FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2080789065> ?p ?o ?g. }

• W2080789065 endingPage "2747" @default.
• W2080789065 startingPage "2738" @default.
• W2080789065 abstract "HomeCirculationVol. 118, No. 25Overview of Late Outcome of Medical and Surgical Treatment for Takayasu Arteritis Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBOverview of Late Outcome of Medical and Surgical Treatment for Takayasu Arteritis Hitoshi Ogino, MD, PhD, Hitoshi Matsuda, MD, PhD, Kenji Minatoya, MD, PhD, Hiroaki Sasaki, MD, PhD, Hiroshi Tanaka, MD, PhD, Yu Matsumura, MD, Hatsue Ishibashi-Ueda, MD, PhD, Junjiro Kobayashi, MD, PhD, Toshikatsu Yagihara, MD, PhD and Soichiro Kitamura, MD, PhD Hitoshi OginoHitoshi Ogino From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author , Hitoshi MatsudaHitoshi Matsuda From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author , Kenji MinatoyaKenji Minatoya From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author , Hiroaki SasakiHiroaki Sasaki From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author , Hiroshi TanakaHiroshi Tanaka From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author , Yu MatsumuraYu Matsumura From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author , Hatsue Ishibashi-UedaHatsue Ishibashi-Ueda From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author , Junjiro KobayashiJunjiro Kobayashi From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author , Toshikatsu YagiharaToshikatsu Yagihara From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author and Soichiro KitamuraSoichiro Kitamura From the Departments of Cardiovascular Surgery (H.O., H.M., K.M., H.S., H.T., Y.M., J.K., T.Y., S.K.) and Pathology (H.I.), National Cardiovascular Center, Osaka, Japan. Search for more papers by this author Originally published16 Dec 2008https://doi.org/10.1161/CIRCULATIONAHA.107.759589Circulation. 2008;118:2738–2747Takayasu arteritis (TA), which is a nonspecific inflammatory disease of unknown origin, causes various types of aortoarterial stenosis/occlusion or dilatation (Figure). Historically, Mikito Takayasu, a Japanese ophthalmologist, described a peculiar wreathlike arteriovenous anastomosis around the papillae of the retina (Takayasu disease) in 1908.1 In the first necropsy case reported in 1940, this ophthalmologic finding was related to cervical vessel occlusion.2,3 Subsequently, this nonspecific panarteritis that affects the intima and the adventitia of the aorta and its main branches was called Takayasu arteritis. Its clinical manifestations are varied and related to the vessel that presents the stenotic or occlusive lesions, such as the aortic arch (pulseless disease),4 descending thoracic or abdominal aorta (atypical coarctation),5 renal arteries,6 coronary arteries,7 and pulmonary arteries. Aortic aneurysm8 and aortic valve regurgitation with ascending aortic dilatation9 may also develop in some instances. Pharmacological treatment with corticosteroids is usually the initial treatment. Some patients require surgical treatment such as bypass grafting and graft replacement or endovascular repair including percutaneous transluminal angioplasty (PTA) and stent grafting, even in the active phase or in the inactive chronic phase with adequate control of the inflammation. Since the 1960s, acceptable early and midterm outcomes of medical and/or surgical treatment have been published. However, the long-term outcome, including that of recently developed endovascular treatment, has not been discussed. In this article, we describe an overview, particularly focusing on the late outcome of treatment for TA. Download figureDownload PowerPointFigure. Three-dimensional computed tomographic findings of an active phase of Takayasu arteritis (21 years, female). Three-dimensional computed tomographic findings include multiple stenotic lesions on the carotid and subclavian arteries (A), aneurysmal dilatation of the ascending aorta to the aortic arch and of the main pulmonary artery (B), aneurysmal dilatation of the descending aorta, stenosis of the right renal artery, and multiple stenoses of the bilateral iliac and femoral arteries (C), and occlusions of the bilateral femoral arteries (D). Under the administration of 25 mg/d of corticosteroids, balloon PTA for stenotic lesions of the right renal artery and the left external iliac artery was performed before surgery. For severe aortic valve regurgitation, composite graft root replacement with the use of a bioprosthetic valve with the miniskirt technique was performed.MethodsSome clinical data in our institute were used in addition to the other authors’ data taken from the references. Our clinical data were published after the approval of the institutional review board in our institute. All of the clinical practices in our