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DISEASES OF AORTIC
PHUNG HUY HOANG, MD MSc
A p r i l 2 0 2 0

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Aorta
Thoracic component
Ascending segment
Arch
Decending segment
Abdominal component
Suprarenal segment
Infrerenal segment

Braverman A. C., Schermerhorn M. (2019), Braunwald’s
Heart Disease: A Textbook Of Cardiovascular Medicine,
Douglas P. Zipes, et al., Editors, Elsevier, pp. 1295-1327
• Aortic root = aortic valve  sinotubular junction
• Aortic isthmus = aortic arch joins descending aorta (~
ligamentum arteriosum): vulnerable to deceleration
trauma  transition between ascending aorta (mobile)
and arch, descending aorta (relatively fixed)
• Abdominal aorta normally < diameter than thoracic

Creager M. A., Loscalzo J. (2018), Harrison's Principles of Internal Medicine, J. Larry Jameson, et al., Editors, McGraw-Hill, pp. 1917-1923

Lang R. M., Goldstein S. A., Kronzon I., et al. (2016), "ASE’s Comprehensive
Echocardiography", Elsevier

Otto C. M., Schwaegler R. G., Freeman R. V. (2016), Echocardiography Review Guide Companion To The Textbook Of Clinical Echocardiography, Elsevier, pp. 334-354

Armstrong W. F., Ryan T. (2019), Feigenbaum’s Echocardiography, Wolters Kluwer

Elefteriades J. A., Olin J. W., Halperin J. L., et al. (2017), Hurst’s The Heart,
Valentin Fuster, et al., Editors, McGraw-Hill, pp. 2157-2194
(in IMH, the D-dimer may not be elevated)

9
AORTIC ANEURYSMS
A p r i l 2 0 2 0

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OVERVIEW
• Aneurysm (Greek aneurysma) = a pathologic dilation of a segment of a blood vessel
• ≠ Ectasia: modest generalized dilation and elongation of the aorta that occurs with aging1
• 2nd most frequent disease of the aorta after atherosclerosis1
• 19th most common cause of death, 15th most common in those older than 652
• Abnormal aortic dilation =  in diameter ≥ 50% (x1.5) than expected for same segment in
unaffected individuals of same age and sex3
• Discription = size, location, morphology, cause
• Thoracoabdominal aortic aneurysm (3-10%): descending thoracic aneurysms extending
distally to involve the abdominal aorta4
1. Goldstein S. A., Evangelista A., Abbara S., et al. (2015), J Am Soc Echocardiogr, 28 (2), pp. 119-82
2. National Center for Injury Prevention and Control. WISQARS leading causes of death reports, 1999–2007. 2015
3. Karthikesalingam A., Bahia S. S., Patterson B. O., et al. (2013), Eur J Vasc Endovasc Surg, 46 (5), pp. 533-41
4. Elefteriades J. A., Olin J. W., Halperin J. L., et al. (2017), Hurst’s The Heart, Valentin Fuster, et al., Editors, McGraw-Hill, pp. 2157-2194

Teo E. P., Isselbacher E. M. (2019), Essential Echocardiography A Companion To Braunwald’s
Heart Disease, Scott D. Solomon, Justina C. Wu, Linda D. Gillam, Editors, pp. 354-369

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• Fusiform: more common, symmetrically dilated with involvement of the entire aortic
circumference.
• Saccular: focal outpouching, intact but dilated aortic wall involving all layers
• Pseudoaneurysms (“false” aneurysms): bleeding  contained periaortic hematoma in
continuity with the aortic lumen.

Elefteriades J. A., Olin J. W., Halperin J. L., et al. (2017), Hurst’s The Heart, Valentin Fuster, et al., Editors, McGraw-Hill, pp. 2157-2194

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OVERVIEW
•  risk of cardiovascular events (mostly unrelated to aneurysm): common risk factors (e.g.
smoking or hypertension), pathways (e.g. inflammation) //  risk of cardiovascular
comorbidities at the time of aneurysm diagnosis
• Aortic aneurysm identified at any location  assessment entire aorta and aortic valve at
baseline and during follow-up (I-C)
Erbel R., Aboyans V., Boileau C., et al. (2014), Eur Heart J, 35 (41), pp. 2873-926

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PATHOPHYSIOLOGY
• Chronic aortic wall inﬂammation
• Increased local expression of proteinases
• Degradation of structural connective tissue proteins

