Aortic dissection

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Sahar Memar Montazerin, M.D.[3] Laith Adnan Allaham, M.D.[4]

Synonyms and keywords: Leaking aneurysm; dissecting aortic aneurysm; aneurysm, dissecting, aorta; aortic aneurysm – dissecting

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Sahar Memar Montazerin, M.D.[3]

Overview

Dr. Frank Nicholls described the first case of aortic dissection in 1761. Later, in 1819, Dr. René Laennec used the term dissecting aneurysm for the first time. The first successful surgical intervention for aortic dissection was done by Dr. Cooley and Dr. Creech in 1954. In 1965, Dr. DeBakey suggested the first classification system for aortic dissection. In 1970, a group of surgeons suggested the simplified classification system of Stanford. In 1996, an international, referral center was registered for acute aortic dissection with the goal of registering patients’ presentation, treatment, and outcome. This registry provides information of more than 1500 patients with acute aortic dissection and may be used as a resource for this disorder. In 2006, another international registry was established in Germany for acute aortic dissection type A (AADA) with the goal of collecting patients’ information for structured follow-up. This registry with more than 2000 patients is now the largest database on AADA worldwide. Several different classification systems have been used to describe aortic dissections. The systems commonly in use are either based on either the anatomy of the dissection (proximal, distal) or the duration of onset of symptoms (acute, chronic) prior to presentation. DeBakey and Stanford’s systems are commonly used classification systems for aortic dissection. European society of cardiology defined another classification system for aortic dissection in 2014. Aortic dissection begins as a tear in the aortic wall in > 95% of patients. The tear is usually transverse, extends through the intima and halfway through the media and involves ~50% of the aortic circumference. An inherent weakness in the tunica media layer predisposes patients to develop a tear in the intima layer. Two thirds of dissections originate in the ascending aorta, and 20% are in the proximal descending aorta. Age-related changes due to atherosclerosis and uncontrolled hypertension are associated with spontaneous dissection, while blunt trauma injury and sudden deceleration in a motor vehicle accident is a major cause of aortic dissection. Aortic dissection is a life threatening entity that must be distinguished from other life threatening entities such as cardiac tamponade, cardiogenic shock, myocardial infarction, and pulmonary embolism. An aortic aneurysm is not synonymous with aortic dissection. Aneurysms are defined as a localized permanent dilation of the aorta to a diameter > 50% of normal. The incidence of aortic dissection is approximately 6 per 100,000 individuals worldwide.The incidence of aortic dissection increases with age, with a mean age of 63 years. Men are more commonly affected by aortic dissection than women. However, the prognosis tends to be worse in women due to unusual presentations. There is no racial predilection to aortic dissection. However, non-white race is associated with worse prognosis. The 30-days mortality rate of aortic dissection type A and B is approximately 47% and 13%, respectively. Common risk factors in the development of aortic dissection include aging, atherosclerosis, diabetes, hypertension and trauma. Less common risk factors include bicuspid aortic valve, cocaine abuse, coarctation of the aorta, cystic medial necrosis, a history of collagen vascular disoders, giant cell arteritis, heart surgery, pseudoxanthoma elasticum, Turner’s syndrome, tertiary syphilis and the third trimester of pregnancy. Screening guidelines state that an EKG should be obtained for all patients who present with symptoms suspicious for aortic dissection. A chest x-ray should be obtained for patients determined to be in low-risk, and moderate-risk categories, and for patients in high-risk categories, TEE, CT Angiography or MRI Angiography should be obtained. The symptoms of aortic dissection usually develop in the fifth decade of life and start with symptoms such as sudden onset chest/back pain. If left untreated, patients with aortic dissection may progress to develop aortic regurgitation, myocardial ischemia, and cardiac tamponade. The complications of aortic dissection include but not limited to aortic rupture, pericardial tamponade, myocardial ischemia, compression of nearby organs and etc. Aortic dissection carries a poor prognosis. Mortality rate differs based on the type of dissection and is higher in type A compared to type B (25% versus 12%). The diagnostic work-up of aortic dissection is highly dependent on the pretest probability of the patients as well as their hemodynamic status. In hemodynamically unstable patients, transesophageal echocardiography has the greatest value. CT scan, MRI, and transesophageal echocardiography have been observed to have similar reliability in the diagnosis of aortic dissection. However, CT and MRI have been preferred modality for assessing the extension and branch involvement in aortic dissection and diagnosing other types of acute aortic syndrome other than dissection as well as traumatic aortic lesions. History of patients with aortic dissection may be positive for factors such as connective tissue disease, known aortic valve disease, recent heart surgery, Known thoracic aortic aneurysm, and family history of the aortic disease. Sudden onset chest/back pain is the most common symptom of aortic dissection. Pain may be of sharp, ripping, tearing, and knife-like quality. Aortic dissection is commonly associated with varying blood pressure (pseudohypotension or hypertension or hypotension), wide pulse pressure (if the aortic root is involved causing aortic insufficiency), tachycardia, pulsus paradoxus, swollen face due to superior vena cava compression (superior vena cava syndrome). Radial-radial delay or radio-femoral delay (deficit) in pulse can be seen in patients depending on the location of dissection. Pulse deficit is commonly seen in females. In proximal dissections involving aortic root, aortic insufficiency is a complication, and on physical examination an early diastolic decrescendo murmur, which is best heard in the right second intercostal space is noted. There is no particular laboratory findings for the diagnosis of aortic dissection. Possible laboratory findings associated with aortic dissection may include troponin elevation, CK-MB elevation, hematuria, and etc. There has been reports of using a smooth muscle myosin heavy chain immunoassay to help diagnose aortic dissection. EKG findings in aortic dissection are usually non-specific. Possible findings include non-specific ST-segment changes, atrioventricular block (second degree), left ventricular hypertrophy, and sinus bradycardia. It worth mentioning that ECG may lead to a delay in the diagnosis. Since clinicians usually follow the diagnosis of coronary artery disease due to its higher prevalence. Chest x-ray may be helpful in the diagnosis of aortic dissection. Findings suggestive of aortic dissection on x-ray include widening of mediastinum, wide aortic contour, tracheal deviation, aortic kinking, and displacement of previous aortic calcification. Chest x-ray has limited sensitivity (64%) and specificity (86%) in the diagnosis of aortic diseases. It also worth mentioning that a normal chest x-ray may not rule out the diagnosis of aortic dissection. A CT scan can be used to diagnose aortic dissection if neither a TEE nor MRI is available in a timely fashion, or if there is a contraindication to their performance. An example would be after hours in an emergency room setting. If the results of the CT scan are non-diagnostic, then TEE or MRI should be performed to confirm the diagnosis. MRI is the imaging modality of choice in the assessment of longstanding aortic disease in a patient who has chronic chest pain who is hemodynamically stable or for the evaluation of a chronic dissection. Type A dissections of the proximal aorta are generally managed with the operative repair. The repair can be done via open surgery vs endovascular repair depending on the extent of dissection. Type B dissections of the descending aorta are generally managed medically. Even patients who are undergoing operative repair require optimal medical management. The two goals in the medical management of aortic dissection are to reduce blood pressure and to reduce the oscillatory shear on the wall of the aorta (the shear-force dP/dt or force of ejection of blood from the left ventricle). The target blood pressure should be a mean arterial pressure (MAP) of 60 to 75 mm Hg. Aortic dissection is the only hypertensive emergency where target BP is less than 120/80 within the first four hours of presentation. Ideally, the target is to control the heart rate to less than 60 per minute. The first line of agents are beta-blockers, esmolol continuous infusion is used preferably as it is short-acting and works for blood pressure as well as heart rate. IV Labetalol or PO propranolol or metoprolol can also be used. The addition of other IV continuous nitroprusside can also be used. Cyanide toxicity is a concern when nitroprusside is used for more than 24 hours. Any dissection that involves the ascending aorta is considered a surgical emergency, and urgent surgical consultation is recommended. There is a 90% 3-month mortality among patients with a proximal aortic dissection who do not undergo surgery. These patients can rapidly develop acute aortic insufficiency (AI), tamponade or myocardial infarction (MI).

Historical Perspective

Dr. Frank Nicholls described the first case of aortic dissection in 1761. Later, in 1819, Dr. René Laennec used the term dissecting aneurysm for the first time. The first successful surgical intervention for aortic dissection was done by Dr. Cooley and Dr. Creech in 1954. In 1965, Dr. DeBakey suggested the first classification system for aortic dissection. In 1970, a group of surgeons suggested the simplified classification system of Stanford. In 1996, an international, referral center was registered for acute aortic dissection with the goal of registering patients’ presentation, treatment, and outcome. This registry provides information of more than 1500 patients with acute aortic dissection and may be used as a resource for this disorder. In 2006, another international registry was established in Germany for acute aortic dissection type A (AADA) with the goal of collecting patients’ information for structured follow-up. This registry with more than 2000 patients is now the largest database on AADA worldwide.

Classification

Several different classification systems have been used to describe aortic dissections. The systems commonly in use are either based on either the anatomy of the dissection (proximal, distal) or the duration of onset of symptoms (acute, chronic) prior to presentation. DeBakey and Stanford’s systems are commonly used classification systems for aortic dissection. European society of cardiology defined another classification system for aortic dissection in 2014.

Pathophysiology

Aortic dissection begins as a tear in the aortic wall in > 95% of patients. The tear is usually transverse, extends through the intima and halfway through the media and involves ~50% of the aortic circumference. An inherent weakness in the tunica media layer predisposes patients to develop a tear in the intima layer. Two thirds of dissections originate in the ascending aorta, and 20% are in the proximal descending aorta.

Causes

Age-related changes due to atherosclerosis and uncontrolled hypertension are associated with spontaneous dissection, while blunt trauma injury and sudden deceleration in a motor vehicle accident is a major cause of aortic dissection.

Differentiating Aortic Dissection from other Diseases

Aortic dissection is a life threatening entity that must be distinguished from other life threatening entities such as cardiac tamponade, cardiogenic shock, myocardial infarction, and pulmonary embolism. An aortic aneurysm is not synonymous with aortic dissection. Aneurysms are defined as a localized permanent dilation of the aorta to a diameter > 50% of normal.

Epidemiology and Demographics

The incidence of aortic dissection is approximately 6 per 100,000 individuals worldwide.The incidence of aortic dissection increases with age, with a mean age of 63 years. Men are more commonly affected by aortic dissection than women. However, the prognosis tends to be worse in women due to unusual presentations. There is no racial predilection to aortic dissection. However, non-white race is associated with worse prognosis. The 30-days mortality rate of aortic dissection type A and B is approximately 47% and 13%, respectively.

Risk Factors

Common risk factors in the development of aortic dissection include aging, atherosclerosis, diabetes, hypertension and trauma. Less common risk factors include bicuspid aortic valve, cocaine abuse, coarctation of the aorta, cystic medial necrosis, a history of collagen vascular disoders, giant cell arteritis, heart surgery, pseudoxanthoma elasticum, Turner’s syndrome, tertiary syphilis and the third trimester of pregnancy.

Screening

Screening guidelines state that an EKG should be obtained for all patients who present with symptoms suspicious for aortic dissection. A chest x-ray should be obtained for patients determined to be in low-risk, and moderate-risk categories, and for patients in high-risk categories, TEE, CT Angiography or MRI Angiography should be obtained.

Natural History, Complications and Prognosis

The symptoms of aortic dissection usually develop in the fifth decade of life and start with symptoms such as sudden onset chest/back pain. If left untreated, patients with aortic dissection may progress to develop aortic regurgitation, myocardial ischemia, and cardiac tamponade. The complications of aortic dissection include but not limited to aortic rupture, pericardial tamponade, myocardial ischemia, compression of nearby organs and etc. Aortic dissection carries a poor prognosis. Mortality rate differs based on the type of dissection and is higher in type A compared to type B (25% versus 12%).

Diagnosis

Diagnostic Study of Choice

The diagnostic work-up of aortic dissection is highly dependent on the pretest probability of the patients as well as their hemodynamic status. In hemodynamically unstable patients, transesophageal echocardiography has the greatest value. CT scan, MRI, and transesophageal echocardiography have been observed to have similar reliability in the diagnosis of aortic dissection. However, CT and MRI have been preferred modality for assessing the extension and branch involvement in aortic dissection and diagnosing other types of acute aortic syndrome other than dissection as well as traumatic aortic lesions.

History and Symptoms

History of patients with aortic dissection may be positive for factors such as connective tissue disease, known aortic valve disease, recent heart surgery, Known thoracic aortic aneurysm, and family history of the aortic disease. Sudden onset chest/back pain is the most common symptom of aortic dissection. Pain may be of sharp, ripping, tearing, and knife-like quality.

Physical Examination

Aortic dissection is commonly associated with varying blood pressure (pseudohypotension or hypertension or hypotension), wide pulse pressure (if the aortic root is involved causing aortic insufficiency), tachycardia, pulsus paradoxus, swollen face due to superior vena cava compression (superior vena cava syndrome). Radial-radial delay or radio-femoral delay (deficit) in pulse can be seen in patients depending on the location of dissection. Pulse deficit is commonly seen in females. In proximal dissections involving aortic root, aortic insufficiency is a complication, and on physical examination an early diastolic decrescendo murmur, which is best heard in the right second intercostal space is noted.

Laboratory Findings

There is no particular laboratory findings for the diagnosis of aortic dissection. Possible laboratory findings associated with aortic dissection may include troponin elevation, CK-MB elevation, hematuria, and etc. There has been reports of using a smooth muscle myosin heavy chain immunoassay to help diagnose aortic dissection.

Electrocardiogram

EKG findings in aortic dissection are usually non-specific. Possible findings include non-specific ST-segment changes, atrioventricular block (second degree), left ventricular hypertrophy, and sinus bradycardia. It worth mentioning that ECG may lead to a delay in the diagnosis. Since clinicians usually follow the diagnosis of coronary artery disease due to its higher prevalence.

Imaging in Acute Aortic Dissection

There are a wide variety of imaging studies that can be used to diagnose aortic dissection, but in general, transesophageal imaging is the imaging modality of choice in the acutely ill patient and CT Angiography, MRI is the imaging modality of choice in the assessment of longstanding aortic disease in a patient who has chronic chest pain who is hemodynamically stable or for the evaluation of a chronic dissection.

Chest X-ray

Chest x-ray may be helpful in the diagnosis of aortic dissection. Findings suggestive of aortic dissection on x-ray include widening of mediastinum, wide aortic contour, tracheal deviation, aortic kinking, and displacement of previous aortic calcification. Chest x-ray has limited sensitivity (64%) and specificity (86%) in the diagnosis of aortic diseases. It also worth mentioning that a normal chest x-ray may not rule out the diagnosis of aortic dissection.

CT

A CT scan can be used to diagnose aortic dissection if neither a TEE nor MRI is available in a timely fashion, or if there is a contraindication to their performance. An example would be after hours in an emergency room setting. If the results of the CT scan are non-diagnostic, then TEE or MRI should be performed to confirm the diagnosis.

MRI

MRI is the imaging modality of choice in the assessment of longstanding aortic disease in a patient who has chronic chest pain who is hemodynamically stable or for the evaluation of a chronic dissection.

