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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
Risk factors for severe cranial ischaemic events in an Italian population-based cohort of patients with giant cell
C Salvarani1, C Della Bella, L Cimino
1Unità Operativa di Reumatologia, Arcispedale S. Maria Nuova, Reggio Emilia, Italy. salvarani.carlo@asmn.re.it
Insights
In Giant Cell Arteritis (GCA), hypertension and prior ischemic heart disease increase the risk of severe cranial ischemic events (CIEs). A low inflammatory response also predicts higher CIE occurrence.
Area of Science:
- Rheumatology
- Neurology
- Cardiology
Background:
- Giant Cell Arteritis (GCA) is a systemic vasculitis affecting large arteries.
- Cranial Ischemic Events (CIEs) are serious complications of GCA.
- Understanding risk factors for CIEs in GCA is crucial for patient management.
Purpose of the Study:
- To investigate the role of cardiovascular risk factors in GCA.
- To assess the impact of carotid atherosclerosis on CIEs in GCA patients.
- To evaluate the effect of anti-platelet/anti-coagulant therapy on CIEs in GCA.
Main Methods:
- Retrospective analysis of 180 biopsy-proven GCA patients.
- Data collection included demographics, clinical features, and laboratory results.
- Evaluation of cardiovascular risk factors, anti-platelet/anti-coagulant use, and carotid atherosclerosis.
Main Results:
- Patients with CIEs had less frequent systemic signs/symptoms and lower ESR/CRP levels at diagnosis.
- Hypertension and ischemic heart disease were more prevalent in patients with CIEs.
- Anti-platelet/anti-coagulant therapy and ischemic heart disease were associated with increased CIE risk.
Conclusions:
- Hypertension is a significant predictor of severe CIEs in GCA.
- A history of ischemic heart disease is associated with a higher risk of CIEs.
- A low inflammatory response at diagnosis may indicate an increased risk for CIEs in GCA.
Objective:
To evaluate the impact of traditional cardiovascular risk factors, carotid atherosclerosis and the effect of anti-platelet/anti-coagulant therapy on the occurrence of severe cranial ischaemic events (CIEs) in GCA.
Methods:
We identified 180 Reggio Emilia (Italy) residents with biopsy-proven GCA diagnosed between 1986 and 2005. We evaluated data on demographics, clinical features, laboratory investigations, cardiovascular risk factors, anti-platelet/anti-coagulant use and carotid atherosclerosis.
Results:
Systemic signs/symptoms were significantly less frequent (P = 0.004) and ESR and C-reactive protein (CRP) values at diagnosis were significantly lower (P = 0.03 and P = 0.04, respectively) in patients with CIEs. The prevalence of hypertension and ischaemic heart disease was significantly higher in patients with CIEs than in those without (P = 0.01 and P = 0.006, respectively). Patients treated with anti-platelet/anti-coagulant therapy were significantly more likely to suffer CIEs than those without (P = 0.03), while CIEs were significantly associated with ischaemic heart disease in this subset of patients (P = 0.02). By multivariate logistic regression, we found that the best predictors for the development of severe CIEs included the absence of high (>5.38 mg/dl) CRP levels at diagnosis (OR = 0.31, 95% CI 0.08, 1.20), the absence of systemic manifestations (OR = 0.30, 95% CI 0.08, 1.08), the presence of hypertension (OR = 7.77, 95% CI 0.83, 72.76), and a past history of ischaemic heart disease (OR = 8.65, 95% CI 0.92, 80.95).
Conclusions:
In GCA, hypertension, a past history of ischaemic heart disease and a low inflammatory response are associated with a higher risk of developing severe CIEs.
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