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ABDOMINAL
AORTIC ANEURYSM

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ABDOMINAL AORTIC ANEURYSM (AAA)
Overview
• Abdominal aorta ≥ 3.0 cm in diameter1
• Most common form of aortic aneurysms2,5
• Most AAAs (>80-90%): infrarenal aorta2,5, most small AAA5
• 10%: may involve pararenal or visceral aorta  extend into thoracoabdominal segment2
• Strongly associated with: age (most occurring ≥ 60 years), male (x5), cigarette smoking,
emphysema, hypertension, hyperlipidemia, diabetes, family history (20%) 2,3.4,5
• Coexisting thoracic aortic aneurysm (25%), iliac and popliteal aneurysms4
1. Moll F. L., Powell J. T., Fraedrich G., et al. (2011), Eur J Vasc Endovasc Surg, 41 Suppl 1, pp. S1-S58
2. Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp. 1295-1327
3. Chaikof E. L., Brewster D. C., Dalman R. L., et al. (2009), J Vasc Surg, 50 (4 Suppl), pp. S2-49
4. Erbel R., Aboyans V., Boileau C., et al. (2014), Eur Heart J, 35 (41), pp. 2873-926
5. Shah J., Braverman A. C. (2009), The Washington Manual Cardiology Subspeciatly Consult, Phillip S. Cuculich, Andrew M. Kates, Thomas M. De Fer, Editors, Wolters Kluwer, pp.
497-518.

Lederle F. A. (2016), Goldman-Cecil Medicine, Lee Goldman , Andrew I. Schafer, Editors, Elsevier Saunders, pp. 492-497

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Clinical features
• Develop insidiously over several years (0.2 to 0.3 cm/year,  as aortic diameter )1
• Back or abdominal pain: most common presenting symptom (severe, abrupt in onset, with
describing a ripping or tearing pain)
• Symptoms rarely, except:
• Distal thromboembolism (from mural thrombi, 2-5%)
• Rapid expansion
• Impending rupture, or rupture
• Physical examination
• Insensitive in detecting (30-40%)2
• Abdominal palpation: pulsatile epigastric or periumbilical mass

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Clinical features
• Predicting rupture
• Aneurysm diameter (most important), wall tension, wall stiffness, peak wall stress
• Female > male at same diameter
• RUPTURE INTO
• Peritoneal cavity: acute hemorrhage, severe abdominal pain, hypotension
• Retroperitoneum: temporarily contained periaortic hematoma (± Cullen, Grey Turner sign,
iliopsoas sign, compress the femoral nerve), severe abdominal or back pain may radiate to
ﬂank or groin
• Aortoenteric fistulas (unexplained, high volume GI bleeding)
• Aortovenous fistulas (cause high-output HF, leg swelling)
• Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp. 1295-1327
• Erbel R., Aboyans V., Boileau C., et al. (2014), Eur Heart J, 35 (41), pp. 2873-926
• Prince L. A., Johnson G. A. (2016), Tintinalli’s Emergency Medicine A Comprehensive Study Guide, Judith E. Tintinalli, et al., Editors, McGraw Hill, pp. 416-420

23
Diagnostic imaging
• US
• Can detect AAAs with high accuracy (> 90%) + inexpensive, noninvasive, avoids
radiation and contrast agents  preferred over CT in screening CT
• CT, MRI
• Detect and measurement of aneurysm diameter accurately
• Useful in demonstrating relationship of AAA to renal, visceral, iliac arteries + patterns of
mural thrombus, calcifcation, or coexisting occlusive atherosclerosis  inﬂuence AAA
repair
• Aassess AAA variants (inﬂammatory AAAs, mycotic aneurysms)

Prince L. A., Johnson G. A. (2016), Tintinalli’s Emergency Medicine A Comprehensive Study Guide, Judith E. Tintinalli, et al., Editors, McGraw Hill, pp. 416-420

25
Treatment indications
• Small AAA < 5.5cm and slow growth (<1cm/y): can be observed safely = imaging surveillance
(various sizes strategy)3,4
• Smoking cessation (slow growth)
• Control hypertension
• Statins and ACE-inhibitors may be considered (IIb-B) ( aortic complications in small AAA)3,4
• REPAIR INDICATIONS (individualize!)
• Asymptomatic, >5.0-5.5 cm in diameter
• Symptomatic of any size
• Rapid growth (>1 cm/yr)

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Treatment
Size (cm) Interval
2.5-2.9 7y
3.0-3.9 3y
4.0-4.9 12m
5.0-5.4 6m
Size (cm) Interval
2.5-2.9 4y
3.0-3.9 3y
4.0-4.4 2y
> 4.5 1y
SVS 2009 ESC 2014