institute were performed under the national health insurance program. Each patient gave informed consent to receive the treatment and to serve as a subject for the study. The clinical data in the other references were used with the informed consent and the approval of the institutional review board in their institutes, as stated in the references.ResultsIncidences and OriginOne of the characteristic features of TA is its predominance in young women. A Japanese nationwide survey demonstrated that 90% of the patients were women,10 although an international survey showed a lower female to male sex ratio even in other Asian countries such as China, India, and Israel and in Western countries.2,3 Another epidemiological feature is the ethnic difference. TA is prevalent in Asian countries and Latin America, although it is reportedly distributed worldwide. It is extremely rare in white people.11 Furthermore, there are also some differences in the sites affected by aortoarteritis among different countries. In Japanese patients, the ascending aorta and aortic arch with its branches are more frequently involved, whereas in patients from Korea, India, and Western countries, the abdominal aorta and renal arteries are most frequently affected.12 Consequently, aortic regurgitation used to be the main cause of mortality of Japanese patients, and cerebrovascular accidents relating to hypertension have been the cause of death in other countries.12–15Although the pathogenesis of TA has long been studied, its cause remains uncertain. In the early years, infection was advocated as its cause,2,3,16 and the relation between TA and tuberculosis was suspected.17 Since the 1960s, autoimmunity has been considered to be involved in its pathogenesis.18 However, the antigens responsible for inciting these events have not been identified. Currently, TA is widely recognized as a multifactorial disease that occurs predominantly in young women and in the Orient. Furthermore, 10 pairs of identical twins having TA have been reported.19 Its characteristic clinical features indicate an important role of genetic factors in its pathogenesis.20 In fact, a significant association with Bw52 and DR12 antigens was found in 50% of Japanese patients, although the finding was not confirmed in Western countries.21 In addition, a high frequency of the same haplotype of HLA A24-B52-DR2 was found in TA and inflammatory abdominal aortic aneurysm.22 Interestingly, patients with this haplotype are prone to experience an accelerated progression of the inflammation, which tends to be refractory to antiinflammatory therapy.23,24 Further investigations are still required to elucidate the pathogenesis of TA.DiagnosisTA is an uncommon disease, even in Asian countries. The disease onset is insidious, and prominent symptoms are nonspecific or absent in two thirds of the patients in the early stage. Diagnosis is then delayed, particularly in the pediatric population.25 Clues for the diagnosis are hypertension, vascular bruits, asymmetrical arm blood pressure, and other ischemic symptoms. The criteria of Ishikawa26 in 1988 have been widely applied, which consist of 1 obligatory criterion (age <40 years), 2 major criteria (left and right mid subclavian artery lesions), and 9 minor criteria (high erythrocyte sedimentation rate, common carotid artery tenderness, hypertension, aortic regurgitation or annuloaortic ectasia, and lesions of the pulmonary artery, left mid common carotid artery, distal brachiocephalic trunk, thoracic aorta, and abdominal aorta).Angiography used to be the most valuable tool for the diagnosis and classification of TA.2,26 Modern noninvasive diagnostic modalities including computed tomography scanning and magnetic resonance angiography, which have replaced angiography, allow an early and easy detection of the details of vascular lesions in 3-dimensional images.27,28 Magnetic resonance angiography is advocated in the pediatric field because it avoids the use of radiation and of an important quantity of nephrotoxic contrast media.25 It allows the measurement of arterial wall thickness and edema due to acute phase TA. However, it also has some limitations in detecting lesions of visceral and renal arteries and the supra-aortic trunk. As an updated diagnostic tool, 18F-fluorodeoxyglucose positron emission computed tomographic imaging coregistered with enhanced computed tomographic imaging has been developed.29 This tool allows the visualization of the distribution of lesions and inflammatory activity in the aorta, its branches, and the pulmonary arteries in active TA, with weak 18F-fluorodeoxyglucose accumulation, which decreases as inflammation disappears in response to therapy. In monitoring TA activity, serum C-reactive protein concentration and an erythrocyte sedimentation rate have generally been