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1 April 1995 | Volume 122 Issue 7 | Pages 502-507
Objective: To determine the frequency of aneurysm and dissection of the aorta in patients with giant cell arteritis and to assess the effects of these events on these patients.
Design: Population-based cohort study.
Setting: A multispecialty and a primary care clinic in southern Minnesota.
Patients: 96 residents of Olmsted County, Minnesota, who developed giant cell arteritis between 1950 and 1985. The presence of aortic aneurysm, dissection, or both was confirmed using computed tomography, ultrasonography, angiography, or autopsy.
Results: 11 of the 96 patients were found to have thoracic aortic aneurysms. In 2 of these patients, the aneurysms were detected when giant cell arteritis was diagnosed. In the remaining 9 patients, the aneurysms occurred a median of 5.8 years after giant cell arteritis was diagnosed. Six of the 11 died suddenly of acute thoracic aortic dissection. Five patients who did not have thoracic aortic aneurysms developed isolated abdominal aortic aneurysms a median of 2.5 years after giant cell arteritis was diagnosed. The incidence of thoracic aortic aneurysm in patients with giant cell arteritis was 999 per 100 000 person-years; the incidence of abdominal aortic aneurysm in these patients was 555 per 100 000 person-years.
Compared with all persons of the same age and sex living in Olmsted County, patients with giant cell arteritis were 17.3 times (95% CI, 7.9 to 33.0) more likely to develop thoracic aortic aneurysm and 2.4 times (CI, 0.8 to 5.5) more likely to develop isolated abdominal aortic aneurysm.
Conclusions: Giant cell arteritis is associated with a markedly increased risk for the development of aortic aneurysm, which is often a late complication and may cause death.
We did a population-based, retrospective cohort study to determine whether the incidence of aortic aneurysm is increased in patients with previously diagnosed giant cell arteritis. We also attempted to identify clinical features of giant cell arteritis that could be associated with an increased risk for aneurysm formation.
All patients from Olmsted County, Minnesota, with a diagnosis of giant cell arteritis between 1950 and 1985 were identified as part of a population-based study of the incidence and clinical presentation of giant cell arteritis; the results of this study were published in 1988 [1]. Patients' medical records were reviewed at entry into that study; for this study, we again reviewed the records and the bases for diagnosis of giant cell arteritis. We obtained laboratory data and information about the signs and symptoms of giant cell arteritis, history of hypertension, and corticosteroid therapy. The entire medical record of each patient after the diagnosis of giant cell arteritis was reviewed to obtain follow-up data. These data included information about the development of aortic aneurysm; aortic valve; insufficiency; the duration and dosage of corticosteroid therapy; and the results of laboratory tests, including the patient's erythrocyte sedimentation rate at the time that the aneurysm, if any, was discovered.
Patients were considered to have an aortic aneurysm only if it was confirmed pathologically, angiographically, by ultrasonography or echocardiography, or by computed tomography. Aneurysms were classified as thoracic or isolated abdominal. Thoracic aneurysms that involved the abdominal portion of the aorta were classified as thoracic aortic aneurysms.
Statistical Methods
Incidence rates were estimated as the ratio of the number of observed events (thoracic aortic or abdominal aortic aneurysm) to the number of person-years of follow-up (x 105). We assumed that the observed events followed a Poisson distribution, and we obtained confidence intervals for the incidence rate.
Expected numbers of events (thoracic aortic or abdominal aortic aneurysm) were obtained by multiplying known age- and sex-specific incidence rates for thoracic aortic or abdominal aortic aneurysm by the corresponding person-years and summing over all person-years. The ratio of observed to expected incidence, referred to as a standardized morbidity ratio, indicates the relation of the incidence in the special cohort to that in the general population. Confidence intervals for the standardized morbidity ratio estimate were obtained on the basis of the Poisson distribution.
Survival was estimated using the Kaplan-Meier method, and expected survival was estimated using the population mortality rates for persons of the same age and sex as those in the study cohort. The two were compared using the one-sample log-rank test.