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Screening
• Most frequent mode of detection: incidental
• Screening = ultrasound + repair of AAAs > size threshold  reduced AAA-related deaths
• SVS (2009): recommends a one-time screening for AAAs in all men and women 65 or older
with a history of tobacco use or a family history of AAA1
• ESC (2014)2
• Recommended in all men >65 yo (I-A)
• Considered in women >65 yo + history of current/past smoking (IIb-C)
• NOT recommended in female nonsmokers without familial history (III-C)
• Considered in first-degree siblings of a patient with AAA (IIa-B)
• Duplex ultrasound for screening of peripheral artery disease and peripheral aneurysms (IIa-
C)21. Chaikof E. L., Brewster D. C., Dalman R. L., et al. (2009), J Vasc Surg, 50 (4 Suppl), pp. S2-49

Bertino R. E., Mustafaraj E. (2018), Diagnostic Ultrasound, Carol M. Rumack , Deborah Levine, Editors, Elsevier, pp. 432-470

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Prognosis
• 30-50% of ruptured AAAs die before hospitalization
• An additional 30-40% die after reaching a hospital but before treatment
• Operative mortality rate for open surgical repair after AAA rupture: 40-50%, may be lower
with EVAR
• Moll F. L., Powell J. T., Fraedrich G., et al. (2011), Eur J Vasc Endovasc Surg, 41 Suppl 1, pp. S1-S58
• Chaikof E. L., Brewster D. C., Dalman R. L., et al. (2009), J Vasc Surg, 50 (4 Suppl), pp. S2-49

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THORACIC
AORTIC ANEURYSM

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THORACIC AORTIC ANEURYSM (TAA)
Overview
• Cause, natural history, treatment vary ∈ location of TAA
• Prevalence1:
• Aortic root or ascending aortic: most common (60%)
• Descending aorta (35%)
• Aortic arch (<10%)
• Majority descending TAA: atherosclerotic2
1. Goldstein S. A., Evangelista A., Abbara S., et al. (2015), J Am Soc Echocardiogr, 28 (2), pp. 119-82

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Pathogenesis
CAUSES OF TAAS
• Heritable disorders
• Genetic (congenital) disorders
• Degenerative (“atherosclerotic”)
• Mechanical
• Inﬂammatory infectious diseases
(syphilis and aortitis)
Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp.
1295-1327
RISK FACTORS FOR TAAS
• Smoking
• Hypertension
• Age
• COPD
• CAD
• Family history

Shah J., Braverman A. C. (2009), The Washington Manual Cardiology Subspeciatly Consult, Phillip S. Cuculich, Andrew M. Kates, Thomas M. De Fer, Editors, Wolters Kluwer, pp. 497-
518

Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp. 1295-1327

39
Manifestation
• Most TAAs: asymptomatic, discovered incidentally
• Suggested physical findings
• Local mass effect
• obstruction of SVC or innominate vein, trachea, bronchus, esophagus
• persistent chest or back pain (compression of intrathoracic structures or erosion into
bone)
• Progressive AR
• Systemic embolization (caused by mural thrombus or atheroembolism)
• Infected TAAs ~ pain, fever, and fistulas

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Manifestation
• Most serious complications
• Dissection (more common)
• Rupture
• Rupture into
• Pleural cavity (usually left) or into the mediastinum: hypotension
• Esophagus: hematemesis
• Bronchus or trachea: hemoptysis

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Diagnosis
• Chest radiographs
• Widened mediastinum, prominent aortic knob, displaced trachea
• Small TAA; Aneurysms involving sinuses of Valsalva and aortic root may not be seen
• TTE: sinuses of Valsalva and often the proximal ascending aorta, aortic arch, and proximal
descending aorta
• TEE: can image most of the thoracic aorta (a small blind spot/ mid-high ascending)
• Contrast-enhanced CT and MRA: provide outstanding detail of aortic and branch vessel
anatomy in TAA disease
Echocardiogram: generally measures internal diameter ≠ CT, MRI measure external diameter
(expected to be 0.2-0.4 cm > internal diameter*,**)
* Goldstein S. A., Evangelista A., Abbara S., et al. (2015), J Am Soc Echocardiogr, 28 (2), pp. 119-82
** Hiratzka L. F., Bakris G. L., Beckman J. A., et al. (2010), Circulation, 121 (13), pp. e266-369

