Acute aortic syndrome describes life-threatening conditions of the thoracic aorta including aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. These conditions involve acute lesions of the aortic tunica media and can be distinguished by imaging techniques. Recent advances in imaging and treatment have increased awareness of these conditions and emphasized the importance of early diagnosis and management. The most common cause is aortic dissection, which occurs when blood tears the intimal layer, separating the media into an inner and outer layer. Other causes include intramural hematoma where blood enters the media without an intimal tear, and penetrating ulcers where atherosclerotic lesions erode the intima and media. Risk factors
1) Acute aortic syndromes include aortic dissection, intramural hematoma, and penetrating aortic ulcer and are characterized by tears in the aortic wall that can lead to life-threatening complications if not diagnosed promptly.
2) MDCT angiography is now the standard of care for diagnosis and treatment planning of acute aortic syndromes as it can identify complications with high sensitivity and specificity. Echocardiography also provides important information but CT or MRI are needed for full anatomical assessment.
3) Rapid diagnosis is key as acute aortic syndromes can present with varied symptoms mimicking other conditions. Delays in diagnosis lead to higher mortality. The choice of initial imaging depends on the clinical
However, it is an invasive procedure that is not straightforward to perform so is often reserved as a problem-solving tool when both the aortic root and valve are the prime source of interest.
Contrast-enhanced, cardiac-gated CT is highly accurate for determining the cause of acute aortic syndrome, which can be due to aortic dissection, intramural hematoma, penetrating atherosclerotic ulcer, or unstable thoracic aneurysm. CT accurately identifies the location and extent of disease and guides urgent surgical or endovascular repair when needed to treat life-threatening conditions such as type A aortic dissection or ruptured aneurysm.
Acute aortic syndrome (AAS) refers to emergency aortic conditions including aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. The common feature is disruption of the aortic media layer allowing blood to enter and separate layers. Aortic dissection occurs when a tear in the intima allows blood to flow between layers. Medical management focuses on controlling blood pressure to limit propagation. Type A dissections involving the ascending aorta require emergency surgery while type B dissections of the descending aorta typically receive medical management. Long term follow up is needed to monitor for complications like aneurysm formation.
This document provides an overview of acute aortic syndrome (AAS), including aortic dissection, intramural hematoma, penetrating aortic ulcer, and ruptured aortic aneurysm. It discusses the pathophysiology, imaging appearance and protocols, classification systems, and reporting considerations for each condition. CT and MRI are highlighted as the primary imaging modalities. The radiologist plays an important role in diagnosing AAS, determining treatment approaches such as endovascular intervention, and evaluating outcomes through follow up imaging. Proper technique and systematic reporting of anatomic details are essential for clinical management of these life-threatening aortic emergencies.
This document discusses acute aortic syndrome (AAS), which includes acute aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. AAS is caused by disruption of the aortic wall layers from tears or ulcers, allowing blood to track within the layers. The most common type is aortic dissection, where blood passes through a tear separating the vessel layers. Presenting symptoms typically include sudden severe chest or back pain. Diagnosis involves imaging like CECT, MRI, or TEE to identify abnormalities. Prognosis depends on factors like involvement of the ascending aorta and complications. Classification systems differentiate type A dissections involving the ascending aorta from type B.
An aortic dissection is a tear within the layers of the aortic wall. It can cause severe chest or back pain and risks damage to organs if blood flow is blocked. Prompt diagnosis through imaging tests and treatment are critical to survival. While type A dissections involving the ascending aorta require emergency surgery, type B dissections of the descending aorta can often be treated through intensive blood pressure control and medication to prevent expansion of the tear. Risk factors include hypertension, genetics, trauma, and certain medical conditions.
Penetrating atherosclerotic ulcer (PAU) is an ulcerating atherosclerotic lesion that penetrates the aortic wall. CT is often used to evaluate PAU, showing features like a focal outpouching with adjacent hematoma. While some cases progress slowly, PAU carries a risk of complications like rupture. Treatment depends on factors like symptoms, expansion rate, and surgical risk. Careful monitoring is important due to variable prognosis.
1) Acute aortic syndromes include aortic dissection, intramural hematoma, and penetrating aortic ulcer and are characterized by tears in the aortic wall that can lead to life-threatening complications if not diagnosed promptly.
2) MDCT angiography is now the standard of care for diagnosis and treatment planning of acute aortic syndromes as it can identify complications with high sensitivity and specificity. Echocardiography also provides important information but CT or MRI are needed for full anatomical assessment.
3) Rapid diagnosis is key as acute aortic syndromes can present with varied symptoms mimicking other conditions. Delays in diagnosis lead to higher mortality. The choice of initial imaging depends on the clinical
However, it is an invasive procedure that is not straightforward to perform so is often reserved as a problem-solving tool when both the aortic root and valve are the prime source of interest.
Contrast-enhanced, cardiac-gated CT is highly accurate for determining the cause of acute aortic syndrome, which can be due to aortic dissection, intramural hematoma, penetrating atherosclerotic ulcer, or unstable thoracic aneurysm. CT accurately identifies the location and extent of disease and guides urgent surgical or endovascular repair when needed to treat life-threatening conditions such as type A aortic dissection or ruptured aneurysm.
Acute aortic syndrome (AAS) refers to emergency aortic conditions including aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. The common feature is disruption of the aortic media layer allowing blood to enter and separate layers. Aortic dissection occurs when a tear in the intima allows blood to flow between layers. Medical management focuses on controlling blood pressure to limit propagation. Type A dissections involving the ascending aorta require emergency surgery while type B dissections of the descending aorta typically receive medical management. Long term follow up is needed to monitor for complications like aneurysm formation.
This document provides an overview of acute aortic syndrome (AAS), including aortic dissection, intramural hematoma, penetrating aortic ulcer, and ruptured aortic aneurysm. It discusses the pathophysiology, imaging appearance and protocols, classification systems, and reporting considerations for each condition. CT and MRI are highlighted as the primary imaging modalities. The radiologist plays an important role in diagnosing AAS, determining treatment approaches such as endovascular intervention, and evaluating outcomes through follow up imaging. Proper technique and systematic reporting of anatomic details are essential for clinical management of these life-threatening aortic emergencies.
This document discusses acute aortic syndrome (AAS), which includes acute aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. AAS is caused by disruption of the aortic wall layers from tears or ulcers, allowing blood to track within the layers. The most common type is aortic dissection, where blood passes through a tear separating the vessel layers. Presenting symptoms typically include sudden severe chest or back pain. Diagnosis involves imaging like CECT, MRI, or TEE to identify abnormalities. Prognosis depends on factors like involvement of the ascending aorta and complications. Classification systems differentiate type A dissections involving the ascending aorta from type B.
An aortic dissection is a tear within the layers of the aortic wall. It can cause severe chest or back pain and risks damage to organs if blood flow is blocked. Prompt diagnosis through imaging tests and treatment are critical to survival. While type A dissections involving the ascending aorta require emergency surgery, type B dissections of the descending aorta can often be treated through intensive blood pressure control and medication to prevent expansion of the tear. Risk factors include hypertension, genetics, trauma, and certain medical conditions.
Penetrating atherosclerotic ulcer (PAU) is an ulcerating atherosclerotic lesion that penetrates the aortic wall. CT is often used to evaluate PAU, showing features like a focal outpouching with adjacent hematoma. While some cases progress slowly, PAU carries a risk of complications like rupture. Treatment depends on factors like symptoms, expansion rate, and surgical risk. Careful monitoring is important due to variable prognosis.
An intramural hematoma (IMH) is a thickening of the aortic wall due to bleeding within the media in the absence of an intimal tear. It is considered a precursor to aortic dissection and is classified as a class 2 aortic dissection. A penetrating atherosclerotic ulcer (PAU) is caused by the erosion of an atherosclerotic plaque through the internal elastic lamina into the media. It is classified as a class 4 aortic dissection. Both IMH and PAU can lead to complications like intramural hematoma expansion, pseudoaneurysm formation, aortic dissection, and rupture. Imaging modalities like CT, MRI, TEE, and IVUS
This document discusses aortic dissection, including:
1. It provides an introduction defining acute aortic syndromes and the types of aortic dissection.
2. It covers the incidence, risk factors, classifications, pathogenesis, natural history, signs and symptoms, diagnostic testing including imaging and labs, and management approaches for aortic dissection.
3. The management focuses on reducing blood pressure and pulse pressure through beta blockers and other antihypertensive drugs to prevent extension of the dissection.
This document discusses the role of MRI in assessing the thoracic aorta. It provides details on various MRI techniques used including CE-MRA, bSSFP, phase contrast, and black-blood sequences. It reviews clinical applications of MRI for thoracic aortic aneurysm, acute aortic syndromes, and large vessel vasculitis. MRI is presented as a good non-invasive alternative to CT for evaluation and serial imaging of thoracic aortic pathology due to lack of ionizing radiation and ability to characterize soft tissues and evaluate flow.
No reflow and slow flow phenomenon during pcirahul arora
This document discusses strategies and prevention of slow flow and no-reflow phenomenon during percutaneous coronary intervention (PCI). It defines no-reflow as inadequate myocardial perfusion through a coronary artery without mechanical obstruction. No-reflow occurs in 8-11% of primary PCIs and is associated with worse clinical outcomes. The pathophysiology involves distal embolization, ischemic injury, reperfusion injury, and individual patient susceptibility. Preventing no-reflow requires reducing thrombus burden, ischemia time, reperfusion injury through anti-inflammatory drugs, and addressing risk factors like diabetes.
This document summarizes various diseases of the thoracic aorta including normal variations, aneurysms, dissections, and other conditions. It describes the pathogenesis, risk factors, imaging appearance and features that help differentiate various thoracic aortic diseases including atherosclerotic aneurysms, mycotic aneurysms, traumatic aortic injuries, acute aortic syndromes like dissections and intramural hematomas, and penetrating atherosclerotic ulcers. Treatment options are mentioned for different conditions based on location and severity of the disease.
1. The document discusses various methods for evaluating aortic aneurysms including CT, MRI, and aortography. CT is useful for determining size and details of the aneurysm but risks radiation exposure, while MRI does not require contrast but has longer scan times and other limitations.
2. Factors such as aneurysm size greater than 5.5cm, shape, wall thickness, and presence of thrombus impact the risk of rupture. Open or endovascular repair options are discussed based on risk factors. Endovascular repair has lower short-term mortality but higher reintervention rates.
3. Details are provided on preparations, techniques, and steps for open surgery to replace the thoracic or thoracoabdom
This document discusses penetrating aortic ulcers (PAUs), which are focal ulcerative lesions in the aortic wall. PAUs have unknown causes but are often associated with atherosclerosis. They can progress to pseudoaneurysms or ruptured aneurysms. Symptomatic PAUs usually require intervention to prevent rupture, while asymptomatic cases may be monitored. Computed tomography is the primary diagnostic tool and endovascular stent grafting is now usually the preferred treatment approach over open surgery due to lower risks, though complications can still occur.