Echocardiography

The echocardiographic changes diagnostic of aortic dissection include Intimal flaps in the aorta obstruction of a false lumen, intimal calcification displacement toward the center of the lumen, separation of intimal layers from the thrombus, and shearing of different wall layers during aortic pulsation. The sensitivity and specificity of transthoracic echocardiography vary based on the type of dissection and are usually lower for the diagnosis of distally located aortic dissection. Echocardiography may also show severe pleural effusion, which is suggestive of the development of cardiac tamponade. Transesophageal echocardiography may be useful in the diagnosis of aortic dissection in patients in whom transthoracic echocardiography has limited efficacy. Prolapse of intimal flap through the aortic valve seen in transesophageal echocardiography is diagnostic of aortic dissection complicated by aortic regurgitation. Sensitivity is usually higher (99%). However, it has limited usage in the diagnosis of dissections involving the distal portion of ascending aorta.

Treatment

Medical Therapy

Type A dissections of the proximal aorta are generally managed with the operative repair. The repair can be done via open surgery vs endovascular repair depending on the extent of dissection. Type B dissections of the descending aorta are generally managed medically. Even patients who are undergoing operative repair require optimal medical management. The two goals in the medical management of aortic dissection are to reduce blood pressure and to reduce the oscillatory shear on the wall of the aorta (the shear-force dP/dt or force of ejection of blood from the left ventricle). The target blood pressure should be a mean arterial pressure (MAP) of 60 to 75 mmHg. Aortic dissection is the only hypertensive emergency where target BP is less than 120/80 within the first four hours of presentation. Ideally, the target is to control the heart rate to less than 60 per minute. The first line of agents are beta-blockers, esmolol continuous infusion is used preferably as it is short-acting and works for blood pressure as well as heart rate. IV Labetalol or PO propranolol or metoprolol can also be used. The addition of other IV continuous nitroprusside can also be used.Cyanide toxicity is a concern when nitroprusside is used for more than 24 hours.

Surgery

Any dissection that involves the ascending aorta is considered a surgical emergency, and urgent surgical consultation is recommended. There is a 90% 3-month mortality among patients with a proximal aortic dissection who do not undergo surgery. These patients can rapidly develop acute aortic insufficiency (AI), tamponade or myocardial infarction (MI).

Secondary Prevention

Proper treatment and control of hardening of the arteries (atherosclerosis) and high blood pressure may reduce risk of aortic dissection. It is very important for patients at risk for dissection to tightly control their blood pressure. Taking safety precautions to prevent injuries can help prevent dissections. Many cases of aortic dissection cannot be prevented. If diagnosed with Marfan or Ehlers-Danlos syndrome, regular follow-up is advisable.

Template:WH Template:WS CME Category::Cardiology

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

Dr. Frank Nicholls described the first case of aortic dissection in 1761. Later, in 1819, Dr. René Laennec used the term dissecting aneurysm for the first time. First successful surgical intervention for aortic dissection was done by Dr. Cooley and Dr. Creech in 1954. In 1965, Dr. DeBakey suggested the first classification system for aortic dissection. In 1970, a group of surgeons suggested the simplified classification system of Stanford. In 1996, an international, referral center was registered for acute aortic dissection with the goal of registering patients presentation, treatment, and outcome. This registry provides information of more than 1500 patients with acute aortic dissection and may be used as a resource for this disorder. In 2006, another international registry was established in Germany for acute aortic dissection type A (AADA) with the goal of collecting patients information for structured follow-up. This registry of more than 2000 patients is now the largest database on AADA worldwide.

Historical Perspective

Discovery

In 1761, Dr. Frank Nicholls described the first case of aortic dissection.^[1]
In 1965, Dr. DeBakey suggested the first classification system for aortic dissection.^[2]

Landmark Events in the Development of Treatment Strategies

First successful surgical intervention for aortic dissection was done by Dr. Cooley and Dr. Creech in 1954.^[3]
In 1970, a group of surgeons suggested the simplified classification system of Stanford.^[4]
In 1996, an international, referral center was registered for acute aortic dissection with the goal of registering patients presentation, treatment, and outcome. This registry provides information of more than 1500 patients with acute aortic dissection and may be used as a resource for this disorder.^[5]
In 2006, another international registry was established in Germany for acute aortic dissection type A (AADA) with the goal of collecting patients information for structured follow-up. This registry of more than 2000 patients is now the largest database on AADA worldwide.^[6]^[7]

Impact on Cultural History

In 1819, Dr. René Laennec used the term dissecting aneurysm for the first time.^[8]

Famous Cases

The following are the famous cases of aortic dissection:^[9]

George II, King of England
Dr. Michael DeBakey

References

↑ “LI. Observations concerning the body of his late Majesty, October 26, 1760”. Philosophical Transactions of the Royal Society of London. 52: 265–275. 1761. doi:10.1098/rstl.1761.0052. ISSN 0261-0523.
↑ DEBAKEY ME, HENLY WS, COOLEY DA, MORRIS GC, CRAWFORD ES, BEALL AC (January 1965). “SURGICAL MANAGEMENT OF DISSECTING ANEURYSMS OF THE AORTA”. J. Thorac. Cardiovasc. Surg. 49: 130–49. PMID 14261867.
↑ De Bakey, Michael E.; Cooley, Denton A.; Creech, Oscar (1955). “Surgical Considerations of Dissecting Aneurysm of the Aorta”. Annals of Surgery. 142 (4): 586–612. doi:10.1097/00000658-195510000-00005. ISSN 0003-4932.
↑ Daily, Pat O.; Trueblood, H. Ward; Stinson, Edward B.; Wuerflein, Robert D.; Shumway, Norman E. (1970). “Management of Acute Aortic Dissections”. The Annals of Thoracic Surgery. 10 (3): 237–247. doi:10.1016/S0003-4975(10)65594-4. ISSN 0003-4975.
↑ Hagan, Peter G.; Nienaber, Christoph A.; Isselbacher, Eric M.; Bruckman, David; Karavite, Dean J.; Russman, Pamela L.; Evangelista, Arturo; Fattori, Rossella; Suzuki, Toru; Oh, Jae K.; Moore, Andrew G.; Malouf, Joseph F.; Pape, Linda A.; Gaca, Charlene; Sechtem, Udo; Lenferink, Suzanne; Deutsch, Hans Josef; Diedrichs, Holger; Marcos y Robles, Jose; Llovet, Alfredo; Gilon, Dan; Das, Sugata K.; Armstrong, William F.; Deeb, G. Michael; Eagle, Kim A. (2000). “The International Registry of Acute Aortic Dissection (IRAD)”. JAMA. 283 (7): 897. doi:10.1001/jama.283.7.897. ISSN 0098-7484.
↑ Conzelmann, L.O.; Krüger, T.; Hoffmann, I.; Rylski, B.; Easo, J.; Oezkur, M.; Kallenbach, K.; Dapunt, O.; Karck, M.; Weigang, E. (2011). “Deutsches Register für akute Aortendissektion Typ A (GERAADA)”. Herz. 36 (6): 513–524. doi:10.1007/s00059-011-3512-x. ISSN 0340-9937.
↑ Weigang, E.; Rylski, B.; Krüger, T.; Easo, J.; Conzelmann, L.O.; Karck, M.; Boening, A. (2016). “German Registry for Acute Aortic Dissection Type A: Structure, Results, and Future Perspectives”. The Thoracic and Cardiovascular Surgeon. 65 (02): 077–084. doi:10.1055/s-0036-1572436. ISSN 0171-6425.
↑ Criado FJ (2011). “Aortic dissection: a 250-year perspective”. Tex Heart Inst J. 38 (6): 694–700. PMC 3233335. PMID 22199439.
↑ Leonard, J C (1979). “Thomas Bevill Peacock and the early history of dissecting aneurysm”. BMJ. 2 (6184): 260–262. doi:10.1136/bmj.2.6184.260. ISSN 0959-8138.

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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Sahar Memar Montazerin, M.D.[3]

Overview

Several different classification systems have been used to describe aortic dissections. The systems commonly in use are either based on either the anatomy of the dissection (proximal, distal) or the duration of onset of symptoms (acute, chronic) prior to presentation. DeBakey and Stanford systems are the commonly used classification systems for aortic dissection. European society of cardiology defined another classification system for aortic dissection in 2014.

Classification

Several classification systems have been suggested for the description of aortic dissection.^[1]^[2]^[3]^[4]
The commonly used classifications for aortic dissection are either based on the timing of the symptoms or the anatomy of the dissection.
DeBakey and Stanford systems are the commonly used classification systems for aortic dissection.

DeBakey Classification System

The DeBakey system classifies aortic dissection based on anatomy of the aorta. It classifies the dissection according to the intimal tear location.^[5]

Type I – Intimal tear is located in ascending aorta, spreads at least to the aortic arch and often beyond it distally.
Type II –Intimal tear is located and limited to the ascending aorta.
Type III – Intimal tear is located in descending aorta, rarely extends proximally.

Type III A: Dissection limited to the descending thoracic aorta
Type III B: Dissection extended below the diaphragm


Percentage	60 %	10-15 %	25-30 %
Type	DeBakey I	DeBakey II	DeBakey III
	Stanford A		Stanford B
	Proximal		Distal
Classification of aortic dissection

Stanford Classification System

Stanford classification system is based on the involvement of ascending aorta.^[6]

A = Type I and II DeBakey
B = Type III Debakey

Dissection of the aorta descendens (3), which starts from the left subclavian artery, reaching to the abdominal aorta (4). Aorta ascendens (1) and aortic arch (2) are not involved.

Aortic dissection may be classified according to the timing of symptom presentation to the following:
- Acute (<14 days)
- Sub-acute (15-90 days)
- Chronic (>90 days)

References

↑ Nienaber CA, Eagle KA (August 2003). “Aortic dissection: new frontiers in diagnosis and management: Part I: from etiology to diagnostic strategies”. Circulation. 108 (5): 628–35. doi:10.1161/01.CIR.0000087009.16755.E4. PMID 12900496.
↑ Tsai TT, Nienaber CA, Eagle KA (December 2005). “Acute aortic syndromes”. Circulation. 112 (24): 3802–13. doi:10.1161/CIRCULATIONAHA.105.534198. PMID 16344407.
↑ DEBAKEY ME, HENLY WS, COOLEY DA, MORRIS GC, CRAWFORD ES, BEALL AC (January 1965). “SURGICAL MANAGEMENT OF DISSECTING ANEURYSMS OF THE AORTA”. J. Thorac. Cardiovasc. Surg. 49: 130–49. PMID 14261867.
↑ Daily PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway NE (September 1970). “Management of acute aortic dissections”. Ann. Thorac. Surg. 10 (3): 237–47. doi:10.1016/s0003-4975(10)65594-4. PMID 5458238.
↑ DeBakey ME, Henly WS, Cooley DA, Morris GC Jr, Crawford ES, Beall AC Jr. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1965;49:130-49. PMID 14261867.
↑ Daily PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway NE. Management of acute aortic dissections. Ann Thorac Surg 1970;10:237-47. PMID 5458238.

Template:WH Template:WS CME Category::Cardiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] Sahar Memar Montazerin, M.D.[3]

Overview

Aortic dissection begins as a tear in the aortic wall in > 95% of patients. The tear is usually transverse, extends through the intima and halfway through the media and involves ~50% of the aortic circumference. Two thirds of dissections originate in the ascending aorta, and 20% are in the proximal descending aorta.

Pathophysiology

Normal Anatomy of the Aorta

As with all other arteries, the aorta is made up of three layers. The layer that is in direct contact with the flow of blood is the tunica intima, commonly called the intima. This layer is made up of mainly endothelial cells. Just deep to this layer is the tunica media, known as the media. This middle layer is made up of smooth muscle cells and elastic tissue. The outermost layer (furthest from the flow of blood) is known as the tunica adventitia or the adventitia. This layer is composed of connective tissue.

Blood penetrates the intima and enters the media layer.

Pathogenesis

Initial Intimal Tear

Aortic dissection begins as a tear in the aortic wall in > 95% of patients.
It is usually transverse, extends through the intima and halfway through the media and involves ~50% of the aortic circumference.

Location of Dissections

The initial tear is usually within 100 mm of the aortic valve.
65% of dissections originate in the ascending aorta, distal to the aortic valve and coronary ostia
10% arise in the transverse aortic arch
20% in the proximal descending aorta
5% in the more distal descending aorta

Propagation of the Intimal Tear

In an aortic dissection, blood penetrates the intima and enters the media layer. The high pressure rips the tissue of the media apart, allowing more blood to enter. This can propagate along the length of the aorta for a variable distance, dissecting either towards or away from the heart or both.

Once a tear develops, blood then passes into the media, and a false lumen is dissected in the outer layer of aortic media involving ~50% of the aortic circumference. This false lumen can enlarge, and compress the true lumen, as well as extend proximally or distally and occlude aortic branches. For some unknown reason, the right lateral wall of the ascending aorta is the most common site for dissection. The right coronary artery can become occluded as a result of this propagation.

Separating the false lumen from the true lumen is a layer of intimal tissue. This tissue is known as the intimal flap. As blood flows down the false lumen, it may cause secondary tears in the intima. Through these secondary tears, the blood can re-enter the true lumen.

Aortic Dissection in the Absence of an Intimal Tear

In about 13% of aortic dissections, there is no evidence of an intimal tear. It is believed that in these cases the inciting event is an intramural hematoma (caused by hemorrhage within the media). Since there is no direct connection between the true lumen and the false lumen in these cases, it is difficult to diagnose an aortic dissection by aortography if the etiology is an intramural hematoma. An aortic dissection secondary to an intramural hematoma should be treated the same as one caused by an intimal tear.

An aortic intramural hematoma can form when the vasa vasorum ruptures into the aortic wall. This is distinguished from dissection by the lack of an intimal tear. This disorder parallels aortic dissection in terms of prognosis when the ascending aorta or aortic arch is involved, and rapid surgical intervention is indicated. Involvement of the descending aorta, however, carries a better prognosis than dissection, and outcome tends to be similar with medical or surgical therapy.

Genetics

Genes involved in the pathogenesis of aortic dissection include:^[1]^[2]

FBN1 (fibrillin-1)
LOX (lysyl oxidase)
MYH11 (smooth muscle myosin heavy chain 11)
ACTA2 (smooth muscle α-actin 2)
MYLK (myosin light chain kinase)
PRKG1 (protein kinase cGMP-dependent type 1)
COL3A1 (α-1 procollagen, type III)
TGFBR1 (TGF-β receptor type I)
TGFBR2 (TGF-β receptor type II)
TGFB2
SMAD3 (mothers against decapentaplegic drosophila homolog 3)

Associated Conditions

Conditions associated with aortic dissection include:^[1]

Gross Pathology

Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Dissecting Aneurysm: Gross fixed tissue external view of heart aortic arch and descending aorta showing dilated first and second portion of arch from anterior projection.
Dissecting Aneurysm: Gross, a very good example of dissection beginning just above aortic ring.
Dissecting Aneurysm: Gross dissection first portion of arch fixed specimen (a good example).

Dissecting Aneurysm: Gross very good example dissected channel has been opened.
Dissecting Aneurysm: Gross external view good appearance from adventitia.
Dissecting Aneurysm: Gross opened false channel.

Dissecting Aneurysm: Gross good example dissection beginning at third portion aortic arch.
Dissecting Aneurysm: Gross cross sections showing thrombus in false lumen. True lumen has been opened longitudinally.
Dissecting Aneurysm: Gross shows origin just above aortic valve false channel shown in descending thoracic aorta (very good example).