The effect of risk factors on the rate at which aneurysms were diagnosed was assessed using the Cox proportional-hazards model.
Giant cell arteritis was diagnosed in 96 Olmsted County residents between 1950 and 1985. Two patients were diagnosed at autopsy and thus were excluded from calculations of incidence rates of aortic aneurysm. Both had died suddenly and unexpectedly of thoracic aortic dissection, and thoracic aortic aneurysms with active giant cell aortitis were found in both at autopsy. One of these patients, an 86-year-old woman, had classic symptoms of giant cell arteritis 4 months before death. At that time, her erythrocyte sedimentation rate was 70 mm/h; a reactive thrombocytosis was also present. The other patient, a 69-year-old man, had aching and morning stiffness in the shoulders and hips consistent with polymyalgia rheumatica and pain in the jaw during chewing consistent with jaw claudication. These symptoms were present for 2 or 3 months before death and had responded promptly, but temporarily, to a corticosteroid injection given by the home physician. The diagnosis of giant cell arteritis, however, was not made in either patient before their sudden deaths. The remaining 94 patients comprised the cohort that was initially described in 1988 [1].
Of the 94 patients in whom giant cell arteritis was diagnosed before death, 88 had artery biopsy specimens that showed giant cell arteritis (87 temporal, 1 occipital). Two patients had biopsy specimens that did not show giant cell arteritis, but they met the classic clinical criteria for the diagnosis of this condition; four met the classic clinical criteria but did not have temporal artery biopsies [8]. All patients fulfilled the American College of Rheumatology clinical criteria for the classification of giant cell arteritis [11]. The age-and sex-adjusted incidence of giant cell arteritis per 100 000 persons aged 50 years and older was 17.0 (95% CI, 13.6 to 20.5). The cohort comprised 78 women and 16 men, ranging in age from 56 to 92 years (median, 75 years) at the time of diagnosis. Twenty of the 94 patients (21%) had a history of hypertension, a proportion that accords with national prevalence figures for hypertension in the elderly [12]. The patients were followed for a median of 8.6 years (range, 1 month to 28.0 years). The median duration of corticosteroid therapy was 12 months (range, < 1 month to 50 months).
Incidence of Thoracic Aortic Aneurysm
After the diagnosis of giant cell arteritis, the 94 patients with no history of aneurysm were followed for 901 person-years. During this follow-up, thoracic aortic aneurysm was diagnosed in 9 patients, producing an incidence rate of 999 per 100 000 person-years (CI, 456.8 to 1898.4) (Tables 1 and 2). The Olmsted County incidence rates of thoracic aortic aneurysm [13] predicted that only 0.52 cases of thoracic aortic aneurysm would have occurred during these person-years of observation to persons of the same age and sex as those in the cohort with giant cell arteritis. Thus, the patients with giant cell arteritis were 17.3 times (CI, 7.9 to 33.0) more likely to develop a thoracic aortic aneurysm than those of the same age and sex in the general population of the county. ARTICLE
Increased Incidence of Aortic Aneurysm and Dissection in Giant Cell (Temporal) Arteritis: A Population-Based Study
Giant cell (temporal) arteritis is a vasculitis that affects large and medium-sized arteries in persons 50 years of age and older. It is among the most common forms of vasculitis, with an age- and sex-adjusted average annual incidence of 17 per 100 000 person-years in Olmsted County, Minnesota [1]. Similar incidence rates have been found in Scandinavian countries [2, 3]. Aortic aneurysmal disease and death from aortic dissection have occasionally been reported as complications of giant cell arteritis [4-8]. Active granulomatous inflammation with multinucleated giant cells has been reported in some aortas at surgery or autopsy, suggesting that aortitis is the mechanism of aneurysm formation [4-8]. Earlier reports are primarily either isolated case reports or small case series reports, mostly from large referral centers. Recently, we described a larger retrospective series of patients with giant cell arteritis and thoracic aortic aneurysm who were seen at our institution over a 40-year period [9]. No previous reports were population based, and referral and selection bias are likely to have been confounding factors, making it difficult to determine the frequency and clinical relevance of purported associations between giant cell arteritis and aortic aneurysm.