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Natural history
• Relatively indolent, # 1-2 mm/yr // marked individual variability1,2
• RAPID GROWTH INFLUENCING FACTORS1,2
• MFS, BAV disease > degenerative aneurysms
• Larger aneurysms > smaller ones
• Descending aorta (2 mm/yr) > ascending aorta (1 mm/yr)
• Dissected TAAs > without dissection
• RISK FACTORS FOR RUPTURE OF TAAS3
• Aortic diameter (most important), rapid aneurysm growth, aortic dissection
• Older age, cigarette smoking, underlying diseases (COPD), family history
1. Oladokun D., Patterson B. O., Sobocinski J., et al. (2016), Eur J Vasc Endovasc Surg, 51 (5), pp. 674-81
3. Hiratzka L. F., Bakris G. L., Beckman J. A., et al. (2010), Circulation, 121 (13), pp. e266-369

Paradigm of“Guilt by Association”for detection of silent thoracic aortic aneurysms
Elefteriades J. A., Sang A., Kuzmik G., et al. (2015), Open Heart, 2 (1), pp. e000169

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Threshold (cm)
Degenerative aneurysm ≥5.5
Bicuspid aortic valve ≥5.5
Bicuspid aortic valve with risk factors or low surgical risk ≥5.0
Bicuspid aortic valve requiring aortic valve replacement >4.5
Marfan syndrome ≥5.0
Marfan syndrome with risk factors >4.5
Loeys-Dietz syndrome 4.0-4.5
Familial thoracic aortic aneurysm syndromes 4.5-5.0
Turner syndrome >2.5 cm/m2
ROOT AND ASCENDING

50
• Bicuspid aortic valve
• with risk factors = family history of dissection, growth rate ≥ 0.5 cm/yr, coarctation of
the aorta, hypertension, root phenotype
• low surgical risk (<4%)
• Marfan syndrome with risk factors = family history of aortic dissection, rapid aortic growth
(>3 mm/yr), severe AR or MR
• If pregnancy desired, consider prophylactic aortic surgery for aortic diameter of 4.0-4.5
cm

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Threshold (cm)
Isolated aortic arch aneurysm ≥5.5
May be considered in patients with aortic arch aneurysm who already have an
indication for surgery of an adjacent aneurysm located in the ascending or
descending aorta
ARCH

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Threshold (cm)
TEVAR when anatomy suitable ≥5.5
When TEVAR is not technically possible, surgery should be considered ≥6.0
DESCENDING

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Size criteria apply only to
asymptomatic aneurysms!

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Prognosis
• < 50% with rupture arrive at the hospital alive
• Mortality at 24 hours reaches 75%
Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp.
1295-1327

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ACUTE AORTIC SYNDROME
A p r i l 2 0 2 0

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CLASSIFICATION
Aortic rupture
(Classic) Aortic dissection (80-90%)
Intramural hematoma (IMH) (10-20%)
Penetrating atherosclerotic ulcer (PAU) (5%)
• Creager M. A., Loscalzo J. (2018), Harrison's Principles of Internal Medicine, J. Larry
Jameson, et al., Editors, McGraw-Hill, pp. 1917-1923
• Nienaber C. A., Powell J. T. (2012), Eur Heart J, 33 (1), pp. 26-35b

Mussa F. F., Horton J. D., Moridzadeh R., et al. (2016), JAMA, 316 (7), pp. 754-63

Lang R. M., Goldstein S. A., Kronzon I., et al. (2016), "ASE’s Comprehensive Echocardiography", Elsevier

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CLASSIC AORTIC DISSECTION

NEW CLASSIFICATION

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AORTIC DISSECTION
Overview
• Intimal disruption  dissection plane in media
• May propagate
• Anterograde (or less often retrograde)
• Adventitial disruption may lead to rupture OR distal tear(s) results in blood reentering
aortic lumen (more frequently)
• A very high early mortality1.
• Factors associated with delay in diagnosis: female, transfer from another hospital, fever,
normal BP2
1. Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp. 1295-
1327
2. Nienaber C. A., Clough R. E. (2015), The Lancet, 385 (9970), pp. 800-811

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AORTIC DISSECTION
Overview
• Age occurrence1
• Type A 50-60 years
• Type B 60-70 years
• Men > women (2:1-5:1)2
1. Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp. 1295-
1327

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AORTIC DISSECTION
Pathophysiology
• Hypothesis
• Primary tear/aortic intima  blood from aortic lumen penetrating into diseased media
 dissection
• Primary rupture of vasa vasorum  hemorrhage in aortic wall  subsequent intimal
disruption  intimal tear
• Malperfusion: dynamic (overpressurized false lumen), static (dissection ﬂap, hematoma,
embolism, or thrombosis  stenosis or occlusion), or mixed
• Dissected aorta may NOT be dilated
• Inflammatory response to thrombus/media  initiate further necrosis + apoptosis of smooth
muscle cells + degeneration of elastic tissue  potentiates risk of medial rupture
• Subsequent aneurysm formation