Dissecting Aneurysm: Gross, an excellent example, starting just above the aortic valve with reflection of aorta to show the dissection tract and some thrombus
Dissecting Aneurysm: Gross shows dilated aorta with extensive atherosclerosis dissection is seen, a small abdominal aorta atherosclerotic aneurysm is present good for association of dilation with dissection
Dissecting Aneurysm: Gross arrow points to start of dissection in first portion aortic arch good but not the best example shows dilation
Dissecting Aneurysm: Gross, very good to show start of dissection above aortic valve and blood in false channel.

Dissecting Aneurysm: Gross, heart with root of aorta to show hemorrhage into pericardium (a very good example).
Dissecting Aneurysm: Gross, of heart and aorta with dissection and large false channel (a good example).
Dissecting Aneurysm: Gross cross section of aorta with two channels (a good example).
Dissecting Aneurysm: Gross good example angular tear above aortic valve.

Dissecting Aneurysm: Gross good example of typical angular tear above aortic valve.
Dissecting Aneurysm: Gross, rather well shown dissection in first portion of the aortic arch
Dissecting Aneurysm: Gross, rather well shown dissection in first portion of the aortic arch
Dissecting Aneurysm: Gross, an excellent example of type I lesion

Dissecting Aneurysm: Gross, external view, an excellent example
Dissecting Aneurysm: Gross, Type I shows false channel
Dissecting Aneurysm: Gross, opened to show false channel (good example)
Dissecting Aneurysm: Gross, large tear in first portion of aortic arch, annuloaortic ectasia

Dissecting Aneurysm: Gross, coagulum of blood in false channel
Dissecting Aneurysm: Gross, aortic valve area dissection (well shown, typical lesion)
Dissecting Aneurysm: Gross, external view of heart and first portion of aortic arch, annuloaortic ectasia, hemorrhage beneath adventitia is evidence of dissection
Dissecting Aneurysm in a patient with Marfan’s syndrome

Dissecting Aneurysm: Gross, fixed tissue, descending thoracic segment dissection opened to show the false channel. The true surface is also visible
Dissecting Aneurysm: Gross natural color descending aorta opened into false channel
Dissecting Aneurysm: Gross natural color close-up view of aortic valve and proximal aortic arch with ruptured intima rather good illustration of this lesion
Dissecting Aneurysm Chronic: Gross natural color first portion of aortic arch with intimal rent well shown with healed margins and view into false channel that shows a surface looking like atherosclerosis which is known to develop in a chronic dissection
Dissecting Aneurysm Chronic: Gross, natural color, closer view of the previous one (a very good example)

Microscopic Pathology

References

↑ ^1.0 ^1.1 Pinard, Amélie; Jones, Gregory T.; Milewicz, Dianna M. (2019). “Genetics of Thoracic and Abdominal Aortic Diseases”. Circulation Research. 124 (4): 588–606. doi:10.1161/CIRCRESAHA.118.312436. ISSN 0009-7330.
↑ Verhagen, Judith M.A.; Kempers, Marlies; Cozijnsen, Luc; Bouma, Berto J.; Duijnhouwer, Anthonie L.; Post, Jan G.; Hilhorst-Hofstee, Yvonne; Bekkers, Sebastiaan C.A.M.; Kerstjens-Frederikse, Wilhelmina S.; van Brakel, Thomas J.; Lambermon, Eric; Wessels, Marja W.; Loeys, Bart L.; Roos-Hesselink, Jolien W.; van de Laar, Ingrid M.B.H. (2018). “Expert consensus recommendations on the cardiogenetic care for patients with thoracic aortic disease and their first-degree relatives”. International Journal of Cardiology. 258: 243–248. doi:10.1016/j.ijcard.2018.01.145. ISSN 0167-5273.
↑ Case courtesy of Wikimedia Commons

Template:WH Template:WS CME Category::Cardiology

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vendhan Ramanujam M.B.B.S [2] Sahar Memar Montazerin, M.D.[3]

Overview

Atherosclerosis and hypertension are associated with spontaneous aortic dissection, while blunt trauma and sudden deceleration in a motor vehicle accident are major causes of traumatic aortic dissection.

Causes

Common Causes

The most common causes of aortic dissection include:^[1]^[2]^[3]^[4]^[5]

Causes by Organ System

Causes of aortic dissection include:^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]^[14]

Cardiovascular	Atherosclerosis, bicuspid aortic valve, hypertension, malignant hypertension, ruptured aortic arch with aberrant left subclavian artery, seat belt aorta, vasculitis
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Methonium
Ear Nose Throat	No underlying causes
Endocrine	Cushing’s syndrome
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	Aneurysms osteoarthritis syndrome, annuloaortic ectasia, bicuspid aortic valve, Ehlers-Danlos syndrome, Erdheim’s cystic medial necrosis, familial aortic dissection, fibromuscular dysplasia, Loeys-Dietz syndrome, Marfan syndrome, mutation of TGF-β receptor genes, mutations in genes encoding α-actin and β-myosin, mutations in SMAD3, mutations in the gene encoding filamin A, Noonan syndrome, osteogenesis imperfecta, pseudoxanthoma elasticum, Turner syndrome
Hematologic	No underlying causes
Iatrogenic	Aortic valve replacement surgery, cardiac catheterization, coronary artery bypass graft surgery, implantation of stent graft, intra-aortic balloon pump, mitral valve replacement surgery, surgical correction of aortic coarctation
Infectious Disease	AIDS, annuloaortic ectasia, aortitis, syphilitic aortitis
Musculoskeletal/Orthopedic	Ehlers-Danlos syndrome, osteogenesis imperfecta
Neurologic	No underlying causes
Nutritional/Metabolic	Homocystinuria
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Ophthalmologic	No underlying causes
Overdose/Toxicity	Cocaine abuse
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	Polycystic kidney disease
Rheumatology/Immunology/Allergy	Aortitis, arteritis, Behçet’s disease, giant cell arteritis, rheumatoid arthritis, scleroderma, systemic lupus erythematosus, Takayasu arteritis, vasculitis
Sexual	No underlying causes
Trauma	Chest trauma, deceleration injuries, motor vehicle accident, seat belt aorta
Urologic	No underlying causes
Miscellaneous	Connective tissue disorders, heavy exercise, idiopathic

For more information on potential risk factors for the development of aortic dissection click here.

References

↑ Penn JL, Martindale JL, Milne LW, Marill KA (2015). “Aortic dissection associated with blunt chest trauma diagnosed by elevated D-dimer”. Int J Surg Case Rep. 10: 76–9. doi:10.1016/j.ijscr.2015.03.027. PMC 4429846. PMID 25805614.
↑ Weissmann-Brenner A, Schoen R, Divon MY (2004). “Aortic dissection in pregnancy”. Obstet Gynecol. 103 (5 Pt 2): 1110–3. doi:10.1097/01.AOG.0000124984.82336.43. PMID 15121626.
↑ Brooke V, Goswami S, Mohanty A, Kasi PM (2012). “Aortic dissection and renal failure in a patient with severe hypothyroidism”. Case Rep Med. 2012: 842562. doi:10.1155/2012/842562. PMC 3399550. PMID 22829842.
↑ “Classification of diabetic retinopathy from fluorescein angiograms. ETDRS report number 11. Early Treatment Diabetic Retinopathy Study Research Group”. Ophthalmology. 98 (5 Suppl): 807–22. 1991. PMID 2062514.
↑ Cury M, Zeidan F, Lobato AC (2013). “Aortic disease in the young: genetic aneurysm syndromes, connective tissue disorders, and familial aortic aneurysms and dissections”. Int J Vasc Med. 2013: 267215. doi:10.1155/2013/267215. PMC 3557640. PMID 23401778.
↑ Larson, Eric W.; Edwards, William D. (1984). “Risk factors for aortic dissection: A necropsy study of 161 cases”. The American Journal of Cardiology. 53 (6): 849–855. doi:10.1016/0002-9149(84)90418-1. ISSN 0002-9149.
↑ Januzzi, James L; Isselbacher, Eric M; Fattori, Rossella; Cooper, Jeanna V; Smith, Dean E; Fang, Jianming; Eagle, Kim A; Mehta, Rajendra H; Nienaber, Christoph A; Pape, Linda A (2004). “Characterizing the young patient with aortic dissection: results from the international registry of aortic dissection (IRAD)”. Journal of the American College of Cardiology. 43 (4): 665–669. doi:10.1016/j.jacc.2003.08.054. ISSN 0735-1097.
↑ “Correspondence”. The Annals of Thoracic Surgery. 67 (2): 593. 1999. doi:10.1016/S0003-4975(99)00037-5. ISSN 0003-4975.
↑ Losenno, Katie L.; Goodman, Robert L.; Chu, Michael W. A. (2012). “Bicuspid Aortic Valve Disease and Ascending Aortic Aneurysms: Gaps in Knowledge”. Cardiology Research and Practice. 2012: 1–16. doi:10.1155/2012/145202. ISSN 2090-8016.
↑ Senaha S, Uezu T, Shimoji M, Akasaki M (March 2015). “[Stanford type B aortic dissection associated with coarctation of the aorta]”. Kyobu Geka (in Japanese). 68 (3): 184–7. PMID 25743550.
↑ Dioguardi GS, Pimenta J, Knoplich J, Ghorayeb N, Ramos LR, Giannini SD (June 1994). “[Risk factors for cardiovascular diseases in physicians. Preliminary data from the VIDAM Project of the Paulista Medical Association]”. Arq. Bras. Cardiol. (in Portuguese). 62 (6): 383–8. PMID 7826227.
↑ Caglayan, Ahmet Okay; Dundar, Munis (2009). “Inherited diseases and syndromes leading to aortic aneurysms and dissections”. European Journal of Cardio-Thoracic Surgery. 35 (6): 931–940. doi:10.1016/j.ejcts.2009.01.006. ISSN 1010-7940.
↑ “Acute aortic dissection: pathogenesis, risk factors and diagnosis”. Swiss Medical Weekly. 147 (3334). 2017. doi:10.4414/smw.2017.14489. ISSN 1424-7860.
↑ Increased maternal cardiovascular mortality associated with pregnancy in women with Turner syndrome.

Template:WH Template:WS CME Category::Cardiology

Differentiating Aortic Dissection from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]Cafer Zorkun, M.D., Ph.D. [3]

Overview

Aortic dissection is a life threatening entity that must be distinguished from other life threatening entities such as cardiac tamponade, cardiogenic shock, myocardial infarction, and pulmonary embolism. An aortic aneurysm is not synonymous with aortic dissection. Aneurysms are defined as a localized permanent dilation of the aorta to a diameter > 50% of normal.

Differentiating Aortic Dissection from other Diseases

Differentiating Aortic Dissection from other Diseases on the Basis of Chest Pain

The following table outlines the major differential diagnoses of Chest Pain..^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]^[14]^[15]^[16]^[17]^[18]^[19]^[20]^[21]^[22]^[23]^[24]^[25]^[26]^[27]^[28]^[29]^[30]^[31]^[32]^[33]^[34]^[35]^[36]

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell); Coronary CT angiography (CCTA); multidetector row scanners (MDCT); Cardiovascular magnetic resonance — CMRI; Myocardial perfusion imaging (MPI); single-photon emission CT (SPECT); Positron emission tomography (PET) scanning; Magnetic resonance (MR) angiography, Computed tomographic (CT) angiography, and Transesophageal echocardiography (TEE), late gadolinium enhancement (LGE); right ventricular hypertrophy (RVH), right atrial enlargement (RAE), functional tricuspid regurgitation (TR), Pulmonary artery systolic pressure (PASP; adenosine deaminase (ADA); Serum amyloid A (SAA), soluble interleukin-2 receptor (sIL2R); High-resolution CT (HRCT) scanning