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Olmsted County, Minnesota, is well suited to population-based epidemiologic studies. The county comprises a stable urban and rural population, which is predominantly white and is representative of the adult white population in the United States [10]. The Mayo Clinic and the Olmsted Medical Group are almost the only sources of medical care within the county. Each of these providers uses a unit record system whereby all medical information for each patient is accumulated in a single record. This unit record contains the details of every inpatient hospitalization, every outpatient office or emergency department visit, every physician contact at a nursing home or private home, all laboratory results, all pathology reports including autopsies, and all correspondence. The potential of this data system for use in population-based studies has been described previously [10].
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Clinical Manifestations
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For the nine patients with a diagnosis of thoracic aortic aneurysm during follow-up, the median time between diagnosis of giant cell arteritis and diagnosis of the aneurysm was 69 months (range, 2.5 to 241 months) (Tables 1 and 2). Four of the nine [44%] died suddenly of thoracic aortic dissection (Table 2); patients 1, 2, 4, and 7).
Three of the nine patients with thoracic aortic aneurysm (33%) also developed symptomatic aortic valve insufficiency. One of the three had aortic valve replacement and aortoplasty. Pathologic examination of the native aortic valve showed the valve cusps to be normal but separated because of aneurysmal dilation of the aortic root.
The aortas of the three patients who developed thoracic aortic aneurysm were examined microscopically. Two aortas were studied at autopsy and one, after surgery; two had microscopic evidence of giant cell aortitis (Table 2, patients 1 and 4), and one showed medial necrosis (Table 2, patient 7). Figures 1 and 2 show radiologic findings in two patients.
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Eleven additional patients were shown to have a "dilated" thoracic aorta on chest radiograph. Because no other confirmatory studies had been done and because the radiographic films were not available for review, we excluded these 11 patients from consideration as patients with thoracic aortic aneurysms. It is likely, however, that at least some of them did indeed have thoracic aortic aneurysms.
Incidence of Abdominal Aortic Aneurysm
During the 901 person-years of follow-up, abdominal aortic aneurysm was diagnosed in five patients, producing an incidence rate of 555 per 100 000 person-years (CI, 180.4 to 1293.4). The Olmsted County incidence rates of abdominal aortic aneurysm [14] predicted that 2.1 cases of abdominal aortic aneurysm would have occurred during these person-years of observation among persons of the same age and sex of those in the cohort. Thus, patients with giant cell arteritis were 2.4 times (CI, 0.8 to 5.5) more likely to develop an abdominal aortic aneurysm than those in the general population of the county of the same age and sex as those in the cohort. Our study, with only five cases of abdominal aortic aneurysm, had an 84% power of detecting a fourfold increase in risk (one-sided 
= 0.05).
These five diagnoses of abdominal aortic aneurysm were made a median of 30 months (range, 16 to 92 months) after the diagnosis of giant cell arteritis. Four of the five abdominal aortic aneurysms were asymptomatic during the follow-up period (Table 2). Patient 12 Table 2 was treated surgically after an unexpected acute aortic rupture; the other four patients were being followed because their aneurysms appeared stable and were not large enough in diameter to indicate surgery.
Survival
The overall survival of the cohort of patients with giant cell arteritis is shown in Figure 3. No statistically significant difference in overall survival was found between patients with giant cell arteritis and persons of identical age and sex living in Olmsted County, despite the sudden death of 4 of the 94 patients from thoracic aortic dissection.
