Nuevos horizontes en el manejo de la Disección … Montero-Bak… · de la Disección Aórtica tipo B ... aortic intramural hematoma or penetrating ... Figure 2 Kaplan-Meier survival

Nuevos horizontes en el manejo de la Disección Aórtica tipo B

M. Montero-Baker

• Patología letal sin terapia


• La mayoría de los pacientes mueren en menos de 3 meses sin tratamiento


• La mayoría de los pacientes mueren en menos de 3 meses sin tratamiento

• De los pocos que sobreviven y llegan ala fase crónica mueren en una ventana de 5 años por degeneración aneurismática.

2003

2003 2012

Tratamiento

• Identificación y optimización médica

• Complicado o no complicado?

Dis Tipo B Complicada

Dis Tipo B Complicada• Malperfusión


• Dolor intratable



• Hipertensión descontrolada




• Degeneración Aórtica >55mm





• Hematoma periaórtico/mediastinal in crescendo






• Derrame pleural hemorrágico (2 CTs subsecuentes)






• Derrame pleural hemorrágico (2 CTs subsecuentes)

25% de las disecciones calzan dentro de estos parámetros

369Annals of cardiothoracic surgery, Vol 3, No 4 July 2014

© AME Publishing Company. All rights reserved. Ann Cardiothorac Surg 2014;3(4):368-374www.annalscts.com

explain acute aortic dissection. The first theory holds that an initial tear in the intima leads to blood from the aortic lumen surging into the media and separating the intima from the aorta and creating a true and false lumen. In contrast, the second theory holds that the vasa vasorum in the more outer portions of the media hemorrhage first, and then secondarily cause intimal rupture. In both theories, it is thought that the pressure of pulsatile blood flow extends the dissection, typically in an anterograde fashion (7). In 10-20% of acute aortic dissection cases, a variant such as an aortic intramural hematoma or penetrating atherosclerotic ulcer occurs (8).

International Registry of Acute Aortic Dissection

Aortic dissection remains a relatively rare but life-threatening disease in the current era, occurring in 3.5 per 100,000 persons per year (9) with recent evidence suggesting an increasing incidence of up to 14 per 100,000 persons per year (10). Up to 30% of these cases are believed to be type B in nature (11). To further elucidate contemporary practice patterns and outcomes of aortic dissection, The International Registry of Acute Aortic Dissection (IRAD) was established in 1996 initially enrolling patients in 12 centers of excellence in six countries with further expansion to 30 centers in 11 countries (Figure 1), and since then has enrolled over 5,000 patients. Since the landmark initial publication in 2000, IRAD publications have steadily

increased improving knowledge and understanding of aortic dissection. Data from IRAD have identified basic risk factors including: bicuspid aortic valve, Marfan syndrome, male gender, age greater than 60, and hypertension (11).

With the large-scale IRAD study, comparisons regarding the demographics and clinical presentations of patients with type A versus type B disease also became possible. Patients with type B dissection are older, have higher rates of atherosclerosis, and are more likely to present with back pain rather than anterior chest pain (11). Importantly, half of type B dissections have an initial abnormal chest radiograph. Furthermore, the in-hospital mortality rate is 13% with the majority of deaths occurring within the first week of hospitalization. Independent predictors of death in type B dissection have been jointly termed the ‘deadly triad’: hypotension/shock, absence of chest/back pain on presentation, and branch vessel involvement (12). In recent years, analyses of IRAD data have gone beyond simply characterizing the patient with acute type B aortic dissection and have attempted to identify the means by which the outcome of such a patient could be improved. Thus, we present herein three areas in which IRAD data has recently advanced our understanding of acute type B aortic dissection.

Temporal classification

Classically, aortic dissection has been classified into two

Figure 1 IRAD centers worldwide. IRAD, International Registry of Acute Aortic Dissection.

369Annals of cardiothoracic surgery, Vol 3, No 4 July 2014


explain acute aortic dissection. The first theory holds that an initial tear in the intima leads to blood from the aortic lumen surging into the media and separating the intima from the aorta and creating a true and false lumen. In contrast, the second theory holds that the vasa vasorum in the more outer portions of the media hemorrhage first, and then secondarily cause intimal rupture. In both theories, it is thought that the pressure of pulsatile blood flow extends the dissection, typically in an anterograde fashion (7). In 10-20% of acute aortic dissection cases, a variant such as an aortic intramural hematoma or penetrating atherosclerotic ulcer occurs (8).