Differentials on the basis of Etiology	Disease	Clinical manifestations										Diagnosis
		Symptoms								Risk factors	Physical exam	Lab Findings	EKG	Imaging	Gold standard
		Onset	Duration	Quality of Pain	Cough	Fever	Dyspnea	Weight loss	Associated Features	Risk factors	Physical exam	Lab Findings	EKG	Imaging	Gold standard
	Stable Angina^[37]	Sudden (acute)	2-10 minutes	Heaviness/pressure/ tightness/squeezing/ burning (Levine’s sign) Retrosternal or left sided chest pain	–	–	+/-	–	Nausea and vomiting Diaphoresis	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	Transient third heart sound (S3 – ventricular filling sound) and fourth heart sound (S4 – atrial filling sound)	Cardiac enzymes normal	Exercise EKG: ST-segment depression	Exercise Stress Testing: Decreased myocardial perfusion Transthoracic echocardiography: Ejection fraction <50 percent	Coronary angiography
	Unstable Angina^[38]^[39]^[40]	Acute	10-20 minutes	Same as stable angina but often more severe	–	–	+	–	Nausea and vomiting Diaphoresis Presyncope Palpitations	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	Reverse splitting of the second heart sound Rales or crackles Elevated jugular venous pressure	Cardiac biomarkers [Cardiac troponin I, cardiac troponin T and MB isoenzyme of creatine kinase (CK-MB)] normal	ST-depression New T wave inversions Transient ST-elevation	Echocardiography: Ejection fraction <50 percent Exercise Stress Testing: Decreased myocardial perfusion	Invasive coronary angiography
	Myocardial Infarction^[1]^[2]^[3]^[4]	Acute	Commonly > 20 minutes	Same as stable angina but often more severe	–	–	+	–	Nausea and vomiting Diaphoresis Presyncope Palpitations Lateral displacement of the apical impulse	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	Hypotension Tachycardia S4 gallop Paradoxical splitting of S2 Mitral regurgitation murmur	Elevated cardiac enzymes ↑B-Type Natriuretic Peptide	ST elevation MI (STEMI) Non-ST elevation MI (NSTEMI) or Non Q wave	Echocardiography: ↓ EF CCTA: Coronory artery stenosis CMRI: Coronory vessels stenosis MPI on SPECT or PET scanning: Decreased myocardial perfusion.	CCTA combined with MPI
Cardiac	Vasospastic/ Prinzmetal/ Variant Angina^[41]^[42]	Gradual in onset and offset	Episodic, gradual in onset and offset	Chest discomfort described as squeezing, tightness, pressure, constriction, strangling, burning, heart burn, fullness in the chest, a band-like sensation, knot in the center of the chest, lump in the throat, ache, and heavy weight on chest	–	–	+	–	Nausea, diaphoresis, dizziness, dyspnea, and palpitations Associated with other vasospastic disorders, such as Raynaud’s phenomenon and migraine headache	Multiple drugs (ephedrine-based products, cocaine, marijuana, alcohol, butane, sumatriptan, and amphetamines) Food-born botulism Guide wire or balloon dilatation while doing PCI Magnesium deficiency	Tachycardia, hypertension, diaphoresis, and a gallop rhythm	Urine drug screen may be positive for cocaine or other drugs	Transient (less than 15 minutes) ischemic ST changes in multiple leads A tall and broad R wave, Disappearance of the S wave A taller T wave Negative U waves	Stress testing: normal noninvasive stress test, exercise-induced spasm with ST-segment elevation, Stress echocardiography with ergonovine provocation: Vasospasm of coronory vessels Coronary arteriography: Epicardial spasm	Coronary arteriography
	Aortic Dissection^[43]^[44]	Sudden severe progressive pain (common) or chronic (rare)	Variable	Tearing, ripping sensation, knife like	–	–	+	–	Focal neurologic deficit Hypotension	Hypertension Genetically mediated collagen disorders Preexisting aortic aneurysm Bicuspid aortic valve Aortic coarctation Turner syndrome Vasculitis (giant cell arteritis, Takayasu arteritis, rheumatoid arthritis, syphilitic aortitis)	Pulse deficit New diastolic murmur Diastolic decrescendo murmur Focal neurologic deficit Hypotension	D-dimer <500 ng/mL rules out aortic dissection ↑Soluble ST2 (sST2) Measurements of soluble elastin fragments, smooth muscle myosin heavy chain, high-sensitivity C-reactive protein, fibrinogen, and fibrillin fragments	Nonspecific ST and T wave changes	CXR: Mediastinal and/or aortic widening CTA: A compressed true lumen MRA: Detects differential flow between the true and false lumens, widening of the aorta with a thickened wall TEE: Intimal dissection flaps, true and false lumens, thrombosis in the false lumen Aortography: Distortion of the normal contrast column, Flow reversal or stasis into a false channel, Failure of major branches to fill, and Aortic valvular regurgitation	CT angiography Digital subtraction aortography (if high suspicion)
	Aortic intramural hematoma	Sudden severe progressive pain (common) or chronic (rare)	Variable	Tearing, ripping sensation, knife like	–	–	+	–	Focal neurologic deficit Hypotension	Hypertension Genetically mediated collagen disorders Preexisting aortic aneurysm Bicuspid aortic valve Aortic coarctation Turner syndrome Vasculitis (giant cell arteritis, Takayasu arteritis, rheumatoid arthritis, syphilitic aortitis)	Pulse deficit New diastolic murmur Diastolic decrescendo murmur Focal neurologic deficit Hypotension	D-dimer <500 ng/mL rules out aortic dissection ↑Soluble ST2 (sST2) Measurements of soluble elastin fragments, smooth muscle myosin heavy chain, high-sensitivity C-reactive protein, fibrinogen, and fibrillin fragments	Nonspecific ST and T wave changes	CXR: Mediastinal and/or aortic widening CTA: A compressed true lumen MRA: Detects differential flow between the true and false lumens, widening of the aorta with a thickened wall TEE: Intimal dissection flaps, true and false lumens, thrombosis in the false lumen Aortography: Distortion of the normal contrast column, Flow reversal or stasis into a false channel, Failure of major branches to fill, and Aortic valvular regurgitation	CT angiography Digital subtraction aortography (if high suspicion)
	Penetrating atherosclerotic aortic ulcer^[45]^[46]^[47]	Sudden severe pain	Variable	Tearing, ripping sensation, knife like	–	–	+	–	Hypotension Back pain Hypovolemic shock	Hypertension Smoking Hyperlipidemia Atherosclerosis Male gender Older age Bicuspid aortic valve Prior aortic surgery Prior aortic dilatation	Hypotension	_	_	CXR: Mediastinal and/or aortic widening, diffuse or focal enlargement of thoracic descending aorta, pleural effusion, and deviated trachea CTA: Presence of false aneurysm	CT angiography Contrast-enhanced CT scan
	Pericarditis^[48]^[49]^[50]	Acute or subacute	May last for hours to days	Sharp & localized retrosternal pain	+	+	+	–	Pericardial friction rub	HIV TB Immunosuppression Acute trauma	Pericardial friction rub heard with the diaphragm of stethoscope	Leukocytosis ↑Troponin level ↑Erythrocyte sedimentation rate ↑C-reactive protein level	EKG changes (typically widespread ST segment elevation or PR depressions)	Chest x-ray typically normal Echocardiogram: normal or pericardial effusion CT scan: Noncalcified pericardial thickening with pericardial effusion CMR: inflamed pericardium and myocarditis	Pericardiocentesis Pericardial biopsy
	Pericardial Tamponade^[51]^[52]	Acute or subacute	May last for hours to days	Sharp and stabbing retrosternal pain	+/-	+	+	–	Pulsus paradoxus Pericardial rub	HIV TB Immunosuppression Acute trauma	Kussmaul sign Beck triad Pulsus paradoxus	Creatine kinase and isoenzymes Abnormal LFTs Antinuclear antibody assay, erythrocyte sedimentation rate and rheumatoid factor HIV testing	EKG findings: Sinus tachycardia Low QRS voltage Electrical alternans	CXR: enlarged cardiac silhouette with clear lung fields Echocardiography: Chamber collapse, Respiratory variation in volumes and flows, IVC plethora Swan-Ganz Catheterization: Equilibration of average intracardiac diastolic pressures (usually between 10 and 30 mmHg)	Echocardiography
	Myocarditis^[53]^[54]^[55]	Acute or subacute	Variable	Sharp & localized retrosternal pain reflects associated pericarditis	+/-	+	+	–	Heart failure Sudden cardiac death Arrythmias	Ischemic heart disease Valvular heart disease	S3 and S4 gallop Cardiac murmurs Pericardial friction rub	Serum cardiac troponin levels ↑ BNP or NT-proBNP level	Nonspecific ST changes, single atrial or ventricular ectopic beats, complex ventricular arrhythmias	CXR: Normal to enlarged with or without pulmonary vascular congestion and pleural effusions Echo: Left ventricular dilation, changes in left ventricular geometry (eg, development of a more spheroid shape), and wall motion abnormalities CMR: T1 and T2 signal intensity consistent with edema, presence of LGE consistent with necrosis or scar Radionuclide ventriculography: ↓ EF Cardiac catheterization: Assessment of hemodynamic status	Endomyocardial biopsy
	Hypertrophic cardiomyopathy^[56]^[57]^[58]	Acute or subacute	Variable	Typical or atypical chest pain	–	–	+	–	HF Arrhythmias Syncope Acute hemodynamic collapse	Positive family history of sudden cardiac death Genetic mutation	S4 Systolic murmurs LV apical impulse Brisk carotid pulse ↑ JVP A parasternal lift	Non-specific	Prominent abnormal Q waves P wave abnormalities Left axis deviation Deeply inverted T waves	Echocardiography: LV hypertrophy Systolic anterior motion of the mitral valve, LVOT obstruction Cardiac catheterization Pressure gradient Augmentation of the gradient Aortic pressure Left ventricular pressure Left atrial or pulmonary capillary wedge pressure Coronary angiography Obstructive epicardial coronary artery disease Genetic testing for HCM: Sarcomere mutation in an athlete with a maximal LV wall thickness in the “grey zone”	Genetic testing for HCM
	Stress (takotsubo) Cardiomyopathy^[59]^[60]^[61]^[62]	Acute	Commonly > 20 minutes	Substernal heaviness or tightness	–	–	+	–	Setting of physical or emotional stress or critical illness	Stress	Murmurs and rales may be present on auscultation in the setting of acute pulmonary edema	Catecholamines transiently elevated ↑TnT level ↑BNP level	ST segment elevation ST depression QT interval prolongation, T wave inversion, abnormal Q waves	Radionuclide myocardial perfusion imaging: Transient perfusion abnormalities in the left ventricular apex	Ventriculography and invasive coronary angiography
	Aortic Stenosis^[63]^[64]^[65]	Acute, recurrent episodes of angina	2-10 minutes	Heaviness/pressure/ tightness/squeezing/ burning (Levine’s sign) Retrosternal	–	–	+	–	Dyspnea and decreased exercise tolerance Dizziness and syncope Angina pectoris	HTN Old age	S2 is soft, single and paradoxically split A2 delayed and tends to occur simultaneously with P2 Aortic ejection click Fourth heart sound (S4) can also be heard Crescendo–decrescendo murmur	Schistiocytes on peripheral blood smear	Non specific (the voltage of the QRS complex is increased showing the presence of left ventricular hypertrophy)	Echocardiography: aortic leaflets thickened and calcified, ↑ pulmonary artery pressure) CMR: Myocardial fibrosis, evaluation of aortic anatomy and size MDCT: Degree of aortic valve calcification PET: Measures active mineralization which correlates with stenosis severity	Echocardiography
	Heart Failure^[66]^[67]^[68]	Subacute or chronic	Variable	Dull Left sided chest pain	+	+/-	+	+	Orthopnea Peripheral edema Hemoptysis	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	S3 Elevated JVP Peripheral edema	Hyponatremia Hypoalbuminemia ↑ Serum brain natriuretic peptide (BNP) or NT-proBNP level A mild elevation in serum bilirubin (total bilirubin <3 mg/dL)	EKG findings are specific according to each cause of heart failure Q waves, ST and T wave abnormalities in patients with prior MI New onset arrhythmias (atrial fibrillation and ventricular tachycardia)	CXR: Cardiomegaly Echocardiography: ↓ EF Right heart catheterization: Pulmonary capillary wedge pressure >20 mmHg, right atrial pressure ≥12 mmHg) and/or decreased cardiac index (≤2.2 L/min/m2	Echocardiography
Differentials on the basis of Etiology	Disease	Clinical manifestations										Diagnosis
		Symptoms								Risk factors	Physical exam	Lab Findings	EKG	Imaging	Gold standard
		Onset	Duration	Quality of Pain	Cough	Fever	Dyspnea	Weight loss	Associated Features	Risk factors	Physical exam	Lab Findings	EKG	Imaging	Gold standard
Pulmonary	Pulmonary Embolism^[69]^[70]	Acute	May last minutes to hours	Sharp or knifelike or pleuritic pain Localized to side of lesion	+	+/-	+	–	Hemoptysis History of venous thromboembolism or coagulation abnormalities.	Hormone replacement therapy Cancer Oral contraceptive pills Stroke Pregnancy Postpartum Prior history of VTE Thrombophilia	S3 or S4 gallop Low grade fever Tachycardia Tachypnea Hypoxia	↑D-dimer ≥500 ng/mL Arterial blood gases (Respiratory alkalosis) ↑Troponin levels Hypercoagulation workup	Tachycardia and nonspecific ST-segment and T-wave changes (70 percent) S1Q3T3 pattern New right bundle branch block Inferior Q-waves (leads II, III, and aVF)	Duplex Ultrasonography: DVT CXR: Westermark sign, Hampton hump, Palla’s sign Echocardiography: RV dilation (ratio of apical 4-chamber RV diameter to left ventricle (LV) diameter > 0.9) RV systolic dysfunction Ventilation-Perfusion Scanning: High probability	CT pulmonary angiography
	Spontaneous Pneumothorax^[71]^[72]	Acute	May last minutes to hours	Sharp Localized pleuritic	–	–	+	–	Respiratory distress Tachypnea Asymmetric lung expansion Hyperresonance on percussion Decreased tactile fremitus Tachycardia Cardiac apical displacement	Smoking Positive family history Marfan syndrome Homocystinuria Thoracic endometriosis.	Decreased breath sounds on involved side Lung sounds transmitted from the unaffected hemithorax are minimal with auscultation at the midaxillary line Adventitious lung sounds (crackles, wheeze; an ipsilateral finding) Pulsus paradoxus	Respiratory alkalosis on ABGs	Rightward shift in the mean electrical axis Loss of precordial R waves Diminution of the QRS voltage Precordial T wave inversions	CXR: White visceral pleural line on the chest radiograph CT: small amounts of intrapleural gas, atypical collections of pleural gas, and loculated pneumothoraces	CT scan
	Tension Pneumothorax^[73]^[74]	Acute	May last minutes to hours	Sharp Pleuritic	–	–	+	–	Hypotension Jugular venous distention Respiratory distress	Trauma	Decreased breath sounds on involved side Lung sounds transmitted from the unaffected hemithorax are minimal with auscultation at the midaxillary line Adventitious lung sounds (crackles, wheeze; an ipsilateral finding) Pulsus paradoxus	Respiratory alkalosis on ABGs	Significant elevation of the ST-T segment from leads V1 to V4	CXR: A distinct shift of the mediastinum to the contralateral side, collapse of the ipsilateral lung, and flattening or inversion of the ipsilateral hemidiaphragm	CT scan
	Pneumonia^[75]^[76]^[77]	Acute or chronic	Variable	Dull Localized to side of lesion	+	+	+	+/-	Altered mental status Tachycardia Rust-colored sputum Green sputum Red currant-jelly sputum Central cyanosis	Long hospital stay Ill contact exposure Aspiration	Wheezing Rhonchi Rales Decreased breath sounds Pleural friction rub	Arterial blood gas : Hypoxia, hypoxemia ↑ Procalcitonin Leukocytosis Sputum evaluation Positive blood cultures	Sinus tachycardia Nonspecific ST-segment or T-wave changes	CXR: Interstitial infiltrates, lobar consolidation, cavitation	CXR
	Tracheitis/ Bronchitis^[78]^[79]^[80]^[81]	Acute	Variable	Dull Substernal	+	+	+	–	Tachypnea Respiratory distress Hoarseness Dyspnea Cyanosis Sore throat Odynophagia Dysphonia	Aspiration Pneumonia	Inspiratory stridor (with or without expiratory stridor) Nasal flaring Wheezing	Gram stain of exudates: Neutrophils	Peaked P-wave	Radiography of the neck: Steeple sign Laryngotracheobronchoscopy: a normal epiglottis with subglottic narrowing, thick and purulent secretions in the trachea, pseudomembranes	Endoscopy
	Pleuritis	Acute or subacute or chronic	May last minutes to hours	Sharp Localized pleuritic	+	+	+	–	Sharp chest pain with breathing Itching in sites on the back Dizziness	Autoimmune conditions Infections	Tachypnea Tachycardia Pleural Rubs Decreased breath sounds	Leukocytosis Arterial blood gas (ABG): Hypoxia Thoracocentesis	EKG done to rule out other causes in differential diagnoses	Chest X Ray: Pleural fluid on one or both sides Computerized tomography (CT) scan: Pleural effusions	CXR
	Pulmonary Hypertension^[82]^[83]^[84]	Acute or subacute or chronic	Variable	Substernal pressure like	+	–	+	–	Dyspnea Symptoms of right heart failure (edema) Past history of heart murmur Deep venous thrombosis (DVT) Arthritis or arthralgias Rash	Smoking HF Heavy snoring Morbid obesity	The intensity of the pulmonic component of the second heart sound (P2) may be increased and the P2 may demonstrate fixed or paradoxical splitting. Systolic ejection murmur A right-sided fourth heart sound (S4) with a left parasternal heave	Abnormal Arterial blood gas Antinuclear antibody (ANA) levels Antineutrophil cytoplasmic antibody (ANCA) Brain natriuretic peptide (BNP of NT-proBNP) HIV testing Iron deficiency Pulmonary Function Testing Polysomnography	Right axis deviation An R wave/S wave ratio greater than one in lead V1 Incomplete or complete right bundle branch block Increased P wave amplitude in lead II (P pulmonale) due to right atrial enlargement	Chest Radiography: Oligemic lung fields Echocardiography: PASP is >50 and the TRV is >3.4 Ventilation-Perfusion (V/Q) Lung Scanning: Abnormal Right-sided cardiac catheterization: Mean PCWP >15 mmHg,	Cardiac catheterization
	Pleural Effusion^[85]^[86]^[87]	Acute or subacute or chronic	Variable	Dull Pleuritic pain	+	+/-	+	+/-	Increasing lower extremity edema Orthopnea Paroxysmal nocturnal dyspnea Night sweats Hemoptysis	Pneumonia	Diminished or inaudible breath sounds Pleural friction rub Egophony (known as “E-to-A” changes)	Pleural fluid LDH levels above 1000 IU/L Nucleated cells – Lymphocytosis – Eosinophilia – Mesothelial cells Pleural fluid culture and cytology Pleural fluid antinuclear antibody and rheumatoid factor	Typically not indicated	Chest X Ray: Pleural fluid on one or both sides Computerized tomography (CT) scan: Detects small pleural effusions, ie, less than 10 mL and possibly as little as 2 mL of liquid in the pleural space, Thickening of the visceral and parietal pleura MRI: Characterize the content of pleural effusions	Computed tomography
