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ACUTE AORTIC SYNDROMES. RAJESH K F. Acute aortic syndromes consist of 3 interrelated conditions with similar clinical characteristics Aortic dissection Intramural hematoma Penetrating aortic ulcer.

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slide2

Acute aortic syndromes consist of 3 interrelated conditions with similar clinical characteristics

  • Aortic dissection
  • Intramural hematoma
  • Penetrating aortic ulcer
slide3

Erbel R, Alfonso F, Boileau C, Dirsch O, Eber B, Haverich A, et al. Diagnosis and management of aortic dissection. Eur Heart J 2001;22:1642-81.

aortic dissection
AORTIC DISSECTION
  • Most common aortic catastrophe
  • Incidence - 5 to 30 per 1 million people/year
  • Primary tear in aortic intima with bleed into diseased media
  • Rupture of vasavasorum - Hemorrhage in aortic wall with subsequent intimal disruption
slide5

Most ascending aortic dissections begin within a few centimeters of aortic valve

  • Most descending aortic dissections have their origin just distal to left subclavianartery
debakey classification
DeBakey classification
  • I: Ascending aorta -> arch +/- descending aorta
  • II: Ascending aorta only
  • III:Descending aorta
  • IIIa: Limited to descending thoracic aorta
  • IIIb: Extending below diaphragm
stanford classification
Stanford classification

Type A

  • Affect ascending aorta, regardless of site of origin

Type B

  • Do not affect ascending aorta
classification
Classification
  • Based on time of onset of initial symptoms to time of presentation
  • Acute dissection < 2 weeks
  • Subacute- between 2 and 6 weeks
  • Chronic > 6 weeks

Behave like aneurysm

Rupture is the risk

Malperfusionis rare

risk factors
RISK FACTORS

Hypertension (75%)

Genetically triggered

• Marfansyndrome

• Bicuspid aortic valve (5 to 10 times risk)

• Loeys-Dietz syndrome

• Hereditary thoracic AA or dissection

• Vascular Ehlers-Danlossyndrome

Congenital diseases or syndromes

• Coarctation of the aorta

• Turner syndrome(dissection at small aortic dimensions)

• Tetralogy of Fallot

Atherosclerosis

• Penetrating atherosclerotic ulcer

Trauma, blunt or iatrogenic

• Catheter or stent

• Intra-aortic balloon pump

• Aortic or vascular surgery

• Motor vehicle accident

• CABG or AVR

Cocaine use

Inflammatory or infectious disease

• Giant cell arteritis

• Takayasu arteritis

• Behcetdisease

• Aortitis

• Syphilis

Pregnancy (typically in third trimester)

slide10

Patients <40years are less likely to have HTN(34%) and more likely to have Marfan’s syndrome, bicuspid aortic valve, or prior aortic surgery

IRAD registery

marfan syndrome ghent criteria
Marfan syndrome -Ghent criteria

CARDIOVASCULAR SYSTEM

MAJOR CRITERIA

•Dilation of ascending aorta

•Aortic dissection

MINOR CRITERIA

•MVP

•Dilation of MPA

•Premature mitral annular calcification (<40yrs)

•Descending thoracic or Abdominal aortic aneurysm(< 50 yrs)

CVS involvement:one minor criterion

OCULAR SYSTEM-MAJOR CRITERION

• Ectopialentis

SKELETAL SYSTEM

MAJOR CRITERIA

Presence of at least four of the following

• Pectuscarinatum

• Pectusexcavatum requiring surgery

• Reduced US to LS ratio (.85to 0.95) or arm span to height ratio > 1.05

• Wrist and thumb signs

•Scoliosis > 20° or spondylolisthesis

•Reduced extension at elbows (<170°)

• Medial displacement of medial malleolus

causing pesplanus

• Protusioacetabulae of any degree

marfan syndrome ghent criteria1
Marfan syndrome -Ghent criteria
  • INDEX CASE: Major criteria in two systems and involvement of a third system
  • FAMILY MEMBER: One major criterion in an organ system and involvement of a second organ system
revised ghent criteria
Revised Ghent criteria

