2018
DOI: 10.1016/j.carpath.2018.04.005
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Molecular and cellular insights into the pathogenesis of coronary artery ectasia

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Cited by 32 publications
(31 citation statements)
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“…The increased prevalence of CAE in recent years has resulted in a greater focus on the incidence and factors in uencing CAE [3];estimates of the incidence of coronary ectasia have varied from 0.3% to 4.7%. However, the etiopathogenetic mechanism of CAE is not yet completely known, although it may be related to systemic in ammation, stimulated nitric oxide production, coronary balloon angioplasty, nodular polyarteritis, and Kawasaki syndrome [4,5].…”
Section: Introductionmentioning
confidence: 99%
“…The increased prevalence of CAE in recent years has resulted in a greater focus on the incidence and factors in uencing CAE [3];estimates of the incidence of coronary ectasia have varied from 0.3% to 4.7%. However, the etiopathogenetic mechanism of CAE is not yet completely known, although it may be related to systemic in ammation, stimulated nitric oxide production, coronary balloon angioplasty, nodular polyarteritis, and Kawasaki syndrome [4,5].…”
Section: Introductionmentioning
confidence: 99%
“…Frequent coexistence of CAE with CAD is the likely reason for the lack of knowledge regarding the exact mechanism of CAE. However, distinct differences between CAE and CAD have been documented in the literature in terms of clinical course and pathophysiologic steps and biomarkers [ 2 , 3 , 4 , 5 , 6 ]. The most promising difference is the increased inflammatory status in patients with CAE compared to those with normal coronary arteries and CAD, as demonstrated by Boles et al Increased cellular activation molecules such as intercellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM), E-selectin, C-reactive protein, and activation markers of macrophages have already been documented as indicating increased inflammation in CAE compared to CAD [ 7 , 8 , 9 , 10 ].…”
mentioning
confidence: 99%
“…On the other hand, the loss of musculoelastic arterial wall components in CAE was noticed to be unrelated to local atheromatous burden [ 38 , 39 ]. Although CAE has been known to be a variant of atherosclerosis in the literature, there are certain pathophysiologic mechanisms or clinical variables differentiating it from atherosclerosis [ 3 , 40 ]. Furthermore, CAE has been supposed to be a local manifestation of systemic vessel wall abnormality.…”
Section: Coronary Artery Ectasiamentioning
confidence: 99%