	Asthma & COPD^[88]^[89]^[90]^[91]	Acute or subacute or chronic	Variable	Tightness	+	+/-	+	+/-	Cyanosis	Smoking HF HTN	Elevated jugular venous pulse (JVP) Hyperinflation (barrel chest) Peripheral edema Clubbing Wheezing Rhonchi Diffusely decreased breath sounds Coarse crackles beginning with inspiration	Leukocytosis Eosinophilia Respiratory alkalosis	Peaked P-wave Reduced amplitude of the QRS complexes Multifocal atrial tachycardia (MAT)	CXR: Hyperinflation Spirometry: ↓ FEV1, PEF, ↓ FEV1/FVC	Spirometry
	Pulmonary Malignancy^[92]^[93]^[94]^[95]	Chronic	Variable	Dull aching	+	+/-	+	+	Bone pain Fatigue Neurologic dysfunction Superior vena cava (SVC) obstruction Hoarseness Hemidiaphragm paralysis Dysphagia Paraneoplastic syndromes Hypercalcemia	Smoking Metastasis	Wheeze Crackles Depending upon complications caused by the spread of cancer	Hypercalcemia	EKG may be performed before cancer treatment to identify any pre-existing conditions, or during treatment to check for possible heart damage	CXR and CT scan: Mass lesion, hilar lymphadenopathy Spirometry: ↓Vt, ↑RV Bronchoscopy: Biopsy	Bronchoscopy
	Sarcoidosis^[96]^[97]^[98]^[99]	Chronic	Days to week	Chest fullness	+	–	+	+	Löfgren syndrome (fever, bilateral hilar lymphadenopathy (BHL), and polyarthralgias) Uveitis Heart block Lymphocytic meningitis Diabetes insipidus Fatigue Hypercalciuria	Black population Autoimmune diseases	Diminished respiratory sounds	↑ ACE level, adenosine deaminase, SAA, sIL2R Hypercalciuria Elevated 1,25-dihydroxyvitamin D levels	AV block Prolongation of the PR interval (first-degree AV block) Ventricular arrhythmias (sustained or nonsustained ventricular tachycardia and ventricular premature beats [VPBs]) Supraventricular arrhythmias	Chest radiograph: Bilateral hilar adenopathy High-resolution CT (HRCT) scanning of the chest: Ground glass opacification, Hilar and mediastinal lymphadenopathy, Bronchial wall thickening	Lung Biopsy
	Acute chest syndrome (Sickle cell anemia)^[100]^[101]^[102]	Acute	May last minutes to hours	Chest tightness	+	+/-	+	–	Sickle cell anemia Vaso-occlusive crisis Pain crises	↑ WBC ↑ Hb levels ↓ fetal hemoglobin levels Smoking Vaso-occlusive pain events	Systolic murmur may be heard over the entire precordium	↑Erythrocyte sedimentation rate Peripheral blood smears: Schistiocytes ↑ Reticulocyte count	EKG typically not indicated	Plain radiography of the extremities: Avascular necrosis	—
Differentials on the basis of Etiology	Disease	Clinical manifestations										Diagnosis
		Symptoms								Risk factors	Physical exam	Lab Findings	EKG	Imaging	Gold standard
		Onset	Duration	Quality of Pain	Cough	Fever	Dyspnea	Weight loss	Associated Features	Risk factors	Physical exam	Lab Findings	EKG	Imaging	Gold standard
Gastrointestinal	GERD, Peptic Ulcer^[103]^[104]^[105]	Acute	Minutes to hours (gastroesophageal reflux) Prolonged (peptic ulcer) 5 to 60 minutes	Burning Substernal Epigastric	+/-	–	–	+/-	Visceral, substernal, worse with recumbency, no radiation, relief with food, antacids Hematemesis or melena resulting from gastrointestinal bleeding Dyspepsia	Prolonged NSAIDs intake Smoking Alcohol abuse Spicy foods H-pylori infection	Not any auscultatory findings associated with this disease Enamel erosion or other dental manifestations	↑Serum Gastrin Level Secretin Stimulation Test H-Pylori testing	EKG usually normal but may show T wave inversions in leads V2 through V4 consistent with myocardial ischemia in patients with peptic ulcer perforation	Upper Gastrointestinal Endoscopy: Biopsy Esophageal Manometry: To exclude an esophageal motility disorder Esophageal impedance pH testing: Monitors esophageal pH	Upper Gastrointestinal Endoscopy
	Diffuse Esophageal Spasm^[106]^[107]^[108]^[109]	Acute	Minutes to hours 5 to 60 minutes	Burning Pressure Visceral, spontaneous, substernal	+	–	+/-	+/-	Associated with cold liquids Relief with nitroglycerin	—	—	Barium swallow: Multiple areas of spasm throughout the length of the esophagus Impedance testing: Higher amplitudes and better transit of swallowed boluses	No ECG findings associated with DES, but ECG is done to exclude variant angina due to higher concurrent association of variant angina with DES	Esophageal manometry : ≥20 percent premature contractions (distal latency <4.5 seconds)	Esophageal manometry
	Esophagitis^[110]^[111]^[112]	Acute	Variable	Burning Epigastric	+	+	–	+/-	Heartburn Abdominal pain	HIV Immunosuppression	No auscultatory finding	Troponin or other cardiac markers Leukopenia ↓CD4 count Human immunodeficiency virus (HIV) test	ECG is done to rule out acute coronary syndrome	Double-contrast esophageal barium study (esophagography) Endoscopy: Biopsy	Endoscopy
	Eosinophilic Esophagitis^[113]^[114]^[115]^[116]^[117]^[118]	Chronic	Variable	Burning Retrosternal Abdominal	+	–	–	–	Dysphagia Food impaction GERD	Allergic diseases Asthma Rinitis Eczema	No auscultatory finding in the this disease	Elevated IgE (>114,000 units/L) Elevated peripheral eosinophils	Typically no finding on EKG	Barium studies: Strictures and a ringed esophagus Endoscopy: Stacked circular rings (“feline” esophagus) ●Strictures ●Linear furrows ●Whitish papules Esophageal biopsy: More than 15 eosinophils per high-power field	Esophageal biopsy
	Esophageal Perforation^[6]	Acute	Minutes to hours	Burning Upper abdominal	–	+/-	+	–	Eating disorders such as bulimia Repeated episodes of retching and vomiting with either recent excessive dietary or alcohol intake Subcutaneous emphysema	Instrumentation/surgery Penetrating or blunt trauma Medications, other ingestions, foreign body Violent retching/vomiting Hernia/intestinal volvulus/obstruction Inflammatory bowel disease Appendicitis Peptic ulcer disease	Mild tachycardia or hypothermia Hamman crunch (crackling sound upon chest auscultation occurs due to pneumomediastinum)	↑Serum amylase ↑C-reactive protein levels	EKG may be indicated to assess for myocardial ischemia due to acute gastrointestinal bleeding, especially if there is coexisting:Cardiovascular disease, significant anemia and advanced age	Plain chest films or chest CT: Pneumomediastinum, Free air under the diaphragm, •Pleural effusion •Pneumothorax (Macklin effect). •Subcutaneous emphysema Plain abdominal films (or abdominal CT scout film):The appearance of pneumoperitoneum -Free air under the diaphragm -Cupola sign (inverted cup) -Rigler sign (double-wall sign) -Psoas sign -Urachus sign	Confirmed by water-soluble contrast esophagram
	Mediastinitis^[119]^[120]^[121]^[122]	Acute, Chronic	Variable	Retrosternal irritation	+/-	+	+	–	Nonspecific	Infection Esophageal perforation Post operative complication	Dysphagia Dysphonia Stridor Hamman sign	Positive organisms in sternal culture Leukocytosis Positive blood cultures	Diffuse ST elevation	CT: Localize the infection and extent of spread MRI: Assesses vascular involvement and complications	CT scan
	Cholelithiasis^[123]^[124]^[125]^[126]	Acute, subacute	Minutes to hours	Burning Colicky Right upper abdomen Substernal epigastric	–	+/-	–	–	Obesity Fertile females in 40’s	The presence of a common bile duct stone on transabdominal ultrasound •Clinical acute cholangitis •A serum bilirubin greater than 4 mg/dL (68 micromol/L)	Murphy sign negative Jaundice	↑ALT ↑AST ↑Amylase levels ↑ALP	Typically not indicated	Transabdominal ultrasound (TAUS): shows gallstones EUS: Detects biliary sludge MRCP: Detects stones >6mm Endoscopic Retrograde Cholangiopancreatography (ERCP): Diagnostic and therapeutic removal of stones	Endoscopic ultrasound and MECP
	Pancreatitis^[127]^[128]^[129]^[130]^[131]	Acute, Chronic	Variable	Epigastric Upper left side of the abdomen Pressure like	–	+	+	+/-	Primary cirrhosis Primary sclerosing cholangitis Cystic fibrosis Autoimmune diseases	Alcohol abuse Smoking Genetic predisposition	Tachypnea Hypoxemia Hypotension Cullen’s sign Grey Turner sign	↑Amylase levels ↑Lipase levels ↑ALT ↑ALP Leukocytosis	T-wave inversion ST-segment depression ST-segment elevation rarely Q-waves	CT: focal or diffuse enlargement of the pancreas MRI: Pancreatic enlargement	CT Scan
	Sliding Hiatal Hernia^[132]^[133]^[134]	Acute	Variable	Epigastric Burning	+	–	+	–	Obstruction Cameron ulcers GERD Dysphagia	Trauma Iatrogenic Congenital malformation	Bowel sounds may be heard in the chest	Non specific	T wave inversion in anterior lead.	Barium swallow: At least three rugal folds traversing the diaphragm Upper endoscopy: A greater than 2-cm separation between the squamocolumnar junction and the diaphragmatic impression High resolution manometry: The separation of the crural diaphragm from the lower esophageal sphincter (LES) by a pressure trough	Upper endoscopy High resolution manometry (for smaller hernias)
Musculoskeletal	Costosternal syndromes (costochondritis)^[135]^[136]^[137]^[138]	Acute, subacute	Days to weeks	Pressure like on anterior part of chest wall	–	+	–	–	History of repeated minor trauma or unaccustomed activity (eg, painting, moving furniture)	Trauma	Pain by palpation of tender areas Maneuvers, such as the “crowing rooster” and horizontal arm flexion maneuver	Non specific	EKG is done to rule out other cardiovascular causes	CXR: To rule out fracture	Pain by palpation of tender areas
	Lower rib pain syndromes^[139]	Chronic	Variable	Aching Lower chest Upper abdomen	–	–	+	–	Common in women with a mean age in the mid-40s	—	Hooking maneuver Reproduces pain by pressing a tender spot on the costal margin	Non specific The workup is done for excluding cardiac disorders and other causes of chest pain	EKG is done to rule out other cardiovascular causes	CXR: To rule out fracture	—
	Sternalis syndrome	Chronic	Variable	Pressure like pain Over the body of sternum Sternalis muscle Left or middle side of the chest wall	–	–	–	–	Cardiac diseases	Daily activities Emotional distress Anxiety	Localized tenderness is found directly over the body of the sternum or overlying sternalis muscle	No specific diagnostic test for this disease The workup is done for excluding cardiac disorders and other causes of chest pain	EKG is done to rule out other cardiovascular causes	X-ray : To rule out fracture	Physical exam
	Tietze’s syndrome^[140]	Acute	Weeks	Pressure like pain over Costosternal joint Sternoclavicular joint Costochondral joint Second and third ribs	–	–	–	–	Most often involve the areas of 2nd and 3rd ribs More common in young adults Sternocostoclavicular hyperostosis Ankylosing spondylitis	Upper respiratory infections Excessive coughing	Painful and localized swelling of the costosternal, sternoclavicular, or costochondral joints most often involving 2nd and 3rd ribs	No specific diagnostic test for this disease The workup is done for excluding cardiac disorders and other causes of chest pain	EKG is done to rule out other cardiovascular causes	X-ray: To rule out fracture	Tests are done to rule out other diseases
	Xiphoidalgia^[141]	Acute	Variable	Pressure like pain over Over the xiphoid process Sternum Xiphisternal joint	–	–	–	–	Symptoms are aggravated by twisting and bending movements	Cough Heavy work	Provocative test	No specific diagnostic test for this disease The workup is done for excluding cardiac disorders and other causes of chest pain	EKG is done to rule out other cardiovascular causes	X-ray: To rule out fracture	Tests are done to rule out other diseases
	Spontaneous sternoclavicular subluxation^[142]	Acute, Chronic	Variable	Aching pain over Sternoclavicular joint	–	–	–	–	More common in middle age women Occurs in dominant hands with repetitive tasks of heavy or moderate quality	Trauma	Palpation of tender areas	No specific diagnostic test for this disease The workup is done for excluding cardiac disorders and other causes of chest pain	EKG is done to rule out other cardiovascular causes	X-ray: Sclerosis of the medial clavicle	X-ray
Differentials on the basis of Etiology	Disease	Clinical manifestations										Diagnosis
		Symptoms								Risk factors	Physical exam	Lab workup	EKG	Imaging	Gold standard
		Onset	Duration	Quality of Pain	Cough	Fever	Dyspnea	Weight loss	Associated Features	Risk factors	Physical exam	Lab workup	EKG	Imaging	Gold standard
Rheumatic	Fibromyalgia^[143]^[144]^[145]	Chronic	Variable	Raynaud phenomenon (RP) Deep ache and burning pain on Shoulders Back of the Neck Chest Lower Back Elbows Hips Shin Knees	–	–	+	–	Somatization Depression IBS	—	Presence of tenderness in soft-tissue anatomic locations	Non specific Normal Blood and urine test (mandatory to rule out other diseases)	P-wave dispersions (Pd)	—	—
	Rheumatoid arthritis^[146]	Chronic	Years	Symmetrical joint pain in Wrist Fingers Knees Feet Ankles	–	+	–	+	Extra-articular involvement of other organ systems Carpal tunnel syndrome Tarsal tunnel syndrome	Old age Smoking Autoimmune conditions	Reduced grip strength Rheumatoid nodules	Positive Rheumatic Factor Anti-CCP body Synovial fluid analysis: WBC between 1500 and 25,000/cubicmm, low glucose, low C3 and C4 complement level. Thrombocytosis Anemia Mild leukocytosis	ECG is done rule out the heart failure as RA is one of the causes of heart failure	Plain film radiography: periarticular osteopenia, joint space narrowing, and bone erosions MRI: Bone erosions Ultrasonography: Degree of inflammation and the volume of inflamed tissue	—
	Ankylosing spondylitis^[147]^[148]^[149]^[150]	Chronic	Years	Intermittent pain in Spine joint Sacroiliac joint	–	–	–	–	Patients with HLA-27 variant Extra-articular joint involvements Restrictive pulmonary disease Acute coronary syndromes (ACS), strokes, venous thromboembolism, conduction abnormalities	Genetics (Monozygotic twins)	Tenderness of the SI Limited spinal ROM Schober test	↑ESR ↑CRP ↑ALP ↑IgA Antigen HLA-27 positive Negative Rheumatic Factor	ECG is done to rule out conductions defects and aortic insufficiency	Plain radiography: Erosions, ankylosis, changes in joint width, or sclerosis. Magnetic resonance imaging (MRI): Osteitis” or “bone marrow edema” (BME)	Plain films of the sacroiliac joints
	Psoriatic arthritis^[149]	Chronic	Years	Asymmetrical intermittent pain in Interphalangeal joints Nails Wrist Knees Ankles Lower Back	–	–	–	–	Psoriasis Enthesitis Tenosynovitis Dactylitis	Psoriasis HLA-B*27 positive	Dactylitis with sausage digits Onycholysis Pitting edema Ocular involvement	Non specific	Longer PR interval	X-ray: “pencil-in-cup” deformity, erosive changes and new bone formation, lysis of the terminal phalanges; fluffy periostitis MRI: Detects articular, periarticular, and soft-tissue inflammation, enthesitis	X-ray
	Sternocostoclavicular hyperostosis (SAPHO syndrome)^[149]^[151]^[152]^[153]^[154]	Chronic	Years	Recurrent and multifocal pain in Sternoclavicular joint	–	+	–	–	Palmoplantar pustulosis (PPP)	Positive family history of: Spondyloarthritis IBD Psoriasis Rheumatoid arthritis Other autoimmune/autoinflammatory disease	Hyperostosis Osteitis Synovitis Pustular eruptions Inflammatory nodules or plaques	Serologic testing to exclude other diseases Non specific	ECG is done to rule out conductions defects and aortic insufficiency	Plain radiography: Hyperostotic changes (thickening of periosteum, cortex, and endosteum), sclerotic lesions, osteolysis, periosteal reaction, and osteoproliferation Bone scan: “bull’s head” change Magnetic resonance imaging: Osteitis and soft tissue involvement Fluorodeoxyglucose positron emission tomography (FDG-PET)/CT: Differentiates active versus inactive lesions	Bone scan
	Systemic lupus erythematosus^[155] ^[156]^[157]	Chronic	Years	Skin Joints (fingers, wrist, knees) Kidneys SLE can affect any organ of the body	+/-	+	+	+	HLA-genetic mutations Female gender Being younger than 50	Autoimmune conditions Genetic predisposition Positive family history	Malar rash Photosensitive rash Discoid rash Arthritis of the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints of the hands Pleuro-pericardial friction rubs Systolic murmurs	Elevation of autoantibodies (ANA, anti-dsDNA, anti-SM, antiphospholipid) Complement levels decreased Anemia	Sinus tachycardia, ST segment changes, and ventricular conduction disturbances	Related to specific organ involvent	Anti-dsDNA antibody test
	Relapsing polychondritis^[158]	Chronic	Years	Intermittent pain in: Tissues that cover the end of the joints Cartilage of costal rib	+	+	+	+	Hodkin’s lymphoma Myelodysplastic syndromes Gastrointestinal disorders Type 1 Diabetes mellitus Auricular chondritis	Autoimmune diseases	Physical examinations findings are seen related to nasal chondritis, ocular inflammation, cardiovascular disease, skin disease, CNS and pulmonary system	Negative rheumatoid factor Anti-type II collagen antibodies Antineutrophil cytoplasmic antibodies	ECG is done to rule out the cardiovascular complications of this disease	Non specific Related to specific organ involvent	No gold standard test for this disease
Psychiatric	Panic attack/ Disorder^[159]^[7]^[160]	Acute or subacute or chronic	Variable	Variable	+	–	+	–	History of Depression Panic attacks Agoraphobia	Psychiatric disorders	Anxious Tachypneic	Thyroid function tests Complete blood count Chemistry panel	Sinus Tachycardia	No any specific radiographic test is done	—
Others	Substance abuse (Cocaine)^[161]^[162]^[163]	Acute (hours)	Minutes to hours	Pressure like pain in the center of chest	+	+	+	+	Anxiety Dyspnea Nausea Palpitations	Psychiatric disorders	Signs of injection drug use Signs of drug inhalation Poor personal hygiene	Serum biomarkers (Troponin I, Troponin T) Toxicologic tests or drug screens of bodily fluids (blood, urine, saliva) and hairs	QT prolongation Sinus Tachycardia Arrhythmias Cardiac conduction abnormalities	—	Gold standard test depends on the type of substance is abuse
Others	Herpes Zoster^[164]^[165]^[166]	Acute or Chronic	Variable	Burning pain on Chest Upper back Lower back	–	+	–	–	People who had chickenpox	Immunosuppression	Painful grouped herpetiform vesicles on an erythematous base distributed in a single dermatome	Viral culture Direct immunofluorescence testing, Polymerase chain reaction assay (PCR)	ECG is done to rule out other cardiovascular causes of chest pain	Magnetic resonance imaging (MRI): To rule out encephalitis	Viral tissue culture