An aortic aneurysm is a localized dilation of the aorta that is at least 50% larger than normal. Risk factors include smoking, family history, and conditions like Marfan syndrome. Aneurysms are classified by location (abdominal, thoracic) and shape (fusiform, saccular). Diagnosis involves imaging like ultrasound, CT, or MRI to measure size. Treatment depends on size and growth rate, and may involve surgery if the risk of rupture increases. Medical management focuses on risk factor modification through smoking cessation, blood pressure control, and statin therapy.
Acute aortic dissection is a potentially life-threatening condition where blood flows into the layers of the aortic wall, splitting it apart. It occurs in approximately 2.9 per 100,000 people per year in the US. There are several classification systems, but the most important distinguishes between type A dissections, which involve the ascending aorta and require surgery, and type B dissections, which do not involve the ascending aorta and can be treated medically. Risk factors include hypertension, connective tissue disorders like Marfan syndrome, bicuspid aortic valves, pregnancy, and trauma. Prompt diagnosis and treatment are crucial as the risk of death is approximately 1% per hour without treatment.
Thoracic aortic aneurysms can occur in the ascending aorta, aortic arch, or descending aorta. They are generally asymptomatic but can potentially rupture or dissect, leading to death. Surgical repair is recommended for thoracic aortic aneurysms over 5.5 cm in the ascending aorta or over 6.5 cm in the descending aorta, or if the aneurysm is growing rapidly. Both open surgical graft replacement and endovascular stent grafting are options for repair, with endovascular approaches having shorter recovery but risk of complications like endoleaks. Untreated thoracic aortic aneurysms have high mortality from rupture.
1) Aortic dissection is a tear in the inner layer of the aorta that allows blood to flow between the layers of the aortic wall, creating a false passageway. It was first documented in King George II of England in 1760.
2) Symptoms include a sudden, severe chest pain that can radiate to the back. Diagnosis is often challenging, but can be made through imaging like CT, MRI, or TEE ultrasound.
3) Type A dissections involving the ascending aorta require emergency surgery, while Type B dissections of the descending aorta can sometimes be treated medically to reduce blood pressure. Without treatment, mortality is high within the first few weeks.
Aneurysms of splanchnic and visceral arteriesTapish Sahu
This document provides information on aneurysms of splanchnic and visceral arteries. It discusses their definition, epidemiology, etiology, clinical presentation, treatment principles, and management approaches for different types of aneurysms including splenic artery aneurysms. The key points are that splanchnic artery aneurysms are rare but lethal, various treatment modalities exist including open surgery, endovascular techniques, and observation depending on the specific aneurysm characteristics and patient factors.
The document describes a case of a 46-year-old male who presented with sudden onset chest and back pain that progressed to weakness in his lower extremities. Imaging revealed an aortic dissection involving the ascending aorta and descending aorta. He underwent surgery to replace the dissected ascending aorta but later developed multiple complications and died. The document also reviews the classification, presentation, risk factors, diagnosis and management of aortic dissections.
presentation will give a idea about management of thoracoabdominal aortic aneurysm, including detail of investigation and treatment options available today.
1. Arterial aneurysms most commonly occur in the abdominal aorta and can be caused by degenerative processes, infections, trauma, or genetic conditions.
2. Abdominal aortic aneurysms are the most prevalent type of aneurysm in the United States and rupture of aneurysms is a serious complication.
3. Aneurysms can be classified by their morphology (fusiform vs. saccular), etiology (degenerative, inflammatory, infectious), and location (aortic, iliac, femoral, etc.). Management depends on the type and severity of the individual aneurysm.
The document discusses aortic aneurysms and stenosis, including definitions, causes, classifications, symptoms, diagnosis, and surgical considerations. It covers topics such as the etiology of aortic diseases, different classification systems for aneurysms and dissections, signs and symptoms, preoperative evaluation and risk assessment, indications for surgery, and management of anesthesia.
The document discusses carotid artery strokes, describing the anatomy of the carotid arteries and causes of stenosis like plaque buildup which can lead to emboli and blockages. Symptoms of carotid artery stenosis or occlusion include transient ischemic attacks (TIAs) or strokes, and treatment options involve lifestyle changes, medications, carotid endarterectomy surgery, or carotid stenting to reopen blocked arteries. Grades of stenosis are defined based on the percentage of blockage.
The document defines no-reflow as inadequate myocardial perfusion through a coronary circulation segment without mechanical vessel obstruction. No-reflow occurs in 30% of patients after reperfusion for myocardial infarction and is associated with worse outcomes. It results from microvascular obstruction from distal embolization, ischemic injury, and reperfusion injury. Diagnosis involves assessing TIMI flow, myocardial blush grade, and imaging techniques. Prevention focuses on reducing embolization using thrombectomy or filters while treatment involves vasodilators like adenosine, verapamil, and glycoprotein IIb/IIIa inhibitors.
This document provides information about a seminar on aortic dissection presented by Monika Devi. It discusses the introduction, types, causes, symptoms, risk factors, diagnosis, treatment, complications and prevention of aortic dissection. The two main types are Type A, which involves the ascending aorta, and Type B, which only involves the descending aorta. Causes include high blood pressure, genetic conditions like Marfan syndrome, and traumatic injury. Symptoms can include chest pain and symptoms of a stroke. Treatment depends on the type but may involve medications to lower blood pressure or surgery to repair the tear in the aorta. Complications can include death, organ damage or stroke if not properly treated.
Stanford Type A Aortic Dissection: a Complex Disease for Patients and Cardiot...Crimsonpublisherssmoaj
Acute type A aortic dissection is a catastrophic event in which blood exits the vascular lumen and dissects the media, creating a false lumen. Surgery is the best possible treatment but it is complex. The surgical team needs to understand the anatomy and physiopathology before dealing with the repair. While there are just a few surgical solutions for the repair of the dissected ascending aorta, debate is still ongoing about the best surgical option for the disease involving the arch and the descending aorta. Late reoperations are relatively common on the aortic valve and/or the distal aorta after primary repair. Results are excellent in specialized centers with high volume and complexity. Lifelong follow-up is required in survivors.
Fatal Condition of Aortic Dissection Produces Symptoms of Sudden and Tearing ...semualkaira
Aortic dissection is a very difficult condition in which the inner
sheath of the aortic wall is torn without tearing the outer sheath.
This causes blood to enter the aortic wall through the tear, which
further splits the mediastinum and creates a new channel in the
aortic wall. The serious and often fatal condition of aortic dissection produces symptoms of sudden and tearing chest pain. Although aortic dissection mostly occurs in people around the age of
60, the peak incidence in people with Marfan syndrome is between
20 and 40 years of age.
Fatal Condition of Aortic Dissection Produces Symptoms of Sudden and Tearing ...semualkaira
Aortic dissection is a very difficult condition in which the inner
sheath of the aortic wall is torn without tearing the outer sheath.
This causes blood to enter the aortic wall through the tear, which
further splits the mediastinum and creates a new channel in the
aortic wall. The serious and often fatal condition of aortic dissection produces symptoms of sudden and tearing chest pain. Although aortic dissection mostly occurs in people around the age of
60, the peak incidence in people with Marfan syndrome is between
20 and 40 years of age.
An intramural hematoma (IMH) is a thickening of the aortic wall due to bleeding within the media in the absence of an intimal tear. It is considered a precursor to aortic dissection and is classified as a class 2 aortic dissection. A penetrating atherosclerotic ulcer (PAU) is caused by the erosion of an atherosclerotic plaque through the internal elastic lamina into the media. It is classified as a class 4 aortic dissection. Both IMH and PAU can lead to complications like intramural hematoma expansion, pseudoaneurysm formation, aortic dissection, and rupture. Imaging modalities like CT, MRI, TEE, and IVUS
This document discusses aortic dissection, including:
1. It provides an introduction defining acute aortic syndromes and the types of aortic dissection.
2. It covers the incidence, risk factors, classifications, pathogenesis, natural history, signs and symptoms, diagnostic testing including imaging and labs, and management approaches for aortic dissection.
3. The management focuses on reducing blood pressure and pulse pressure through beta blockers and other antihypertensive drugs to prevent extension of the dissection.
This document discusses the role of MRI in assessing the thoracic aorta. It provides details on various MRI techniques used including CE-MRA, bSSFP, phase contrast, and black-blood sequences. It reviews clinical applications of MRI for thoracic aortic aneurysm, acute aortic syndromes, and large vessel vasculitis. MRI is presented as a good non-invasive alternative to CT for evaluation and serial imaging of thoracic aortic pathology due to lack of ionizing radiation and ability to characterize soft tissues and evaluate flow.
No reflow and slow flow phenomenon during pcirahul arora
This document discusses strategies and prevention of slow flow and no-reflow phenomenon during percutaneous coronary intervention (PCI). It defines no-reflow as inadequate myocardial perfusion through a coronary artery without mechanical obstruction. No-reflow occurs in 8-11% of primary PCIs and is associated with worse clinical outcomes. The pathophysiology involves distal embolization, ischemic injury, reperfusion injury, and individual patient susceptibility. Preventing no-reflow requires reducing thrombus burden, ischemia time, reperfusion injury through anti-inflammatory drugs, and addressing risk factors like diabetes.
This document summarizes various diseases of the thoracic aorta including normal variations, aneurysms, dissections, and other conditions. It describes the pathogenesis, risk factors, imaging appearance and features that help differentiate various thoracic aortic diseases including atherosclerotic aneurysms, mycotic aneurysms, traumatic aortic injuries, acute aortic syndromes like dissections and intramural hematomas, and penetrating atherosclerotic ulcers. Treatment options are mentioned for different conditions based on location and severity of the disease.
1. The document discusses various methods for evaluating aortic aneurysms including CT, MRI, and aortography. CT is useful for determining size and details of the aneurysm but risks radiation exposure, while MRI does not require contrast but has longer scan times and other limitations.
2. Factors such as aneurysm size greater than 5.5cm, shape, wall thickness, and presence of thrombus impact the risk of rupture. Open or endovascular repair options are discussed based on risk factors. Endovascular repair has lower short-term mortality but higher reintervention rates.
3. Details are provided on preparations, techniques, and steps for open surgery to replace the thoracic or thoracoabdom
This document discusses penetrating aortic ulcers (PAUs), which are focal ulcerative lesions in the aortic wall. PAUs have unknown causes but are often associated with atherosclerosis. They can progress to pseudoaneurysms or ruptured aneurysms. Symptomatic PAUs usually require intervention to prevent rupture, while asymptomatic cases may be monitored. Computed tomography is the primary diagnostic tool and endovascular stent grafting is now usually the preferred treatment approach over open surgery due to lower risks, though complications can still occur.