J Med Genet 2010 47: 476-485

loeys dietz aneurysm syndrome
Loeys-Dietz aneurysm syndrome
  • Autosomal dominant
  • Mutations in TGFBR1 or TGFBR2
  • Arterial tortuosity, hypertelorism, bifid or broad uvula,cleft palate
  • Soft, velvety skin and easily visible veins
  • Aortic dissection and aneurysm involving branch vessels
familial thoracic aortic aneurysm and dissection
Familial thoracic aortic aneurysm and dissection
  • Autosomal dominant disorder
  • Mutations in various genes including ACTA 2, MYH11, TGFBR1 and TGFBR2, FBN1
  • Thoracic aortic aneurysm and dissection
  • May be associated with PDA, cerebral aneurysm, BAV or livedoreticularis
vascular ehlers danlos syndrome type 4
VascularEhlers-Danlos syndrome (type 4)
  • Autosomal dominant
  • Mutation in gene COL3A1
  • Abnormal type III procollagen synthesis
  • Hyperflexible fingers, hyperlucent skin with visible veins, easy bruisability and varicose veins
  • Hisk for spontaneous arterial dissection and rupture, often in medium sized arteries
aortic dissection clinical presentation
Aortic dissection clinical presentation
  • Usual age is sixth or seventh decades of life
  • Chestpain or backpain or both
  • Most severe at its onset
  • Migratory Pain
  • Ripping, tearing, stabbing, or sharp quality
  • Patients on steroids and Marfan syndrome prone for painless presentation (6.4%)
high risk examination features
High-risk examination features
  • Loss of peripheral pulse
  • SBP limb differential greater than 20 mm Hg
  • Focal neurologic deficit
  • New AR murmur

International Registry of Acute Aortic Dissection (IRAD) Physical Findings of 591 Patients With Type A Aortic Dissection

slide21

Most type B dissection are hypertensive on presentation

  • Type A dissection may present with normal BP or hypotension
  • Loss of peripheral pulse
  • are reported in 10% to 30% of acute dissections
  • May be intermittent -Dynamic movement of dissection flap

Dynamic obstruction

aortic regurgitation
Aortic regurgitation
  • In 40% with acute type A dissection
  • Mechnisms of AR

• Malcoaptation of aortic leaflets - dilation of aortic root and annulus

• Distortion of alignment

• Aortic leaflet prolapse

• Prolapse of intimal flap across aortic valve

neurologic manifestations
Neurologic manifestations
  • Most common in dissection type A
  • May dominate clinical presentation
  • Neurologic syndromes include

• Persistent or transient ischemic stroke

• Spinal cord ischemia

• Ischemic neuropathy

• Hypoxic encephalopathy

syncope
Syncope
  • Reported in 13% of patients in IRAD
  • Indicate development of dangerous complications
  • Acute hypotension - Cardiac tamponade (10% of acute type A dissections) or aortic rupture
  • Cerebral vessel obstruction or activation of cerebral baroreceptors
vascular insufficiency
Vascular insufficiency
  • Renal artery - 5% to 10%
  • Renal ischemia,infarction, renal insufficiency or refractory hypertension
  • Mesenteric ischemia or infarction in 5%
  • Extension to iliac arteries -acute limb ischemia
acute myocardial infarction
Acute myocardial infarction
  • Flap causing malperfusionof coronary artery
  • Occurs in 1% to 7% of acute type A dissections
  • RCA is most commonly involved
slide27

Left-sided pleural effusion

  • Usually related to inflammatory response
  • Acute hemothorax
chest radiography
Chest radiography
  • Widening mediastinum (80% to 90% of cases (83%, type A; 72%, type B)
  • Obliteration of aortic knob 
  • Displaced intimal calcification (>5 mm) -calcium sign 20%
  • Displacement of trachea to right
  • Distortion of left main-stem bronchus
  • Pleural effusion (more common left sided)
  • Cardiomegaly
  • Normal in 12% to 15% of cases
d dimer levels
D-dimer levels
  • Rise in acute aortic dissection as in pulmonary embolism
  • Level >1,600 ng/mL within first 6 hours - positive likelihood ratio of 12.8 for dissection
  • In first 24 hours after symptom onset - D-dimer level < 500 ng/Ml has negative predictive value of 95%
imaging
IMAGING