Cotarlan V., Austin J. J. (2015), Principles of Critical Care, Gregory A. Schmidt Jesse B.
Hall, John P. Kress, Editor, McGraw Hill Education, pp. 356-368

Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of
Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp. 1295-1327

71
AORTIC DISSECTION
Causes and pathogenesis
• 75% of all patients with aortic dissection have hypertension1
• MFS: high risk for aortic root aneurysm and especially type A dissection1,2
• BAV: important risk factor for ascending aortic aneurysm and dissection3
• Late pregnancy or early postpartum period (most have unknown underlying aortopathy)4
• TAA have risk for aortic dissection, with risk for dissection and rupture = aortic diameter, age,
sex, body size, and rate of aortic growth, mechanical and hemodynamic factors5
1. Pape L. A., Awais M., Woznicki E. M., et al. (2015), J Am Coll Cardiol, 66 (4), pp. 350-8
3. Wojnarski C. M., Svensson L. G., Roselli E. E., et al. (2015), Ann Thorac Surg, 100 (5), pp. 1666-73; discussion 1673-4
4. Wanga S., Silversides C., Dore A., et al. (2016), Can J Cardiol, 32 (1), pp. 78-85.

Shah J., Braverman A. C. (2012), The Washington Manual Of Critical Care, Warren Isakow Marin H. Kollef, Editor, Lippincott Williams & Wilkins, pp. 155-162.

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AORTIC DISSECTION
Classification
• Based on location of dissection: 2 major classifcation schemes DeBakey and Stanford
• ∈ risk of sudden death from the dissection, highest in type A1
• Based on duration from symptoms onset
• Occurence1,2
• Ascending 65% (15% of transverse arch and 5% of descending aortic tears will involve the
ascending aorta by retrograde dissection)
• Descending 30%
• Aortic arch < 10%
• Isolated abdominal aortic dissection rare (1%), associated with existing AAA or an iatrogenic
cause
1. Cotarlan V., Austin J. J. (2015), Principles of Critical Care, Gregory A. Schmidt Jesse B. Hall, John P. Kress, Editor, McGraw Hill Education, pp. 356-368
2. Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp.
1295-1327

Braverman A. C., Schermerhorn M. (2019), Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes, et al., Editors, Elsevier, pp. 1295-1327
• Acute dissections: very high-risk lesions with an estimated mortality for type A of 50% for the
first 48 hours (~1% per hour)
Cotarlan V., Austin J. J. (2015), Principles of Critical Care, Gregory A. Schmidt Jesse B. Hall, John P. Kress, Editor, McGraw Hill Education, pp. 356-368

77
AORTIC DISSECTION
Clinical manifestations
• Abrupt onset of severe chest or back pain (90%)
• Chest pain: more commonly ~ Type A
• Back or abdomen pain: more commonly ~ Type B
• “Painless” aortic dissection in (4-15%) of patients, more common in those with diabetes,
previous aortic aneurysm, prior cardiac surgery1,2
• Blood pressure
• Hypertension
• Hypotension (cardiac tamponade, acute aortic rupture, CHF related to acute severe AR)
• Pseudohypotension (altered arm circulation due to dissection)
• Normotension
1. Hagan P. G., Nienaber C. A., Isselbacher E. M., et al. (2000), JAMA, 283 (7), pp. 897-903

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AORTIC DISSECTION
• Pulse deficits, AR, neurologic manifestations: more characteristic of ascending than
descending dissection2
• Absence NOT RULE OUT!!
1295-1327

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AORTIC DISSECTION
• Complications related to the dissection
• HF (<10%)  acute AR (incomplete coaptation, aortic leaflet prolapse  dissection flap,
extensive or circumferential dehiscing intimal flap into LVOT/diasystole, preexisting AR)
• Syncope (9%)  acute hypotension (cardiac tamponade, severe AR, or aortic rupture),
obstruction of a cerebral vessel, or activation of cerebral baroreceptors
• Neurological deficits (6%)  persistent or transient ischemic stroke, spinal cord ischemia,
ischemic neuropathy, hypoxic encephalopathy
• Acute MI (10-15%, mostly invole RCA)  false lumen or dissection flap compressing coronary
ostium
• Abdominal vascular complications and malperfusion (mesenteric, renal,…)
1295-1327

Cotarlan V., Austin J. J. (2015), Principles of Critical Care, Gregory A. Schmidt Jesse B. Hall, John P. Kress, Editor, McGraw Hill Education, pp. 356-368

Newby D., Grubb N. (2018), Davidson’s Principles and Practice of Medicine, Stuart H Ralston, et al., Editors, Elsevier, pp. 441-544

