2014
DOI: 10.1016/j.ijcme.2014.03.002
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Microvascular inflammation in atherosclerosis

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Cited by 27 publications
(17 citation statements)
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“…62 Evidence linking microvascular and inflammatory responses to risk factors indicates that oxidative stress, reduced nitric-oxide (NO)-bioavailability, and endothelial activation are common early features of coronary microvascular responses to atherosclerosis risk factors. 63 …”
Section: Pathophysiologymentioning
confidence: 99%
“…62 Evidence linking microvascular and inflammatory responses to risk factors indicates that oxidative stress, reduced nitric-oxide (NO)-bioavailability, and endothelial activation are common early features of coronary microvascular responses to atherosclerosis risk factors. 63 …”
Section: Pathophysiologymentioning
confidence: 99%
“…The pathophysiology of atherosclerosis is now clearly related to chronic inflammation with periods of minor plaque rupture, erosion, and distal embolism resulting in MI . Evidence linking microvascular and inflammatory responses to risk factors indicates that oxidative stress, reduced nitric oxide (NO) bioavailability, and endothelial activation are common early features of coronary microvascular responses to atherosclerosis risk factors . Essentially, all INOCA patients with chronic angina studied by intravascular ultrasound (IVUS) to date have some coronary atherosclerosis .…”
Section: Pathophysiologymentioning
confidence: 99%
“…25 Evidence linking microvascular and inflammatory responses to risk factors indicates that oxidative stress, reduced nitric oxide (NO) bioavailability, and endothelial activation are common early features of coronary microvascular responses to atherosclerosis risk factors. 26 Essentially, all INOCA patients with chronic angina studied by intravascular ultrasound (IVUS) to date have some coronary atherosclerosis. 27,28 A greater burden of risk factors is associated with more atherosclerosis, concealed by compensatory positive remodeling, yielding diffuse nonobstructive CAD.…”
Section: Atherosclerosismentioning
confidence: 99%
“…[4][5][6] In various animal and human model of atherosclerosis, circulating blood components like neutrophil, lymphocyte, platelets, and other inflammatory mediators were found in the lesions. 7 Pathophysiology of atherosclerosis involves chemotactic proteins and adhesion molecules mediated recruitment of circulating leucocytes and platelets to the injured endothelium site. 8 Damage to the endothelium upsets the balance between vasoconstriction and vasodilation that promotes the endothelial permeability, platelet aggregation, leukocyte adhesion, and generation of cytokines ultimately initiating deleterious events of atherosclerosis.…”
Section: Introductionmentioning
confidence: 99%