1 Establish presence of AD or variant (IMH,PAU)

2 Location of the dissection (Type A, Type B)

3 Anatomical features

a Extent of dissection

b Sites of entry and reentry

c False lumen patency, partial thrombosis, thrombosis

4 Complications of dissection

a Type A

i Aortic regurgitation

ii Coronary artery involvement

iii Pericardial effusion/hemopericardium

b Aortic rupture or leaking

c Branch vessel involvement

d Malperfusion

contrast enhanced ct
Contrast-enhanced CT
  • Most commonly used
  • Sensitivity and specificity of 95% to 98%
  • ECG gating or multi detector scanning eliminate pulsation artifacts
  • Intravenous contrast is necessary to visualize true and false channels
  • Visualize hemopericardium, aortic rupture, and branch vessel involvement
slide32
MRI
  • Sensitivity of 98% and specificity of 98% with diagnostic odds ratio of 6.8
  • Capable of multiplanar imaging with 3D reconstruction
  • Cine MRI visualize blood flow, differentiating slow flow and clot and AR
  • MRA -detect and quantify AR & branch vessel morphology
slide33
TTE
  • 78.3% sensitivity and 83.0% specificity for diagnosing proximal dissection
  • 2 lumens separated by flap
slide34
TEE
  • Accurately visualise entire thoracic aorta (sensitivity 98.0%, specificity 95.0%, diagnostic odds ratio 6.1)
  • 2 lumens separated by flap
  • Visualize coronary ostia
  • AR
  • Pericardial effusion
  • LV & RV function
  • May not adequately visualize distal ascending aorta and aortic arch
aortography
Aortography
  • Identify intimal flap, true and false lumen
  • Thickened wall (thrombosed false lumen)
  • AR, branch vessel involvement
  • Diagnostic accuracy 90-95%
  • 5-10% false negative rate

– thrombosed false lumen

– simultaneous opacification of both lumens

– misses IMH

  • Risks of procedure
slide36

Comparative study with nonhelical CT, 0.5 Tesla MR and TEE showed

  • 100% sensitivity for all modalities,
  • Better specificity of CT (100%) than for TEE and MR
  • False-negative studies can and do occur

Shiga T, Wajima Z, Apfel CC, Inoue T, Ohe Y. Diagnostic accuracy of transesohageal echocardiography, helical computed tomography,andmagnetic resonance imaging for suspected thoracic aortic dissection. Arch Intern Med. 2006;166:1350-6.

initial management
INITIAL MANAGEMENT
  • IV beta blockade -Target HR of 60 /min or less(LOE : C)
  • Esmolol -Initial bolus of 500microg/kg and continuous infusion of 50 to 200 microg/kg/min
  • Labetolol-Initial dose of 20 mg IV over 2 minutes and 40 to 80 mg IV every 15 minutes (max 300 mg), continuous infusion 2 to 8 mg/min
  • Propranolol and metoprolol–IV or oral
  • BBs blockers- compensatory tachycardia in acute AR
slide39

CIs to BB-Nondihydropyridine CCB(LOE : C)

  • IV diltiazem0.25 mg/kg over 2 minutes > infusion 5 to 15 mg/hr
  • SBP > 120 mm Hg after adequate HR control- ACEI and/or other vasodilators IV (LOE : C)
  • Should not be initiated prior to rate control - reflex tachycardia increase aortic wall stress (LOE : C)
slide40

IV sodium nitroprusside - most established agent, rapidly titratable , 20 microg/min, with titration to 0.5 to 5 microg/kg/min

