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Conclusions: Aortitis continues to be a conundrum; however, good results are achievable with surgery.
Intervention should be based on a clearer understanding of the histologic pattern and extent of disease, which
helps in subsequent targeted disease management. (J Thorac Cardiovasc Surg 2014;-:1-6)
infections at sites of calcification, old grafts, penetrating
ulcers, or areas of turbulence. Furthermore, the subgroup of
patients with noninfectious aortitis are considered to have
acute phases, often missed subacute phases, and chronic
phases, the latter with some risk of repeated flare-ups. There
is, however, considerable overlap of histologic findings between the noninfective labeled types and chronic infective
types such as syphilis, tuberculosis, human immunodeficiency disease, and rickettsialike etiologies. This clearly raises the question of potential undetected subclinical infective
etiologies by bacteria that have not been defined, such as
the more recently discovered archaic or extremophile organisms and organisms detected in tumors.21 In the early nineties,
Svensson and Crawford20 did attempt to group patients with
Takayasu arteritis according to anatomic extent of their disease on the basis of reported histologic patterns. That analysis
was based on a smaller study of patients and observations.
This analysis from the Cleveland Clinic, in contrast, is based
on a larger series of more than 7500 patients, 12% of whom
were found to have inflammatory aortitis proved by histologic
analysis.22
MATERIALS AND METHODS
Between 1996 and 2012, we operated on 7551 patients with ascending
or arch disease. Of these patients, 279 had inflammatory disease, and
156 (2%) were found to have aortitis proved by histologic examination
and are the subject of this report. The study was approved by the institutional review board of the Cleveland Clinic, with patient consent waived.
Svensson et al
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Sex
Male
Female
Age (y)
Range
Mean SD
Diagnosis
Preoperative
Immunosuppressant
Preoperative
Postoperative
Comorbidities
DM
Carotid artery
COPD
CVA
Hypertension
PVD
Preoperative dialysis
History of smoking
History of MI
History of CHF
Preoperative AF
Aneurysm
Intramural hematoma
Penetrating ulcer
Acute dissection
Chronic dissection
Preoperative ascending diameter (mm, mean SD)
Preoperative descending diameter (mm, mean SD)
Giant cell
(n 50; 32%)
Takayasu
(n 8; 5%)
Isolated
(n 92; 58%)
Other
(n 6; 3%)
Total
(n 156)
13 (26%)
37 (74%)
2 (25%)
6 (75%)
23 (25%)
69 (75%)
5 (83.3%)
1 (16.7%)
43 (27.5%)
113 (72.5%)
44.08-84.14
69.6 9
23.16-56.4
36.2 13.5
19.82-86.91
66.8 14
65.19-79.5
70.1 4.9
20-87
66.2 14.3
20
26 (18%)
12
37
3
7
1
7
6
5
22 (14.1%)
57 (36.54%)
2 (4%)
10 (20%)
10 (20%)
3 (6%)
41 (82%)
9
0
25
6
8
4
43
1
1
4
1
53.2 6.7
39.6 10.4
0
0
2 (25%)
0
5 (62.5%)
1
0
4
0
1
0
8
0
0
0
0
55 12.6
36.2.7 12.9
10 (10.8%)
23 (25%)
28 (30.4%)
11 (12%)
71 (77.1%)
18
0
55
12
15
6
77
2
6
0
7
56.6 9
43 14.6
1 (16.6%)
1 (16.6%)
2 (33.3%)
0
6 (100%)
2
0
3
1
1
0
5
0
1
0
0
47.1 12.7
39.1 12.8
13 (8.3%)
34 (21.8%)
42 (27%)
13 (8.3%)
123 (78.8%)
30 (19.2%)
0
87 (55.7%)
19 (12.8%)
25 (16%)
10 (6.4%)
134
3
8
4
8
55.5 9.2
41.6 13.5
All data represent number of patients with percentage unless otherwise indicated. DM, Diabetes mellitus; COPD, chronic obstructive pulmonary disease; CVA, cerebrovascular
accident; PVD, peripheral vascular disease; MI, myocardial infarction; CHF, congestive heart failure; AF, atrial fibrillation; SD, standard deviation.
