While clinical signs and symptoms of giant cell arter it is improve promptly after starting glucocorticoid therapy, reports have suggested that the vascular inflammation may persist. To assess the duration and quality of his to pathologic changes in treated patients, we prospectively obtained second temporal artery biopsies in patients treated for 3 to 12 months after their first diagnostic biopsy. 40 patients (28 women, 12 men, median age 77 years) agreed to have a second temporal artery biopsy randomly assigned to 3, 6, 9, or 12 months subsequent to the first. Clinical and laboratory evaluation of the patient cohort revealed a typical rapid response and continued suppression of clinical manifestations as a result of glucocorticoid treatment. His to pathologic findings, evaluated in a blinded fashion by a cardiovascular pathologist, showed unequivocal findings of vasculitis in 7/10 patients with second temporal artery biopsy at 3 months, 9/12 at 6 months, 4/9 at 9 months, and 4/9 at 12 months. Lymphocytes were present in all positive initial biopsies and remained the dominant cell population in chronically treated patients. Granulomatous inflammation decreased in a time-dependent fashion from 78%-100% at initial biopsy to 50% at 9 months and 25% at 12 months. The increased medial fibrosis noted in the second biopsies (60% vs. 33% in primary temporal artery biopsies) suggested that the finding may represent a chronic finding in arteritis. In summary, the response to glucocorticoids in giant cell arteritis was frequently discordant. Clinical manifestations were readily suppressed, but vascular changes were gradual and often incomplete.

Objectives To assess the prognostic significance of high vs. low grade coronary artery ectasia (CAE) and the impact of antithrombotic or anticoagulant therapy on adverse cardiac outcomes. Background There is paucity of knowledge on the impact of angiographic characteristics in CAE or that of antithrombotic or anticoagulant therapy on outcomes. Methods and results In this retrospective study, we reviewed angiograms and medical records of all cases of confirmed CAE (2001–2011). Extent of CAE was categorized using the Markis classification. Types 1 and 2 were categorized as high‐grade and types 3 and 4 as low‐grade CAE. Angiographic flow was recorded as normal or sluggish (

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