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THU0285 The Association of Giant Cell Arteritis and its Histopathology with all-Cause and Cardiovascular Mortality
  1. G. Tomasson1,
  2. J. Björnsson2,
  3. Y. Zhang3,
  4. V. Gudnason4,
  5. P.A. Merkel5
  1. 1University of Iceland, Reykjavik
  2. 2Akureyri Regional Hospital, Akureyri, Iceland
  3. 3Boston University, Boston, United States
  4. 4Icelandic Heart Association, Kopavogur, Iceland
  5. 5University of Pennsylvania, Philadelphia, United States

Abstract

Background There is scant information on how histopathology findings are associated with outcomes of patients with giant cell arteritis (GCA).

Objectives To measure the effect of GCA and its histopathology on all-cause and cardiovascular mortality within a population cohort with detailed information on temporal artery biopsies (TABs).

Methods Data from the Reykjavik Study (RS), a population-based study focused on cardiovascular disease, were used. Residents who lived in the greater Reykjavik area in 1967 and were born between 1908 and 1935 were invited to join the study. Subjects who underwent TAB prior to their initial RS visit were excluded. GCA status was defined from examination of TAB by a single expert pathologist by re-examination of all TAB obtained from members of the RS cohort. Original histological diagnosis was obtained from the original pathology report. Level of inflammatory intensity in TABs consistent with GCA was visually graded as mild, moderate, or severe. Subjects were followed from study visit or age 50, whichever occurred later, until death or December 31, 2008, whichever came first. Cardiovascular mortality was assessed from death certificates. Subjects contributed unexposed person-time until they met diagnostic criteria for GCA. Effect of GCA and levels of inflammatory intensity on mortality risks compared to those who did not undergo TAB is expressed as incidence rate ratios (IRR) with 95% confidence intervals (CI) standardized by age and sex.

Results Of 19,196 subjects (51% women) who came for a RS study visit from 1967 to 1994, 692 underwent TAB (71% women) and 196 had GCA (70% women). At study visit the mean age was 54.3 (8.7) years. Mean age of subjects with GCA at the time of TAB was 73.3 (6.8) years. The median follow-up time was 7.1 (IQR: 3.5-12.4) years for subjects after the diagnosis of GCA and 24.3 (IQR: 17.6-29.8) years for referent subjects, respectively. GCA was associated with an increased all-cause (IRR=1.45, 95% CI: 1.20-1.75) and cardiovascular (IRR=1.50, 95% CI: 1.13-1.99) mortality. Subjects with GCA per review of biopsy but who had an original TAB pathology report read as negative for GCA and those with mild inflammatory intensity has substantially elevated mortality risks (Table).

Table 1

Conclusions GCA is associated with modest increases in both all-cause mortality and cardiovascular mortality, driven by patients whose original TAB was reported as negative (and in Iceland therefore, likely not treated for GCA). The level of inflammation seen on TAB is inversely associated with mortality risks

Disclosure of Interest None declared

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