An aortic aneurysm is a localized dilation of the aorta that is at least 50% larger than normal. Risk factors include smoking, family history, and conditions like Marfan syndrome. Aneurysms are classified by location (abdominal, thoracic) and shape (fusiform, saccular). Diagnosis involves imaging like ultrasound, CT, or MRI to measure size. Treatment depends on size and growth rate, and may involve surgery if the risk of rupture increases. Medical management focuses on risk factor modification through smoking cessation, blood pressure control, and statin therapy.
Acute aortic dissection is a potentially life-threatening condition where blood flows into the layers of the aortic wall, splitting it apart. It occurs in approximately 2.9 per 100,000 people per year in the US. There are several classification systems, but the most important distinguishes between type A dissections, which involve the ascending aorta and require surgery, and type B dissections, which do not involve the ascending aorta and can be treated medically. Risk factors include hypertension, connective tissue disorders like Marfan syndrome, bicuspid aortic valves, pregnancy, and trauma. Prompt diagnosis and treatment are crucial as the risk of death is approximately 1% per hour without treatment.
Thoracic aortic aneurysms can occur in the ascending aorta, aortic arch, or descending aorta. They are generally asymptomatic but can potentially rupture or dissect, leading to death. Surgical repair is recommended for thoracic aortic aneurysms over 5.5 cm in the ascending aorta or over 6.5 cm in the descending aorta, or if the aneurysm is growing rapidly. Both open surgical graft replacement and endovascular stent grafting are options for repair, with endovascular approaches having shorter recovery but risk of complications like endoleaks. Untreated thoracic aortic aneurysms have high mortality from rupture.
1) Aortic dissection is a tear in the inner layer of the aorta that allows blood to flow between the layers of the aortic wall, creating a false passageway. It was first documented in King George II of England in 1760.
2) Symptoms include a sudden, severe chest pain that can radiate to the back. Diagnosis is often challenging, but can be made through imaging like CT, MRI, or TEE ultrasound.
3) Type A dissections involving the ascending aorta require emergency surgery, while Type B dissections of the descending aorta can sometimes be treated medically to reduce blood pressure. Without treatment, mortality is high within the first few weeks.
Aneurysms of splanchnic and visceral arteriesTapish Sahu
This document provides information on aneurysms of splanchnic and visceral arteries. It discusses their definition, epidemiology, etiology, clinical presentation, treatment principles, and management approaches for different types of aneurysms including splenic artery aneurysms. The key points are that splanchnic artery aneurysms are rare but lethal, various treatment modalities exist including open surgery, endovascular techniques, and observation depending on the specific aneurysm characteristics and patient factors.
The document describes a case of a 46-year-old male who presented with sudden onset chest and back pain that progressed to weakness in his lower extremities. Imaging revealed an aortic dissection involving the ascending aorta and descending aorta. He underwent surgery to replace the dissected ascending aorta but later developed multiple complications and died. The document also reviews the classification, presentation, risk factors, diagnosis and management of aortic dissections.
presentation will give a idea about management of thoracoabdominal aortic aneurysm, including detail of investigation and treatment options available today.
1. Arterial aneurysms most commonly occur in the abdominal aorta and can be caused by degenerative processes, infections, trauma, or genetic conditions.
2. Abdominal aortic aneurysms are the most prevalent type of aneurysm in the United States and rupture of aneurysms is a serious complication.
3. Aneurysms can be classified by their morphology (fusiform vs. saccular), etiology (degenerative, inflammatory, infectious), and location (aortic, iliac, femoral, etc.). Management depends on the type and severity of the individual aneurysm.
The document discusses aortic aneurysms and stenosis, including definitions, causes, classifications, symptoms, diagnosis, and surgical considerations. It covers topics such as the etiology of aortic diseases, different classification systems for aneurysms and dissections, signs and symptoms, preoperative evaluation and risk assessment, indications for surgery, and management of anesthesia.
The document discusses carotid artery strokes, describing the anatomy of the carotid arteries and causes of stenosis like plaque buildup which can lead to emboli and blockages. Symptoms of carotid artery stenosis or occlusion include transient ischemic attacks (TIAs) or strokes, and treatment options involve lifestyle changes, medications, carotid endarterectomy surgery, or carotid stenting to reopen blocked arteries. Grades of stenosis are defined based on the percentage of blockage.
The document defines no-reflow as inadequate myocardial perfusion through a coronary circulation segment without mechanical vessel obstruction. No-reflow occurs in 30% of patients after reperfusion for myocardial infarction and is associated with worse outcomes. It results from microvascular obstruction from distal embolization, ischemic injury, and reperfusion injury. Diagnosis involves assessing TIMI flow, myocardial blush grade, and imaging techniques. Prevention focuses on reducing embolization using thrombectomy or filters while treatment involves vasodilators like adenosine, verapamil, and glycoprotein IIb/IIIa inhibitors.
This document provides information about a seminar on aortic dissection presented by Monika Devi. It discusses the introduction, types, causes, symptoms, risk factors, diagnosis, treatment, complications and prevention of aortic dissection. The two main types are Type A, which involves the ascending aorta, and Type B, which only involves the descending aorta. Causes include high blood pressure, genetic conditions like Marfan syndrome, and traumatic injury. Symptoms can include chest pain and symptoms of a stroke. Treatment depends on the type but may involve medications to lower blood pressure or surgery to repair the tear in the aorta. Complications can include death, organ damage or stroke if not properly treated.
Stanford Type A Aortic Dissection: a Complex Disease for Patients and Cardiot...Crimsonpublisherssmoaj
Acute type A aortic dissection is a catastrophic event in which blood exits the vascular lumen and dissects the media, creating a false lumen. Surgery is the best possible treatment but it is complex. The surgical team needs to understand the anatomy and physiopathology before dealing with the repair. While there are just a few surgical solutions for the repair of the dissected ascending aorta, debate is still ongoing about the best surgical option for the disease involving the arch and the descending aorta. Late reoperations are relatively common on the aortic valve and/or the distal aorta after primary repair. Results are excellent in specialized centers with high volume and complexity. Lifelong follow-up is required in survivors.
Fatal Condition of Aortic Dissection Produces Symptoms of Sudden and Tearing ...semualkaira
Aortic dissection is a very difficult condition in which the inner
sheath of the aortic wall is torn without tearing the outer sheath.
This causes blood to enter the aortic wall through the tear, which
further splits the mediastinum and creates a new channel in the
aortic wall. The serious and often fatal condition of aortic dissection produces symptoms of sudden and tearing chest pain. Although aortic dissection mostly occurs in people around the age of
60, the peak incidence in people with Marfan syndrome is between
20 and 40 years of age.
Fatal Condition of Aortic Dissection Produces Symptoms of Sudden and Tearing ...semualkaira
Aortic dissection is a very difficult condition in which the inner
sheath of the aortic wall is torn without tearing the outer sheath.
This causes blood to enter the aortic wall through the tear, which
further splits the mediastinum and creates a new channel in the
aortic wall. The serious and often fatal condition of aortic dissection produces symptoms of sudden and tearing chest pain. Although aortic dissection mostly occurs in people around the age of
60, the peak incidence in people with Marfan syndrome is between
20 and 40 years of age.
The document discusses thoracic aortic aneurysms (TAAs), including:
1. TAAs can be true aneurysms involving all vessel layers, or pseudoaneurysms where the intimal and medial layers are disrupted. Common types are fusiform and saccular.
2. Etiologies include atherosclerosis, cystic medial necrosis from conditions like Marfan syndrome, infections, vasculitides, trauma, and congenital factors.
3. Imaging plays a key role in evaluating TAAs to characterize morphology, size, relationships to other structures, and signs of rupture risk. Management depends on aneurysm location and size.
The document discusses vascular imaging and interventional radiology. It provides an overview of imaging modalities used for vascular imaging like ultrasound, CT, MRI and angiography. It describes the layers of artery and vein walls and how diseases can affect the walls. Examples of interventional procedures are provided like angioplasty, stent placement, aneurysm embolization and stent graft implantation. Equipment used for these procedures includes catheters, guidewires, balloons and embolic agents.
1. CT is the imaging modality of choice for diagnosing aortic dissection, allowing visualization of the intimal flap and differentiation of the true and false lumens.
2. Key CT findings include an intimal flap that separates the true and false lumens, as well as complications such as periaortic hematoma.
3. ECG gating is important to minimize motion artifacts and accurately characterize the proximal extent of the dissection and involvement of coronary arteries.
This document presents a rare case report of a 30-year-old woman diagnosed with Takayasu arteritis who presented with both aneurysmal dilation and stenosis of the right common carotid artery. Imaging revealed aneurysmal dilation of the right innominate and proximal right common carotid arteries as well as a 75% focal stenosis in the right common carotid artery distal to the dilation. Treatment with prednisone resulted in improvement of symptoms and normalization of inflammation markers. The concurrent presence of aneurysmal dilation and stenosis from Takayasu arteritis in the same vessel is an exceptionally rare finding.
AORTIC DISSECTION and management of aortic dissectiondrhanifmohdali
Aortic emergencies are life-threatening conditions involving the aorta that require timely diagnosis and management. Aortic dissection, a tear in the aortic wall that causes blood to flow abnormally within the wall, is a common aortic emergency. It is usually caused by high blood pressure damaging the aortic wall. Symptoms include a sudden, severe chest pain and pulse abnormalities. Diagnosis involves imaging tests like CT, MRI, or angiography. Treatment aims to lower blood pressure and heart contractility to prevent dissection progression, often using beta blockers. Surgery is usually recommended for type A dissections involving the ascending aorta, while type B dissections of the descending aorta may be treated medically or
Aortitis refers to inflammation of the aortic wall that can be infectious or non-infectious. Non-infectious aortitis includes large vessel vasculitides like giant cell arteritis (GCA) and Takayasu arteritis. GCA most commonly involves the cranial arteries and affects older adults, while Takayasu arteritis typically causes stenosis of the aorta and its major branches and is more common in younger Asian females. Imaging plays a key role in diagnosis and monitoring of aortitis. CT, MR, and PET scanning can detect wall abnormalities and assess disease activity.
Acute aortic syndrome (AAS) refers to emergency aortic conditions including aortic dissection, intramural hematoma, and penetrating ulcers that have similar clinical presentations. AAS is classified using the DeBakey or Stanford systems based on the location and extent of disease. Imaging with CT, MRI, or TEE is used to establish the diagnosis and guide treatment, which may involve medical management or emergent surgery depending on the specific condition and complications. Prognosis depends on factors like age, hypertension status, and involvement of other organs. Long term follow-up is needed due to risks of progressive aortic disease.
The document describes the anatomy of the carotid arteries and their branches, evaluation and imaging of carotid artery disease, and treatment strategies including lifestyle modifications to reduce risk factors, carotid endarterectomy to remove plaques from significantly stenotic arteries, and outcomes data from clinical trials on endarterectomy for symptomatic and asymptomatic carotid stenosis. Imaging modalities like carotid duplex ultrasound, CTA, and MRA are described for evaluating the degree of carotid stenosis. The benefits of carotid endarterectomy are greater for symptomatic high-grade stenosis while more moderate for asymptomatic disease.
