophysiological process leading to type A aortic dissection: a narrative review – Uimonen – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/55926/html

  Pathophysiology of the TAAD is related to biochemical and histological as well as mechanical and hemodynamic alterations leading to a degeneration of the aortic wall via inflammatory response. […] The degradative mechanisms of aortic wall structures and the mechanical forces, to which the wall is predisposed, are interrelated and influence one another. […] The relativity between the factors influencing aortic wall strength and healing capacity, and factors influencing mechanical stress on the aortic wall suggest that the risk of TAAD is not a linear but rather a dynamic phenomenon. […] The chain of events leading to TAAD through aortic wall degeneration is a complex phenomenon regulated by several molecular, cellular, and mechanical pathways. Inflammation in the aortic wall has been shown to play a key role in the development of degeneration.

• #99 Synthesis of multidimensional pathophysiological process leading to type A aortic dissection: a narrative review – Uimonen – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/55926/html

  Increased oxidative and mechanical stress of VSMC facilitate the transformation of VSMC phenotype from contractile to synthetic. […] The subsequent cascade causes elastin fragmentation and cleaving of cross-links between the ECM fibers as well as attachments of VSMC to ECM structures. […] The impaired force transmitting properties of degraded elastin and swelled glycosaminoglycans predisposes the aortic wall to localized unequal distribution of stress load during the cardiac cycle. […] These modifications lead to reductions in the aortic wall strength to resist dissecting. […] The definitive evidence on the mechanisms determining whether the excessive stress on the aortic wall leads to aortic dilatation or TAAD is lacking. […] The ability of the aorta to conform with the stress under which it is exposed derives from an equilibrium of the strength and the healing capacity of aortic wall structures and the intensity of the stress. […] The continuum from a healthy aorta to a complete dissection may be conceptualized in a two-dimensional model with three steps of aortic disease.

• #100 Synthesis of multidimensional pathophysiological process leading to type A aortic dissection: a narrative review – Uimonen – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/55926/html

  Increased oxidative and mechanical stress of VSMC facilitate the transformation of VSMC phenotype from contractile to synthetic. […] The subsequent cascade causes elastin fragmentation and cleaving of cross-links between the ECM fibers as well as attachments of VSMC to ECM structures. […] The impaired force transmitting properties of degraded elastin and swelled glycosaminoglycans predisposes the aortic wall to localized unequal distribution of stress load during the cardiac cycle. […] These modifications lead to reductions in the aortic wall strength to resist dissecting. […] The definitive evidence on the mechanisms determining whether the excessive stress on the aortic wall leads to aortic dilatation or TAAD is lacking. […] The ability of the aorta to conform with the stress under which it is exposed derives from an equilibrium of the strength and the healing capacity of aortic wall structures and the intensity of the stress. […] The continuum from a healthy aorta to a complete dissection may be conceptualized in a two-dimensional model with three steps of aortic disease.

• #101 Synthesis of multidimensional pathophysiological process leading to type A aortic dissection: a narrative review – Uimonen – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/55926/html

  Increased oxidative and mechanical stress of VSMC facilitate the transformation of VSMC phenotype from contractile to synthetic. […] The subsequent cascade causes elastin fragmentation and cleaving of cross-links between the ECM fibers as well as attachments of VSMC to ECM structures. […] The impaired force transmitting properties of degraded elastin and swelled glycosaminoglycans predisposes the aortic wall to localized unequal distribution of stress load during the cardiac cycle. […] These modifications lead to reductions in the aortic wall strength to resist dissecting. […] The definitive evidence on the mechanisms determining whether the excessive stress on the aortic wall leads to aortic dilatation or TAAD is lacking. […] The ability of the aorta to conform with the stress under which it is exposed derives from an equilibrium of the strength and the healing capacity of aortic wall structures and the intensity of the stress. […] The continuum from a healthy aorta to a complete dissection may be conceptualized in a two-dimensional model with three steps of aortic disease.

• #102 KAKEN — Research Projects | Molecular mechanism of aortic dissection : regulation of aortic wall tensile strength through cell-cell interactions (KAKENHI-PROJECT-24390334)

  https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-24390334/

  Aortic dissection (AD) is a frequently fatal medical emergency for which molecular pathogenesis is largely unknown. […] Activation of JAK/STAT in smooth muscle cells caused proliferation of adventitial fibroblast, deposition of collagen fibers and reinforcement of the tensile strength of aortic walls, thus preventing AD. […] Our findings indicate that JAK/STAT signaling is activated in AD and plays cell type-specific roles. […] Molecular pathogenesis of aortic dissection: The failure of protective mechanism of aortic walls. […] Macrophage IL-6 Signaling is Critically Involved in the Pathogenesis of Acute Aortic Dissection. […] Involvement of IL-6 in Pathogenesis of Abdominal Aortic Aneurysm.

