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Ann Thorac Surg 2005;80:101-105
© 2005 The Society of Thoracic Surgeons

Original article: Cardiovascular

Annuloaortic Ectasia and Giant Cell Arteritis

Sandro Gelsomino, MDa,*, Stefano Romagnoli, MDb, Franca Gori, MDc, Gabriella Nesi, MDc, Chiara Anichini, MDc, Carlo Sorbara, MDb, Pierluigi Stefàno, MDa, Gian Franco Gensini, MDd

a Department of Cardiac Surgery, Careggi Hospital, Florence, Italy
b Department of Anesthesia, Careggi Hospital, Florence, Italy
c Department of Pathology, University of Florence, Florence, Italy
d Department of Clinical Medicine and Cardiology, University of Florence, Florence, Italy

Accepted for publication January 7, 2005.

* Address reprint requests to Dr Gelsomino, Cardiac Surgery Unit, Careggi Hospital, Viale Morgagni 85, 50134, Florence, Italy (Email: sandrogelsomino{at}virgilio.it).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Thoracic aortic aneurysm, aortic dissection and aortic valve regurgitation have been widely described in patients with Horton disease, also known as giant cell arteritis. We present our midterm experience with patients with these features.

METHODS: A total of 386 cases of ascending aorta and aortic valve replacement performed for thoracic aortic aneurysm and aortic insufficiency between 1998 and 2004 were reviewed. Among them 10 cases of histopathologically confirmed GAA were identified. Patients were predominantly female (90%); the mean age was 74.5 ± 4.6 years.

RESULTS: Eight patients (80%) showed typical annuloaortic ectasia, leading to significant aortic valve regurgitation. These subjects underwent a Bentall operation. Two patients whose sinuses seemed undilated and macroscopically normal had separate valve graft replacement at first operation and underwent reoperation due to dilatation of the native sinuses. Eight patients had partial aortic arch replacement (hemiarch), and 1 underwent total arch replacement. Six-year survival was 0.9 ± 0.09; freedom from reoperation at 6 years was 0.77 ± 0.13.

CONCLUSIONS: Annuloaortic ectasia is a common finding in giant cell arteritis. In patients with Horton disease, the aortic root should always be replaced regardless of macroscopic findings.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Giant cell arteritis (GCA), also known as temporal arteritis, cranial arteritis, granulomatous arteritis, and Horton disease, is a chronic systemic vasculitis of unknown etiology, affecting medium- and large-sized arteries [1–3].

Typically GCA occurs in patients older than 50 years of age, and women seem to be affected twice as much as males [4, 5], although this is still debated [6, 7]. However, temporal arteritis is the most common primary systemic vasculitis in populations with predominantly northern European ancestry, with an annual incidence as high as 15 to 33 cases per 100,000 persons of middle age or older [8–10]. The temporal arteries or other cranial arteries are most commonly affected. Nonetheless, the aorta, with any of its primary or secondary branches, may be involved. In fact, aortic aneurysm [11], aortic dissection [12, 13], and large artery and arm or leg artery stenoses [14, 15] have been widely described in GCA. It has been reported that as many as 15% of patients with temporal arteritis might have angiographic evidence of aortic involvement [16], and that patients with GCA are 17.3 times more likely to develop a thoracic aortic aneurysm compared with the general population [17].

We retrospectively analyzed our midterm experience with aortic root replacement in patients with GCA, thoracic aortic aneurysm, and aortic regurgitation.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
A total of 386 cases of ascending aorta and aortic valve replacement performed for thoracic aortic aneurysm and aortic insufficiency between 1998 and 2004 were reviewed. Among them, 10 cases of histopathologically confirmed GCA were identified. To define clinically manifested GCA, the American College of Rheumatology (ACR) criteria were followed [18]. Furthermore, because of the close relationship between temporal arteritis and polymyalgia rheumatica, all patients were considered for this association. The current diagnostic criteria for polymyalgia rheumatica empirically formulated by Chuang and coworkers [19] and and Healey [20] were employed. Secondary (occult) manifestations were defined following published criteria [21].