The mechanisms by which acute aortic dissection cause
death:
• intrapericardial rupture and tamponade
• acute aortic insufficiency
• free rupture into left pleural space
• occlusion of a branch of the aorta
Elefteriades J. A., Olin J. W., Halperin J. L., et al. (2017), Hurst’s The Heart, Valentin Fuster,
et al., Editors, McGraw-Hill, pp. 2157-2194

85
AORTIC DISSECTION
Laboratory findings
• CXR
• Abnormal aortic contour or widening of the aortic silhouette in 80% of cases
• Pleural effusions 20%
• Normal chest radiograph CANNOT EXCLUDE presence of aortic dissection1,2
• ECG: nonspecifc, indicate acute complications (myocardial ischemia or infarction, low-voltage
QRS complexes ~ hemopericardium)
• Patients with high probability (risk score 2 or 3) of AD  D-dimers not recommended (III-C)3
2. Hiratzka L. F., Bakris G. L., Beckman J. A., et al. (2010), Circulation, 121 (13), pp. e266-369.

87
AORTIC DISSECTION
Laboratory findings
• Diagnostic methods: TTE (initial), CECT (1st choice for definitive), MRI, TEE
• In case of initially (-) imaging + persistence of suspicion  repetitive imaging (CT or MRI)
is recommended (I-C)
• In case of uncomplicated Type B AD treated medically  repeated imaging (CT or MRI)
during 1st days is recommended (I-C)

Ptaszek L. M., Isselbacher E. M., Spooner A. E. (2012), Irwin and Rippe’s Intensive Care Medicine Richard S. Irwin , James M. Rippe, Editors, Wolters Kluwer, pp. 358-373

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AORTIC DISSECTION
Evaluation
• Hemodynamic state
• Pre-test probability
• Choice of imaging diagnostic modality

97
AORTIC DISSECTION
Management
Minimize effects of dissection // rapidly evaluating patient’s candidacy for surgical repair, if
indicated
• Medical therapy (ALL PATIENTS)
• Blood pressure control
• Pain relief
• Complications management
• Definitive treatment

98
AORTIC DISSECTION
Management
• MEDICAL THERAPY (ALL PATIENTS)
• Blood pressure control
• Reduced to as low a level as possible, target HR # 60 bpm
• Care should be taken to avoid vasodilators, in absence of negative chronotropic
medications (may induce reflex tachycardia   dP/dt extend dissection)
• If hypotension persists: pressors of choice = norepinephrine or phenylephrine
• Coacine intoxication: selective beta blockers (esmolol), or mixed agents (labetalol)
(non-selective beta blockers alone  unopposed alpha stimulation  worsening
hypertension)*
• Pain relief  patient comfort,  adrenergic tone
*Manning W. J., Blac J. H. (2019), UpToDate

Elefteriades J. A., Olin J. W., Halperin J. L., et al. (2017), Hurst’s The Heart, Valentin Fuster, et al., Editors, McGraw-Hill, pp. 2157-2194
Use only in presence of beta blocker

102
AORTIC DISSECTION
Management
• Medical therapy
• COMPLICATIONS MANAGEMENT*
• Cardiac tamponade
• Urgent pericardiocentesis: may be harmful > beneficial (can precipitate hemodynamic
collapse and death)
• If marked hypotension  aspiration of minimum volume of fluid  raise BP to lowest
level acceptable
• Definitive treatment (Endovascular therapy, Surgery)
* Nienaber Christoph A., Eagle Kim A. (2003), Circulation, 108 (6), pp. 772-778

108
AORTIC DISSECTION
Follow-up
• Lifestyle modifcations, education
• Control of patient’s blood pressure
• Regular imaging
• Screening patient and 1st degree relatives for heritable disorders

109
AORTIC DISSECTION
Follow-up
CONTROL OF PATIENT’S BLOOD PRESSURE
• Lowest level capable of sustaining normal organ function (sensorium, urine output,…)
• Life-long

110
AORTIC DISSECTION
Follow-up
REGULAR IMAGING
• Close observation for development of late aneurysm
• Risk factors: aortic dilation, hypertension, nonresection of false lumen, larger false lumen
diameter (>22 mm), entry tear diameter > 10 mm, partial false lumen thrombosis1
• CT scan at 3 months  in 6 months  annually if stable2
• Known patent false lumens: must be watched very closely (estimated aortic expansion
rate of 1-4.3 mm/y)1,2
2. Cotarlan V., Austin J. J. (2015), Principles of Critical Care, Gregory A. Schmidt Jesse B. Hall, John P. Kress, Editor, McGraw Hill Education, pp. 356-368

