Background/Purpose:

Involvement of large arteries leading to stenosis is well-documented in giant cell arteritis (GCA), but limited data are available on the risk of coronary events.  We estimated the risk of newly diagnosed MI events among incident cases with GCA compared to controls from the general population. We also explored time trends for MI since GCA diagnosis.

Methods:

Our data included all visits to health professionals and hospital admissions covered by the comprehensive provincial medical services plan from January 1, 1990 until December 31, 2010 for all individuals. We conducted a matched cohort analysis among patients satisfying the following criteria: a) 40 years of age or older; b) new diagnosis of GCA on at least 2 visits within a 2-year period between Jan 1996 and Dec 2010; and c) use of oral glucocorticoids between 1 month before and 6 months after the diagnosis date.  Ten non-GCA controls matched by birth year, sex, and calendar year of follow-up were selected from the general population for each case.  Our outcome was risk of incident MI events based on hospitalization records or death certificate.  We estimated the relative risks (RRs) of MI compared with the matched non-GCA comparison cohort, adjusting for history of angina, COPD, obesity, cardiovascular disease, diabetes, hormone replacement therapy, dyslipidemia, non-steroidal anti-inflammatory drug use, COX-2 inhibitor use, number of hospitalizations, and Charlson Comorbidity Index at baseline.

Results:

Among 835 individuals with incident GCA (74% female, mean age of 75 years), 109 developed MI (incidence rate = 49.8 per 1000 person years) (Table 1).  Compared with non-GCA individuals, the age-, sex-, and entry time-matched RRs were 3.3 (95% CI; 2.6-4.1).  After adjusting for covariates, the RR remained similar (3.0; 95% CI, 2.3-4.1) (Table 1).  The risk of developing an MI was highest in the first year following diagnosis of GCA and decreased over time, with no increased risk observed after 5 years.

Conclusion:

This large population-based study indicates a substantially increased risk of MI among GCA patients.  The risk was 7 fold higher than that observed in non-GCA controls within the first year of the disease, suggesting that a high level of inflammation or associated therapy at the time of GCA diagnosis may be the culprit.  These findings support the need for increased screening for MI and managing cardiovascular risk factors in GCA, particularly in the period following diagnosis.

Table 1.  Risk of Incident MI according to GCA Status