Preoperative patient characteristics are shown in Table 1. Three patients (30%) reflected ACR criteria for the diagnosis of GCA. Specifically, all these subjects were older than 50 years of age and had new onsets of headaches; 2 had abnormal temporal artery biopsies and 1 showed an erythrocyte sedimentation rate greater than 50 mm/h. Eighty percent of patients presented at observation with cardiovascular symptoms including chest pain, dyspnea, and tachycardia. Two (20%) had signs of congestive heart failure. Secondary manifestations occurred in 3 patients as neurologic symptoms (transient ischemic attack), Raynaud phenomenon, and fever of unknown origin. Jaw claudication, girdle pain, polymyalgia rheumatica, and visual symptoms were uncommon in our cohort. Two subjects had preoperative diagnoses of GCA; they had abnormal biopsies of the temporal artery and underwent preoperative corticosteroid therapy. In the others, the diagnoses were made after routine histologic examination of aortic wall specimens. All tissue obtained at surgery was processed by hematoxylin and eosin staining. Specimens of the aortic wall showed signs of chronic inflammation with typical inflammatory infiltrate of mononuclear cells with giant cell formation within the media of the arterial wall. The sinuses of Valsalva showed slight signs of inflammation in all patients; however, the inflammatory cellular infiltrate did not show giant cells. The aortic cusps showed dystrophic changes with mononuclear cellular infiltrate but without granulomatouslike inflammatory reaction and multinucleated giant cells.


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  		Table 1. Preoperative Patient Characteristics (n = 10)
 
Laboratory tests, which were reconsidered after histology analysis, demonstrated an increase in inflammatory indices in only 2 patients.

All subjects underwent preoperative computed tomography scan and angiography, the latter showing unaffected coronary arteries in the entire study population. Finally, echocardiography was performed preoperatively and before hospital discharge.

All surviving patients were routinely followed up and had a computed tomography scan at 6 months and 1 year from surgery. All information was obtained by review of medical records, written or telephone communication, or both, and outpatient appointments.

All data were analyzed with the SPSS for Windows, release 8.0 (SPSS, Chicago, Illinois) statistical package. Death and event-free survival estimates were calculated by the product-limit method of Kaplan and Meier and reported with 95% confidence limit; the Mantel-Cox (log-rank) test was used to test survival differences. A p value less than 0.05 was considered significant.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
Table 2 shows the operative data. Indications for surgery included cardiac symptoms (dyspnea on exertion, angina) in 2 patients (20%) and congestive heart failure in 2 patients (20%); in the rest of the cases, the indication was given on the basis of aneurysm size. At surgical inspection, either the ascending aorta and the aortic arch were commonly affected. In only 1 patient was there no disease involvement. In 1 patient, the aneurysm extended to the descending aorta. Eight patients (80%) showed typical features of annuloaortic ectasia, leading to significant aortic regurgitation. These subjects underwent a Bentall procedure. In all patients, the St. Jude valve graft prosthesis (St Jude Medical, Minneapolis, Minnesota) was used. In 2 patients, the sinuses seemed macroscopically normal, and the annulus was undilated. These patients underwent separate graft valve replacement and received, respectively, a 23-mm and 25-mm Carpentier-Edwards biological prosthesis (Edwards Lifescience, Irvine, California) because of their advanced age. Eight patients had partial aortic arch replacement (hemiarch), and 1 underwent total arch replacement. For these patients, deep hypothermic (22°C) circulatory arrest was used in 1, retrograde cerebral perfusion was used in 1, and selective antegrade cerebral perfusion was used in 8 patients. No other cardiac procedure was performed.