International Registry of Acute Aortic Dissection

Aortic dissection remains a relatively rare but life-threatening disease in the current era, occurring in 3.5 per 100,000 persons per year (9) with recent evidence suggesting an increasing incidence of up to 14 per 100,000 persons per year (10). Up to 30% of these cases are believed to be type B in nature (11). To further elucidate contemporary practice patterns and outcomes of aortic dissection, The International Registry of Acute Aortic Dissection (IRAD) was established in 1996 initially enrolling patients in 12 centers of excellence in six countries with further expansion to 30 centers in 11 countries (Figure 1), and since then has enrolled over 5,000 patients. Since the landmark initial publication in 2000, IRAD publications have steadily

increased improving knowledge and understanding of aortic dissection. Data from IRAD have identified basic risk factors including: bicuspid aortic valve, Marfan syndrome, male gender, age greater than 60, and hypertension (11).

With the large-scale IRAD study, comparisons regarding the demographics and clinical presentations of patients with type A versus type B disease also became possible. Patients with type B dissection are older, have higher rates of atherosclerosis, and are more likely to present with back pain rather than anterior chest pain (11). Importantly, half of type B dissections have an initial abnormal chest radiograph. Furthermore, the in-hospital mortality rate is 13% with the majority of deaths occurring within the first week of hospitalization. Independent predictors of death in type B dissection have been jointly termed the ‘deadly triad’: hypotension/shock, absence of chest/back pain on presentation, and branch vessel involvement (12). In recent years, analyses of IRAD data have gone beyond simply characterizing the patient with acute type B aortic dissection and have attempted to identify the means by which the outcome of such a patient could be improved. Thus, we present herein three areas in which IRAD data has recently advanced our understanding of acute type B aortic dissection.

Temporal classification

Classically, aortic dissection has been classified into two

Figure 1 IRAD centers worldwide. IRAD, International Registry of Acute Aortic Dissection.

370 Patel et al. Acute type B dissection: insights from IRAD


groups based upon on the time of symptom onset. Acute dissection has been diagnosed when clinical symptoms have lasted for 14 days or less, while greater than two weeks of symptom duration has been considered to be chronic. Although this distinction was made in an era prior to the advent of modern diagnostic and surgical and nonsurgical management strategies, this categorization has continued to guide contemporary care of aortic dissection. Recently, Booher et al. analyzed the IRAD database and developed Kaplan-Meier survival curves for type B aortic dissection identifying distinct inflection points and creating four distinct time periods: hyperacute (symptom onset to 24 hours), acute (2-7 days), subacute (8-30 days) and chronic (>30 days) (Figure 2). Cumulative survival continued to decline throughout all four of these temporal groups regardless of treatment modality: 94-99%, 82-93%, 77-92%, and 73-91% respectively (13). The finding that survival continues to decrease significantly, even up to 30 days post-symptom onset into what has been traditionally considered the chronic phase, is novel. While current guidelines for the management of patients with type B aortic disease utilize the traditional acute vs. chronic time periods with differing classification for various interventions in acute and chronic type B aortic dissection, it is expected that this new IRAD classification system will assist in improving ‘best practice’ for management (14).

Optimal treatment of aortic dissection in the 15-30 days from symptom onset time period remains uncertain. As

such, the question remains of how to best treat patients presenting with subacute type B aortic dissection. The INSTEAD trial attempted to answer this question by randomizing patients with uncomplicated type B aortic dissection between 2 and 52 weeks from onset into either medical therapy or thoracic endovascular aortic repair (TEVAR) therapy. Though the study was initially found to be underpowered, 5-year all-cause mortality appeared favorable for TEVAR at 11.1% versus best medical therapy alone at 19.3% (P=0.13). Additionally, aorta-specific 5-year mortality was significantly lower in the TEVAR group at 6.9% versus 19.3% (P=0.04) (15). It appears that TEVAR, in addition to optimal medical therapy, is associated with delayed disease progression resulting in improved long-term survival. Akin et al. have suggested that instability in subacute or chronic type B dissection as evidenced by permanent thoracic pain, uncontrolled hypertension, or aortic diameter increasing beyond 55-60 mm (or at an annual rate >4 mm) would be appropriate indications for TEVAR intervention (16). However, in truth there remains paucity of data and our current views of best practices are likely transient. Future trials based upon the defined temporal subgroups are needed to further inform the optimal management and prognosis of acute vs. subacute vs. chronic type B aortic dissection.

