TY - JOUR
T1 - Risk factors for severe cranial ischaemic events in patients with giant cell arteritis
AU - Grossman, Chagai
AU - Barshack, Iris
AU - Koren-Morag, Nira
AU - Ben-Zvi, Ilan
AU - Bornstein, Gil
N1 - Publisher Copyright:
© Clinical and Experimental Rheumatology 2017.
PY - 2017
Y1 - 2017
N2 - Objective. Cranial ischaemic events constitute a significant component in the clinical spectrum of giant cell arteritis (GCA). Our aim was to investigate whether cardiovascular risk factors, specific medications and baseline clinical features are associated with the development of severe cranial ischaemic events in GCA patients. Methods. Retrospective analysis of GCA patients. Information collected included baseline clinical and laboratory data, comorbidities, cardiovascular risk factors and medications. GCA Patients with and without severe cranial ischaemic complications were compared. Results. A total of 83 patients with GCA were included in the study. Among them, 24 (29%) patients developed severe cranial ischaemic events. Compared with patients without severe cranial ischaemic events, those with severe cranial ischaemic events had lower erythrocyte sedimentation rate (ESR) levels at diagnosis (81±17 vs. 93±21, p=0.018) and were more likely to have jaw claudication (37.5% vs. 17%, p=0.043). Rate of cardiovascular risk factors and rate of use of anti-platelets and statins were similar between the two groups. The use of β blockers was higher among patients with severe ischaemic events (46% vs. 20%, p=0.019). Logistic regression analysis showed that lower ESR levels (OR=0.967, 95% CI, 0.94,0.99) and β blockers use (OR=4.35, 95% CI, 1.33,14.2) predicted development of severe cranial ischaemic complications. Conclusions The present study demonstrated that GCA patients with severe cranial ischaemic events had lower inflammatory responses and were more likely to have been treated with β-blockers. Cardiovascular risk factors and antiplatelet therapy had no effect on the occurrence of severe cranial ischaemic events.
AB - Objective. Cranial ischaemic events constitute a significant component in the clinical spectrum of giant cell arteritis (GCA). Our aim was to investigate whether cardiovascular risk factors, specific medications and baseline clinical features are associated with the development of severe cranial ischaemic events in GCA patients. Methods. Retrospective analysis of GCA patients. Information collected included baseline clinical and laboratory data, comorbidities, cardiovascular risk factors and medications. GCA Patients with and without severe cranial ischaemic complications were compared. Results. A total of 83 patients with GCA were included in the study. Among them, 24 (29%) patients developed severe cranial ischaemic events. Compared with patients without severe cranial ischaemic events, those with severe cranial ischaemic events had lower erythrocyte sedimentation rate (ESR) levels at diagnosis (81±17 vs. 93±21, p=0.018) and were more likely to have jaw claudication (37.5% vs. 17%, p=0.043). Rate of cardiovascular risk factors and rate of use of anti-platelets and statins were similar between the two groups. The use of β blockers was higher among patients with severe ischaemic events (46% vs. 20%, p=0.019). Logistic regression analysis showed that lower ESR levels (OR=0.967, 95% CI, 0.94,0.99) and β blockers use (OR=4.35, 95% CI, 1.33,14.2) predicted development of severe cranial ischaemic complications. Conclusions The present study demonstrated that GCA patients with severe cranial ischaemic events had lower inflammatory responses and were more likely to have been treated with β-blockers. Cardiovascular risk factors and antiplatelet therapy had no effect on the occurrence of severe cranial ischaemic events.
KW - Cardiovascular risk factors
KW - Giant cell arteritis
KW - Severe cranial ischaemic events
UR - http://www.scopus.com/inward/record.url?scp=85018243756&partnerID=8YFLogxK
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C2 - 28466802
AN - SCOPUS:85018243756
SN - 0392-856X
VL - 35
SP - 88
EP - 93
JO - Clinical and Experimental Rheumatology
JF - Clinical and Experimental Rheumatology
ER -