used. However, these are nonspecific inflammatory markers and therefore lack sensitivity and specificity.30 Matrix metalloproteinases are reportedly useful markers of disease activity. Matrix metalloproteinase 2 can be helpful in diagnosing TA, and matrix metalloproteinases 3 and 9 serve as activity markers.31 It is also important to differentiate TA from other similar diseases such as giant cell arteritis, atherosclerotic disease, congenital coarctation of the aorta, and Behçet’s disease.2Pathology and ClassificationNasu32 summarized the criteria for the pathological diagnosis of TA. One of the characteristic findings is a “skipped lesion” consisting of a mixture of both active, productive inflammatory lesions and old fibrous lesions.33 Inflammation originates in the vasa vasorum followed by cellular infiltration composed mainly of T cells invading the outer layer of the media and/or its neighboring adventitia. Once the inflammation invades the intima, edematous changes occur, resulting in infiltration of lipids and blood cells. Eventually, these inflammatory changes cause atherosclerosis. Calcification and a thickened intima are also characteristic. It is then difficult to differentiate TA from atherosclerosis. Calcification, a useful index of aging, is found >5 years after the onset of the disease. With the rapid progression of these changes, the artery or aorta becomes dilated, forming aneurysms. Healed lesions show progressive intimal and adventitial fibrosis. The histological pattern is classified into granulomatous type, diffuse proliferative type, and fibrous type.32 Documentation of atherosclerotic complications in young females generally free from atherosclerotic risk factors may constitute clinical evidence of the importance of inflammation as a risk factor for atherogenesis.33 TA has recently been shown to affect the parenchyma of various organs: mesangial proliferative, membranoproliferative, crescentic glomerulonephritis, and amyloidosis.34 Dilated cardiomyopathy, myocarditis, and pericarditis have also been reported.The disease is subdivided into the early or active phase and the late, chronic, or inactive phase. Nakao et al35 first proposed a classification based on angiographic findings, and Ueno et al36 revised it, stressing the clinical significance of aneurysms. After that, TA was classified into 4 types37: lesions in the arch and its branches, “pulseless disease” (type I), the descending and abdominal aorta and its branches, “atypical coarctation” (type II), manifestation of features of type I and II (type III), and combination of features type I through III with pulmonary artery disease (type IV). At the XIth International Conference on TA in 1994, a newer classification was established38: the aortic branches are involved (type I); the ascending aorta, arch, and its branches (type IIa); the ascending aorta, arch with its branches, and thoracic descending aorta (type IIb); the thoracic descending aorta, abdominal aorta, and/or renal arteries (type III); only the abdominal aorta and/or renal arteries (type IV); and the combined features of type IIb and IV (type V). A comparison of affected lesions showed that the incidence of types I and IIa was higher in Japan, whereas the incidence of type IV was higher in India.38 Among the aortic arch vessels, the left subclavian artery was affected in 60%, followed by the left common carotid artery in 40%, and the innominate artery in 19%. Among the patients, 28% had abdominal aortic lesions, 13% had renal arteries lesions, and 15% had pulmonary arteries lesions.39 Coronary artery involvement was first demonstrated at necropsy in 1951.7,40 Further postmortem studies have revealed coronary artery disease in 9% to 10% of patients.40 The predominant lesions were on the coronary orifices, as indicated by the presence of intimal hypertrophy. Occlusion of the proximal ostium of the anastomosis resulting from intimal hypertrophy is the most frequent problem in coronary artery bypass grafting. A Japanese institute reported 38.3% of coronary artery involvement in TA.41 The ostium was most frequently affected in 87.5%. Kimoto8 was the first to describe aneurysm as a complication of TA. In the phase of acute progression, destruction of the arterial media leads to aneurysmal dilatation.42 Aneurysmal disease reportedly occurs with much higher frequency in Asian countries than in Western countries.20,21,43 In a Japanese angiographic study of 113 patients with TA,42 fusiform or saccular aneurysms were found in 31.9%. Aortic regurgitation also develops and is a risk factor for mortality in Japan.9,44 In the previous Japanese nationwide epidemiological surveys, the occurrence of aortic regurgitation was 19% for the 1973–1975 period and 24.8% for the 1982–1984 period.10 Aortic regurgitation occurs primarily because