Behcet s disease new concepts in vascular involvementsuvcd
This document discusses Behcet's disease, a inflammatory disorder characterized by recurrent oral and genital ulcers. It was first described by Dr. Hulusi Behcet in 1937. The document summarizes the epidemiology, pathophysiology, clinical manifestations especially related to vascular involvement, treatment approaches, and the author's experience treating vascular complications through endovascular and open surgical procedures. Key points are that Behcet's disease has higher prevalence along the Silk Road, vascular involvement can include aneurysms and thrombosis, and endovascular repair may be preferable to open surgery for treating aneurysms to avoid complications from anastomoses.
This document discusses various aortic diseases and considerations for their assessment and treatment. It begins by outlining the objectives to discuss different aortic conditions, including acute syndromes, aneurysms, genetic diseases, and tumors. It then covers important anatomical considerations like the thoracic and abdominal divisions of the aorta. Subsequent sections provide details on endovascular zones, normal dimensions, histology, pathologies, clinical exam findings, imaging modalities like CT and their roles in evaluating the aorta.
Carotid blowout syndrome (CBS) is an uncommon but dreaded complication that occurs in patients treated for head and neck cancer. CBS is the result of necrosis of the arterial wall, which can occur following resection, after reirradiation for a recurrent or second primary tumor, by direct tumor invasion of the carotid artery wall or by a combination of these factors.
Acute Pericarditis Diagnosis and Management Summary.docxwrite22
Acute Pericarditis Diagnosis and Management Summary examines the diagnosis and management of acute pericarditis. It discusses how acute pericarditis is diagnosed using a combination of clinical features, electrocardiography, chest X-ray, and echocardiography. Treatment involves the use of nonsteroidal anti-inflammatory drugs to reduce pain and inflammation. Corticosteroids may also be used in some cases. The prognosis is generally good if the underlying cause is identified and treated appropriately.
Spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic separation of the coronary arterial walls, creating a false lumen. It predominantly affects young to middle-aged women and can lead to myocardial ischemia. Diagnosis is challenging as angiographic findings can mimic atherosclerosis. Intravascular ultrasound and optical coherence tomography provide better visualization of the dissection and intimal tears. Management involves antiplatelet therapy but thrombolysis and anticoagulation should be avoided due to risk of extension. Prognosis is generally good but recurrence risk remains.
Similar to Anesthesia and perioperative care for aortic surgery (18)
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Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
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Unit 4: MRA 103T Regulatory affairs
This guideline is directed principally toward new Molecular Entities that are
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Examples-Measures of central tendency Dispersion, Variance, Standard Deviation (SD), Absolute Error, Mean Absolute Error (MAE), Eigen Value
2. C.M. Wells and K. Subramaniam
Pathologically, classic aortic dissections
(class I) are characterized by an intimal tear with
separation of the aortic media into two layers, the
inner two thirds and outer one third. This separa-
tion extends for a variable distance in both
circumferential and longitudinal fashion. The
vast majority of dissections originate from inti-
mal tears in the ascending aorta within several
centimeters of the sinuses of Valsalva where tor-
sional movement of the aortic annulus provokes
additional downward traction in the aortic root
and increases longitudinal stress in that segment
of aorta. The other common site for an intimal
tear to originate is in the descending aorta just
distal to the origin of the subclavian artery at the
Fig. 2.1 Classification of acute aortic syndromes (Reprinted with permission from Berger F et al.30
)
Table 2.1 Classification of acute aortic syndrome
Class I – Classic aortic dissection
Class II – Intramural hematoma
Class III – Localized dissection, intimal tear without
extensive intimal flap formation, localized bulge in the
aortic wall
Class IV – Penetrating aortic ulcers
Class V – Iatrogenic or post-traumatic dissection
Fig.2.2 Progression of one type of acute aortic syndrome
to another type
18
3. 2 Acute Aortic Syndrome
site of the ligamentum arteriosum. Tears occur in
the isthmus area because of increased tension at
the union of the relatively mobile aortic arch with
the fixed descending thoracic aorta. From this
point, blood under pressure extends the dissec-
tion in an antegrade direction although retrograde
extension is also possible, thus forming a false
lumen and double channel aorta. A further reen-
trance tear allows blood to circulate in the false
lumen and communicate with the true lumen.
Reentry tears are often located in the abdominal
aorta, iliac arteries, or other aortic branches.
These small communications, normally less than
2 mm in diameter, represent intercostal and
lumbar arteries severed by the dissection pro-
cess.4
The true lumen is most often the smaller of
the two and is surrounded by calcifications if
present. The false lumen is located along the
outer curve of the aortic arch and from the aortic
isthmus, a dissection adopts a spiral route involv-
ing the left border of the descending thoracic
aorta and the left posterior region of the infradia-
phragmatic and infrarenal aorta (Fig. 2.4). From
there, a dissection may involve any branches of
aorta including the arch vessels, the left intercos-
tal, renal, and iliac vessels, most often, it is the
left renal and iliac artery which are involved.
The celiac, superior mesenteric, and right renal
arteries usually communicate with the true lumen.
Dissections rarely extend to the common femoral
arteries.
Class III dissections are characterized by the
presence of an intimal tear without a flap or
hematoma formation. Patients often present with
the classic symptoms of dissection and may have
associated aneurysms, aortic regurgitation, or
Fig. 2.3 Types of acute
aortic syndromes based on
the site of aortic involve-
ment (Reprinted with
permission from
Springer4
)
Table 2.2 Risk factors for aortic dissection
Long-standing hypertension
Male
Advanced age
Prior cardiac surgery
Known aortic aneurysm or prior dissection
Cardiac catheterization/surgery
Connective tissue disorders
Marfan’s syndrome
Ehlers−Danlos syndrome
Bicuspid aortic valve
Coarctation of the aorta
Hereditary thoracic aortic disease
Vascular inflammation
Deceleration injury
Cocaine
Peripartum
19
4. C.M. Wells and K. Subramaniam
pericardial effusion. Imaging techniques such as
CT, MRI, or TEE may fail to detect this type of
dissection since each of these modalities depends
on the presence and identification of an intimal
flap or true and false lumen for diagnosis.
Aortography may show an eccentric bulge in the
aorta, which should raise the suspicion of this
class of dissection. Treatment is similar to that
for classic aortic dissection.1
Class V aortic dissections are caused by
traumatic or iatrogenic injury. Traumatic dissec-
tions are described in detail in another chapter.
Iatrogenic aortic dissections may result from
cardiac surgery, percutaneous coronary interven-
tions, or endovascular procedures. Dissections
resulting from cardiac surgical procedures may
occur during the procedure, early in the postop-
erative period, or their presentation may be
delayed for years.5,6
The incidence varies between
0.12% and 0.35% of cardiac surgeries, but the
mortality is high unless recognized early. Injury
to the aorta can occur at the site of cross-clamp
placement, cannulation and decannulation, aorto-
tomy, cardioplegic cannulation, or aortocoronary
anastomosis. Preexisting atherosclerotic or con-
nective tissue disease, increased aortic diameter,
previous heart surgery, a history of hypertension
and elevated CPB pressures are all risk factors.
There is a growing concern of an increased inci-
dence of aortic dissection following off-pump
coronary artery bypass grafting compared to on-
pump CABG related to the application of a side-
biting clamp under higher blood pressure and
pulsatility.7
Intraoperative TEE and epiaortic
ultrasound may help in the prevention and
early diagnosis of this potentially lethal compli-
cation. Type A dissections have been reported
after diagnostic coronary angiography (0.01%)
and other percutaneous interventions (0.03%).8,9
Isolated coronary artery dissections and localized
aortic dissections (less than 40 mm of ascending
aortic involvement) can be treated with intracoro-
nary or aortic stenting. However, a failed stenting
procedure or progression of a dissection must be
surgically treated. Retrograde type A dissections
after endograft placement for type B dissections
havebeenreportedwithanincidenceof10–27%.10
The presentation may be acute or delayed for sev-
eral months. Various etiological factors include
wire and sheath manipulation in the arch, repeated
balloon dilatations, oversizing of grafts, injury to
a diseased aorta at the margin of inflexible grafts,
and progression of disease unrelated to stent
grafting. Surgical replacement with tube grafts is
recommended in these patients and mortality is
high (27%). Other procedures associated with an
increased risk of aortic dissection include the
insertion of intra-aortic balloon pumps, percuta-
neous angioplasty, and stenting for coarctation of
the aorta.11
Fig. 2.4 CT reconstruction of a type A dissection follow-
ing graft placement in the ascending aorta. The dissection
that extends into the descending aorta demonstrates how
the defects spiral around the aorta
20
5. 2 Acute Aortic Syndrome
Intramural Hematoma
Aortic intramural hematomas (IMH) account for
up to 20% of all cases of AAS and represent a
variant of dissection characterized by the absence
of an intimal flap, reentrant tear, or double
channel with false lumen flow. IMH often occur
in patients with severe atherosclerotic disease in
which penetrating aortic ulcers or atherosclerotic
plaques rupture causing intimal injury with blood
entering the media. In patients with mild or no
atherosclerosis, spontaneous rupture of the vasa
vasorum may initiate aortic wall degeneration,
which leads to hematoma formation in the aortic
wall, splitting of the medial layer, and dissection
formation without an intimal tear (Class II).12
Patients in the first group tend to be older and
have coexisting coronary and peripheral vascular
disease. Absence of intimal tears is not manda-
tory in the diagnosis of IMH since small com-
munications may be seen indicating rupture as a
decompressing mechanism.13
The presence of
large intimal erosions or deep ulcer-like lesions
in the intima is associated with a progressive dis-
ease course and poor outcome.14
IMH evolution is difficult to predict (Fig. 2.5).
In some cases, the hematoma does not change in
size. Resolution occurs in fewer than 10% of
cases, but is more likely with less hematoma and
aortic wall thickness.2
When an IMH resolves, a
localized aneurysm may develop because of a
weakened media and remodeling, requiring close
surveillance. Progression of IMH may lead to
weakening and disruption of the intimal layer
causing a classic dissection. Progression to dis-
section has been shown to occur in 16–47% of
patients with IMH.15
A few patients may demon-
strate IMH and dissection in different segments of
aorta, known as a hybrid case. Increasing aortic
diameter (>50 mm) causing aneurysm formation
is a poor prognostic factor associated with IMH.16
In addition, increased permeability of the aortic
wall may lead to pericardial or pleural effusions
or a mediastinal hemorrhage. Most effusions will
resolve. However, large and progressive fluid
accumulations are an ominous signs. Weakening
of the adventitial layer may lead to aortic rupture,
while a contained rupture from disintegration of
the outer medial layers with intact adventitia is
not uncommon.17
Similar to aortic dissections, the
Fig. 2.5 Evolution of
intramural hematoma
(Reprinted with permis-
sion from Springer4
)
21
6. C.M. Wells and K. Subramaniam
most common underlying condition associated
with IMH is hypertension.