The series consisted of 36% male and 64% female patients with a mean
(SD) age of 66.4 14.3 years. Preoperative indications for surgery
included aortic degenerative diseases (84%), acute aortic syndrome
(10%), chronic dissection (5%), and aortic rupture (1%) (Table 1). Among
those excluded were 34 patients with Takayasu arteritis who did not need
aortic surgical replacement. The study was approved by the institutional review board of the Cleveland Clinic, with patient consent waived. Data from
both the prospectively collected cardiovascular database and chart review
were combined. Late mortality data were obtained from regular prospective
interval follow-up and cross-checking with the Social Security Death Index
for death.
Aortitis was defined as a nonatherosclerotic and noninfectious
inflammatory process involving the tunica media with or without
involvement of the adventitia of the aorta.
In 4 patients with aortitis, we examined the microorganism signatures
and compared these with those from 3 patients without aortitis and found
a clustering of patients with aortitis.21
RESULTS
Of the total number of patients who underwent ascending
and/or arch aortic surgery (n 7551), 156 (12%) of them
had historically proven aortitis. Among these 156 patients,
2
Svensson et al
Index procedure
Isolated root replacement
Ascending aortic repair
Hemiarch repair
Total arch replacement
Stage 1 ET
Other
Frozen ET
Reverse frozen ET
Aortoplasty
Aortic biopsy
Concomitant procedures
Aortic valve repair
Aortic valve replacement
Concomitant root replacement
Hemiarch
Total arch replacement
ET
CABG
Mitral valve repair
Tricuspid valve repair
Atrial fibrillation surgery
Other congenital correction
Subsequent aortic replacement after index
TEVAR
Thoracoabdominal repair
Proximal aortic repair
Index as reintervention
Root plus ascending
Total arch
ET
Stage 2 ET (n 25; 53%)
EEC
OEC
Complications
Death (in-hospital and 30 d)
Stroke
Spinal paralysis
Renal dialysis
Reoperation for bleeding
Myocardial infarction
Giant cell
(n 50; 32%)
Takayasu
(n 8; 5%)
Isolated
(n 92; 58%)
Other
(n 6; 3%)
Total
(n 156)
3
16
12
3
12
0
0
3
3
2
5
27
21
5
32
0
1
1
3
1
8
44
37
14
47
0
0
1
3
0
0
0
0
1
1
0
0
0
0
0
0
7
26
0
5
8
41
0
3
1
1
1
3
181
15
75
3
0
1
2
1
1
9
0
4
0
0
0
4
3
0
0
1
1
2
3
2
0
1
0
1
0
2
0
0
0
0
1
0
0
0
0
6
2
0
1
12
3
1
0
1
1
0
0
2
0
0
0
0
0
0
0
4
2
0
3
6
0
0
0
0
0
0
0
14
1
6
39
10
5
9
7
17
5
8
4
4
1
1
2
46
19
6
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Variable
5 (3.2%)
3 (1.9%)
0
3
8 (5.1%)
0
All data represent number of patients. ET, Elephant trunk; CABG, coronary artery bypass grafting; TEVAR, total endovascular aortic repair; EEC, endovascular elephant trunk
completion; OEC, open elephant trunk completion.
Svensson et al
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including 12 (77%) receiving methotrexate (an antimetabolite and antifolate immunosuppressive and immunomodulatory agent similar to mycophenolate mofetil, and
azathioprine but with different metabolic pathways
affected). Some 49 patients required late reoperation, with
no difference in etiology types.
There were 5 in-hospital deaths (3.2%), and stroke
occurred in 3 patients (1.9%). There was reoperation for
bleeding in 7 cases (5.1%). The Kaplan-Meier survival
was 54.7% at 8 years, and reoperations increased with
time (Figure 1). Freedoms from reintervention at 30 days,
1 year, 5 years, and 8 years were 98.9%, 83.1%, 82.1%,
and 77.6%, respectively.