Surveillance imaging for any type B aortic dissection is thought by many to provide benefit regardless of temporal or risk stratification or even treatment applied (17). In

Figure 2 Kaplan-Meier survival curves for type B dissection stratified by time (13).

0 1 4 8 12 16 20 24 28 32 36 40 44 48 52 56 60

Time from symptom onset (days)

0-24 hours(hyperacute)

8-30 days(subacute)

Greater than 30 days(chronic)

Surgical management

Medical management

Endovascular management

Log rank Chi-Sq P<0.001between management types

2-7 days(acute)

Sur

viva

l

1.00

0.95

0.90

0.85

0.80

0.75

0.70

Endo reparación

• Objetivos

• Reparación del desgarro principal

• Promover la trombosis del lúmen falso

• Remodelación aórtica a mediano plazo

• Evitar la degeneración aneurismática

Y los no complicados?

¿Existe la posiblidad de disminuir la mortalidad relacionada a las complicaciones tardías aórticas?

Louis Labrousse, Rossella Fattori and Hüseyin InceZipfel,Guenther Kundt, Aenne Glass, Dierk Scheinert, Martin Czerny, Tilo Kleinfeldt, Burkhart

Christoph A. Nienaber, Stephan Kische, Hervé Rousseau, Holger Eggebrecht, Tim C. Rehders,Investigation of Stent Grafts in Aortic Dissection Trial

Endovascular Repair of Type B Aortic Dissection: Long-Term Results of the Randomized

Print ISSN: 1941-7640. Online ISSN: 1941-7632 Copyright © 2013 American Heart Association, Inc. All rights reserved.

Avenue, Dallas, TX 75231is published by the American Heart Association, 7272 GreenvilleCirculation: Cardiovascular Interventions

published online August 6, 2013;Circ Cardiovasc Interv.

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Nienaber et al Long-Term F/U After Stent Grafts in Aortic Dissection 7

complications, such as expansion, rupture, and late crossover/conversion to emergent TEVAR, conveying a higher aorta-specific mortality. The notion of uncomplicated type B dis-section may in fact be a misnomer and should be reconsidered because the need for late repair of critical expansion and pro-gression of dissection is common.6,10,26,27 Thus, initial clinical stability does not preclude emergent silent expansion and even rupture; both events are preventable by endovascular manage-ment in the early phase.

Despite encouraging early and mid-term survival of uncom-plicated type B dissection with medical management,5,6,17 chronic expansion and late rupture even without critical expansion were not heralded; although TEVAR in an early complicated scenario reveals immediate therapeutic resolu-tion of the complication, elective TEVAR embodies a preemp-tive element requiring long-term observation to prove benefit. Finally, the association between TEVAR and aortic remodel-ing suggests concordance of healing with clinical outcomes.

INSTEAD-XL reveals, with elective TEVAR of aortic dis-section, an association with favorable aortic remodeling and long-term survival despite early hazard, although medical

management was associated with failure to prevent progres-sive expansion or late complications triggering steady cross-over to TEVAR at 5 years. Conversely, reinterventions after primary TEVAR were few and clustered in the first year. Such long-term stability in patients with stented aorta may be dissection specific and explained by healing, and thereby different from less encouraging experience in aneurysmatic disease.28 Although elective crossover and endovascular rein-tervention were generally safe, corroborating observations in chronic type B dissection,14 emergency TEVAR portends con-siderable mortality29,30; emergencies may in fact be avoided by both imaging surveillance and elective TEVAR.

The concept of TEVAR already embraced to replace open surgery for managing complications of type B dissection (even without any randomized data)2,4,31–33 may now be extended to manage stable (initially uncomplicated) type B dissection because the potential to remodel dissected aorta and prevent late expansion and malperfusion has been confirmed.21,34 With completed 5-year surveillance in all survivors, any discordance of aortic remodeling with clinical outcomes after TEVAR was