of annular or ascending aortic dilatation.9,44 Its secondary mechanism is aortic valve change due to TA, including fibrous thickening, rolling, retraction, and calcification. Aortic regurgitation is progressive, and therefore surgical treatment is often required. Hypertension develops frequently as a result of reduced elasticity of the arterial wall (wind-kettle), atypical coarctation (proximal hypertension), and renovascular stenosis (renovascular hypertension). The association rate of hypertension was 55.7% in Japan during the 1982–1984 period,10 and it constitutes a substantive problem in regard to the long-term prognosis because prolonged hypertension results in cerebrovascular accident, congestive heart failure, aneurysmal dilatation, and rupture.10TreatmentAccording to the 1982–1984 Japanese survey, pharmacological treatment was predominantly provided, whereas surgery was attempted in 13.3% (pharmacological in 75.2%, pharmacological and surgical in 11.7%, surgical in 1.6%, no treatment in 3.9%, and unknown in 7.7%).10 Because of recent technical advances, the most common treatment at present has shifted slightly toward prompt surgery or less invasive endovascular treatment such as angioplasty or updated endovascular aneurysmal repair.Medical TreatmentCorticosteroids are still used in the active phase of TA. There is evidence that adequate, long-term prednisolone therapy contributes to an angiographic improvement.45,46 The guidelines established in 1987 by the Systemic Vascular Disorders Research Committee from the Ministry of Health and Welfare of Japan consist of 2 parts: the first deals with antiinflammatory treatment with adrenocorticosteroids and the second with treatments for thrombosis and hypertension.47AntiinflammationThe guidelines recommend 30 mg/d of adrenocorticosteroids as the initial dose for adult patients with active TA.47 The initial dose is tapered at a rate of 5 mg every 2 weeks down to 10 mg and thereafter at a rate of 2.5 mg every 2 weeks until withdrawal or to the minimum required dose to control inflammation, while the erythrocyte sedimentation rate and serum C-reactive protein concentration are monitored. When withdrawal from corticosteroids is difficult, immunosuppressive drugs such as cyclophosphamide or azathioprine are used.47 The efficacy of other immunosuppressive agents including methotrexate,48 mycophenolate mofetil,49 and infliximab50 has been described. In case of persistent inflammation, even in the chronic phase, the administration of corticosteroids should be continued to control systemic inflammation with <1.0 mg/dL of serum C-reactive protein concentration and 20 mm/h of erythrocyte sedimentation.47Other Treatments Including Antithrombosis and AntihypertensionThe active phase of TA is often complicated by thrombosis in the affected vessels with stenotic/occlusive lesions.51 In the active phase, platelets may be sensitive not only to collagen but also to prostacyclin because of endothelial dysfunction. Plasma thromboxane B2 levels are higher, whereas cAMP levels are lower.52 Long-term aspirin therapy is then recommended to prevent thrombus formation in vessels with endothelial damage.52 Antihypertensive agents are frequently used because >70% of the patients have hypertension related to atypical coarctation or renovascular hypertension.47 In the 1982–1984 Japanese nationwide survey, the pharmacological treatment was found to include aspirin and antiplatelet agents as well as adrenocorticosteroids (54.1%), hypotensive agents consisting of calcium antagonists, β-blockers, and hypotensive diuretics, cardiac glycoside, coronary vasodilator agents, and other agents.10Percutaneous Transluminal AngioplastyWith recent advances in endovascular treatment, PTA has become particularly attractive for inactive stenotic/occlusive arterial or aortic lesions due to TA (Table).53–72Table. Balloon PTA for Takayasu ArteritisStudy, Year, and LocationNo. of PatientsSiteSite No.Initial Success Rate, %Follow-UpRestenosisNA indicates not available; LMT, left main trunk lesion; and DES, drug-eluting stent.Martin et al, 1980, US532Renal artery, subclavian artery250.01 yNoneSaddekni et al, 1980, US541Renal artery1100.0NANAHodgins et al, 1982, Canada551Subclavian artery1100.0NANAYagura et al, 1984, Japan561Descending aorta1100.0NANAKhalilullah et al, 1987, India574Descending aorta, abdominal aorta4100.08.5±4.1 moNoneGu et al, 1988, China589Abdominal aorta9100.03–28 moNone (incomplete data)Dong et al, 1987, China5922Renal artery22NA6 moNAPark et al, 1989, Korea608Coronary artery: 1; renal artery: 9; subclavian artery: 1; abdominal aorta: 31485.77–38 mo21.4%Kumar et al, 1989, India6116Renal artery: 9; subclavian artery: 5; innominate artery: 1; abdominal aorta: 2; descending aorta: 21974.02–33 moNoneSharma et al, 1990, India6211Renal artery: 