  • Renal insufficiency or prolonged use-cyanide toxicity
  • IV enalaprilat,nitroglycerin,nicardipine,nitroglycerin, fenoldopam
  • Refractory hypertension - consider renal artery hypertension due to dissection causing renal malperfusion
  • Appropriate analgesia – opiate
slide41

Surgical Therapy Acute type A aortic dissection

Retrograde dissection into ascending aorta

Surgical Therapy and/or Endovascular Therapy

Acute type B aortic dissection complicated by

• Visceral ischemia

• Limb ischemia

• Rupture or impending rupture

• Aneurysmal dilation

• Refractory pain

Medical Therapy Uncomplicated type B aortic dissection

Uncomplicated isolated arch dissection

goals of surgery
GOALS OF SURGERY
  • Excise intimal tear
  • Obliterate false channel by oversewingaortic edges
  • Reconstitute aorta,usuallyby placing a dacron interposition graft
type a aortic dissection
Type A aortic dissection
  • Replace affected ascending aorta with or without aortic arch with prosthetic graft
  • In-hospital mortality 15-35%
  • Proximal extension of dissection to aortic valve or ostia of coronary arteries may require replacement or resuspension of aortic valve (24% )or coronary artery bypass (15% )

Valve sparing -David or Yacoub Procedures

slide44

• AVR required if annular supports of leaflets damaged (composite graft or homograft)

• AVR required if aortic root >5 cm

Modified Bentall’s operation

preoperative prediction model of surgical mortality risk
Preoperative Prediction Model of Surgical Mortality Risk

From Rampoldi V, Trimarchi S, Eagle KA, et al: Simple risk models to predict surgical mortality in acute type A aortic dissection: The International Registry of Acute Aortic Dissection score. Ann ThoracSurg 83:55, 2007.

uncomplicated acute type b aortic dissection
Uncomplicated acute type B aortic dissection
  • Drug treatment alone can result in 78% three year survival
  • Medical management remains the gold standard
  • Endovascular treatment is increasingly possible with low mortality

[IRAD]: New insights into an old disease. JAMA 283:897, 2000.)

adsorb trial
ADSORB trial
  • Acute Dissection: Stent graft OR Best medical therapy
  • Acute uncomplicated type B aortic dissection
  • Stent graft OR Best medical therapy
  • 250 subjects ,125 test / 125 control
  • Follow-up – 3 years

<55mm

slide52

No 30-day deaths stroke or paraplegia were reported in either treatment group

  • Aortic remodelling at 1 year (p<0.001) favoured TAG+BMT
complicated acute type b dissection
Complicated acute type B dissection
  • Complications such as malperfusion, shock -mortality rate is 25% to 50%
  • Conventional open surgery- 30 day mortality of 30%
  • Meta-analysis has shown that endovascular treatment( TEVAR)-30 day mortality of 9.8%

30-day mortality in patients with acute type B-AD undergoing stent–graft placement in comparison with medically and surgically treated type B-AD patients derive d from IRAD

Eggebrecht H, Nienaber CA, Neuhauser M, Baumgart D, Kische S, Schmermund A, et al. Endovascular stent-graft placement in aortic dissection: a meta-analysis. Eur Heart J 2006;27:489-98.

tevar
TEVAR
  • Treatment modality of choice in complicated acute type B AD
  • Focus is occlusion of primary entry tear
  • Size of stent graft should be based on diameter of aorta proximal to dissected segment, applying almost no oversizing
  • Sufficient length (1.5–2 cm) of proximal landing zone
  • Ballooning is not recommended even if stent graft is not fully expanded-Retrograde dissection and rupture of dissection membrane
chronic type b dissection
Chronic type B dissection
  • Managed conservatively
  • 15% complicated by aneurysm
  • Conventional open surgery has an appreciable death rate and poses considerable physiological challenges
  • Endovascular approach is associated with less morbidity and mortality
  • Endovascular surgery 93%; open surgery 79%

Subramanian S, Roselli EE. Thoracic aortic dissection: long-term results of endovascular and open repair. SeminVascSurg2009;22:61-8.