• #103 Challenges in thoracic aortic aneurysm and dissection – Aoki – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/24753/html

  The importance of SMCs is evidenced by the fact that mutations in SMC-specific genes also manifest TAAD phenotype. […] Although genetic evidence clearly indicates the importance of ECM, TGF- and SMCs, how these pieces of the puzzle are put together to form the maintenance mechanism of the aortic tissue mechanism, or how the abnormality of the mechanism leads to TAAD phenotype is largely unknown. […] The importance of SMCs is also shown by the fact that smooth muscle-specific deficiency of Sirtuin-1 or Akt2 confers susceptibility to TAAD in mice. […] Abnormal aortic tissue integrity and aortic stress seem to culminate in proinflammatory response and tissue destruction. […] SmgGDS is likely to maintain the destruction-resistant phenotype of the aortic tissue. […] These finding may be relevant with human TAAD, because expression of SmgGDS was reduced in human TAAD tissue compared to normal aorta. […] If this hypothesis holds true, TAAD can be regarded as a network disease, where a defect in a part of the network component leads to the disruption of the aortic wall integrity, making it susceptible to the acute or chronic destruction due to the hemodynamic and neurohumoral stress.

• #104 Aortic aneurysms: current pathogenesis and therapeutic targets | Experimental & Molecular Medicine

  https://www.nature.com/articles/s12276-023-01130-w

  Furthermore, these biological mechanisms are thought to initiate the degradation of elastic fibers and alterations in collagen composition, ultimately compromising the structural integrity and reducing the flexibility of the aortic wall. […] The loss of structural integrity due to vascular SMC dysfunction, including apoptosis and ECM degradation, leads to weakness and dilatation of the aortic wall, which are hallmarks of aortic aneurysm. […] An imbalance in reparative/ECM production and inflammatory/ECM degradation in SMCs that underwent phenotypic switching and are known as synthetic SMCs in response to constant pathological stimuli damages the aortic wall, leading to dilatation and rupture in aortic aneurysms. […] The components of the transforming growth factor- (TGF-) signaling pathway, including receptors and SMAD proteins, are fundamental for synthesizing SMC contractile proteins, ECM proteins, elastin, and collagen.

• #105 Challenges in thoracic aortic aneurysm and dissection – Aoki – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/24753/html

  The importance of SMCs is evidenced by the fact that mutations in SMC-specific genes also manifest TAAD phenotype. […] Although genetic evidence clearly indicates the importance of ECM, TGF- and SMCs, how these pieces of the puzzle are put together to form the maintenance mechanism of the aortic tissue mechanism, or how the abnormality of the mechanism leads to TAAD phenotype is largely unknown. […] The importance of SMCs is also shown by the fact that smooth muscle-specific deficiency of Sirtuin-1 or Akt2 confers susceptibility to TAAD in mice. […] Abnormal aortic tissue integrity and aortic stress seem to culminate in proinflammatory response and tissue destruction. […] SmgGDS is likely to maintain the destruction-resistant phenotype of the aortic tissue. […] These finding may be relevant with human TAAD, because expression of SmgGDS was reduced in human TAAD tissue compared to normal aorta. […] If this hypothesis holds true, TAAD can be regarded as a network disease, where a defect in a part of the network component leads to the disruption of the aortic wall integrity, making it susceptible to the acute or chronic destruction due to the hemodynamic and neurohumoral stress.

• #106 Synthesis of multidimensional pathophysiological process leading to type A aortic dissection: a narrative review – Uimonen – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/55926/html

  Pathophysiology of the TAAD is related to biochemical and histological as well as mechanical and hemodynamic alterations leading to a degeneration of the aortic wall via inflammatory response. […] The degradative mechanisms of aortic wall structures and the mechanical forces, to which the wall is predisposed, are interrelated and influence one another. […] The relativity between the factors influencing aortic wall strength and healing capacity, and factors influencing mechanical stress on the aortic wall suggest that the risk of TAAD is not a linear but rather a dynamic phenomenon. […] The chain of events leading to TAAD through aortic wall degeneration is a complex phenomenon regulated by several molecular, cellular, and mechanical pathways. Inflammation in the aortic wall has been shown to play a key role in the development of degeneration.

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