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  		Table 2. Operative Data (n = 10)
 
There was an in-hospital death occurring 10 days after surgery caused by multiorgan failure. Six-year survival (Fig 1) was 0.9 ± 0.09 (SE [hazard = 0.10 ± 0.1]). Mean survival time was 64.8 months. Two patients (20%) underwent reoperation for dilatation of the native sinuses. Freedom from reoperation at 6 years was 0.77 ± 0.13 (hazard = 0.25 ± 0.1). Freedom from reoperation resulted to be significantly higher in the Bentall procedure (Fig 2). Actuarial freedom from thromboembolic events and anticoagulant-related hemorrhage was 100%. Two patients underwent 1-year postoperative steroid therapy. The initial dose was 40 mg of prednisone followed by a daily dose of 10 mg for 6 months and 5 mg within 1 year. These patients remained asymptomatic with erythrocyte sedimentation rate and C-reactive protein levels normal. Among nontreated patients, 2 had fever with high inflammation indices at 34 and 56 months postoperatively, respectively, and 1 patient exhibited headaches and transitory visual loss 16 months after surgery. In 1 patient, an abdominal aortic aneurysm developed and required surgery. No patient showed signs of dissection or stenosis of the large arteries.



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  		Fig 1. Six-year survival after aortic root replacement in patients with giant cell arteritis. (H = hazard; S = survival; SE(H) = standard error hazard; SE(S) = standard error survival.)

 


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  		Fig 2. Freedom from reoperation after aortic root replacement in patients with giant cell arteritis. Freedom from reoperation was found to be significantly higher in Bentall. Diamonds = all; squares = Bentall; triangles = separate valve graft replacement. (Yrs. = years.)

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
Giant cell arteritis is a chronic systemic vasculitis of unknown etiology with a distinct tropism for large and medium-sized arteries with well developed elastic membranes [22]. Its incidence rises with increasing age and is higher among whites than blacks, Hispanic, or Asians. The highest incidence rates are described in Scandinavian countries and North American populations of the same descent [23]. Symptoms include headache, jaw claudication, visual symptoms, fever, and an abnormal (pulseless, enlarged) temporal artery [21]. In addition, weak extremity pulses, arm claudication, and Raynaud phenomenon type may occur; these symptoms result from the narrowing or occlusion of branches of the thoracic aorta. Polymyalgia rheumatica and GCA are closely related entities, and approximately 40% of patients with arteritis have polymyalgia rheumatica [24]. However, the range of presenting features is enormous, and 40% of patients do not present with the classic signs and symptoms [25]. Although an elevated erythrocyte sedimentation rate is such a common feature that it constitutes one of the five ACR criteria for the classification of the disease [18], the prevalence of low or normal erythrocyte sedimentation rate in GCA has been reported to vary from 0% to 22.5% [4, 26]. Typical histopathologic findings are disruption of the internal elastic lamina and an inflammatory cellular infiltrate with giant cells [27]. Involvement of medium-size arteries tends to be predominantly focal with some skipped lesions, whereas aortic involvement tends to be continuous and diffuse [28]. The temporal arteries are most commonly affected; nonetheless, GCA may lead to weakening of the aortic wall and eventual aneurysm formation or dissection [17]. Although this association is not new and aortic involvement in GCA was first reported in 1937 [29], it has recently gained renewed attention. Thoracic aortic aneurysms are usually a late complication of GCA; however, they can occur at any time during the course of the disease, and rupture or dissection of the aortic wall as well as aortic regurgitation might be an initial manifestation of temporal arteritis [30]. Patients presenting with acute aortic pathology as the first clinical manifestation showed a mortality rate as high as 80% after 2 weeks [30]; nonetheless, these catastrophic complications are infrequent in GCA-diagnosed patients [31] whereas active aortitis caused by occult GCA seems to occur more commonly than previously appreciated and to represent an important clinical variant of the disease, often requiring a prompt diagnosis and early referral to surgery [32].