Table 4. Morphological Characteristics Over Time

Characteristics OMT (n=68)OMT+TEVAR

(n=72) P Value

Baseline type B dissection

Maximum aortic diameter 43.6±9.2* 44.1±9.6 0.65

True lumen diameter at level A 20.3±9.3* 19.4±8.0* 0.55

False lumen diameter at level A 27.7±11.6* 29.3±12.4* 0.65

True lumen diameter at level B 17.3±8.7 17.4±10.7* 0.91

False lumen diameter at level B 24.0±10.4* 26.9±10.9* 0.13

2-y follow-up

Maximum aortic diameter 46.3±9.9 43.9±11.4 0.24

True lumen diameter at level A 22.7±10.9 32.4±5.5 <0.0001

False lumen diameter at level A 25.4±14.8 8.6±13.4 <0.0001

True lumen diameter at level B 19.1±8.6 29.7±7.0 <0.0001

False lumen diameter at level B 24.3±12.2 11.5±13.7 <0.0001

False lumen thrombosis at 2 y†

Complete, n (%) 13/67 (19.4) 63/69 (91.3) <0.0001

Partial‡, n (%) 6/66 (9.1) 6/69 (8.7) 1.00

5-y follow-up

Maximum aortic diameter 56.4±6.8 44.5±11.5 <0.0001






Complete, number (%) 11/50 (22.0) 48/53 (90.6) <0.0001

Partial‡, number (%) 6/50 (12.0) 5/53 (9.4) 0.76

Values are mean±SD, numbers in parenthesis reflect percentage; OMT indicates optimal medical treatment; and TEVAR, thoracic endovascular aortic repair.

*P<0.001 vs 2 y and 5 y (repeated measures analysis).†Throughout the level of the descending thoracic aorta.‡Partial false lumen thrombosis used as defined in Tsai et al40 with residual

(retrograde) perfusion of the false lumen despite evidence of layered thrombosis.

Figure 3. Gadolinium-enhanced sagittal MR angiogram of type B dissection before randomization (top) and 5 years after endovas-cular repair (bottom). Sagittal maximum intensity projection (A and C) and 3-dimensional reconstructed scans (B and D) show complete aortic remodeling with time; the left subclavian artery is filled by collaterals after intentional coverage with the endograft.

by guest on September 22, 2014http://circinterventions.ahajournals.org/Downloaded from

8 Circ Cardiovasc Interv August 2013

refuted. These initial findings are promising and may prelude a paradigm shift in managing type B aortic dissection.

Nonetheless, with 3 conversions to open surgery in both groups within 2 years, and 2 cases of spinal injury, TEVAR is not always safe35,36; however, procedural risk may be lowered by referral to high-volume centers, preemptive carotido-subclavian bypass and dissection-specific endoprosthetic technology. Moreover, elective TEVAR within 90 days of dissection benefits from ongoing aortic plasticity with better remodeling.37

Thus, different from early outcomes, INSTEAD-XL sug-gests survival benefit from preemptive TEVAR in patients surviving type B dissection in addition to OMT and surveil-lance. Considering the few cases of progression after 2 years of elective TEVAR, surveillance may be tapered once remod-eling was documented. Finally, remodeling of dissected aorta seems in concordance with long-term vascular survival.

INSTEAD-XL was initiated assuming 35% late mortality in type B dissection6,10,22 with medical management; how-ever, with surveillance, adjusted medication, and an option to crossover, OMT outcomes were better than in previous regis-tries, further explaining the need for long-term follow-up to demonstrate the impact of preemptive TEVAR. Although real world 5-year cumulative mortality of type B dissection is 28% with β-blockers, and 25% with calcium antagonists compared with 33% and 36% without those drugs,10 21.6% mortality with OMT was even lower in INSTEAD-XL, reflecting the nature of a controlled trial. INSTEAD-XL confirms standard-ized care with blood pressure control for patients with distal dissection regardless of symptoms but eventually encourages elective TEVAR in suitable patients for long-term benefit.

LimitationsFor stable survivors of type B dissection, benefits of TEVAR begin to show after 2 years of follow-up. Landmarking at 2 years of follow-up was selected a priori in anticipation of events both before and after 2 years.17 Nevertheless, with Landmark analysis, findings become observational because some confounders may not be accounted for, and early events may be omitted, thus rendering the analysis susceptible to time point–specific results and loss of power.38 The risk of depen-dence on any lack of proportionality of hazards, however, was partly defused by additional Landmarking at 12 months and at 1 month of follow-up with consistent results with late benefit of TEVAR (Figure IIA–IIC in the online-only Data Supplement).

Nevertheless, for some very old patients, the benefit may not emerge during expected lifetime; yet, preemptive TEVAR seems useful for younger patients, although advanced age

and severe comorbidities may still favor medical manage-ment. Similarly, patients with hereditary connective tis-sue disease will probably require open surgery. Conversely, advancing TEVAR technology and growing operator skills may avoid procedure-related risks and lower the threshold for early TEVAR to avoid late complications.39 Before preemp-tive scaffolding is widely accepted, asymptomatic patients at risk, for example, with partial false lumen thrombosis ideally addressed by cine-MRI,40 critical false lumen diameter,41 or a large entry tear should be considered for TEVAR.