Penetrating Aortic Ulcer
The term penetrating atherosclerotic ulcer (PAU)
describes a condition in which ulceration of an
atherosclerotic lesion penetrates the intima and
extends into the media, eroding the inner elastic
layer of the aortic wall. The reason why most ath-
erosclerotic ulcers do not penetrate the internal
elastic lamina and few penetrate the media and
adventitia is not clear. PAUs are focal lesions
most often located in the descending thoracic
aorta, which correlates with a greater disease bur-
den in that region. These patients tend to be older
with severe systemic atherosclerosis but without
connective tissue diseases. Multiple PAUs are
often found in a single patient. Imaging of PAU
most often reveals extensive atherosclerosis with
severe intimal calcification and plaque. A crater
or extravasation of contrast is often visualized.18
Occasionally, PAU may progress (Fig. 2.6).
This may precipitate a localized, intramural hem-
orrhage following progressive erosion and rupture
of the vasa vasorum.19
Further penetration to the
adventitia may lead to the formation of a saccular
aneurysm or pseudoaneurysm.20
Symptomatic
ulcers with signs of deep erosion are more prone to
aortic rupture.21
In rare cases, PAU may lead to
aortic dissection, but those dissections arising from
a PAU tend to be less extensive and demonstrate a
thick, calcified static flap in a location atypical for
entrance tears. Longitudinal spread of aortic dis-
sections arising from PAU is limited by medial
fibrosis and calcification.20
Acute Expanding Aneurysms
Also included in many discussions of acute aortic
pathology are symptomatic aortic aneurysms
which may represent impending rupture. The
acute expansion of an aortic aneurysm accounts
for a significant number of patients who present
with the sudden onset of chest pain. As aneu-
rysms increase in size, the dilatation results in
greater wall tension and a more rapid rate of
expansion. In addition, aneurysms may be associ-
ated with progressive dissections, IMH, or PAU,
all of which cause weakening of the aortic wall.
Etiopathogenesis
The physiopathological mechanism that precipi-
tates the appearance of each of these entities var-
ies somewhat; however, both acquired and genetic
conditions share an underlying pathology that
involves breakdown of the intimal layer and
weakening of the aortic media, both of which
lead to higher wall stress. In addition, it is
common for there to be progression from one
Fig. 2.6 Evolution of
penetrating aortic ulcers
(Reprinted with permis-
sion from Springer4
)
22
7. 2 Acute Aortic Syndrome
type of lesion to another and some patients may
concurrently manifest multiple types of lesions.
Hypertension and Mechanical Forces
The most common risk factor for aortic dissec-
tion is hypertension. Chronic exposure of the
aorta to high pressures leads to intimal thicken-
ing, fibrosis, calcification, and extracellular fatty
acid deposition. The extracellular matrix also
undergoes accelerated degradation, apoptosis,
and elastolysis. Both mechanisms lead to intimal
weakening and medial degeneration.22
At any site
where there is tissue thickening and fibrosis, there
is compromise of nutrient and oxygen supply to
the arterial wall. Eventually, there is necrosis of
smooth muscle cells and fibrosis of elastic tissue
in the vessel wall. The resulting stiffness increases
the risk of aortic pathology when exposed to the
chronic trauma of arterial hypertension.
Genetic Predisposition
Marfan’s syndrome, Ehlers–Danlos syndrome,
familial forms of aortic aneurysm and dissection,
as well as bicuspid aortic valve are genetic condi-
tions that predispose patients to develop an acute
aortic syndrome and correlate with earlier
presentations. Among these, Marfan’s syndrome
is the most prevalent connective tissue disorder
with an incidence of one in 7,000. The underly-
ing defect is a mutation on the fibrillin-1 gene,
which results in defective fibrillin in the extracel-
lular matrix.22
Ehlers–Danlos syndrome is another inherited
connective tissue disorder characterized by tissue
fragility. The familial form of aortic disease has
been localized to mutations on the fibrillin-1
gene,similartoMarfan’ssyndrome.Characteristic
to each of the different genetic disorders is a sim-
ilar pathophysiology that includes a dedifferenti-
ation of vascular smooth muscle cells and
enhanced elastolysis of aortic wall components.
In addition, increased expression of metallopro-
teinases promotes fragmentation of elastic tissue
in the medial layer.22
Matrix Metalloproteins
The matrix metalloproteins are a group of proteins
whose primary function is to degrade extracellu-
lar matrix. Patients with thoracic aortic disease
have been shown to have increased levels of these
enzymes, which favor proteolysis within the aor-
tic wall. There are still many unanswered ques-
tions related to the role these enzymes play in
AAS; however, they may serve as a marker for
aortic pathology or their inhibition may slow the
progression of disease.23
Clinical Presentation
AAS is characterized clinically by “aortic pain,”
most often in a patient with a coexisting history
of hypertension. The early recognition of pain
associated with progressive aortic lesions is of
paramount importance. Table 2.3 lists various
presenting symptoms and signs of AAS and
Table 2.4 lists the most common associated con-
ditions. The characteristic findings listed may
Table 2.3 Presenting features of acute aortic syndrome
Chest pain – abrupt, severe, tearing, radiating
Anterior pain or radiation to neck – associated with
ascending aorta
Radiation to back or abdomen – associated with
descending aorta
Syncope or cerebrovascular accident
Hypertension – SBP > 150 mmHg
Shock or tamponade
Diastolic murmur
Pressure differential in upper extremities
Pulse deficits
End-organ ischemia
Table 2.4 Comorbid conditions associated with acute
aortic syndrome
History of hypertension
Smoking
Known coronary artery disease
Thoracic or abdominal aortic aneurysm
Peripheral arterial disease
Prior stroke
Chronic renal insufficiency
23
8. C.M. Wells and K. Subramaniam
vary or be absent, emphasizing the necessity of a
high level of suspicion in order to avoid diagnos-
tic delays and poor outcomes.
The pain caused by PAU and IMH is similar to
classic aortic dissection. The various types of
AAS cannot be reliably differentiated on clinical
grounds alone. Aortic pain is described as
severely intense, acute, tearing, throbbing, and
radiating.24
In contrast to the increasing intensity
of dull cardiac pain, AAS is described as being
more abrupt and at maximal intensity from the
onset. In addition, 4.5% of patients deny having
any pain on presentation.25
Pain located in the
anterior chest and neck is related to involvement
of the ascending aorta and may be easily con-
founded with that of ischemic syndromes. Back
and abdominal pain may indicate that there is
involvement of the descending aorta. Syncope
may be the presenting symptom in up to 20% of
cases and is associated with a proximal dissec-
tion. The onset of syncope or central neurologi-
cal deficits indicates probable complications such
as obstruction of cerebral vessels, cardiac tam-
ponade, or activation of cerebral baroreceptors.
Other presenting features of AAS may include
end-organ ischemia or pulse deficits.3
Two types
ofdistalvisceralorganmalperfusionaredescribed
(Fig. 2.7). In static obstruction, the dissection
flap enters the origin of the branch and encroaches
on the lumen. If there is no reentry, then the true
lumen will be narrowed to cause ischemia. In
dynamic obstruction, the flap prolapses and
obstructs the origin of the vessel without entering
the vessel. Static and dynamic obstruction may
be combined to contribute to branch obstruction.
Diagnostic Evaluation
As diagnostic modalities have improved over the
past 2 decades, the awareness of AAS has
increased significantly. PAU and IMH were virtu-
ally unknown in the prior era of aortic imaging by
aortography. These disorders were not classified
as being distinct entities until the mid-1980s.
In the current era of three-dimensional, high-
resolution imaging by computerized tomography
(CT), magnetic resonance (MR) imaging, and
Fig. 2.7 Types of visceral
organ malperfusion with
aortic dissections
(Reprinted with permis-
sion from Springer4
)
24
9. 2 Acute Aortic Syndrome
transesophageal echocardiography (TEE), these
two disorders have become increasingly recog-
nized. The sensitivity and specificity of different
imaging techniques and their comparison are
given in Table 2.5.26
The goals of diagnostic
imaging in patients with suspected AAS are con-
firmation of the diagnosis, classification and type
of aortic pathology, tear localization, and identifi-
cation of signs indicating the need for emergent
intervention (pericardial, mediastinal, or pleural
hemorrhage).2
Additional information includes
arch and branch vessel involvement. Each imag-
ing modality has distinct advantages (Table 2.6)
and most patients require multiple imaging stud-
ies to diagnose and characterize the underlying
aortic pathology.27
Electrocardiogram
An ECG is an important first diagnostic test
performed for all patients presenting with acute
chest pain, whether typical or atypical for an
acute aortic syndrome. The differentiation of
AAS from acute coronary syndrome (ACS) is
important; however, it must be remembered the
ACS may occur as a result of AAS.
Chest Radiography
While rapid imaging plays a crucial role in the
diagnosis of AAS, the role of chest radiography
has become limited, especially for conditions
Table2.5 Results of meta-analysis – diagnostic accuracy of different imaging modalities for suspected aortic dissection
(Reprinted with permission from American Medical Association16
)
Imaging
technique
Number
of studies Sensitivity Specificity
Positive
likelihood ratio
Negative
likelihood ratio
TEE 10 98 (95–99) 95 (92–97) 14.1 (6.0–33.2) 0.04 (0.02–0.08)
Helical CT 3 100 (96–100) 98 (87–99) 13.9 (4.2–46.0) 0.02 (0.01–0.11)
MRI 7 98 (95–99) 98 (95–100) 25.3(11.1–57.1) 0.05 (0.03–0.10)
Data reported with 95% confidence intervals. Likelihood ratios greater than 10 and less than 0.1 are considered strong
evidence to confirm or ruling out the diagnosis of aortic dissection
Table 2.6 Comparison of imaging modalities (Reproduced with permission from Oxford University press and the
primary author Professor Raimund Erbel56
)
TTE/TEE CT MRI Angiography IVUS
Sensitivity ++ ++ +++ ++ +++
Specificity +++ ++ +++ ++ +++
Classification +++ ++ ++ + ++
Tear localization +++ − ++ + +
Aortic regurgitation +++ − ++ ++ −
Pericardial effusion +++ ++ ++ − −
Mediastinal hematoma ++ +++ +++ − +
Side branch
involvement
+ ++ ++ +++ +++
Coronary artery
involvement
++ − + +++ ++
X-ray exposure − ++ − +++ −
Patient comfort + ++ + + +
Follow-up studies ++ ++ +++ − −
Intraoperative
availability
+++ − − (+) (+)
TTE/TEE – transthoracic/transoesophageal echocardiography; CT – computed tomography; MRI – magnetic resonance
imaging; IVUS – intravascular ultrasound
25
10. C.M. Wells and K. Subramaniam
confined to the ascending aorta. In a study of 216
patients over a 6-year period, the sensitivity for
aortic disease was 64%, with a specificity of 86%.