12; iliac artery: 1; abdominal aorta: 21586.71–16 mo20.0%Tyagi et al, 1992, India6336Abdominal aorta: 26; descending aorta: 144094.443±9.4 mo2.8% (incomplete data)Tyagi et al, 1993, India6454Renal artery7589.314.2±7.8 mo13.5%Rao et al, 1993, India6516Abdominal aorta: 11; descending aorta: 617100.02–41 mo18.8%Sawada et al, 1994, Japan672Abdominal aorta2100.010 mo and 8 mo, eachNone (balloon angioplasty with stenting)Sharma et al, 1996, India6624 childrenRenal artery4095.033±22 mo20.0%Sharma et al, 1998, India6866Renal artery9695.0 (89)22±17 mo16.0%Sharma et al, 2000, India6920Coronary artery: 1; carotid artery: 5; renal artery: 5; subclavian artery: 5, aorta: 132995.04–10 mo10.5% (balloon angioplasty with stenting)Bali et al, 2000, India706Descending aorta6100.022.8±4.0 moNone (balloon angioplasty with stenting); pseudoaneurysm: 1Furukawa et al, 2005, Japan711Coronary (LMT)1100.06 moNone (DES)Amir et al, 2006, US721Coronary (LMT)1100.03 moNone (DES)Carotid, Subclavian, Renal, and Other Peripheral ArteriesSuccessful PTA for subclavian and renal arteries was first reported in 1980.53,54 The initial results of PTA of the carotid, subclavian, and renal arteries, reported predominantly from Asian countries, were encouraging because they were associated with minimum morbidity and mortality, and costs were low compared with surgical revascularization.53–55,59,66 The indication for PTA was symptomatic stenosis of >70% or a peak systolic gradient of >50 mm Hg.68Atypical CoarctationThe first attempt was reported in 1984,56 and it was followed by several reports dealing with small series.57,58,60-63,65 Tyagi et al63 reported from India the largest series of 36 patients with favorable initial and midterm outcome, especially in dilatating discrete-type aortic stenoses.Surgical TreatmentSurgery has been associated with low mortality and morbidity except for surgery of aortic aneurysm, especially a ruptured aneurysm.73 Although <20% of adult patients requires surgical treatment,74,75 in the pediatric field, 80% of the patients need surgery for stenotic/occlusive lesions because 70% are in the active phase and on steroid therapy.25 The major surgical procedures in the Japanese nationwide surveys were aortocervical bypass, cervicosubclavian bypass, aortic replacement, aortocoronary bypass, replacement of aortic aneurysm, aortoaortic bypass, aortorenal bypass, reconstruction of renal vessel, and nephrotomy.10Cerebrovascular LesionIschemic symptoms are common even in the young patient population because of the involvement of the arch vessel.10 Stroke occurs from a reduction in cerebrovascular blood flow due to total occlusion of ≥1 arch vessel rather than from emboli. Aortocervical bypass originating in the ascending aorta (not in the subclavian artery) and anastomosed to the carotid bulb with the use of saphenous vein grafts is recommended.76Atypical CoarctationTA is one of the causes of a much less common variety of aortic coarctation, the middle aortic syndrome, apart from the more common congenital coarctation of the aorta. This atypical coarctation occurs anywhere along the length of the aorta except the ascending aorta, whereas coarctation of the aorta is typically located around the aortic isthmus. An aortoaortic bypass with the use of a 10- to 16-mm prosthetic graft was the most common procedure. The satisfactory long-term survival after surgery was described in 33 patients followed up from 1960 to 2004.77 In that series, the outcome of 29 patients with aortic coarctation proximal to the origin of the renal arteries and hypertension in the upper half of the body was reviewed.Renal Artery Stenosis (Renovascular Hypertension)Hypertension is a common occurrence in TA and is related to major complications such as congestive heart failure, cardiomyopathy, hemorrhagic stroke, hypertensive encephalopathy, and myocardial infarction.2,10 Renal artery stenosis as well as atypical coarctation or reduced elasticity of the arterial wall can cause hypertension. Less invasive PTA is today the first choice therapy (Table). If it is unsuccessful or technically impossible, prompt renal artery bypass with the use of a saphenous vein graft with aortic inflow or relief of atypical coarctation with bypass grafting should be performed to lower blood pressure. In renal artery bypass, another available inflow is that from the in situ hepatic or splenic artery close to the kidney.Coronary Artery DiseaseCoronary artery involvement was reported to be 10%.40 The ostium was most frequently involved in 87.5% of the patients, 95.8% of whom were treated surgically.41 In the experience with surgery for stenotic/occlusive lesions at the authors’ institute (1979–1998), obstructive coronary artery disease was found in 41.3% (n=19).78 Coronary artery bypass grafting was performed in 10 and coronary ostial