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↑ Prat F, Meduri B, Ducot B, Chiche R, Salimbeni-Bartolini R, Pelletier G (March 1999). “Prediction of common bile duct stones by noninvasive tests”. Ann. Surg. 229 (3): 362–8. PMC 1191701. PMID 10077048.
↑ Tse F, Barkun JS, Barkun AN (September 2004). “The elective evaluation of patients with suspected choledocholithiasis undergoing laparoscopic cholecystectomy”. Gastrointest. Endosc. 60 (3): 437–48. PMID 15332044.
↑ Dickson AP, Imrie CW (October 1984). “The incidence and prognosis of body wall ecchymosis in acute pancreatitis”. Surg Gynecol Obstet. 159 (4): 343–7. PMID 6237447.
↑ Yadav D, Agarwal N, Pitchumoni CS (June 2002). “A critical evaluation of laboratory tests in acute pancreatitis”. Am. J. Gastroenterol. 97 (6): 1309–18. doi:10.1111/j.1572-0241.2002.05766.x. PMID 12094843.
↑ Fortson MR, Freedman SN, Webster PD (December 1995). “Clinical assessment of hyperlipidemic pancreatitis”. Am. J. Gastroenterol. 90 (12): 2134–9. PMID 8540502.
↑ Lecesne R, Taourel P, Bret PM, Atri M, Reinhold C (June 1999). “Acute pancreatitis: interobserver agreement and correlation of CT and MR cholangiopancreatography with outcome”. Radiology. 211 (3): 727–35. doi:10.1148/radiology.211.3.r99jn08727. PMID 10352598.
↑ Stimac D, Miletić D, Radić M, Krznarić I, Mazur-Grbac M, Perković D, Milić S, Golubović V (May 2007). “The role of nonenhanced magnetic resonance imaging in the early assessment of acute pancreatitis”. Am. J. Gastroenterol. 102 (5): 997–1004. doi:10.1111/j.1572-0241.2007.01164.x. PMID 17378903.
↑ Weston AP (October 1996). “Hiatal hernia with cameron ulcers and erosions”. Gastrointest. Endosc. Clin. N. Am. 6 (4): 671–9. PMID 8899401.
↑ Bredenoord AJ, Weusten BL, Timmer R, Smout AJ (February 2006). “Intermittent spatial separation of diaphragm and lower esophageal sphincter favors acidic and weakly acidic reflux”. Gastroenterology. 130 (2): 334–40. doi:10.1053/j.gastro.2005.10.053. PMID 16472589.
↑ Kahrilas PJ, Kim HC, Pandolfino JE (2008). “Approaches to the diagnosis and grading of hiatal hernia”. Best Pract Res Clin Gastroenterol. 22 (4): 601–16. doi:10.1016/j.bpg.2007.12.007. PMC 2548324. PMID 18656819.
↑ Wolf E, Stern S (February 1976). “Costosternal syndrome: its frequency and importance in differential diagnosis of coronary heart disease”. Arch. Intern. Med. 136 (2): 189–91. PMID 1247350.
↑ Fam AG, Smythe HA (September 1985). “Musculoskeletal chest wall pain”. CMAJ. 133 (5): 379–89. PMC 1346531. PMID 4027804.
↑ Bösner S, Becker A, Hani MA, Keller H, Sönnichsen AC, Karatolios K, Schaefer JR, Haasenritter J, Baum E, Donner-Banzhoff N (August 2010). “Chest wall syndrome in primary care patients with chest pain: presentation, associated features and diagnosis”. Fam Pract. 27 (4): 363–9. doi:10.1093/fampra/cmq024. PMID 20406787.
↑ Zaruba RA, Wilson E (June 2017). “IMPAIRMENT BASED EXAMINATION AND TREATMENT OF COSTOCHONDRITIS: A CASE SERIES”. Int J Sports Phys Ther. 12 (3): 458–467. PMC 5455195. PMID 28593100.
↑ Scott EM, Scott BB (July 1993). “Painful rib syndrome–a review of 76 cases”. Gut. 34 (7): 1006–8. PMC 1374244. PMID 8344569.
↑ Aeschlimann A, Kahn MF (1990). “Tietze’s syndrome: a critical review”. Clin. Exp. Rheumatol. 8 (4): 407–12. PMID 1697801.
↑ LIPKIN M, FULTON LA, WOLFSON EA (October 1955). “The syndrome of the hypersensitive xiphoid”. N. Engl. J. Med. 253 (14): 591–7. doi:10.1056/NEJM195510062531403. PMID 13266001.
↑ van Holsbeeck M, van Melkebeke J, Dequeker J, Pennes DR (September 1992). “Radiographic findings of spontaneous subluxation of the sternoclavicular joint”. Clin. Rheumatol. 11 (3): 376–81. PMID 1458785.
↑ Almansa C, Wang B, Achem SR (March 2010). “Noncardiac chest pain and fibromyalgia”. Med. Clin. North Am. 94 (2): 275–89. doi:10.1016/j.mcna.2010.01.002. PMID 20380956.
↑ Disla E, Rhim HR, Reddy A, Karten I, Taranta A (November 1994). “Costochondritis. A prospective analysis in an emergency department setting”. Arch. Intern. Med. 154 (21): 2466–9. PMID 7979843.
↑ Wise CM, Semble EL, Dalton CB (February 1992). “Musculoskeletal chest wall syndromes in patients with noncardiac chest pain: a study of 100 patients”. Arch Phys Med Rehabil. 73 (2): 147–9. PMID 1543409.
↑ Rodríguez-Henríquez P, Solano C, Peña A, León-Hernández S, Hernández-Díaz C, Gutiérrez M, Pineda C (July 2013). “Sternoclavicular joint involvement in rheumatoid arthritis: clinical and ultrasound findings of a neglected joint”. Arthritis Care Res (Hoboken). 65 (7): 1177–82. doi:10.1002/acr.21958. PMID 23335586.
↑ Ramonda R, Lorenzin M, Lo Nigro A, Vio S, Zucchetta P, Frallonardo P, Campana C, Oliviero F, Modesti V, Punzi L (September 2012). “Anterior chest wall involvement in early stages of spondyloarthritis: advanced diagnostic tools”. J. Rheumatol. 39 (9): 1844–9. doi:10.3899/jrheum.120107. PMID 22798267.
↑ Wendling D, Prati C, Demattei C, Loeuille D, Richette P, Dougados M (July 2013). “Anterior chest wall pain in recent inflammatory back pain suggestive of spondyloarthritis. data from the DESIR cohort”. J. Rheumatol. 40 (7): 1148–52. doi:10.3899/jrheum.121460. PMID 23678156.
↑ ^149.0 ^149.1 ^149.2 Jurik AG (1992). “Seronegative anterior chest wall syndromes. A study of the findings and course at radiography”. Acta Radiol Suppl. 381: 1–42. PMID 1488919.
↑ Guglielmi G, Cascavilla A, Scalzo G, Salaffi F, Grassi W (2009). “Imaging of sternocostoclavicular joint in spondyloarthropaties and other rheumatic conditions”. Clin. Exp. Rheumatol. 27 (3): 402–8. PMID 19604431.
↑ Saghafi M, Henderson MJ, Buchanan WW (February 1993). “Sternocostoclavicular hyperostosis”. Semin. Arthritis Rheum. 22 (4): 215–23. PMID 8484129.
↑ Magrey M, Khan MA (October 2009). “New insights into synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome”. Curr Rheumatol Rep. 11 (5): 329–33. PMID 19772827.
↑ Colina M, Govoni M, Orzincolo C, Trotta F (June 2009). “Clinical and radiologic evolution of synovitis, acne, pustulosis, hyperostosis, and osteitis syndrome: a single center study of a cohort of 71 subjects”. Arthritis Rheum. 61 (6): 813–21. doi:10.1002/art.24540. PMID 19479702.
↑ Carneiro S, Sampaio-Barros PD (May 2013). “SAPHO syndrome”. Rheum. Dis. Clin. North Am. 39 (2): 401–18. doi:10.1016/j.rdc.2013.02.009. PMID 23597971.
↑ Turner-Stokes L, Turner-Warwick M (April 1982). “Intrathoracic manifestations of SLE”. Clin Rheum Dis. 8 (1): 229–42. PMID 6749397.
↑ Hunder GG, McDuffie FC, Hepper NG (March 1972). “Pleural fluid complement in systemic lupus erythematosus and rheumatoid arthritis”. Ann. Intern. Med. 76 (3): 357–63. PMID 5015911.
↑ Porcel JM, Ordi-Ros J, Esquerda A, Vives M, Madroñero AB, Bielsa S, Vilardell-Tarrés M, Light RW (2007). “Antinuclear antibody testing in pleural fluid for the diagnosis of lupus pleuritis”. Lupus. 16 (1): 25–7. doi:10.1177/0961203306074470. PMID 17283581.
↑ Chopra R, Chaudhary N, Kay J (May 2013). “Relapsing polychondritis”. Rheum. Dis. Clin. North Am. 39 (2): 263–76. doi:10.1016/j.rdc.2013.03.002. PMID 23597963.
↑ Fleet RP, Martel JP, Lavoie KL, Dupuis G, Beitman BD (2000). “Non-fearful panic disorder: a variant of panic in medical patients?”. Psychosomatics. 41 (4): 311–20. doi:10.1176/appi.psy.41.4.311. PMID 10906353.
↑ Simpson RJ, Kazmierczak T, Power KG, Sharp DM (August 1994). “Controlled comparison of the characteristics of patients with panic disorder”. Br J Gen Pract. 44 (385): 352–6. PMC 1238951. PMID 8068393.
↑ Grant BF, Goldstein RB, Saha TD, Chou SP, Jung J, Zhang H, Pickering RP, Ruan WJ, Smith SM, Huang B, Hasin DS (August 2015). “Epidemiology of DSM-5 Alcohol Use Disorder: Results From the National Epidemiologic Survey on Alcohol and Related Conditions III”. JAMA Psychiatry. 72 (8): 757–66. doi:10.1001/jamapsychiatry.2015.0584. PMC 5240584. PMID 26039070.
↑ Cosci F, Schruers KR, Abrams K, Griez EJ (June 2007). “Alcohol use disorders and panic disorder: a review of the evidence of a direct relationship”. J Clin Psychiatry. 68 (6): 874–80. PMID 17592911.
↑ George DT, Nutt DJ, Dwyer BA, Linnoila M (February 1990). “Alcoholism and panic disorder: is the comorbidity more than coincidence?”. Acta Psychiatr Scand. 81 (2): 97–107. PMID 2183544.
↑ Dworkin RH, Johnson RW, Breuer J, Gnann JW, Levin MJ, Backonja M, Betts RF, Gershon AA, Haanpaa ML, McKendrick MW, Nurmikko TJ, Oaklander AL, Oxman MN, Pavan-Langston D, Petersen KL, Rowbotham MC, Schmader KE, Stacey BR, Tyring SK, van Wijck AJ, Wallace MS, Wassilew SW, Whitley RJ (January 2007). “Recommendations for the management of herpes zoster”. Clin. Infect. Dis. 44 Suppl 1: S1–26. doi:10.1086/510206. PMID 17143845.
↑ Oxman MN (December 1995). “Immunization to reduce the frequency and severity of herpes zoster and its complications”. Neurology. 45 (12 Suppl 8): S41–6. PMID 8545018.
↑ Jumaan AO, Yu O, Jackson LA, Bohlke K, Galil K, Seward JF (June 2005). “Incidence of herpes zoster, before and after varicella-vaccination-associated decreases in the incidence of varicella, 1992-2002”. J. Infect. Dis. 191 (12): 2002–7. doi:10.1086/430325. PMID 15897984.