The sensitivity for lesions of the ascending aorta
was 47%, while that for disease involving distal
aortic segments was 77%.28
A chest X-ray may
show widening of the aortic contour, displaced
calcification, aortic kinking, or opacification of
the aortopulmonary window (Fig. 2.8a and b).
Computerized Tomography (CT)
When AAS is suspected based on clinical presen-
tation and an acute coronary syndrome has been
excluded, cardiac-gated, contrast-enhanced mul-
tidetector CT angiography is nearly 100% sensi-
tive and specific in the diagnosis, differentiation
and staging of AAS.29
Modern CT machines have
up to 64 rows of detectors, and this enables them
to generate multiple simultaneous images with a
slice thickness of less than 1 mm. Multidetector
CT is also extremely fast with spiral imaging
of the entire thorax can be done in a single
breath-hold, which eliminates respiratory motion
artifact. Cardiac gating is done to avoid artifacts
produced because of the imaging being obtained
during different phases of cardiac cycle. CT
allows for a complete diagnostic evaluation of the
thoracic aorta, including the lumen, aortic wall,
and periaortic region. Both unenhanced and
enhanced images are valuable. Unenhanced scans
depict intramural hematoma (crescent shaped or
circumferential wall thickening) and thrombosis
of the false lumen. Contrast-enhanced imaging
allows demonstration of an intimal flap, which is
the most reliable finding in the diagnosis of dis-
section (Fig. 2.9a and b). Contrast differences
between arterial and venous phase can help
differentiate true and false lumens. Interestingly,
it can be difficult to differentiate an aneurysm
with thrombus from a dissection with a throm-
bosed false lumen. Intimal calcifications are
displaced by a false lumen in the latter case.30
The diagnosis of IMH and PAU are also highly
accurate with CT.31,32
The diagnosis of PAU is
made by the demonstration of an outpouching
of the aortic wall with rough edges (Fig. 2.10).
Fig. 2.8 PA (a) and lateral Chest X-Rays (b) demonstrating a dilated thoracic aorta and widened mediastinum
26
11. 2 Acute Aortic Syndrome
The ulcer is usually surrounded by extensive ath-
erosclerotic plaques. CT imaging of the aorta
should include the iliac arteries for possible endo-
vascular intervention and aortic arch branches to
evaluate the extent of dissection and possible
neurological complications. Other benefits of CT
are its availability and noninvasiveness. The
major drawbacks of CT are the exposure to large
doses of ionizing radiation and contrast agents.29
In addition, CT does not offer the capability to
assess for aortic insufficiency or involvement of
the coronary arteries.
Magnetic Resonance Imaging (MRI)
MRI is a valuable diagnostic tool for the diagno-
sis of acute aortic syndrome. MRI can be highly
accurate even without the use of contrast.
Although MRI has the highest sensitivity and
specificity for the detection of all forms of aortic
pathology and provides superior anatomic detail
when compared to other imaging modalities, it is
limited by availability, expense, and patient
restrictions such as pacemakers, aneurysm clips,
or other metal devices. Prolonged scanning time
and limited access to unstable patients are other
limitations. For these reasons, MRI is not a
widely used tool (<5% of patients in IRAD)3
(Fig. 2.11).
Fig. 2.9 Contrast-enhanced chest CT clearly depicting a type A dissection. The intimal flap is seen in the ascending
and descending aorta (a) as well as the aortic arch (b)
Fig. 2.10 CT reconstructions demonstrating PAU of the
arch and descending aorta as indicated by arrows
27
12. C.M. Wells and K. Subramaniam
Echocardiography
Transthoracic echocardiography (TTE) can be
used as screening tool for the diagnosis of AAS
of the proximal aorta. TTE is useful in the rapid
evaluation of aortic insufficiency, pericardial
tamponade, arch vessel involvement, and left
ventricular systolic function. Hemodynamically
unstable patients in whom TTE has shown peri-
cardial effusion to be present should be taken to
the operating room for airway stabilization and
further TEE evaluation. Thus, cardiac surgeons
rely on echocardiography more than other
imaging modalities including CTA in emer-
gency situations.33
A TEE can be done while
the surgeon simultaneously prepares to open
the chest.
Transesophageal echocardiography (TEE) is
highly sensitive and specific in diagnosing tho-
racic aortic pathologies. The only limitation is in
the distal ascending aorta and proximal arch
which are not clearly visualized by TEE in
most patients. Evaluation of the aortic valve and
suitability for repair can be done with TEE.
The diagnosis of an IMH is characterized by
crescentric aortic wall thickening, the absence of
an intimal flap and a lack of false lumen color
flow typical of dissection. The primary limiting
factor in the use of TEE is the requirement for a
skilled echocardiographer to be immediately
available to perform and interpret results in emer-
gency situations.29
A further detailed description
of TEE examinations for aortic pathology is
described elsewhere in this textbook.
Aortography
Since the development of newer, noninvasive
imaging modalities, there has been a shift away
from invasive techniques for imaging the aorta.
Traditionally, aortography had been the gold
standard for the diagnosis of aortic dissection. Its
primary limitations include its invasive nature
and further risk of intimal damage, the use of
contrast agents, as well as limited visualization of
thrombosed dissections, IMH, and occluded
branch vessels. The specificity for diagnosing
aortic dissection is >95%, but the sensitivity only
averages 90%.2
Intravascular ultrasound (IVUS)
with high-frequency transducers (8–10 MHz) has
been used to complement conventional angiogra-
phy in the diagnosis of acute dissection. IVUS
probes are advanced through guidewire and guid-
ing catheters under fluoroscopy to evaluate the
aorta from inside and provide useful information
about the vessel wall and pathology.
Management
Once there is a suspicion of AAS, patients should
be rapidly stabilized and transported to a tertiary
care center with adequate aortic surgical and
endovascular surgical expertise. It is there that
further imaging and management should take
place. Figure 2.12 provides an algorithm for the
rapid evaluation and treatment of patients
presenting with a suspected AAS.29,34
Fig. 2.11 MRI of the chest showing a descending aortic
dissection
28
14. C.M. Wells and K. Subramaniam
Although the treatment of AAS remains a ther-
apeutic challenge, diverse surgical and percutane-
ous strategies continue to evolve. There are many
factors that affect management decision as listed
in Table 2.7. One third of the mortality associated
with AAS is the result of end-organ failure, which
emphasizes the importance of early intervention.
The goal of treatment is to prevent the progres-
sion of the disease and its lethal complications.
The initial management of all patients with
AAS involves pain relief and aggressive blood
pressure control. In normalizing the blood pres-
sure, the goal is to reduce the force of left ven-
tricular ejection (dP/dt), which is the primary
cause of dissection extension and aortic rupture.
Beta-blockers are the preferred agents because
they not only reduce systemic pressure but also
lower heart rate. For most patients, the goal is a
systolic pressure between 100 and 120 mmHg
and heart rate <60 bpm or the lowest tolerable
levels that provide adequate cerebral, coronary,
and renal perfusion. Less is known about the role
of calcium channel blockers for patients who are
-blocker intolerant, but they should reduce
blood pressure without causing reflex tachycar-
dia. If neither of the above agents is adequate to
control the blood pressure, vasodilators may be
added. However, they should never be used as an
initial form of therapy before starting -blockers
because of the reflex tachycardia and increase in
the force of left ventricular ejection leading to
increased aortic wall stress.
Type A Aortic Dissection
Acute ascending aortic pathology (acute dissec-
tion, IMH, and PAU) should be treated as a surgi-
cal emergency because of the possible risk of
life-threatening complications including aortic
rupture, pericardial tamponade, and high early
mortality (Fig. 2.13). Surgery is also aimed
to relieve aortic regurgitation and reestablish
coronary and branch vessel perfusion. Acute type
A dissection has a mortality rate of 1–2% per
hour during the first hours of symptom onset and
without surgical treatment, the mortality rate is
20% by 24 h, 30% by 48 h, 40% at 1 week, and
50% at 1 month.35
Even with surgical treatment,
Table 2.7 Patient factors affecting management
decisions
Disease location – type A or B
Retrograde extension into the arch and/or ascending
aorta
Rupture or impending rupture
Site of entry and reentry
Involvement of side branches
Branch origin from true or false lumen
Risk of end-organ damage
Complications – rupture, coronary occlusion, aortic
insufficiency, neurological
Diameters of the true and false lumens
Areas of normal vessel for stent-graft placement
Fig. 2.13 Management of
acute aortic dissection
(Reprinted with permis-
sion from Springer4
)
30
15. 2 Acute Aortic Syndrome
the mortality rate is as high as 10% by 24 h and
20% at 1 month.36,37
Aortic arch and descending thoracic intimal
tears are seen in 20–30% of patients with type A
dissection and if left untreated predisposes to
later distal reoperation.38,39
Patients who require
partial or total arch replacement with reconnec-
tion of supraaortic vessels to the graft must often
undergo deep hypothermic circularoty arrest with
antegrade or retrograde cerebral perfusion. If a
dissection extends into the descending thoracic
aorta, an elephant trunk extension of the arch
graft is an option.40
In a later procedure, the ele-
phant trunk portion of the graft may be connected
to the distal descending aorta, a tubular graft or
endovascular graft. There are reports of endovas-
cular repair of the ascending aorta in highly
selected patients, but this has most often been for
the purpose of temporizing symptoms and pre-
venting disease progression before a more defini-
tive open repair could be performed. It is most
often not possible due to the anatomic restrictions
of securing the graft in the ascending aorta. The
placement of stent grafts has been applied to treat
aortic branch occlusions in both type A and B
acute aortic dissections. In type A dissections
with visceral malperfusion, treatment of the leak-
ing aorta and aortic valve take precedence over
visceral malperfusion. However, patients with
prolonged limb or bowel ischemia may be
unsuitable for proximal aortic surgery, and endo-
vascular treatment to restore perfusion to critical
organs is recommended.
Type B Aortic Dissection
Uncomplicated Type B Dissection
Medical management (analgesics and antihyper-
tensive therapy) still remains the main stay of
therapy for patients with uncomplicated type B
disease. It is safe to treat these patients medically
with close follow-up for ischemic complications,
disease progression, or aneurysmal enlargement.
