¹University of Lübeck, Department of Rheumatology and Clinical Immunology, Lübeck
²Christian-Albrechts University Kiel, Institute of Experimental Medicine, Kiel
³University of Lübeck, Lübeck Institute of Experimental Dermatology, Lübeck
⁴University of Lübeck, Department of Dermatology, Lübeck
⁵University of Lübeck, Cardioimmunology Research Group, Lübeck
⁶Independent Researcher, Groß Grönau

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Introduction: In spite of significantly improved therapy during the last years, long-term mortality and cardiovascular morbidity have remained high in giant cell arteritis (GCA). Cardiovascular diseases are the leading causes of death within the first year after diagnosis [1], [2]. National population-based database and cohort analyses suggest an increased risk for cerebrovascular events in GCA [3], [4]. This study aimed to assess the risk of death and cardiovascular outcomes in GCA using a large global electronic health record database for biomedical and clinic research (TriNetX) [5].

Methods: This retrospective cohort study analysed data samples from an electronic health record database of the US-based TriNetX network. Patients (aged ≥18 years) with the diagnostic codes of giant cell arteritis (GCA), polymyalgia rheumatica without signs of vasculitis (so-called clinically pure PMR), and giant cell arteritis with polymyalgia rheumatica (GCA-PMR) (International Classification of Diseases [ICD]) were included. Patients without GCA and/or PMR served as negative controls and were matched 1:1 with the cases. Propensity score matching for demographic variables (age, gender, family history of ischemic heart disease and other disease of the circulatory system, personal history of nicotine dependence) and cardiovascular and metabolic comorbidities (diagnostic codes for nicotine dependence, overweight and obesity, dyslipoproteinaemia, arterial hypertension, chronic lower respiratory diseases, chronic kidney disease, neoplasms, diabetes mellitus) was performed to optimize between-group comparability. Hazard ratios (HR) related to death and cardiovascular outcomes were calculated using univariate Cox regression after analysis of the matched cohort using the Kaplan-Meier method. P values were determined by the Log-rank test.

Results: We identified 51,507 patients with GCA, 114,603 with PMR without vasculitis (pure PMR), and 8,169 with GCA-PMR. The unadjusted and adjusted relative risk (RR) of mortality was increased in GCA (RR 19.75%), PMR (RR 17.66%), and GCA-PMR (RR 22.62%) compared to matched controls (GCA: HR: 1.84, 95%CI: 1.77 to 1.90, P < 0.0001, PMR: HR: 1.54 95%CI: 1.50 to 1.58, P < 0.0001, GCA-PMR: HR: 1.50 95%CI: 1.39 to 1.62; P < 0.0001). The overall risk for cardiac and vascular events was increased in GCA, PMR, and GCA-PMR compared to matched controls (P < 0.0001). In contrast to PMR, the risk for cerebrovascular events was increased in GCA and GCA-PMR compared to matched controls (ischaemic stroke: GCA HR: 2.01, 95%CI: 1.91 to 2.12, PMR HR: 1.35, 95%CI: 1.30 to 1.40, GCA-PMR HR: 1.64, 95%CI: 1.45 to 1.85; haemorrhagic stroke: GCA HR: 1.93, 95%CI: 1.77 to 2.11, PMR HR: 1.24 95%CI: 1.17 to 1.32, GCA-PMR HR: 1.46, 95%CI: 1.20 to 1.79; cerebrovascular diseases: GCA HR: 2.35 95%CI: 2.22 to 2.48, PMR HR: 1.43 95%CI: 1.37 to 1.49, GCA-PMR HR: 1.43 95%CI: 1.37 to 1.49).

Conclusion: The overall risk for death and cardiovascular events was increased in patients with GCA with and without PMR and in clinically pure PMR. In contrast to PMR, cerebrovascular events were increased in patients with GCA with or without PMR.

Literatur

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