Template:WH Template:WS CME Category::Cardiology

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sahar Memar Montazerin, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]

Overview

The incidence of aortic dissection is approximately 6 per 100,000 individuals worldwide.The incidence of aortic dissection increases with age, with a mean age of 63 years. Men are more commonly affected by aortic dissection than women. However, the prognosis tends to be worse in women due to unusual presentations. There is no racial predilection to aortic dissection. However, non-white race is associated with worse prognosis. The 30-days mortality rate of aortic dissection type A and B is approximately 47% and 13%, respectively.

Epidemiology and Demographics

Incidence

The incidence of aortic dissection is approximately 6 per 100,000 individuals worldwide.^[1]

Age

The incidence of aortic dissection increases with age, with a mean age of 63 years.^[2]^[3]

Race

There is no racial predilection to aortic dissection. However, non-white race is associated with worse prognosis.^[4]

Gender

Men are more commonly affected by aortic dissection than women. However, the prognosis tends to be worse in women due to unusual presentations.^[2]

Mortality rate

The 30-days mortality rate of aortic dissection type A and B is approximately 47% and 13% affected individuals, respectively.^[1]

References

↑ ^1.0 ^1.1 Howard, Dominic P.J.; Banerjee, Amitava; Fairhead, Jack F.; Perkins, Jeremy; Silver, Louise E.; Rothwell, Peter M. (2013). “Population-Based Study of Incidence and Outcome of Acute Aortic Dissection and Premorbid Risk Factor Control”. Circulation. 127 (20): 2031–2037. doi:10.1161/CIRCULATIONAHA.112.000483. ISSN 0009-7322.
↑ ^2.0 ^2.1 Olsson, Christian; Thelin, Stefan; Ståhle, Elisabeth; Ekbom, Anders; Granath, Fredrik (2006). “Thoracic Aortic Aneurysm and Dissection”. Circulation. 114 (24): 2611–2618. doi:10.1161/CIRCULATIONAHA.106.630400. ISSN 0009-7322.
↑ “Correspondence”. The Annals of Thoracic Surgery. 67 (2): 593. 1999. doi:10.1016/S0003-4975(99)00037-5. ISSN 0003-4975.
↑ Harris, Donald; Klyushnenkova, Elena; Kalsi, Richa; Garrido, Danon; Bhardwaj, Abhishek; Rabin, Joseph; Toursavadkohi, Shahab; Diaz, Jose; Crawford, Robert (2016). “Non-White Race Is an Independent Risk Factor for Hospitalization for Aortic Dissection”. Ethnicity & Disease. 26 (3): 363. doi:10.18865/ed.26.3.363. ISSN 1945-0826.

Template:WH

Template:WS CME Category::Cardiology

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Raviteja Guddeti, M.B.B.S. [3] Sahar Memar Montazerin, M.D.[4]

Overview

Common risk factors in the development of aortic dissection include aging, atherosclerosis, diabetes, hypertension and trauma. Less common risk factors include bicuspid aortic valve, cocaine abuse, coarctation of the aorta, cystic medial necrosis, a history of collagen vascular disoders, giant cell arteritis, heart surgery, pseudoxanthoma elasticum, Turner’s syndrome, tertiary syphilis and the third trimester of pregnancy.

Risk Factors

Common risk factors in the development of aortic dissection include:^[1]^[2]^[3]

Aging with the highest incidence in individuals who are 50 to 70 years old
Atherosclerosis and its associated risk factors like diabetes
Bicuspid aortic valve especially important in ascending aorta dissection^[4]
- The risk of dissection in individuals with bicuspid aortic valve is not associated with the degree of stenosis of the valve.
Chest trauma including blunt trauma and iatrogenic (for example during cardiac catheterization or due to an intra-aortic balloon pump)
Coarctation of the aorta^[5]

Less Common Risk Factors

Less common risk factors in the development of aortic dissection include:^[6]^[7]^[8]^[9]

Cocaine abuse
Cystic medial necrosis
Deceleration trauma most commonly causes aortic rupture, not dissection
Diabetes
A history of collagen vascular disorders such as:
- Ehlers-Danlos syndrome
- Marfan syndrome
Familial hypercholesterolemia
Giant cell arteritis
Heart surgery particularly aortic valve replacement
Hypertension most frequently in those with type III dissection
Male gender
Preexisting aortic aneurysm
Preexisting aortic valve disease
Prior aortic aneurysm repair
Prior aortic dissection
Prior aortic dissection repair
Pseudoxanthoma elasticum
Tertiary syphilis
Tetralogy of Fallot
Third trimester of pregnancy
Turner’s syndrome due to aortic root dilatation in this syndrome
Vasculitis (inflammation (rarely)

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease (DO NOT EDIT)^[10]

Estimation of Pretest Risk of Thoracic Aortic Dissection (DO NOT EDIT)^[10]

Class I
“1. Providers should routinely evaluate any patient presenting with complaints that may represent acute thoracic aortic dissection to establish a pretest risk of disease that can then be used to guide diagnostic decisions. This process should include specific questions about medical history, family history, and pain features as well as a focused examination to identify findings that are associated with aortic dissection, including:
a. High-risk conditions and historical features^[11] (Level of Evidence: B): Marfan syndrome, Loeys-Dietz syndrome, vascular Ehlers-Danlos syndrome, Turner syndrome, or other connective tissue disease. Patients with mutations in genes known to predispose to thoracic aortic aneurysms and dissection, such as FBN1, TGFBR1, TGFBR2, ACTA2, and MYH11. Family history of aortic dissection or thoracic aortic aneurysm. Known aortic valve disease. Recent aortic manipulation (surgical or catheter-based). Known thoracic aortic aneurysm.
b. High-risk chest, back, or abdominal pain features^[12]^[11]^[13]^[14]^[15]^[16]^[17](Level of Evidence: B): Pain that is abrupt or instantaneous in onset. Pain that is severe in intensity. Pain that has a ripping, tearing, stabbing, or sharp quality.
c. High-risk examination features^[12]^[18]^[13]^[17]^[19]^[20]^[21] (Level of Evidence: B): Pulse deficit. Systolic blood pressure limb differential greater than 20 mm Hg. Focal neurologic deficit. Murmur of aortic regurgitation (new).”
“2. Patients presenting with sudden onset of severe chest, back, and/or abdominal pain, particularly those less than 40 years of age, should be questioned about a history and examined for physical features of Marfan syndrome, Loeys-Dietz syndrome, vascular Ehlers-Danlos syndrome, Turner syndrome, or other connective tissue disorders associated with thoracic aortic disease.^[11] (Level of Evidence: B)”
“3. Patients presenting with sudden onset of severe chest, back, and/or abdominal pain should be questioned about a history of aortic pathology in immediate family members as there is a strong familial component to acute thoracic aortic disease.^[11] (Level of Evidence: B)”
“4. Patients presenting with sudden onset of severe chest, back, and/or abdominal pain should be questioned about recent aortic manipulation (surgical or catheter-based) or a known history of aortic valvular disease, as these factors predispose to acute aortic dissection. (Level of Evidence: C)”
“5. In patients with suspected or confirmed aortic dissection who have experienced a syncopal episode, a focused examination should be performed to identify associated neurologic injury or the presence of pericardial tamponade. (Level of Evidence: C)”
“6. All patients presenting with acute neurologic complaints should be questioned about the presence of chest, back, and/or abdominal pain and checked for peripheral pulse deficits as patients with dissection related neurologic pathology are less likely to report thoracic pain than the typical aortic dissection patient.^[20]

References

↑ Larson, Eric W.; Edwards, William D. (1984). “Risk factors for aortic dissection: A necropsy study of 161 cases”. The American Journal of Cardiology. 53 (6): 849–855. doi:10.1016/0002-9149(84)90418-1. ISSN 0002-9149.
↑ Januzzi, James L; Isselbacher, Eric M; Fattori, Rossella; Cooper, Jeanna V; Smith, Dean E; Fang, Jianming; Eagle, Kim A; Mehta, Rajendra H; Nienaber, Christoph A; Pape, Linda A (2004). “Characterizing the young patient with aortic dissection: results from the international registry of aortic dissection (IRAD)”. Journal of the American College of Cardiology. 43 (4): 665–669. doi:10.1016/j.jacc.2003.08.054. ISSN 0735-1097.
↑ “Correspondence”. The Annals of Thoracic Surgery. 67 (2): 593. 1999. doi:10.1016/S0003-4975(99)00037-5. ISSN 0003-4975.
↑ Losenno, Katie L.; Goodman, Robert L.; Chu, Michael W. A. (2012). “Bicuspid Aortic Valve Disease and Ascending Aortic Aneurysms: Gaps in Knowledge”. Cardiology Research and Practice. 2012: 1–16. doi:10.1155/2012/145202. ISSN 2090-8016.
↑ Senaha S, Uezu T, Shimoji M, Akasaki M (March 2015). “[Stanford type B aortic dissection associated with coarctation of the aorta]”. Kyobu Geka (in Japanese). 68 (3): 184–7. PMID 25743550.
↑ Dioguardi GS, Pimenta J, Knoplich J, Ghorayeb N, Ramos LR, Giannini SD (June 1994). “[Risk factors for cardiovascular diseases in physicians. Preliminary data from the VIDAM Project of the Paulista Medical Association]”. Arq. Bras. Cardiol. (in Portuguese). 62 (6): 383–8. PMID 7826227.
↑ Caglayan, Ahmet Okay; Dundar, Munis (2009). “Inherited diseases and syndromes leading to aortic aneurysms and dissections”. European Journal of Cardio-Thoracic Surgery. 35 (6): 931–940. doi:10.1016/j.ejcts.2009.01.006. ISSN 1010-7940.
↑ “Acute aortic dissection: pathogenesis, risk factors and diagnosis”. Swiss Medical Weekly. 147 (3334). 2017. doi:10.4414/smw.2017.14489. ISSN 1424-7860.
↑ Increased maternal cardiovascular mortality associated with pregnancy in women with Turner syndrome.
↑ ^10.0 ^10.1 Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE; et al. (2010). “2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine”. Circulation. 121 (13): e266–369. doi:10.1161/CIR.0b013e3181d4739e. PMID 20233780.
↑ ^11.0 ^11.1 ^11.2 ^11.3 Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, Evangelista A, Fattori R, Suzuki T, Oh JK, Moore AG, Malouf JF, Pape LA, Gaca C, Sechtem U, Lenferink S, Deutsch HJ, Diedrichs H, Marcos y Robles J, Llovet A, Gilon D, Das SK, Armstrong WF, Deeb GM, Eagle KA (February 2000). “The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease”. JAMA. 283 (7): 897–903. doi:10.1001/jama.283.7.897. PMID 10685714.
↑ ^12.0 ^12.1 Coady MA, Davies RR, Roberts M, Goldstein LJ, Rogalski MJ, Rizzo JA, Hammond GL, Kopf GS, Elefteriades JA (April 1999). “Familial patterns of thoracic aortic aneurysms”. Arch Surg. 134 (4): 361–7. doi:10.1001/archsurg.134.4.361. PMID 10199307.
↑ ^13.0 ^13.1 von Kodolitsch Y, Schwartz AG, Nienaber CA (October 2000). “Clinical prediction of acute aortic dissection”. Arch. Intern. Med. 160 (19): 2977–82. doi:10.1001/archinte.160.19.2977. PMID 11041906.
↑ Mészáros I, Mórocz J, Szlávi J, Schmidt J, Tornóci L, Nagy L, Szép L (May 2000). “Epidemiology and clinicopathology of aortic dissection”. Chest. 117 (5): 1271–8. doi:10.1378/chest.117.5.1271. PMID 10807810.
↑ Spittell PC, Spittell JA, Joyce JW, Tajik AJ, Edwards WD, Schaff HV, Stanson AW (July 1993). “Clinical features and differential diagnosis of aortic dissection: experience with 236 cases (1980 through 1990)”. Mayo Clin. Proc. 68 (7): 642–51. doi:10.1016/s0025-6196(12)60599-0. PMID 8350637.
↑ Mehta RH, O’Gara PT, Bossone E, Nienaber CA, Myrmel T, Cooper JV, Smith DE, Armstrong WF, Isselbacher EM, Pape LA, Eagle KA, Gilon D (August 2002). “Acute type A aortic dissection in the elderly: clinical characteristics, management, and outcomes in the current era”. J. Am. Coll. Cardiol. 40 (4): 685–92. doi:10.1016/s0735-1097(02)02005-3. PMID 12204498.
↑ ^17.0 ^17.1 Klompas M (May 2002). “Does this patient have an acute thoracic aortic dissection?”. JAMA. 287 (17): 2262–72. doi:10.1001/jama.287.17.2262. PMID 11980527.
↑ Januzzi JL, Isselbacher EM, Fattori R, Cooper JV, Smith DE, Fang J, Eagle KA, Mehta RH, Nienaber CA, Pape LA (February 2004). “Characterizing the young patient with aortic dissection: results from the International Registry of Aortic Dissection (IRAD)”. J. Am. Coll. Cardiol. 43 (4): 665–9. doi:10.1016/j.jacc.2003.08.054. PMID 14975480.
↑ Armstrong WF, Bach DS, Carey LM, Froehlich J, Lowell M, Kazerooni EA (December 1998). “Clinical and echocardiographic findings in patients with suspected acute aortic dissection”. Am. Heart J. 136 (6): 1051–60. doi:10.1016/s0002-8703(98)70162-0. PMID 9842019.
↑ ^20.0 ^20.1 Gaul C, Dietrich W, Friedrich I, Sirch J, Erbguth FJ (February 2007). “Neurological symptoms in type A aortic dissections”. Stroke. 38 (2): 292–7. doi:10.1161/01.STR.0000254594.33408.b1. PMID 17194878.
↑ Roberts WC, Ko JM, Moore TR, Jones WH (August 2006). “Causes of pure aortic regurgitation in patients having isolated aortic valve replacement at a single US tertiary hospital (1993 to 2005)”. Circulation. 114 (5): 422–9. doi:10.1161/CIRCULATIONAHA.106.622761. PMID 16864725.