OutlookOur current picture of best medical care for aortic dissection may be supplanted by growing insight into disease progres-sion regardless of symptoms or complications. Uncomplicated aortic dissection seems a misnomer, and any distal dissection may be considered a vascular complication requiring repair by an effective strategy.

AcknowledgmentsWe thank our referring physicians for encouraging their patients to continue a structured long-term follow-up for INSTEAD-XL; more-over, continued support at participating centers and diligent patient care is highly valued. Finally, the authors are indebted to Gitta Knoop and Melanie Elste for preparing this article.

Sources of FundingThe 5 years follow-up of INSTEAD-XL was partially funded by Medtronic, Inc, Santa Rosa, CA; the United States; and by Institutional Research Funds of the University of Rostock.

DisclosuresAll authors disclose their individual interaction with industry, but report no conflict of interest. Dr Nienaber has received lecture and consulting fees from Boston Scientific, Inc, Cook, Inc, and Medtronic, Inc; Dr Rousseau has received lecture fees from Gore, Inc, and Medtronic, Inc; Dr Eggebrecht has received lecture fees from Bolton, Inc, and from Medtronic, Inc; Dr Kische has received lecture fees from Medtronic, Inc; Dr Fattori has received lecture fees from Medtronic, Inc; Dr. Scheinert has received honoraria from Medtronic, Inc; Dr Czerny has received honoraria from Bolton, Inc; Dr Zipfel has received lecture fees from Jotec GmbH and Bolton, Inc; Dr Labrousse has received lecture fees from Gore, Inc; Dr Ince has received honoraria from Medtronic, Inc. Christoph A. Nienaber received honoraria from Cook, Inc, amount: <$10 000; Medtronic Inc, amount: <$10 000; Boston Scientific Inc, amount: <$10 000; and Expert Witness: John-Ritter-Case in 2008. Stephan Kische received honoraria from Medtronic Inc, amount: <$10 000; Hervé Rousseau from Medtronic Inc, amount: <$10 000 and from Gore Inc, amount: <$10 000. Holger Eggebrecht received honoraria from Bolton, Inc, amount: <$10 000 and Medtronic Inc, amount: <$10 000. Tim C. Rehders received honoraria from Medtronic Inc, amount: <$10 000; Dierk Scheinert from Medtronic Inc, amount: <$10 000; and Martin Czerny from Bolton Inc, amount: <$10 000. Burkhart Zipfel received honoraria from Jotec GmbH, amount: <$10 000 and Bolton Inc, amount: <$10 000. Louis Labrousse received honoraria from Gore Inc, amount: <$10 000; Rossella Fattori from Medtronic Inc, amount: <$10 000; and Hüseyin Ince from Medtronic Inc, amount: <$10 000.

References 1. Dake MD, Kato N, Mitchell RS, Semba CP, Razavi MK, Shimono

T, Hirano T, Takeda K, Yada I, Miller DC. Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med. 1999;340:1546–1552.

2. Nienaber CA, Kische S, Ince H, Fattori R. TEVAR in complicated type B aortic dissection. J Vasc Surg. 2011;340:1529–1533.

Table 5. Aortic Morphology at 5 Years

OMT OMT+TEVAR P Value

FL thrombosis 11/50 (22.0%) 48/53 (90.6%) <0.0001

Partial FL/no FL thrombosis 39/50 (78.0%) 5/53 (9.4%) <0.0001

Remodeling of thoracic aorta* 5/50 (10.0%) 42/53 (79.2%) <0.0001

Critical expansion of thoracic aorta† 33/50 (66.0%) 11/53 (20.8%) <0.0001

FL indicates false lumen; OMT, optimal medical treatment; and TEVAR, thoracic endovascular aortic repair.

*Based on aortic morphology as assessed vs baseline.†Occurring within long-term follow-up.


Nienaber et al Long-Term F/U After Stent Grafts in Aortic Dissection 7

complications, such as expansion, rupture, and late crossover/conversion to emergent TEVAR, conveying a higher aorta-specific mortality. The notion of uncomplicated type B dis-section may in fact be a misnomer and should be reconsidered because the need for late repair of critical expansion and pro-gression of dissection is common.6,10,26,27 Thus, initial clinical stability does not preclude emergent silent expansion and even rupture; both events are preventable by endovascular manage-ment in the early phase.