There was no significant difference in outcomes by age,
sex, race, greater vessel or cerebrovascular disease, nor
procedure, suggesting that the results can be generalized
arch, with variable degrees of descending or thoracoabdominal dilation. Greater vessel involvement is variable but
often involves carotid disease at the bifurcation or more
distally. For those patients, there is little distinction between
giant cell and isolated aortitis, and thus these patients as a
group should be considered for prophylactic elephant trunk
procedures because their natural progression is continued
distal dilation with time that would necessitate repeated
intervention. Type 2 disease typically consists of ascending
aortic disease with proximal greater vessel involvement
proximal to the carotid bifurcation or proximal innominate
or subclavian involvement. Takayasu arteritis is typical of
the type 2 classification, and these patients should be
considered for greater vessel bypasses with prosthetic rather
than biologic material beyond the arch artery origins and
mechanical valve replacement for moderate or severe aortic
valve disease. Type 3 disease usually consists of thoracoabdominal disease with variable dilatation or atheroma or
atherosclerosis and proximal greater arch vessel or visceral
abdominal involvement. These patients require either specific procedures, such as bypasses or stenting of the greater
vessels, before thoracoabdominal aortic repairs to the
greater vessels or concurrent prosthetic material bypasses
to visceral arteries or left subclavian bypass. Type 4 disease
includes that group of subdiaphragmatic inflammatory aneurysms that may have variable visceral artery involvement
and appear to have a different type of etiology, possibly
related to lymphatic vessel disease. Pulmonary stenotic disease appears to represent a separate, rare disease group.
In short, the aim of surgical intervention for aortitis
should be to correct the anatomic disease problem, to
reduce the risk of pseudoaneurysm formation, to prevent
perivalvular aortic valve leaks, to prevent continued
destruction from the disease, and to prepare for later
disease progression. Greater vessel bypasses allow for later
extrathoracic cavity bypasses to be done, and prophylactic
elephant trunk procedures allow for safer second-stage
procedures, either open or by stenting. Vein grafts and biologic material, including aortic valve replacement, should
be avoided because of the high risk of failure.
Limitations
This is a retrospective study concentrating on histologically based diagnoses of aortitis. We are preparing
a separate article that is based on disease diagnosis
groups and medical or surgical treatment. Ideally,
continuing research will contribute to a better understanding of the disease etiology and determine the medications
and techniques that should be developed to halt disease
progression as well as potential complications with time.
References
1. Miller DV, Isotalo PA, Weyand CM, Edwards WD, Aubry MC, Tazelaar HD.
Surgical pathology of noninfectious ascending aortitis: a study of 45 cases
with emphasis on an isolated variant. Am J Surg Pathol. 2006;30:1150-8.
2. Hunder GG, Bloch DA, Michel BA, Stevens MB, Arend WP, Calabrese LH, et al.
The American College of Rheumatology 1990 criteria for the classification of
giant cell arteritis. Arthritis Rheum. 1990;33:1122-8.
3. Grayson PC, Maksimowicz-McKinnon K, Clark TM, Tomasson G,
Cutherbertson D, Carette S, et al; Vasculitis Clinical Research Consortium.
Distribution of arterial lesions in Takayasus arteritis and giant cell arteritis.
Ann Rheum Dis. 2012;71:1329-34.
4. Maksimowicz-McKinnon K, Clark TM, Hoffman GS. Takayasu arteritis and
giant cell arteritis: a spectrum within the same disease? Medicine (Baltimore).
2009;88:2216.
5. Pipitone N, Salvarani C. Idiopathic aortitis: an under recognized vasculitis.
Arthritis Res Ther. 2011;13:119.
6. Rojo-Leyva F, Ratliff NB, Cosgrove DM III, Hoffman GS. Study of 52 patients
with idiopathic aortitis from a cohort of 1,204 surgical cases. Arthritis Rheum.
2000;43:901-7.
7. Zehr KJ, Mathur A, Orszulak TA, Mullany CJ, Schaff HV. Surgical treatment of
ascending aortic aneurysms in patients giant cell aortitis. Ann Thorac Surg. 2005;
79:1512-7.
8. Lee A, Luk A, Phillips KR, Lim KD, David TE, Butany J. Giant cell aortitis: a
difficult diagnosis assessing risk for the development of aneurysms and
dissections. Cardiovasc Pathol. 2011;20:247-53.
