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ACUTE AORTIC SYNDROMES

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1 ACUTE AORTIC SYNDROMES
RAJESH K F

2 Acute aortic syndromes consist of 3 interrelated conditions with similar clinical characteristics
Aortic dissection Intramural hematoma Penetrating aortic ulcer

3 Erbel R, Alfonso F, Boileau C, Dirsch O, Eber B, Haverich A, et al
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:

4 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 vasa vasorum - Hemorrhage in aortic wall with subsequent intimal disruption

5 Most ascending aortic dissections begin within a few centimeters of aortic valve
Most descending aortic dissections have their origin just distal to left subclavian artery

6 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

7 Stanford classification
Type A Affect ascending aorta, regardless of site of origin Type B Do not affect ascending aorta

8 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 Malperfusion is rare

9 RISK FACTORS Hypertension (75%) Genetically triggered • Marfan syndrome • Bicuspid aortic valve (5 to 10 times risk) • Loeys-Dietz syndrome • Hereditary thoracic AA or dissection • Vascular Ehlers-Danlos syndrome 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 • Behcet disease • Aortitis • Syphilis Pregnancy (typically in third trimester)

10 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

11 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 • Ectopia lentis SKELETAL SYSTEM MAJOR CRITERIA Presence of at least four of the following • Pectus carinatum • Pectus excavatum 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 pes planus • Protusio acetabulae of any degree

12 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

13 Revised Ghent criteria
J Med Genet :

14 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

15 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 livedo reticularis

16 Vascular Ehlers-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 Clinical appearance of our patient. Note the translucent skin with visible underlying vasculature, slightly extensible skin, acrogeria, small joint hypermobility, characteristic facies, ecchymosis on the legs,genu valgum, elongated upper extremities, and dorsal kyphosis.

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19 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%)

20 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

21 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

22 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 These mechanisms include dilatation of the aortic root and annulus (Figure 5A), pressure of a false lumen on 1 cusp causing asymmetrical cusp coaptation (Figure 5B), flail of an aortic cusp attributable to annular support disruption (Figure 5C), and prolapse of a mobile intimal flap through the aortic valve (Figure 5D). 4

23 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

24 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

25 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

26 Acute myocardial infarction
Flap causing malperfusion of coronary artery Occurs in 1% to 7% of acute type A dissections RCA is most commonly involved

27 Left-sided pleural effusion
Usually related to inflammatory response Acute hemothorax

28 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

29 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%

30 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

31 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

32 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

33 TTE 78.3% sensitivity and 83.0% specificity for diagnosing proximal dissection 2 lumens separated by flap

34 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

35 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

36 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,and magnetic resonance imaging for suspected thoracic aortic dissection. Arch Intern Med. 2006;166:

37 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

38 BB Action

39 CIs to BB-Nondihydropyridine CCB(LOE : C)
IV diltiazem 0.25 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)

40 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

41 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

42 GOALS OF SURGERY Excise intimal tear
Obliterate false channel by oversewing aortic edges Reconstitute aorta,usually by placing a dacron interposition graft

43 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

44 • AVR required if annular supports of leaflets damaged (composite graft or homograft) • AVR required if aortic root >5 cm Modified Bentall’s operation

45 Preoperative Prediction Model of Surgical Mortality Risk
VARIABLE OVERALL TYPE A (%) AMONG SURVIVORS (%) AMONG DEATH (%) COEFFICIENT SCORE ASSIGNED P VALUE ODDS RATIO, DEATH (95% CI) Age ≥ 70 yr 27.3 24.1 37.4 0.68 0.7 <0.01 1.98 ( ) History of aortic valve replacement 4.5 3.8 6.6 1.44 1.5 4.21 ( ) Presenting hypotension, shock, or tamponade 28.8 22.4 49.0 1.17 1.2 3.23 ( ) Migrating chest pain 13.8 12.1 19.3 0.88 0.9 2.42 ( ) Preoperative cardiac tamponade 15.5 11.7 28.2 0.97 1.0 2.65 ( ) Any pulse deficit 28.6 25.7 37.8 0.56 0.6 0.03 1.75 ( ) 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 Thorac Surg 83:55, 2007.

46 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.)

47 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

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52 No 30-day deaths stroke or paraplegia were reported in either treatment group
Aortic remodelling at 1 year (p<0.001) favoured TAG+BMT

53 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:

54 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

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56 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. Semin Vasc Surg 2009;22:61-8.

57 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

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59 No difference in rate of death between two treatment groups
Patients receiving endovascular grafts -higher rate of false-lumen thrombosis

60 Systematic review of mid-term outcomes of endovascular treatment
Reintervention for 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 Vasc Endovasc Surg 2011;42:632-47

61 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

62 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

63 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,

64 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 Vasc Surg 2012;55:629-40)

65 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

66 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

67 Hybrid approach One segment of aorta, such as the aortic arch, is treated surgically, descending aorta receives an endovascular graft

68 Zone 3:Carotid Bypass+TEVAR
Zone 4: TEVAR Zone 3:Carotid Bypass+TEVAR Zone 2:Ascending aorta Bypass(elephant trunk extension) +TEVAR

69 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

70 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

71 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

72 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

73 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

74 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

75 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

76 PAU may stabilize or lead to complications including
IMH Distal embolization Aortic rupture Pseudoaneurysm (contained rupture) Aortic dissection Saccular or fusiform aneurysm

77 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

78 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

79 Recommendations for Thoracic Stent Graft Insertion

80 REFERENCES The diagnosis and management of aortic dissection Sri G Thrumurthy, Alan Karthikesalingam, Benjamin O Patterson, Peter J E Holt,Matt M Thompson BMJ | 14 JANUARY 2012 | VOLUME 344 Aortic dissection:Prompt diagnosis 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 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: IRAD Registry JAMA February 16th 2000 ,vol 283 no,7 The INvestigation of STEnt Grafts in Aortic Dissection (INSTEAD) Trial Christoph A. Nienaber, MD, PhD; etalCirculation. 2009;120: Management of Aortic Dissection----New classification and Mid-term results Dinghua Yi, et al, Division of Cardiovascular Surgery ,Xijing Hospital, Xi’an, China Thoracic Endovascular Aortic Repair (TEVAR)for the treatment of aortic diseases: a positionstatement from 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's Heart Disease Ninth Edition Hurst,s THE HEART 13TH edition

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82 (CAPTIVIA (NCT01181947) and VIRTUE (NCT01213589)


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