Despite encouraging early and mid-term survival of uncom-plicated type B dissection with medical management,5,6,17 chronic expansion and late rupture even without critical expansion were not heralded; although TEVAR in an early complicated scenario reveals immediate therapeutic resolu-tion of the complication, elective TEVAR embodies a preemp-tive element requiring long-term observation to prove benefit. Finally, the association between TEVAR and aortic remodel-ing suggests concordance of healing with clinical outcomes.

INSTEAD-XL reveals, with elective TEVAR of aortic dis-section, an association with favorable aortic remodeling and long-term survival despite early hazard, although medical

management was associated with failure to prevent progres-sive expansion or late complications triggering steady cross-over to TEVAR at 5 years. Conversely, reinterventions after primary TEVAR were few and clustered in the first year. Such long-term stability in patients with stented aorta may be dissection specific and explained by healing, and thereby different from less encouraging experience in aneurysmatic disease.28 Although elective crossover and endovascular rein-tervention were generally safe, corroborating observations in chronic type B dissection,14 emergency TEVAR portends con-siderable mortality29,30; emergencies may in fact be avoided by both imaging surveillance and elective TEVAR.

The concept of TEVAR already embraced to replace open surgery for managing complications of type B dissection (even without any randomized data)2,4,31–33 may now be extended to manage stable (initially uncomplicated) type B dissection because the potential to remodel dissected aorta and prevent late expansion and malperfusion has been confirmed.21,34 With completed 5-year surveillance in all survivors, any discordance of aortic remodeling with clinical outcomes after TEVAR was

Table 4. Morphological Characteristics Over Time

Characteristics OMT (n=68)OMT+TEVAR

(n=72) P Value

Baseline type B dissection

Maximum aortic diameter 43.6±9.2* 44.1±9.6 0.65

True lumen diameter at level A 20.3±9.3* 19.4±8.0* 0.55

False lumen diameter at level A 27.7±11.6* 29.3±12.4* 0.65

True lumen diameter at level B 17.3±8.7 17.4±10.7* 0.91

False lumen diameter at level B 24.0±10.4* 26.9±10.9* 0.13

2-y follow-up

Maximum aortic diameter 46.3±9.9 43.9±11.4 0.24






Complete, n (%) 13/67 (19.4) 63/69 (91.3) <0.0001

Partial‡, n (%) 6/66 (9.1) 6/69 (8.7) 1.00

5-y follow-up

Maximum aortic diameter 56.4±6.8 44.5±11.5 <0.0001






Complete, number (%) 11/50 (22.0) 48/53 (90.6) <0.0001

Partial‡, number (%) 6/50 (12.0) 5/53 (9.4) 0.76

Values are mean±SD, numbers in parenthesis reflect percentage; OMT indicates optimal medical treatment; and TEVAR, thoracic endovascular aortic repair.

*P<0.001 vs 2 y and 5 y (repeated measures analysis).†Throughout the level of the descending thoracic aorta.‡Partial false lumen thrombosis used as defined in Tsai et al40 with residual

(retrograde) perfusion of the false lumen despite evidence of layered thrombosis.

Figure 3. Gadolinium-enhanced sagittal MR angiogram of type B dissection before randomization (top) and 5 years after endovas-cular repair (bottom). Sagittal maximum intensity projection (A and C) and 3-dimensional reconstructed scans (B and D) show complete aortic remodeling with time; the left subclavian artery is filled by collaterals after intentional coverage with the endograft.


Nienaber et al 2013 - Circ

Cuáles no complicados?

HAY QUE INCOPORAR EL CONCEPTO DE ALTO RIESGO O BAJO RIESGO DE

DEGENERACION AORTICA

ALTO RIESGO

ALTO RIESGO• Desgarro mayor a 10mm


• Localización del desgarro en la curvatura menor Ao



• Diámetro Aórtico total mayor a 40mm




• Diámtero del lumen falso mayor a 22mm





• Trombosis parcial del lumen falso






• Marui fusiform index (MFI) mayor a 0.64






• Marui fusiform index (MFI) mayor a 0.64

POTENCIALES CANDIDATOS PARA TRATAMIENTO MAS AGRESIVO

IT CAN GO TERRIBLY WRONG!

Avoid free struts, and AVOID POST DILATION

M. Montero-Baker, MD

@monteromiguel [email protected]

mailto:[email protected]

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Nuevos horizontes en el manejo de la Disección … Montero-Bak… · de la Disección Aórtica tipo B ... aortic intramural hematoma or penetrating ... Figure 2 Kaplan-Meier survival