Pathophysiology and Clinical Manifestations of Giant Cell Arteritis

Vascular Inflammation and Remodeling

The American College of Rheumatology notes that histopathological hallmarks of GCA include arterial wall thickening with narrowed lumen, presence of mononuclear inflammatory cells with invasion of the media layer, and multinucleated giant cells in the media 1
The European League Against Rheumatism reports that the inflammatory process leads to destruction and remodeling of the arterial wall, resulting in intimal hyperplasia and progressive occlusion of the arterial lumen, with manifestations including headache, scalp tenderness, jaw claudication, and potentially vision loss in 14-18% of patients 3

The American Heart Association states that less common ischemic complications of GCA include stroke, cranial nerve palsy, and scalp necrosis 1
GCA may also be complicated by large-vessel aneurysms and vascular stenoses, according to the American College of Cardiology 1

The American College of Rheumatology recommends that inflammatory markers, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), be used to diagnose GCA, with ESR typically exceeding 40 mm/h and CRP elevated in most cases 1
A platelet count >400 × 10³/μL is common and has diagnostic value, as reported by the European League Against Rheumatism 4

The American Thoracic Society notes that respiratory involvement occurs in <10% of GCA cases, with chronic cough being the most frequent respiratory symptom 5