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Risk Factors for Aneurysm
We attempted to identify clinical features of patients with giant cell arteritis that might predict aneurysm formation. The number of symptoms related to giant cell arteritis at diagnosis, the presence of anemia at diagnosis, the duration of corticosteroid therapy, the patient's age and sex, and the presence or history of hypertension were each evaluated independently. None of these factors was associated with a statistically significant increased risk for aneurysm formation (data not shown). None had extensive peripheral atherosclerosis, a history of recent trauma, or a history of a heritable disorder of structural proteins. All patients with histories of hypertension were receiving therapy, and their blood pressure levels were normal in the period before the diagnosis of aortic aneurysm.
Discussion
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In our study, 9 of 94 patients in a community population with a diagnosis of giant cell arteritis developed thoracic aortic aneurysms or dissections, or both, and an additional 5 patients developed abdominal aortic aneurysms. This constitutes a more than 17-fold increase in risk for thoracic aortic aneurysms and an almost 2.5-fold increase in risk for abdominal aortic aneurysm compared with those in Olmsted County of the same age and sex [13, 14]. By way of comparison, the increase in risk for cancer in male smokers (the association between smoking and increased risk for cancer being accepted as a strong one) is 10-fold [17]. As noted above (see Results), 11 patients with chest radiographs that showed "dilated" thoracic aortas were excluded because the actual films had been discarded and we were unable to review them. Some of these patients probably also had aortic aneurysms. Two patients with giant cell arteritis who died of ruptures of thoracic aortic aneurysms were also excluded from incidence calculations because their condition was not diagnosed before death.
Although dissecting and nondissecting aortic aneurysms may have different properties, we grouped them together to compare our results with those of the previous population study [14]. In that study, as in this report, half of the patients had dissecting and half had nondissecting thoracic aortic aneurysms; thus, our finding of a high frequency of aortic abnormalities in patients with giant cell arteritis has not been altered.
Evidence for the diagnosis of giant cell arteritis was firm in all patients, including those with aortic aneurysms. All nine patients who developed thoracic aortic aneurysms and the five with abdominal aortic aneurysms had positive temporal artery biopsy results [11].
Evidence of aortitis was documented histologically in two of four incidence patients whose aortic specimens were examined. One of these two died of dissection Table 2, patient 1) and another at the time of surgery Table 2, patient 4). Histologic examination of aorta specimens did not show aortitis in an additional patient who died of rupture Table 2, patient 7) or in one who died at the time of surgery Table 2, patient 12). However, in patient 7 Table 2, the markedly elevated erythrocyte sedimentation rate (98 mm/h) shortly before death suggests the presence of continued active vasculitis. The tissue samples of these two patients may have been taken from sites not involved by arteritis, the inflammation may have resolved before the specimens were examined, or the aneurysms may not have been the result of aortitis. Focal or segmental involvement of inflammation in giant cell arteritis is well recognized [18, 19]. The difficulty of showing inflammation in all instances, even when specimens are available, is shown in patient 4, who had aortitis at surgery but, when she died 2 years later of aortic dissection, had only noninflammatory medial necrosis in the portion of the aorta examined histologically. Giant cell arteritis may have remitted after surgery, or only uninvolved samples of the aorta may have been examined at the time of this patient's death. In an earlier survey of thoracic aortic aneurysms in patients with giant cell arteritis, half of the aortic specimens available for histologic examination showed arteritis [9].
Five patients with thoracic aortic aneurysms and four with abdominal aortic aneurysms were alive at the end of our study and have not had aortic surgery. Erythrocyte sedimentation rates were calculated when the aortic aneurysms were discovered in four of these nine patients and were elevated in all (Table 2); patients 6, 10, 11, and 13), indicating the possible persistence of giant cell arteritis.
No risk factors other than arteritis, including differences in corticosteroid therapy, uncontrolled hypertension, and congenital abnormalities of structural proteins, were present to account for aneurysms in any patient. Analysis of risk factors was limited by the small number of patients in our study. Although death was caused by aortic rupture in 6 of the 96 patients, no statistically significant decrease in overall survival was shown in patients with giant cell arteritis compared with persons of identical age and sex living in Olmsted County, perhaps because of the small number of patients and the relatively short overall life span in this age group.