endarterectomy in 9. There were no hospital deaths. Six patients died from arrhythmia, myocardial infarction,2 cerebral bleeding, surgery for a thoracic aneurysm, or unknown reason during a follow-up of 117 (4 to 240) months. In 9 patients subjected to ostial endarterectomy, only 2 died from arrhythmia or unknown origin, and no restenosis has been found. Coronary ostial endarterectomy is a useful option, particularly in conjunction with ascending aortic surgery. Otherwise, successful angioplasty, especially with a drug-eluting stent, was recently reported for proximal coronary disease in patients with TA (Table).71,72Aortic AneurysmAneurysm formation is considered one of the major complications related to the prognosis in TA.74 In Japan, the incidence of aneurysmal formation was reported to be higher, between 22.2% and 31.9%,8,42 although the incidence of aneurysm rupture seems to be low.42 Kieffer et al79 reported satisfactory surgical outcome of descending thoracic and thoracoabdominal aortic aneurysm in 33 patients with TA between 1974 and 2001, despite the extent of aneurysmal lesions and high frequency of association with visceral and supra-aortic vessel lesions.Aortic RegurgitationAortic regurgitation, which is another major complication influencing prognosis, is also prevalent in Japan.80–82 It is often associated with ascending aortic or root dilation, which requires concomitant root and aortic valve replacement. Composite graft root replacement has been considered a gold standard procedure.80–82 However, prosthetic graft detachment (anastomotic false aneurysm) including a coronary disorder is the most serious morbidity in the long term, particularly in patients with persisting inflammation.80–83 Since 1987, we have used a novel “miniskirt technique,” in which the prosthetic valve is not attached directly to the fragile annulus, for the composite graft root replacement to treat aortic regurgitation with root dilatation.81,82 Ando et al81 and Matsuura et al82 published details of surgical series of aortic regurgitation with or without root dilatation due to TA. In the latter report,82 prosthetic valve detachment (perivalvular leakage) occurred in 11.1% of the patients after aortic valve replacement alone and in only 3.7% of those subjected to composite graft root replacement. Thus, compared with aortic valve replacement alone or composite graft root replacement with the standard technique, the mechanical stress to the fragile inflamed annulus is expected to be less with the miniskirt technique. On the other hand, homograft root replacement83–86 is one option to prevent the detachment by reducing the mechanical stress to the fragile aortic annulus due to inflammatory diseases. In particular, with the use of steroidal antiinflammatory therapy, a longer durability of homograft might be expected, although there have been no studies on this. Full root replacement with a stentless aortic valve xenograft is another option for this setting87; however, no one has described its long durability. In our experience with more troublesome Behçet’s disease, valve detachment after aortic valve replacement occurred in 4 (40%) of 10 patients.88 Proximal anastomotic detachment occurred in 1 (20%) of the first 5 patients who underwent composite graft root replacement with the standard technique, whereas there was no detachment in the later 5 patients operated on with the miniskirt technique. At other anastomotic sites such as those for coronary and distal aortic reconstruction, no anastomotic false aneurysms occurred, presumably because of routine external Teflon (polytetrafluoroethylene) felt reinforcement.81,82 In addition, late dilatation of the residual ascending aorta occurred in 10.3% after isolated aortic valve replacement compared with 3.7% after composite graft root replacement.82 Thus, for aortic regurgitation with some root dilatation, composite graft root replacement is preferable. The size threshold of the root for composite graft root replacement is ≈45 mm. On the other hand, modern aortic valve-sparing surgery is not recommended very often for root dilatation with or without aortic regurgitation due to TA. There have been no reports regarding this issue. In our experience with 4 patients, 3 of them subsequently required aortic valve replacement due to aortic regurgitation within 5 years. Aortic regurgitation associated with TA primarily develops not o" @default.
• W2080789065 created "2016-06-24" @default.
• W2080789065 creator A5012464194 @default.
• W2080789065 creator A5035020564 @default.
• W2080789065 creator A5037693086 @default.
• W2080789065 creator A5041978602 @default.
• W2080789065 creator A5042321088 @default.
• W2080789065 creator A5056106260 @default.
• W2080789065 creator A5059240436 @default.
• W2080789065 creator A5059264165 @default.