Template:WH Template:WS CME Category::Cardiology

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]; Raviteja Guddeti, M.B.B.S. [3]; Laith Adnan Allaham, M.D.[4]

Overview

Screening guidelines state that an EKG should be obtained for all patients who present with symptoms suspicious for aortic dissection. A chest x ray should be obtained in patients determined to be at low-risk and moderate-risk. In patients in high-risk categories, TEE, CT or MRI should be obtained.

Screening

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease (DO NOT EDIT)^[1]

Class I
“1. An electrocardiogram should be obtained on all patients who present with symptoms that may represent acute thoracic aortic dissection.
a. Given the relative infrequency of dissection-related coronary artery occlusion, the presence of ST-segment elevation suggestive of myocardial infarction should be treated as a primary cardiac event without delay for definitive aortic imaging unless the patient is at high risk for aortic dissection.^[2]^[3] (Level of Evidence: B)”
“2. The role of chest x-ray in the evaluation of possible thoracic aortic disease should be directed by the patient’s pretest risk of disease as follows:
a. Intermediate risk: Chest x-ray should be performed on all intermediate-risk patients, as it may establish a clear alternate diagnosis that will obviate the need for definitive aortic imaging. (Level of Evidence: C)
b. Low risk: Chest x-ray should be performed on all low-risk patients, as it may either establish an alternative diagnosis or demonstrate findings that are suggestive of thoracic aortic disease, indicating the need for urgent definitive aortic imaging. (Level of Evidence: C)”
“3. Urgent and definitive imaging of the aorta using transesophageal echocardiogram, computed tomographic imaging, or magnetic resonance imaging is recommended to identify or exclude thoracic aortic dissection in patients at high risk for the disease by initial screening.^[4]^[5]^[6]^[7]^[8]^[9]^[10] (Level of Evidence: B)”

Class III (No Benefit)
“1. A negative chest x-ray should not delay definitive aortic imaging in patients determined to be high risk for aortic dissection by initial screening. (Level of Evidence: C)”

Genetic Syndromes of Familial Thoracic Aortic Aneurysms and Dissections (DO NOT EDIT) ^[1]

Class IIa
“1. Sequencing of the ACTA2 gene is reasonable in patients with a family history of thoracic aortic aneurysms and/or dissections to determine if ACTA2 mutations are responsible for the inherited predisposition.^[11]^[12]^[13]^[14]^[15]^[16] (Level of Evidence: B)”

Class IIb
“1. Sequencing of other genes known to cause familial thoracic aortic aneurysms and/or dissection (TGFBR1, TGFBR2, MYH11) may be considered in patients with a family history and clinical features associated with mutations in these genes.^[11]^[12]^[13]^[14]^[15]^[16] (Level of Evidence: B)”
“2. If one or more first-degree relatives of a patient with known thoracic aortic aneurysm and/or dissection are found to have thoracic aortic dilatation, aneurysm, or dissection, then referral to a geneticist may be considered. (Level of Evidence: C)”

References

↑ ^1.0 ^1.1 Hiratzka LF, Bakris GL, Beckman JA; et al. (2010). “2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine”. Circulation. 121 (13): e266–369. doi:10.1161/CIR.0b013e3181d4739e. PMID 20233780. Unknown parameter |month= ignored (help)
↑ Hagan PG, Nienaber CA, Isselbacher EM; et al. (2000). “The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease”. JAMA. 283 (7): 897–903. PMID 10685714. Unknown parameter |month= ignored (help)
↑ Klompas M (2002). “Does this patient have an acute thoracic aortic dissection?”. JAMA. 287 (17): 2262–72. PMID 11980527. Unknown parameter |month= ignored (help)
↑ Yoshida S, Akiba H, Tamakawa M; et al. (2003). “Thoracic involvement of type A aortic dissection and intramural hematoma: diagnostic accuracy–comparison of emergency helical CT and surgical findings”. Radiology. 228 (2): 430–5. doi:10.1148/radiol.2282012162. PMID 12819341. Unknown parameter |month= ignored (help)
↑ Sommer T, Fehske W, Holzknecht N; et al. (1996). “Aortic dissection: a comparative study of diagnosis with spiral CT, multiplanar transesophageal echocardiography, and MR imaging”. Radiology. 199 (2): 347–52. PMID 8668776. Unknown parameter |month= ignored (help)
↑ Zeman RK, Berman PM, Silverman PM; et al. (1995). “Diagnosis of aortic dissection: value of helical CT with multiplanar reformation and three-dimensional rendering”. AJR Am J Roentgenol. 164 (6): 1375–80. PMID 7754876. Unknown parameter |month= ignored (help)
↑ Shiga T, Wajima Z, Apfel CC, Inoue T, Ohe Y (2006). “Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging for suspected thoracic aortic dissection: systematic review and meta-analysis”. Arch. Intern. Med. 166 (13): 1350–6. doi:10.1001/archinte.166.13.1350. PMID 16831999. Unknown parameter |month= ignored (help)
↑ Nienaber CA, von Kodolitsch Y, Nicolas V; et al. (1993). “The diagnosis of thoracic aortic dissection by noninvasive imaging procedures”. N. Engl. J. Med. 328 (1): 1–9. doi:10.1056/NEJM199301073280101. PMID 8416265. Unknown parameter |month= ignored (help)
↑ Erbel R, Engberding R, Daniel W, Roelandt J, Visser C, Rennollet H (1989). “Echocardiography in diagnosis of aortic dissection”. Lancet. 1 (8636): 457–61. PMID 2563839. Unknown parameter |month= ignored (help)
↑ Börner N, Erbel R, Braun B, Henkel B, Meyer J, Rumpelt J (1984). “Diagnosis of aortic dissection by transesophageal echocardiography”. Am. J. Cardiol. 54 (8): 1157–8. PMID 6496346. Unknown parameter |month= ignored (help)
↑ ^11.0 ^11.1 Pannu H, Fadulu VT, Chang J, Lafont A, Hasham SN, Sparks E; et al. (2005). “Mutations in transforming growth factor-beta receptor type II cause familial thoracic aortic aneurysms and dissections”. Circulation. 112 (4): 513–20. doi:10.1161/CIRCULATIONAHA.105.537340. PMID 16027248.
↑ ^12.0 ^12.1 Guo DC, Pannu H, Tran-Fadulu V, Papke CL, Yu RK, Avidan N; et al. (2007). “Mutations in smooth muscle alpha-actin (ACTA2) lead to thoracic aortic aneurysms and dissections”. Nat Genet. 39 (12): 1488–93. doi:10.1038/ng.2007.6. PMID 17994018.
↑ ^13.0 ^13.1 Zhu L, Vranckx R, Khau Van Kien P, Lalande A, Boisset N, Mathieu F; et al. (2006). “Mutations in myosin heavy chain 11 cause a syndrome associating thoracic aortic aneurysm/aortic dissection and patent ductus arteriosus”. Nat Genet. 38 (3): 343–9. doi:10.1038/ng1721. PMID 16444274.
↑ ^14.0 ^14.1 Loeys BL, Schwarze U, Holm T, Callewaert BL, Thomas GH, Pannu H; et al. (2006). “Aneurysm syndromes caused by mutations in the TGF-beta receptor”. N Engl J Med. 355 (8): 788–98. doi:10.1056/NEJMoa055695. PMID 16928994.
↑ ^15.0 ^15.1 Stheneur C, Collod-Béroud G, Faivre L, Gouya L, Sultan G, Le Parc JM; et al. (2008). “Identification of 23 TGFBR2 and 6 TGFBR1 gene mutations and genotype-phenotype investigations in 457 patients with Marfan syndrome type I and II, Loeys-Dietz syndrome and related disorders”. Hum Mutat. 29 (11): E284–95. doi:10.1002/humu.20871. PMID 18781618.
↑ ^16.0 ^16.1 Guo DC, Papke CL, Tran-Fadulu V, Regalado ES, Avidan N, Johnson RJ; et al. (2009). “Mutations in smooth muscle alpha-actin (ACTA2) cause coronary artery disease, stroke, and Moyamoya disease, along with thoracic aortic disease”. Am J Hum Genet. 84 (5): 617–27. doi:10.1016/j.ajhg.2009.04.007. PMC 2680995. PMID 19409525.

Template:WH Template:WS CME Category::Cardiology

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Sahar Memar Montazerin, M.D.[3]

Overview

The symptoms of aortic dissection usually develop in the fifth decade of life and start with symptoms such as sudden onset chest/back pain. If left untreated, patients with aortic dissection may progress to develop aortic regurgitation, myocardial ischemia, and cardiac tamponade. The complications of aortic dissection include but not limited to aortic rupture, pericardial tamponade, myocardial ischemia, compression of nearby organs and etc. Aortic dissection carries a poor prognosis. Mortality rate differs based on the type of dissection and is higher in type A compared to type B (25% versus 12%).

Natural History, Complications, and Prognosis

Natural History

The symptoms of aortic dissection usually develop in the fifth decade of life and start with symptoms such as sudden onset chest/back pain.^[1]
If left untreated, patients with aortic dissection may progress to develop aortic regurgitation, myocardial ischemia, and cardiac tamponade.

Complications

The complications of aortic dissection include:^[2]^[3]^[4]^[5]^[6]^[7]

Cardiovascualr Complications

Aortic rupture
Pericardial tamponade
Acute aortic regurgitation
Myocardial ischemia
Thoracic aortic aneurysm
Renal ischemia
Superior mesenteric artery dissection and resultant visceral ischemia
Pleural effusion
Claudication due to an extension of the dissection into the iliac arteries

Neurologic Complications

Ischemic cerebrovascular accident (CVA) due to dissection into the head vessels
Hemiplegia due to dissection into the spinal arteries
Hemianesthesia due to dissection into the spinal arteries

Compression of Nearby Organs

Superior vena cava syndrome due to compression of the superior vena cava
Horner syndrome (compression of the superior cervical ganglia)
Dysphagia due to (compression of the esophagus)
Stridor and wheezing (compression of the airway)
Hemoptysis (compression of and erosion into the bronchus)
Vocal cord paralysis and hoarseness (compression of the recurrent laryngeal nerve)

Prognosis

Aortic dissection carries a poor prognosis.^[8]
Mortality rate differs based on the type of dissection and is higher in type A compared to type B (25% versus 12%).

References

↑ Juang, Derek; Braverman, Alan C.; Eagle, Kim (2008). “Aortic Dissection”. Circulation. 118 (14). doi:10.1161/CIRCULATIONAHA.108.799908. ISSN 0009-7322.
↑ Cambria, Richard P.; Brewster, David C.; Gertler, Jonathan; Moncure, Ashby C.; Gusberg, Richard; Tilson, M.David; Darling, R.Clement; Hammond, Grahme; Megerman, Joseph; Abbott, William M. (1988). “Vascular complications associated with spontaneous aortic dissection”. Journal of Vascular Surgery. 7 (2): 199–209. doi:10.1016/0741-5214(88)90137-1. ISSN 0741-5214.
↑ Fadahunsi, Opeyemi; Romeo, Michael (2014). “Cardiac tamponade – presentation of type A aortic dissection”. Journal of Community Hospital Internal Medicine Perspectives. 4 (5): 25449. doi:10.3402/jchimp.v4.25449. ISSN 2000-9666.
↑ Cai, Jingjing; Cao, Yu; Yuan, Hong; Yang, Kan; Zhu, Yuan-Shan (2012). “Inferior myocardial infarction secondary to aortic dissection associated with bicuspid aortic valve”. Journal of Cardiovascular Disease Research. 3 (2): 138–142. doi:10.4103/0975-3583.95370. ISSN 0975-3583.
↑ Siegelman, Stanley S.; Sprayregen, Seymour; Strasberg, Zeno; Attai, Lari A.; Robinson, George (1970). “Aortic Dissection and the Left Renal Artery”. Radiology. 95 (1): 73–78. doi:10.1148/95.1.73. ISSN 0033-8419.
↑ Blanco, M.; Díez-Tejedor, E.; Larrea, J. L.; Ramírez, U. (1999). “Neurologic complications of type I aortic dissection”. Acta Neurologica Scandinavica. 99 (4): 232–235. doi:10.1111/j.1600-0404.1999.tb07352.x. ISSN 0001-6314.
↑ Arata, Kenichi; Imagama, Itsumi; Shigehisa, Yoshiya; Mukaihara, Kousuke; Toyokawa, Kenji; Matsuba, Tomoyuki; Imoto, Yutaka (2015). “Aortic Fenestration for Type B Chronic Aortic Dissection Complicated with Lower Limb Malperfusion Induced by Walking Exercise”. Annals of Vascular Diseases. 8 (1): 29–32. doi:10.3400/avd.cr.14-00101. ISSN 1881-641X.
↑ “Correspondence”. The Annals of Thoracic Surgery. 67 (2): 593. 1999. doi:10.1016/S0003-4975(99)00037-5. ISSN 0003-4975.

Template:WH Template:WS CME Category::Cardiology

Diagnosis

Treatment

Medical Therapy | Surgery | Secondary Prevention |

Special Scenarios

Management During Pregnancy

Case Studies

Case #1

Related Chapters

Template:WikiDoc Sources CME Category::Cardiology

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[3] Case courtesy of Wikimedia Commons

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Aortic dissection

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Aortic Dissection from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Imaging in Acute Aortic Dissection

Chest X-ray

CT

MRI

Echocardiography

Treatment

Medical Therapy

Surgery

Secondary Prevention

Overview

Historical Perspective

Discovery

Landmark Events in the Development of Treatment Strategies

Impact on Cultural History

Famous Cases

References

Overview

Classification

DeBakey Classification System

Stanford Classification System

References

Overview

Pathophysiology

Normal Anatomy of the Aorta

Pathogenesis

Initial Intimal Tear

Location of Dissections

Propagation of the Intimal Tear

Aortic Dissection in the Absence of an Intimal Tear

Genetics

Associated Conditions

Gross Pathology

Microscopic Pathology

References

Overview

Causes

Common Causes

Causes by Organ System

References

Overview

Differentiating Aortic Dissection from other Diseases

Differentiating Aortic Dissection from other Diseases on the Basis of Chest Pain

References

Overview

Epidemiology and Demographics

Incidence

Age

Race

Gender

Mortality rate

References

Overview

Risk Factors

Less Common Risk Factors

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease (DO NOT EDIT)[10]

Estimation of Pretest Risk of Thoracic Aortic Dissection (DO NOT EDIT)[10]

References

Overview

Screening

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease (DO NOT EDIT)[1]

Genetic Syndromes of Familial Thoracic Aortic Aneurysms and Dissections (DO NOT EDIT) [1]

References

Overview

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease (DO NOT EDIT)^[10]

Estimation of Pretest Risk of Thoracic Aortic Dissection (DO NOT EDIT)^[10]

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease (DO NOT EDIT)^[1]

Genetic Syndromes of Familial Thoracic Aortic Aneurysms and Dissections (DO NOT EDIT) ^[1]