111
AORTIC INTRAMURAL
HEMATOMA (IMH)

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IMH
Overview
• Hematoma develops in medial layer of aortic wall + no evidence of intimal ﬂap or false lumen
• Imaging studies: circular or crescentic thickening ≥ 5 mm in aortic wall1
• Higher incidence in Asian studies than Western cohorts2
• Occurrence1
• Ascending 30%
• Arch 10%
• Descending 60-70%
• Result from rupture of vasa vasorum  mural hemorrhage
• Classifed as type A or type B (as for classic aortic dissection)
2. Harris K. M., Braverman A. C., Eagle K. A., et al. (2012), Circulation, 126 (11 Suppl 1), pp. S91-6

113
IMH
Overview
• Tend to be older, have more atherosclerotic disease > AD
• 2/3 of IMH cases: type B (≠ AD)
Ptaszek L. M., Isselbacher E. M., Spooner A. E. (2012), Irwin and Rippe’s Intensive Care Medicine Richard S. Irwin , James M. Rippe, Editors, Wolters Kluwer, pp. 358-373.

114
IMH
Pathophysiology
• Rupture of vasa vasorum in aortic wall (may be
the result of medial degeneration)
• Invasion of a PAU beyond internal elastic lamina
of the vessel, compromising the integrity of media
Mussa F. F., Horton J. D., Moridzadeh R., et al. (2016), JAMA, 316 (7), pp. 754-63

115
IMH
Risk factors, presentation
• Symptoms, risk factors = aortic dissection
• Ascending IMH  AR, hemopericardium, rupture, BUT malperfusion less common1
• Proximity of IMH to adventitia  frequent coexistence of pleural effusion, pericardial
effusion, periaortic hematoma, higher risk for aortic rupture2

117
IMH
Natural history
• Progression to AD (in type A IMH, may be as high as 25-50%)
• Complete resolution of the hematoma
• Persistence and stabilization of the hematoma
• Progression to aortic aneurysm
Shah J., Braverman A. C. (2009), The Washington Manual Cardiology Subspeciatly Consult, Phillip S. Cuculich, Andrew M. Kates, Thomas M. De Fer, Editors,
Wolters Kluwer, pp. 497-518

118
IMH
Diagnosis
• TTE: very low sensitivity
• Diagnosis
• TEE: focal crescentic or circumferential aortic wall thickening ≥ 5 mm, eccentric aortic lumen,
displaced intimal calcifcation, areas of echolucency within aortic wall, no intimal ﬂap or ﬂow in
aortic wall
• NCECT = area of high attenuation (bleeding)/wall of aorta
• CECT = low attenuation (no contrast material enters the wall)
• MRI
• IMH has a smooth lumen and curvilinear wall ≠ Aneurysm with mural thrombus

Lang R. M., Goldstein S. A., Kronzon I., et al. (2016), "ASE’s Comprehensive Echocardiography", Elsevier.

121
IMH
Management
• Elderly patients or those with significant
comorbidities: initial medical treatment with a
‘wait-and-watch strategy’ (optimal medical therapy
with blood pressure and pain control and repetitive
imaging) may be a reasonable option, particularly
in the absence of aortic dilation (< 50 mm) and IMH
thickness < 11 mm

122
IMH
Prognosis
• Overall long-term prognosis of IMH more favourable than AD1
• TYPE A IMH2
• High risk for complications = aortic dissection (25-50%), hemopericardium, rupture, with
• Mortality > 30% with medical therapy alone
• TYPE B IMH
• Average 30-day mortality rate 4% (medically treated) and 16% (those require surgery)3
• Complete resolution > 50%3
• Predictors of resolution = younger age, smaller aortic diameter (<4-4.5 cm), hematoma
thickness < 1 cm, postoperative use of beta blockers2,3
1. Timperley J., Ferguson J. D., Niccoli G., et al. (2003), American Journal of Cardiology, 91 (6), pp. 777-780

124
PENETRATING ATHEROSCLEROTIC
AORTIC ULCER (PAU)

126
PAU
Overview
• Atherosclerotic lesion penetrates through internal elastic lamina into the media
• Often associated with a variable degree of IMH formation
• May lead to pseudoaneurysm, dissection, aortic rupture, late aneurysm
• Single or multiple
• Range from 5-25 mm in diameter and 4-30 mm in depth1
• More common: middle to distal descending > arch, ascending, abdominal2
• Typically elderly, + coexisting vascular disease, + concomitant aneurysmal dilation of the
aorta elsewhere (especially abdominal)1,3
• Uncertain natural history
3. Shah J., Braverman A. C. (2009), The Washington Manual Cardiology Subspeciatly Consult, Phillip S. Cuculich, Andrew M. Kates, Thomas M. De Fer, Editors, Wolters Kluwer, pp.
497-518.