instead trial
INSTEAD trial
  • Investigation of Stent Grafts in Aortic Dissection
  • 140 patients with uncomplicated type B dissection >2 weeks
  • Compared drug therapy with endovascular stent grafting
  • 2 years of follow-up
slide59

No difference in rate of death between two treatment groups

  • Patients receiving endovascular grafts -higher rate of false-lumen thrombosis
slide60

Systematic review of mid-term outcomes of endovascular treatment

Reinterventionfor late morbidities

  • Endoleak(8.1%)
  • Formation of a distal aneurysm (7.8%)
  • Rupture (3.0%)
  • Postoperative surveillance is mandatory

Thrumurthy SG, Karthikesalingam A, Patterson BO, Holt PJ, Hinchliffe RJ, Loftus IM, et al. A systematic review of mid-term outcomes of Thoracic Endovascular Repair (TEVAR) of chronic type B aortic dissection. Eur J VascEndovascSurg2011;42:632-47

endovascular therapy in aortic dissection
Endovascular therapy in aortic dissection
  • Fenestration of aorta and stenting of branch vessels -earliest techniques used in complicated type B dissection
  • By fenestrating intimal flap, blood flow from false lumen into true lumen,decompressing distended false lumen
endovascular stenting
Endovascular stenting
  • Acute aortic rupture, malperfusion syndromes and rapidly enlarging false lumens
  • Endovascular grafts cover area of a primary intimal tear
  • Promote false-lumen thrombosis
stable trial
STABLE trial
  • Petticoat technique-entry point is sealed with endograft and remaining thoracic and potentially abdominal aorta is stented open
  • Decrease chance of true lumen collapse, enhance aortic remodeling, and promote false lumen thrombosis

Zenith Dissection Endovascular System,

slide64

Evaluates safety and effectiveness of a unique composite thoracic endovascular aneurysm repair (TEVAR) construct (proximal TX2 stent graft and distal BMS) (Zenith Dissection Endovascular System; Cook Medical) for treatment of patients with complicated type B AD

  • Enrolled 40 patients
  • Acute 24 pts (60%), subacute (15-30 days) six pts (15%) and chronic (31-90 days) in 10 pts (25%)

( J VascSurg 2012;55:629-40)

slide65

30-day mortality rate was 5% (2 of 40)

  • Two deaths occurred after 30 days, leading to a 1-year survival rate of 90%
  • Morbidity occurring within 30 days included stroke (7.5%), TIA(2.5%), paraplegia (2.5%), retrograde progression of dissection (5%) and renal failure (12.5%)
  • Four patients (10%) underwent secondary interventions within 1 year
slide66

Favorable aortic remodeling was observed during the course of follow-up

  • Increase in true lumen size and a concomitant decrease in false lumen size
  • Completely thrombosed thoracic false lumen observed in 31% of patients at 12 months as compared to 0% at baseline
hybrid approach
Hybrid approach
  • One segment of aorta, such as the aortic arch, is treated surgically, descending aorta receives an endovascular graft
slide68

Zone 4: TEVAR

Zone 3:Carotid Bypass+TEVAR

  • Zone 2:Ascending aorta Bypass(elephant trunk extension)

+TEVAR

follow up
FOLLOW UP
  • ESC recommendations
  • Regular cross sectional imaging of aorta, preferably with MRA, at 1,3 and 12 months after discharge and every six to 12 months thereafter, depending on aortic size
  • All patients should receive lifelong antihypertensive treatment, including β blockers, with a target BP of 120/80 mm Hg
intramural hematoma
Intramural Hematoma
  • 10% to 20% acute aortic syndromes
  • Common in older patients
  • Clinical picture of dissection
  • Imaging show no blood flow in false lumen or intimal lesion
  • Hemorrhage of vasa vasorum in medial layer of aorta or hematoma arises from microscopic tears in aortic intima
  • Most (50% to 85%) are located in the descending aorta
  • Typically associated with hypertension
slide71