We believe that the increased incidence of aortic aneurysm and dissection cannot be explained by ascertainment bias. The association between giant cell arteritis and aortic aneurysm has not been considered common at our center, and patients with giant cell arteritis have not been screened or followed for the development of aneurysms. Because, in most cases, many years had elapsed since giant cell arteritis had been diagnosed, nearly all physicians caring for patients in this study at the time aneurysms were recognized were generalists and may not have known that the patients had histories of giant cell arteritis. Epidemiologic studies of Olmsted County patients have indicated that two thirds of persons in Olmsted County aged 65 years and older are seen at Mayo Clinic each year, and nearly all are seen during any 5-year period [20]. Thus, most older Olmsted County residents see their physicians frequently. The discovery of aortic complications was made incidentally in the course of routine interval care, as a result of symptoms that led patients to seek care, or at autopsy. Furthermore, the previously published studies of the incidence of aneurysm in Olmsted County used the same population and were probably influenced in a similar way. However, our results may not be applicable to patient populations in different geographic areas.
Thoracic and abdominal aortic aneurysms were described previously in patients with giant cell arteritis, but the frequency of occurrence had not been determined [4-9]. Approximately 85 patients with thoracic aortic aneurysms or rupture, or both, considered to be related to giant cell arteritis have been documented in the literature [9]. Except for our earlier report on a series of 41 patients [9], most reports describe single cases or small series. In a few patients, thoracic aortic aneurysms were the presenting manifestation of giant cell arteritis or they occurred with other symptoms at the time of diagnosis, as in the two patients we describe who were not included in the cohort. However, in most patients for whom information was available, aortic aneurysm was a late complication, possibly a late outcome of chronic inflammation in patients with persistent active disease. In others, the specific cause of the aneurysms is unknown. It could be speculated that aneurysm is the result of structural weakening and degeneration in an aorta previously damaged by arteritis [9]. We found no association in our patients or in previous reports between thoracic aortic aneurysm and occlusive changes in the subclavian or cervical arteries, other specific clinical manifestations, delay from onset of symptoms to diagnosis of giant cell arteritis, or inadequate therapy.
An aortic aneurysm may be one end of the spectrum of aortitis in giant cell arteritis, found in those patients with more severe or prolonged active disease, or both. Aortitis may explain fever, anemia, and high erythrocyte sedimentation rates in the absence of focal symptoms or findings in some patients with giant cell arteritis [21, 22]. Awareness of the possible presence of aortic aneurysm in giant cell arteritis may aid prompt recognition and therapy, not only during the active phase of the disease, but also after other symptoms of giant cell arteritis have relented. Surgical resection of an enlarging aortic aneurysm may prevent rupture and death, and aortic valve replacement may prevent death from congestive heart failure [9, 23]. Surgical treatment was successful in patients 4 and 12 and in patients in earlier series [9].
The surprisingly high rate of thoracic aneurysm in patients with giant cell arteritis has led us to wonder whether we should screen all patients with giant cell arteritis for the development of aneurysm. This is a difficult question to answer, especially considering the high prevalence of comorbid conditions and the short life expectancy of patients in this age group. Currently, we do not believe that the routine use of computed tomography or ultrasonography is justified by our data. On the other hand, a radiograph of the chest with a lateral view is relatively inexpensive and may help to identify an otherwise unsuspected thoracic aneurysm. The decision to do any screening tests at all, however, should be an individual one, made on the basis of the patient's overall health, functional status, and wishes about surgical intervention if an is aneurysm found. On the basis of our results, we recommend an annual physical examination, including palpation of the abdominal aorta, and an annual radiograph of the chest, including a lateral view, for all of our patients with a history of giant cell arteritis. We have not changed our current practice with regard to corticosteroid therapy.
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1. Machado EB, Michet CJ, Ballard DJ, Hunder GG, Beard CM, Chu CP, et al. Trends in incidence and clinical presentation of temporal arteritis in Olmsted County, Minnesota, 1950-1985. Arthritis Rheum. 1988; 31:745-9.
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