127
PAU
Imaging
• CT, MRI, TEE, aortography
• Focal aortic ulceration, associated IMH, a calcifed, displaced intima
• Diffcult to differentiate: PAU + IMH ≠ IMH + ulcerlike projection
Lang R. M., Goldstein S. A., Kronzon I., et al. (2016), "ASE’s
Comprehensive Echocardiography", Elsevier.

Lang R. M., Goldstein S. A., Kronzon I., et al. (2016), "ASE’s Comprehensive
Echocardiography", Elsevier.
CT, computed tomography: IMH, intramural
hematoma; MRI, magnetic resonance imaging; PAU,
penetrating atherosclerotic ulcer; TEE,
transesophageal echocardiography; ULP, ulcer-like
projections
Numbers 1, 2, and 3 refer to first-line, second-line,
and third-line imaging modalities

130
PAU
Management

CHIEF REFERENCES
1. Braverman A. C., Schermerhorn M. (2019), "Diseases of the Aorta", Braunwald’s Heart Disease: A Textbook Of Cardiovascular Medicine, Douglas P. Zipes,
et al., Editors, Elsevier, pp. 1295-1327.
2. Cotarlan V., Austin J. J. (2015), "Aortic Dissection", Principles of Critical Care, Gregory A. Schmidt Jesse B. Hall, John P. Kress, Editor, McGraw Hill
Education, pp. 356-368.
3. Creager M. A., Loscalzo J. (2018), "Diseases of the Aorta", Harrison's Principles of Internal Medicine, J. Larry Jameson, et al., Editors, McGraw-Hill, pp.
1917-1923.
4. Elefteriades J. A., Olin J. W., Halperin J. L., et al. (2017), "Diseases Of The Aorta", Hurst’s The Heart, Valentin Fuster, et al., Editors, McGraw-Hill, pp.
2157-2194.
5. Erbel R., Aboyans V., Boileau C., et al. (2014), "2014 ESC Guidelines on the diagnosis and treatment of aortic diseases: Document covering acute and
chronic aortic diseases of the thoracic and abdominal aorta of the adult. The Task Force for the Diagnosis and Treatment of Aortic Diseases of the
European Society of Cardiology (ESC)", Eur Heart J, 35 (41), pp. 2873-926.
6. Hiratzka L. F., Bakris G. L., Beckman J. A., 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), pp. e266-369.
7. Johnson G. A., Prince L. A. (2016), "Aortic Dissection and Related Aortic Syndromes", Tintinalli’s Emergency Medicine A Comprehensive Study Guide, Judith
E. Tintinalli, et al., Editors, McGraw Hill, pp. 412-416.
8. Lederle F. A. (2016), "Diseases Of The Aorta", Goldman-Cecil Medicine, Lee Goldman , Andrew I. Schafer, Editors, Elsevier Saunders, pp. 492-497.
9. Mussa F. F., Horton J. D., Moridzadeh R., et al. (2016), "Acute Aortic Dissection and Intramural Hematoma: A Systematic Review", JAMA, 316 (7), pp.
754-63.
10. Nienaber C. A., Clough R. E. (2015), "Management of acute aortic dissection", The Lancet, 385 (9970), pp. 800-811.
11. Nienaber C. A., Powell J. T. (2012), "Management of acute aortic syndromes", Eur Heart J, 33 (1), pp. 26-35b.

CHIEF REFERENCES
12. Prince L. A., Johnson G. A. (2016), "Aneurysmal Disease", Tintinalli’s Emergency Medicine A Comprehensive Study Guide, Judith E. Tintinalli, et al., Editors,
McGraw Hill, pp. 416-420.
13. Ptaszek L. M., Isselbacher E. M., Spooner A. E. (2012), "Acute Aortic Syndromes", Irwin and Rippe’s Intensive Care Medicine Richard S. Irwin , James M.
Rippe, Editors, Wolters Kluwer, pp. 358-373.
14. Shah J., Braverman A. C. (2012), "Aortic Dissection", The Washington Manual Of Critical Care, Warren Isakow Marin H. Kollef, Editor, Lippincott Williams
& Wilkins, pp. 155-162.
15. Shah J., Braverman A. C. (2009), "Diseases of the Aorta", The Washington Manual Cardiology Subspeciatly Consult, Phillip S. Cuculich, Andrew M. Kates,
Thomas M. De Fer, Editors, Wolters Kluwer, pp. 497-518.

133
DISEASES OF AORTIC
A p r i l 2 0 2 0

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