• W2080789065 creator A5075824931 @default.
• W2080789065 creator A5089977442 @default.
• W2080789065 date "2008-12-16" @default.
• W2080789065 modified "2023-10-15" @default.
• W2080789065 title "Overview of Late Outcome of Medical and Surgical Treatment for Takayasu Arteritis" @default.
• W2080789065 cites W140050721 @default.
• W2080789065 cites W1927917530 @default.
• W2080789065 cites W1967408929 @default.
• W2080789065 cites W1967946307 @default.
• W2080789065 cites W1974314273 @default.
• W2080789065 cites W1976016205 @default.
• W2080789065 cites W1978405729 @default.
• W2080789065 cites W1980453608 @default.
• W2080789065 cites W1981994310 @default.
• W2080789065 cites W1985634518 @default.
• W2080789065 cites W1986654609 @default.
• W2080789065 cites W1990318876 @default.
• W2080789065 cites W1995104711 @default.
• W2080789065 cites W1995430847 @default.
• W2080789065 cites W1995677442 @default.
• W2080789065 cites W1998328846 @default.
• W2080789065 cites W2002333802 @default.
• W2080789065 cites W2002813185 @default.
• W2080789065 cites W2002956404 @default.
• W2080789065 cites W2004278522 @default.
• W2080789065 cites W2005345769 @default.
• W2080789065 cites W2005534362 @default.
• W2080789065 cites W2007228319 @default.
• W2080789065 cites W2009089124 @default.
• W2080789065 cites W2011581627 @default.
• W2080789065 cites W2012007044 @default.
• W2080789065 cites W2012236545 @default.
• W2080789065 cites W2012729198 @default.
• W2080789065 cites W2013482185 @default.
• W2080789065 cites W2013779255 @default.
• W2080789065 cites W2017379569 @default.
• W2080789065 cites W2018545053 @default.
• W2080789065 cites W2021998085 @default.
• W2080789065 cites W2026652728 @default.
• W2080789065 cites W2035007206 @default.
• W2080789065 cites W2036403371 @default.
• W2080789065 cites W2037133126 @default.
• W2080789065 cites W2038667316 @default.
• W2080789065 cites W2044258895 @default.
• W2080789065 cites W2045137142 @default.
• W2080789065 cites W2048587516 @default.
• W2080789065 cites W2056065325 @default.
• W2080789065 cites W2057507810 @default.
• W2080789065 cites W2058055698 @default.
• W2080789065 cites W2065866793 @default.
• W2080789065 cites W2069845698 @default.
• W2080789065 cites W2071981187 @default.
• W2080789065 cites W2077746806 @default.
• W2080789065 cites W2079349579 @default.
• W2080789065 cites W2079744656 @default.
• W2080789065 cites W2080348269 @default.
• W2080789065 cites W2085402016 @default.
• W2080789065 cites W2088121986 @default.
• W2080789065 cites W2089266745 @default.
• W2080789065 cites W2091676891 @default.
• W2080789065 cites W2093796640 @default.
• W2080789065 cites W2102026201 @default.
• W2080789065 cites W2116825674 @default.
• W2080789065 cites W2120379347 @default.
• W2080789065 cites W2123315938 @default.
• W2080789065 cites W2142991076 @default.
• W2080789065 cites W2144171672 @default.
• W2080789065 cites W2146689481 @default.
• W2080789065 cites W2157685116 @default.
• W2080789065 cites W2158206944 @default.
• W2080789065 cites W2159281419 @default.
• W2080789065 cites W2163547851 @default.
• W2080789065 cites W2324064761 @default.
• W2080789065 cites W2988095612 @default.
• W2080789065 cites W3147995045 @default.
• W2080789065 cites W4234837152 @default.
• W2080789065 cites W4238228430 @default.
• W2080789065 cites W4299509385 @default.
• W2080789065 cites W4321429408 @default.
• W2080789065 doi "https://doi.org/10.1161/circulationaha.107.759589" @default.
• W2080789065 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19106398" @default.
• W2080789065 hasPublicationYear "2008" @default.
• W2080789065 type Work @default.
• W2080789065 sameAs 2080789065 @default.
• W2080789065 citedByCount "138" @default.
• W2080789065 countsByYear W20807890652012 @default.
• W2080789065 countsByYear W20807890652013 @default.
• W2080789065 countsByYear W20807890652014 @default.

• next