In a group of 384 patients with type B dissec-
tions, 73% were treated medically with a 10%
in-hospital mortality. Long-term survival is
60–80% at 5 years.3
Surgical repair has not been
shown to improve outcomes in this group of
patients. Recently, a completed randomized study
(Investigation of stent grafts in patients with type
B aortic dissection-INSTEAD) examined the use
of endografts versus medical therapy in uncom-
plicated dissections. The results did not show any
survival benefit at 2 years.41
Complicated Type B Dissections
Complicated type B aortic disease is differentiated
by the presence of a distal malperfusion syndrome
or rapid disease progression. Indications for inter-
vention are similar to those for type A diseases;
the prevention of life-threatening complications
such as organ or limb ischemia, aneurysm expan-
sion and risk of rupture, periaortic blood collec-
tion, intractable pain, aneurysm expansion or
uncontrolled hypertension. The mortality rate for
open surgical repair (graft replacement, fenestra-
tion, or bypass procedures) is 30–35% and even
higher with the presence of visceral malperfu-
sion.42,43
Aortic endovascular grafting may be par-
ticularly beneficial in this group and has shown
improved mortality rates (16%). The goals of
endograft treatment include reconstruction of the
aortic segment containing the entry tear, induction
of thrombosis in the false lumen, and the
reestablishment of flow in the true lumen and
branches.44
In one series, false lumen thrombosis
was achieved in 85–100% of patients.
An additional benefit of stent grafts is the abil-
ity to relieve dynamic and combined static and
dynamic obstructions successfully in compli-
cated acute type B dissections.45,46
Static obstruc-
tions are relieved by placing the graft in the
branch vessel and dynamic obstructions may
benefit from stents in the true lumen. Endografts
have also been used in patients with retrograde
type A dissection with intimal tear in the descend-
ing aorta to induce false lumen thrombosis.47
Surgical treatment may be the only option in
patients with failed endografts or patients unsuit-
able for this less-invasive technique.
With either surgical, endograft, or medical
management, the risk of further dissection is
never eliminated. Therefore, close, regular moni-
toring, most likely with CT imaging, is necessary
to assess for progression or complications.
31
16. C.M. Wells and K. Subramaniam
Intramural Hematoma
Type A Disease
The recommended treatment for patients with
Type A IMH is prompt surgical intervention.
Proximal IMH are independently associated with
potential progression to dissection, aneurysm,
and rupture as well as poor clinical outcomes.17
The risk of a nonsurgical approach to type A IMH
demonstrates an early mortality of 55% compared
with 8% following surgical repair.17
However, for
patients with significant comorbidities and
uncomplicated type A IMH (no dissection or inti-
mal tear, thickness less than 11 mm, aortic diam-
eter less than 50 mm), medical treatment with
follow-up imaging and timed surgical interven-
tion has been recommended.
Type B Disease
The management of IMH involving the descend-
ing aorta is similar to that recommended for type
B dissections. The current literature supports
medical management. However, if complications
arise (ulceration, expansion, and dilatation),
endograft placement may be considered although
limited data exists. Endografts may cause erosion
of the intima during the acute phase. IMH of the
descending aorta have been associated with an
in-hospital mortality rate of 10%, similar to that
of type B aortic dissection, further emphasizing
the importance of correct diagnosis and proper
treatment.
Penetrating Aortic Ulcers
There are multiple important factors to identify
when diagnosing PAU. One must determine the
number (single or multiple), location (type A or
B), and associated complications (IMH, dissec-
tion, pseudoaneurysm, and rupture). Type A PAU
should be treated surgically. Medical therapy is
indicated in stable patients with type B PAU.48
Very few centers advocate any surgical interven-
tion in uncomplicated type B patients because
there is a high risk of organ failure and poor
prognosis due to the high likelihood of extensive
atherosclerotic disease. For patients with symp-
tomatic or progressive disease, focal PAU in the
descending aorta are ideal targets for endograft
placement. In a meta-analysis of 58 patients from
13 studies, complete sealing of the ulcer was pos-
sible in 94% of patients. Neurologic complica-
tions were present in 6% and the in-hospital
mortality rate was 5%.49
Long-term results are
not known at this time.
Natural History and Prognosis
The outcomes of patients treated for AAS have
improved significantly, although there still
remains a high mortality rate in the acute phase.
Table 2.8 lists predictors of in-hospital death.50
Early clinical suspicion and greater surgical
expertise appear to be the most important factors
in reducing mortality.
Type A aortic dissections are highly lethal.
Overall, mortality at 1 month is 20% with and
50% without surgical treatment for type A dis-
sections. The risk of death is higher if there are
complications of pericardial tamponade, involve-
ment of the coronary arteries causing acute myo-
cardial ischemia, or a malperfusion syndrome.
Age greater than 70 has been identified as an
independent risk factor for hospital death for
acute type A dissection. Shock, hypotension, and
tamponade are other risk factors for increased
mortality.37
For type B dissections, the overall mortality
rate is 10% with medical treatment. Circulatory
shock and visceral ischemia predispose to a
higher mortality in type B dissection.51
Table 2.8 Predictors of in-hospital death
Age >70
Abrupt onset of pain
Hypotension/cardiac tamponade/shock
Abnormal EKG
Kidney failure
Pulse deficits
Iatrogenic cause
32
17. 2 Acute Aortic Syndrome
Following the acute-phase, mid- to long-term
survival depends not only on the underlying
aortic disease but also other comorbidities. In
patients with surgically corrected type A dissec-
tions, survival differences were based on the
presence or absence of distal false lumen flow. In
one study, the absence of a false lumen was
achieved in 53% of patients compared to 10–20%
in most series. In patients with absent false lumen
flow, the survival was 85% at 6 years compared
to 62% in patients with persistent false lumen
flow.37
At 10 years, the survival rate was 44% for
corrected type A dissections compared to 32% in
medically treated type B dissections.51
The pri-
mary reasons for higher, long-term mortality in
type B dissections were aneurysmal expansion
and rupture. Dilatation in the descending aorta
was greater in medically treated type B dissec-
tions compared to operated type A dissections.
Dilatation occurs at a faster rate in patients with
false lumen flow when compared to absent false
lumen flow in type B dissections.52
Junoven et al.
described rupture in 18% and rapid expansion
requiring surgery in 20% of patients with type B
dissection at 3 years.53
The impact of early endo-
vascular treatment on the long-term survival of
type B dissections is yet to be determined.
In patients with type A IMH, Kaji et al.54
reported that surgery was required in 43% of
patients during the acute phase and, among those
discharged without surgery (57%), complete res-
olution occurred in 40% of patients. Type B IMH
has a better long-term prognosis than type B dis-
sections with 5-year survival reported between
43% and 90%.17,55
Close follow-up with imaging
techniques is recommended in patients undergo-
ing medical treatment to look for complications
(dilatation, pseudoaneurysm formation, and
dissection).
Prevention and Follow-Up
At a time when there is an increasing elderly
population, the awareness of such conditions as
AAS is likely to continue to rise. This is due to
improvements in diagnostic modalities, longer
life expectancy, and longer exposure to elevated
blood pressure. In order to best treat these
patients, continued improvements in diagnostic
imaging and therapeutic strategies are necessary,
and a focus on surveillance and prevention will
further reduce the morbidity and mortality asso-
ciated with aortic pathology.
One possibility for the surveillance of patients
at risk for the development or progression of
AAS is the development of biomarkers, which
would enable serum diagnosis. In addition, this
would provide a fast and economic means of dif-
ferentiating patients who present to the emer-
gency room with chest pain. Possible markers
currently include an assay for circulating smooth
muscle myosin heavy chain protein, soluble elas-
tin fragments and acute-phase reactants such as
C-reactive protein, fibrinogen, and D-dimer.
All patients with a known aortic disease
require close surveillance following discharge.
Lifelong treatment of hypertension is required
and regular assessments of the aorta should be
performed at 1, 3, 6, 9, and 12 months as well as
every 6–12 months thereafter, depending on the
aortic size. The most important findings on imag-
ing are aortic diameter, signs of aneurysm forma-
tion, and hemorrhage at surgical anastamosis or
stent-graft sites. The close follow-up emphasizes
the fact that aortic disease progression is not easy
to predict. Repeated surgery is required in
12–30% of patients due to extension or recur-
rence of dissection, aneurysm formation, graft
dehiscence, aortic insufficiency, or infection.26
Conclusion
Significant advances have been made in the diag-
nosis and management of acute aortic dissections
over the past 2 decades. These advancements
have led to a better understanding of aortic pathol-
ogy and led to the discovery of variants that are
collectively termed acute aortic syndrome.
Despite a persistent level of uncertainty in the
diagnosis and management of this lethal disorder,
advances are being made and patient outcomes
are improving.
33
18. C.M. Wells and K. Subramaniam
Key Notes
1. The clinical progress of patients with AAS is
unpredictable. A high level of suspicion is
required for early diagnosis and crucial for
patient survival.
2. The most common risk factor for AAS is
hypertension, with men being affected more
often.
3. Any mechanism that causes intimal damage
and leads to weakening of the medial layers
of the aortic wall can result in dissection,
IMH, or PAU.
4. Acute aortic dissection, the most common
etiology of AAS, is characterized by an inti-
mal tear which is often preceded by medial
wall degeneration or cystic medial necrosis.
5. IMH, a variant of aortic dissection, originates
from a disruption of the vasa vasorum within
the media. They are treated similar to dissec-
tions and have a similar prognosis.
6. PAU is associated with atherosclerotic dis-
ease and can lead to dissection or perfora-
tion. Both IMH and PAU are found most
often in the descending aorta.
7. AAS may present in many ways. Most often
there is the sudden onset of severe, sharp
chest pain or back pain.
8. Type A aortic dissections are associated with
high mortality rates and without surgery,
30-day mortality exceeds 50%.
9. Uncomplicated type B dissections have a
30-day mortality of 10% and may be man-
aged medically. Complications require surgi-
cal intervention or endovascular stenting.
10. CT, MRI, and TEE are all accurate in the
diagnosis of AAS.
11. The initial treatment of all patients with AAS
is blood pressure control in order to decrease
the force of left ventricular contraction and
lower the risk of dissection extension or rup-
ture. Beta-blockers are the preferred first-line
agent to achieve a systolic pressure <120
mmHg and heart rate <60 bpm.
12. Surgery is the definitive treatment of type A
acute aortic pathology. The goal is to prevent
life-threatening complications such as aortic
rupture or pericardial tamponade.
13. Medical therapy with -blockers and
antihypertensive agents is the recommended
therapy for patients with uncomplicated type
B aortic dissection, IMH, or PAU.
14. The advent and incorporation of less-invasive
endovascular treatments has opened up new
perspectives in the treatment of acute aortic
disease and continued advances will result in
improved patient outcomes.
References
1. Svensson LG, Labib SB, Eisenhauer AC, Butterly JR.
Intimal tear without hematoma: an important variant
of aortic dissection that can elude current imaging
techniques. Circulation. 1999;99:1331–1336.
2. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syn-
dromes. Circulation. 2005;112:3802–3813.
3. Hagan PG, Nienaber CA, Isselbacher EM, et al. The
International Registry of Acute Aortic Dissection
(IRAD): new insights into an old disease. JAMA.
2000;283:897–903.
4. Evangelista A, Gonzalez-Alujas T. Pathophysiology
of aortic dissection. In: Rousseau H, Verhoye JP,
Heautot JF, eds. Thoracic aortic Diseases. 1st ed.
