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Text
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URL Address
<a href="http://doi.org/10.2174/1381612811319130004" target="_blank" rel="noreferrer noopener">http://doi.org/10.2174/1381612811319130004</a>
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Pages
2366-2374
Issue
13
Volume
19
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Title
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Microvascular Function/dysfunction Downstream A Coronary Stenosis
Publisher
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Current Pharmaceutical Design
Date
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2013
2013-04
Subject
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artery disease; blood-flow; ca2+-activated k+ channels; Coronary microcirculation; coronary stenosis; endothelial dysfunction; flow-induced dilation; function; iib/iiia receptor blockade; left-ventricular wall; myocardial ischemia; myocardial-perfusion; nitric-oxide; Pharmacology & Pharmacy; resistive vessel; unstable angina
Creator
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Guarini G; Capozza P G; Huqi A; Morrone D; Chilian W M; Marzilli M
Description
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For decades coronary macrovascular atherosclerosis has been considered the principal manifestation of coronary heart disease, with most of our effort dedicated to identifying and removal of coronary stenosis. However, growing body of literature indicates that coronary microcirculation also contributes substantially to the pathophysiology of cardiovascular disease. An understanding of mechanisms regulating microvascular function is of critical importance in understanding its role in disease, especially because these regulatory mechanisms vary substantially across species, vascular bed and due to comorbidities. Indeed, the most obvious consequence of coronary stenosis is that it may limit blood supply to the dependent myocardium to the point of causing ischaemia during exercise or even at rest. However, this flow limiting effect is not only due to the passive hydraulic effect of a narrowed conduit, but also to active responses in the coronary microcirculation triggered by the presence of an epicardial stenosis. To understand this problem it is important to review the inter-related mechanisms that regulate flow to the left ventricular wall and modulate transmural distribution of flow. These regulatory mechanisms operate hierarchically and are heterogeneously distributed along the coronary vascular tree. It is also important to discuss the effect of myocardial performance in modulating both blood flow demands and coronary resistance. Some of the interactions between coronary stenosis and microcirculation are transient, like those documented in acute coronary syndromes or during percutaneous interventions. However, microcirculatory remodeling may be triggered by a chronic coronary stenosis, leading to a sustained impairment of blood supply even after successful removal of the epicardial stenosis. A deeper understanding of these phenomena may explain paradoxical findings in patients undergoing coronary revascularization, particularly when functional tests are used in their assessment. These aspects are discussed in detail in this review.
Identifier
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<a href="http://doi.org/10.2174/1381612811319130004" target="_blank" rel="noreferrer noopener">10.2174/1381612811319130004</a>
Format
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Journal Article or Conference Abstract Publication
2013
artery disease
blood-flow
ca2+-activated k+ channels
Capozza P G
Chilian W M
Coronary microcirculation
coronary stenosis
Current Pharmaceutical Design
endothelial dysfunction
flow-induced dilation
Function
Guarini G
Huqi A
iib/iiia receptor blockade
Journal Article or Conference Abstract Publication
left-ventricular wall
Marzilli M
Morrone D
myocardial ischemia
myocardial-perfusion
nitric-oxide
Pharmacology & Pharmacy
resistive vessel
unstable angina