Coronary Artery Disease and Systemic Vasculitis: Case Report and Review

Extensive phenotyping of vascular damage in non-infectious primary vasculitides with the use of non-invasive vascular biomarkers: prevalence, pathogenesis and response to treatment

“…2 Prior to the introduction of corticosteroids, the natural history of untreated NIPSV was that of a rapidly progressive and RESEARCH PROTOCOLS-PROPOSAL usually fatal disease. 3,4 Nowadays, the causes of death include cancer and infections due to chronic immune activation and/or to immunosuppressive therapy. 4,6 Vascular complications (involving both micro-and macro-circulation) are major sources of morbidity and mortality in NIPSV.…”

“…5 Macrovascular complications (e.g., coronary artery disease, stroke, aneurysm formation and rupture) are major causes of morbidity and mortality especially in medium and large vessel vasculitides. 3,4,5 Lumen stenosis, occlusion or aneurysmal dilatation of blood vessels due to intramural inflammation and necrosis represent the major vascular pathology in NIPSV. 3 Mural fibrin deposition in arterioles or venules, as well as angiocentric inflammatory cell infiltration are the hallmarks of biopsy-proven diagnosis.…”

“…3,4,5 Lumen stenosis, occlusion or aneurysmal dilatation of blood vessels due to intramural inflammation and necrosis represent the major vascular pathology in NIPSV. 3 Mural fibrin deposition in arterioles or venules, as well as angiocentric inflammatory cell infiltration are the hallmarks of biopsy-proven diagnosis. 3 The early steps in the immunological process of vascular damage in NIPSV cannot be considered to be uniform, since various discrete mechanisms such as endothelial activation and dysfunction, autoantibodies to endothelial cell-surface antigens or neutrophil components and abnormal IgA tissue deposition are involved.…”

“…3 Mural fibrin deposition in arterioles or venules, as well as angiocentric inflammatory cell infiltration are the hallmarks of biopsy-proven diagnosis. 3 The early steps in the immunological process of vascular damage in NIPSV cannot be considered to be uniform, since various discrete mechanisms such as endothelial activation and dysfunction, autoantibodies to endothelial cell-surface antigens or neutrophil components and abnormal IgA tissue deposition are involved. 5 Beyond the NIPSV specific pathways of vascular damage, numerous evidence suggests that the classical pathways of arterial damage, namely, atheromatosis (i.e., atheromatic plaque formation), inappropriate arterial remodeling (e.g., arterial hypertrophy / distention) and arteriosclerosis (i.e., arterial stiffening), are accelerated, thus participating in the development of micro-and macro-vascular complications in NIPSV.…”

Inflammatory mediators of coronary artery ectasia

“…45 Coronary vasculitis can even be present in the acute phase of acute renal failure and rheumatic heart disease, and may also be associated with CAE. 46 Aydin et al…”