Berlin Heidelberg, Germany: Springer; 2006:33–53.
5. Fleck T, Ehrlich M, Czerny M, et al. Intraoperative
iatrogenic type A aortic dissection and perioperative
outcome. Interact Cardiovasc Thorac Surg. 2006;
5:11–14.
6. Elitz T, Kawohl M, Fritzsche D, et al. Aortic dissec-
tion after previous coronary artery bypass grafting.
J Card Surg. 2003;18:519–523.
7. De Smet JM, Stefanidis C. Acute aortic dissection
after off pump coronary artery surgery. Eur
J Cardiothorac Surg. 2003;24:315–317.
8. Okamoto R, Makino K, Saito K, et al. Aorto-
coronary dissection during angioplasty in a patient
with myxedema. Jpn Circ J. 2000 Apr;64(4):316–320.
9. Wyss CA, Steffel J, Lüscher TF. Isolated acute iatro-
genic aortic dissection during percutaneous coronary-
intervention without involvement of the coronary
arteries. J Invasive Cardiol. 2008 Jul;20(7):380–382.
10. Kpodonu J, Preventza O, Ramaiah VG, et al.
Retrograde type A dissection after endovascular stent-
ing of the descendingthoracic aorta. Is the risk real?
Eur J Cardiothorac Surg. 2008 Jun;33(6):1014–1018.
Epub 2008 Apr 21.
11. Panten RR, Harrison JK, Warner J, Grocott HP. Aortic
dissection after angioplasty and stenting of an aortic
coarctation:detection by intravascular ultrasonogra-
phy but not transesophageal echocardiography. J Am
Soc Echocardiogr. 2001 Jan;14(1):73–76.
12. Sheldon WS, Vandervoort PM, Black IW, Grimm RA,
Stewart WJ. Aortic intramural hematoma in
patients evaluated for aortic dissection: clinical,
34
19. 2 Acute Aortic Syndrome
echocardiographic,radiologicandpathologicfindings.
Circulation. 1994;90(Suppl I):I385.
13. Vilacosta I, de Dios RM, Pinto AG. Aortic intramural
hematoma during coronary angioplasty: insights into
the pathogenesis of intramedial hemorrhage. J Am
Soc Echocardiogr. 2000;13:403–406.
14. Ganaha F, Miller DC, Sugimoto K, et al. Prognosis of
aortic intramural hematoma with and without pene-
trating atherosclerotic ulcer: a clinical and radiologi-
cal analysis. Circulation. 2002 Jul 16;106(3):
342–348.
15. Nienaber CA, Sievers HH. Intramural hematoma in
acute aortic syndrome: more than on variant of dissec-
tion? Circulation. 2002;106:284–285.
16. Kaji S, Nishigami K, Akasaka T, et al. Prediction of
progression or regression of type A aortic intramural
hematoma bycomputed tomography. Circulation.
1999 Nov 9;100(19 Suppl):II281–II286.
17. Von Kodolitsch Y, Csösz SK, Koschyk DH, et al.
Intramural hematoma of the aorta: predictors of pro-
gression to dissection and rupture. Circulation. 2003
Mar 4;107(8):1158–1163.
18. Hayashi J, Matsuoka Y, Sakamoto I, et al. Penetrating
atherosclerotic ulcer of the aortoa: imaging features
and disease concept. RadioGraphics. 2000;20:
995–1005.
19. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating
atherosclerotic ulcers of the thoracic aorta: natural
history and clinicopathologic correlations. Ann Vasc
Surg. 1986;1:15–23.
20. Vilacosta I, San Román JA, Aragoncillo P, et al.
Penetrating atherosclerotic aortic ulcer: documenta-
tion by transesophagealechocardiography. J Am Coll
Cardiol. 1998;32:83–89.
21. Ando Y, Minami H, Muramoto H, Narita M, Sakai S.
Rupture of thoracic aorta caused by penetrating aortic
ulcer. Chest. 1994;106:624–626.
22. Nienaber CA. Pathophysiology of acute aortic syn-
dromes. In: Baliga RR, Nienaber CA, Isselbacher
EM, Eagle KA, eds. Aortic Dissection and Related
Syndromes. 1st ed. NewYork: Springer Science;
2007:17–44.
23. Botta DM, Elefteriades JA. Matrix metalloproteinases
in aortic aneurysm and dissection. In: Elefteriades JA,
ed. Acute Aortic Disease. 1st ed. NewYork: Informa
Healthcare; 2007:131–146.
24. Wooley CF, Sparks EH, Boudoulas H. Aortic pain.
Prog Cardiovasc Dis. 1998;40:563–589.
25. Ahmad F, Cheshire N, Hamady M. Acute aortic syn-
drome: pathology and therapeutic strategies. Postgrad
Med J. 2006;82:305–312.
26. Shiga T, Wajima Z, Apfel CC, Inoue T, Ohe Y.
Diagnostic accuracy of transesophageal echocardiog-
raphy, helical computed tomography, and magnetic
resonance imaging for suspected thoracic aortic dis-
section: systematic review and meta-analysis. Arch
Intern Med. 2006;166:1350–1356.
27. Kapustin AJ, Litt HI. Diagnostic imaging for aortic
dissection. Semin Thorac Cardiovasc Surg. 2005;17:
214–223.
28. Von Kodolitsch Y, Nienbar CA, Dieckmann C, et al.
Chest radiography for the diagnosis of acute aortic
syndrome. Am J Med. 2004;116:73–77.
29. Smith AD, Schoenhagen P. CT imaging for acute
aortic syndrome. Cleve Clin J Med. 2008;75:7–9.
30. Berger F, Smithuis R, van Delden O. Thoracic Aorta –
the Acute Aortic Syndrome. www.radiologyassistant.
nl/en. Accessed May 25, 2009.
31. Reddy GP. Multidetector CT of acute aortic syndrome.
Imag Decision. 2006;2:22–26.
32. Manghat NE, Morgan-Hughes GJ, Roobottom CA.
Multi-detector row computed tomography: imaging in
acute aortic syndrome. Clin Radiol. 2005;60:1256–1267.
33. Svensson LG. Acute aortic syndromes: time to talk of
many things. Cleve Clin J Med. 2008;75:25–29.
34. Meredith EL, Masani ND. Echocardiography in the
emergency assessment of acute aortic syndromes. Eur
J Echocardiogr. 2009;10:i31–i39.
35. Hagan PG, Nienaber CA, Isselbacher EM, et al. The
International Registry of Acute Aortic Dissection
(IRAD): new insights into an old disease. JAMA.
2000;283:897–903.
36. Mehta RH, O’Gara PT, Bossone E, et al. Acute type A
aortic dissection in the elderly: clinical characteris-
tics, management, and outcomes in the current era.
J Am Coll Cardiol. 2002;40:685–692.
37. Mehta RH, Suzuki T, Hagan PG, et al. Predicting
death in patients with acute type A aortic dissection.
Circulation. 2002;105:200–206.
38. Ergin MA, O’Connor J, Guinto R, Griepp RB.
Experience with profound hypothermia and circula-
tory arrest in the treatment of aneurysms of the aortic
arch. Aortic arch replacement for acute arch dissec-
tions. J Thorac Cardiovasc Surg. 1982;84:649–655.
39. Nguyen B, Müller M, Kipfer B, et al. Different tech-
niques of distal aortic repair in acute type A dissec-
tion: impacton late aortic morphology and reoperation.
Eur J Cardiothorac Surg. 1999;15:496–500.
40. Borst HG, Walterbusch G, Schaps D. Extensive aortic
replacement using elephant trunk prosthesis. Thorac
Cardiovasc Surg. 1983;31:37–40.
41. Isselbacher EM. Dissection of the descending thoracic
aorta: looking into the future. J Am Coll Cardiol.
2007;50:805–807.
42. Heinemann MK, Buehner B, Schaefers HJ, Jurmann
MJ, Laas J, Borst HG. Malperfusion of the thoracoab-
dominal vasculature in aortic dissection. J Card Surg.
1994;9:748–755.
43. Borst HG, Laas J, Heinemann M. Type A aortic dis-
section: diagnosis and management of malperfusion
phenomena. Semin Thorac Cardiovasc Surg.
1991;3:238–241.
44. Ince H, Nienaber CA. The concept of interventional
therapy in acute aortic syndrome. J Card Surg.
2002;17:135–142.
45. Slonim SM, Miller DC, Mitchell RS, Semba CP,
Razavi MK, Dake MD. Percutaneous balloon fenes-
tration and stenting for life-threatening ischemic
complications in patients with acute aortic dissection.
J Thorac Cardiovasc Surg. 1999;117:1118–1126.
35
20. C.M. Wells and K. Subramaniam
46. Slonim SM, Nyman UR, Semba CP, Miller DC,
Mitchell RS, Dake MD. True lumen obliteration in
complicated aortic dissection: endovascular treat-
ment. Radiology. 1996;201:161–166.
47. Kato N, Shimono T, Hirano T, Ishida M, Yada I,
Takeda K. Transluminal placement of endovascular
stent-grafts for the treatment of type A aortic dissec-
tion with an entry tear in the descending thoracic
aorta. J Vasc Surg. 2001;34:1023–1028.
48. Tittle SL, Lynch RJ, Cole PE, et al. Midterm follow-up
of penetrating ulcer and intramural hematoma of the
aorta. J Thorac Cardiovasc Surg. 2002;123:1051–1059.
49. Eggebrecht H, Baumgart D, Schmermund A, et al.
Penetrating atherosclerotic ulcer of the aorta: treat-
ment by endovascular stent-graft placement. Curr
Opin Cardiol. 2003;18:431–435.
50. Song JK, Kang SJ, Song JM, et al. Factors associated
with in-hospital mortality in patients with acute aortic
syndrome involving the ascending aorta. Int J Cardiol.
2007;115:14–18.
51. Nienaber CA, Eagle KA. Aortic dissection:new
frontiers in diagnosis and management. Circulation.
2003;108:628–635.
52. Sueyoshi E, Sakamoto I, Hayashi K, Yamaguchi T,
Imada T. Growth rate of aortic diameter in patients
with type B aortic dissection during the chronic phase.
Circulation. 2004;110(11 Suppl 1):II256–II261.
53. Junoven T, Ergin MA, Galla JD, et al. Risk factors for
rupture of chronic type B dissections. J Thoac
Cardiovasc Surg. 1999;117:776–786.
54. Kaji S, Akasaka T, Boribata Y, et al. Long term prog-
nosis of patients with type A intramural hematoma.
Circulation. 2002;106:248–252.
55. Kaji S, Akasaka T, Katayama M, et al. Long term
prognosis of patients with type B intramural hema-
toma. Circulation. 2003;108:307–331.
56. Erbel R, Alfonso F, Boileau C, et al. Diagnosis and
management of aortic dissection: task force on aortic
dissection, European society of cardiology. Eur Heart
J. 2001;22:1642–1681.
36