Crescentic or circular thickening of aortic wall with maximal thickness > 7 mm on TEE without intimal flap or tear or longitudinal flow in false lumen

type A IMH

slide72

Hematoma may

  • Entirely resolve (10%)
  • Convert to a classic dissection(3% to 14% of cases of descending aorta and in 11% to 88% of cases of ascending aorta)
  • Aorta may enlarge and potentially rupture
management
Management
  • Surgery in patients with acute IMH involving ascending aorta
  • Aggressive medical therapy is advocated in patients with acute IMH involving the descending aorta

IRAD

In-hospital mortality for IMH according to site of origin

penetrating aortic ulcer
PENETRATING AORTIC ULCER
  • Atherosclerotic lesion penetrates internal elastic lamina into media
  • Associated with variable degree of IMH
  • May lead to pseudoaneurysm formation, aortic rupture, or late aneurysm
  • Range from 5 mm to 25 mm in diameter and 4 mm to 30 mm in depth
  • More common in thoracic and abdominal aorta
slide75

2% to 8% of acute aortic syndrome

  • 25% of PAUs are found incidentally
  • Typical symptoms include acute chest or back pain, similar to dissection
  • Imaging show crater-like outpouching with irregular edges in setting of heavy atherosclerosis
  • 80% of patients have some degree of IMH
slide76

PAU may stabilize or lead to complications including

  • IMH
  • Distal embolization
  • Aortic rupture
  • Pseudoaneurysm(contained rupture)
  • Aortic dissection
  • Saccularor fusiform aneurysm
management1
Management
  • Ascending PAUs are treated with surgical resection
  • Stable patients with type B PAUs medical management, with strict follow-up and serial imaging
  • Rrefractory or recurrent pain have increased risk of disease progression, rapid increase in aortic dimension are at risk for rupture should be treated surgically or with endovascular stent grafts
slide78

Indications for surgery or endovascular therapy (imaging )

  • Interval development of hemorrhage
  • Periaortic hematoma
  • Expanding pseudoaneurysm and rupture
  • Increasing aortic wall thickness
  • Ulcer craters more than 20 mm in diameter or 10 mm in depth
  • Increasing aortic hematoma
  • Increasing pleural effusion
  • More aggressive approach to type B PAU than classic type B dissection because of concern of increased risk of rupture
  • Relatively focal aortic segment involved -suitable for endovascular therapy
references
REFERENCES
  • The diagnosis and management of aortic dissection Sri G Thrumurthy, Alan Karthikesalingam, Benjamin O Patterson, Peter J E Holt,MattM Thompson BMJ | 14 JANUARY 2012 | VOLUME 344
  • Aortic dissection:Promptdiagnosis and emergency treatment are critical ALAN C. BRAVERMAN, MD c l e v e l a n d c l i n i c j o u r n a l o f m e d i c i n e v o l u m e 7 8 • n u m b e r 1 0 o c t o b e r 2 0 1 1
  • 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease Circulation April 6, 2010
  • Acute Aortic Syndromes Thomas T. Tsai, MD; Christoph A. Nienaber, MD; Kim A. Eagle, MDCirculation. 2005;112:3802-3813
  • IRAD Registry JAMA February 16th 2000 ,vol 283 no,7
  • The INvestigation of STEnt Grafts in Aortic Dissection (INSTEAD) Trial ChristophA. Nienaber, MD, PhD; etalCirculation. 2009;120:2519-2528
  • Management of Aortic Dissection----New classification and Mid-term results Dinghua Yi, et al, Division of Cardiovascular Surgery ,XijingHospital, Xi’an, China
  • Thoracic Endovascular Aortic Repair (TEVAR)for the treatment of aortic diseases: a positionstatementfrom the European Association for Cardio-Thoracic Surgery (EACTS)and the European Society of Cardiology (ESC),in collaboration with the European Association of Percutaneous Cardiovascular Interventions (EAPCI)†Martin Grabenwo¨ ger1, European Heart Journal Advance Access published May 4, 2012
  • Braunwald'sHeart Disease Ninth Edition
  • Hurst,s THE HEART 13TH edition