9. Tso E, Flamm SD, White RD, Schvartzman PR, Mascha E, Hoffman GS.
Takayasu arteritis: utility and limitations of magnetic resonance imaging in
diagnosis and treatment. Arthritis Rheum. 2002;46:1634-42.
10. Blockmans D, Stroobants S, Maes A, Mortelmans L. Positron emission
tomography in giant cell arteritis and polymyalgia rheumatica: evidence for
inflammation of the aortic arch. Am J Med. 2000;108:246-9.
11. Rahman MS, Storrar N, Anderson LJ. FDG-PET/CT in the diagnosis of aortitis
in fever of unknown origin with severe aortic incompetence. Heart. 2013;99:
435-6.
12. Gornik HL, Creager MA. Aortitis. Circulation. 2008;117:3039-51.
13. Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE Jr, et al;
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; Society for Vascular Medicine. 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. 2010;121:e266-369. Erratum in: Circulation.
2010;122:e410.
14. Wang H, Smith RN, Spooner AE, Isselbacher EM, Cabria RP, MacGillivray TE,
et al. Giant cell aortitis of the ascending aorta without signs or symptoms
of systemic vasculitis is associated with elevated risk of distal aortic events.
Arthritis Rheum. 2012;64:317-9.
15. Mennander AA, Miller DV, Liang KP, Warrington KJ, Connolly HM, Schaff HV,
et al. Surgical management of ascending aortic aneurysm due to non-infectious
aortitis. Scand Cardiovasc J. 2008;42:417-24.
16. Nuenninghoff DM, Hunder GG, Christianson TJ, McClelland RL, Matteson EL.
Mortality of large-artery complication (aortic aneurysm, aortic dissection, and/or
large-artery stenosis) in patients with giant cell arteritis: a population-based study
over 50 years. Arthritis Rheum. 2003;48:3532-7.
17. Evans JM, OFallon WM, Hunder GG. Increased incidence of aortic aneurysm
and dissection in giant cell (temporal) arteritis. A population-based study. Ann
Intern Med. 1995;122:502-7.
18. Idrees J, Albacker TB, Gordon SM, Shin J, Menon V, Roselli EE. Bartonella
infective endocarditis of a prosthetic aortic valve with a subvalvular abscess.
J Card Surg. 2011;26:483-5.
19. Frank MW, Mehlman DJ, Tsai F, Lomasney JW, Joob AW. Syphilitic aortitis.
Circulation. 1999;100:1582-3.
20. Svensson LG, Crawford ES. Cardiovascular and vascular disease of the aorta.
1st ed. Philadelphia: WB Saunders; 1997:105-83.
21. Bebek G, Bennett KL, Funchain P, Campbell R, Seth R, Scharpf J, et al.
Microbiomic subprofiles and MDR1 promoter methylation in head and neck
squamous cell carcinoma. Hum Mol Genet. 2012;21:1557-65.
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Svensson et al
22. Svensson LG, Nadolny EM, Kimmel WA. Multimodal protocol influence on
stroke and neurocognitive deficit prevention after ascending/arch aortic
operations. Ann Thorac Surg. 2002;74:2040-6.
23. Svensson LG, Rushing GD, Valenzuela ES, Rafael AE, Batizy LH,
Blackstone EH, et al. Modifications, classification, and outcomes of
elephant-trunk procedures. Ann Thorac Surg. 2013;96:548-58.
24. Svensson LG, Kim KH, Blackstone EH, Alster JM, McCarthy PM,
Greenberg RK, et al. Elephant trunk procedure: newer indications and uses.
Ann Thorac Surg. 2004;78:109-16; discussion 109-16.
25. Roselli EE, Subramanian S, Sun Z, Idrees J, Nowicki E, Blackstone EH, et al.
Endovascular versus open elephant trunk completion for extensive aortic disease.
J Thorac Cardiovasc Surg. 2013;146:1408-16.
26. Roselli EE, Qureshi A, Idrees J, Lima B, Greenberg RK, Svensson LG, et al.
Open, hybrid, and endovascular treatment for aortic coarctation and postrepair
Svensson et al
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28.
29.
30.
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