In the present study, we reviewed patients with thoracic aortic aneurysm and aortic regurgitation operated on between 1998 and 2004. Ten cases of histopathologically confirmed GAA were identified, and the incidence of GCA was 2.6% among patients with thoracic aortic aneurysm/aortic regurgitation. Older women were strongly prevalent, and the ascending aorta and aortic arch were mainly affected. In the same period, we encountered 2 patients with GCA with a thoracic aortic aneurysm without aortic regurgitation; the incidence of aortic regurgitation in our GCA patients was very high (83.3%), and annuloaortic ectasia was the most common pathologic finding in GCA as first reported in our previous study [32].

Eighty percent of our cohort underwent a Bentall procedure; contrastingly, 2 patients with sinuses macroscopically normal and annulus undilated at surgical inspection, received a separate valve graft replacement. These patients underwent reoperation because of redilatation (true aneurysm) of native sinuses. Thus, our experience suggests that in patients with Horton disease, the aortic root should always be replaced regardless of macroscopic findings.

Another point of interest is the mechanism of aortic regurgitation, which is reported to vary from 9.8% to 33% among patients with GCA [17, 32]. In all patients in our cohort, valve cusps were macroscopically normal, and valve incompetence was presumably caused by lack of leaflets coaptation secondary to aneurismal dilatation of the aortic root [17]. Thus a "valve-sparing" operation could be indicated in these patients. Nonetheless, at histologic examination, aortic leaflets showed signs of inflammation with mononuclear cellular infiltrate, even though we failed to find a true granulomatouslike inflammatory reaction with multinucleated giant cells. However, owing to the advanced age of the patients and the mild dystrophic changes of the cusps, a Bentall operation remains, in our opinion, the treatment of choice for these patients.

Six-year survival was 0.9 ± 0.09 and freedom from reoperation at 6 years was 0.77 ± 0.13, with results comparable with, in our experience, those of aortic root replacement performed in non-GCA patients.

Only 2 patients in the present series received corticosteroids preoperatively. That is mainly because for most patients the diagnosis is not made until the operation; in fact, only a small number of subjects had been diagnosed preoperatively and received preoperative steroid therapy. The overlap of atherosclerosis with GCA may render the evaluation of both angiographic and pathologic findings more difficult. Thus, active aortitis caused by GCA probably occurs more commonly than previously appreciated.

In our experience, however, we failed to detect any difference between these patients and subjects who did not receive corticosteroids. Contrastingly, we found that subjects receiving postoperative steroid therapy remained asymptomatic, with erythrocyte sedimentation rate and C-reactive protein levels that were normal. In contrast, among nontreated patients, 2 had fever with high inflammation indices, and 1 patient was symptomatic.

The major shortcoming of our study is the small number of patients. Nonetheless, considering that the incidence of diagnosed GCA in our country is 6.9/100,000 [4], that approximately 15% of them [16] have thoracic aortic aneurysm, and that only a small percentage will be referred to surgery [33], our small cohort may be sufficiently representative of a disease that is infrequent at our latitude. Given that the population in developing countries is increasingly getting older, however, the number of people at risk can be expected to double in the next 25 years; Therefore, probably we will face this disease much more in the future.

Conclusions
Patients with a typical history of Horton disease should be closely followed up to ensure the early detection of large-vessel pathology, which could be responsible for life-threatening complications such as aortic dissection or rupture, severe aortic incompetence, and ischemic syndrome of the upper and lower extremities [17, 26, 30]. Moreover, when cardiologist are faced with an aortic aneurysm in older patients, particularly women, GCA should at least be suspected and other elements sought in the patient’s clinical history in order to ascertain the nature of the aortopathy. When a GCA is suspected, an investigation of the superficial temporal arteries by duplex ultrasonography may also be of value [34].

However, in presence of diagnosed or suspected GCA, the aortic root should always be replaced regardless of macroscopic findings. Nonetheless, further larger series are necessary to confirm our conclusions.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
We gratefully acknowledge Dr Judith Wilson for the English revision of the manuscript.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

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