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High Coronary Shear Stress in Patients With Coronary Artery Disease Predicts Myocardial Infarction Evolving insights into the role of local shear stress in late stent failure from neoatherosclerosis formation and plaque destabilization Role of local coronary blood flow patterns and shear stress on the development of microvascular and epicardial endothelial dysfunction and coronary plaque Implications of the local hemodynamic forces on the formation and destabilization of neoatherosclerotic lesions Role of endothelial dysfunction in determining angina after percutaneous coronary intervention: Learning from pathophysiology to optimize treatment TAVI Represents an Anti-Inflammatory Therapy via Reduction of Shear Stress Induced, Piezo-1-Mediated Monocyte Activation Transcatheter Aortic Valve Implantation Represents an Anti-Inflammatory Therapy Via Reduction of Shear Stress-Induced, Piezo-1-Mediated Monocyte Activation Endothelial ACKR3 drives atherosclerosis by promoting immune cell adhesion to vascular endothelium
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Review Article2018 Jun 25.[Epub ahead of print]

JOURNAL：Curr Pharm Des. Article Link

Coronary Microcirculation in Ischemic Heart Disease

Pries AR, Kuebler WM, Habazettl H. Keywords: Angioadaptation; Heterogeneity; Inflammation; Leucocyte-Endothelium Interaction; Microvessels; vascular Permeability

ABSTRACT

BACKGROUND - Ischemic heart disease has long been considered to be exlusively caused by stenosis or occlusion. However, the coronary microcirculation too may play an important role in ischemic conditions. Also, the crucial role of microvessels in not only regulating blood flow on a local level but also mediating vascular permeability or inflammatory responses has been recognized.


OBJECTIVE - To review important physiological and pathophysiological mechanisms of coronary microcirculatory control with focus on heterogeneity of local perfusion, microvascular permeability and inflammation.

METHOD - Selective research of the literature.

RESULTS - Heterogeneity is a characteristic of microvascular networks and affects structural and functional parameters such as vessel diameter, length, and connection pattern, flow velocity, wall shear stress, and oxygenation. The networks are optimized to meet the metabolic demand of all tissue compartments. This requires continuous vascular adaptation regulated by local hemodynamic and metabolic stimuli. Compromising this regulation results in functional arterio-venous shunting and tissue areas with either hyperperfusion or hypoxia in close proximity. In ischemia-reperfusion, increased microvascular permeability may aggravate tissue hypoxia by increasing extravascular pressure and seems to contribute to adverse myocardial remodeling. Transendothelial transport mechanisms and deterioration of the endothelial glycocalyx seem to be major contributors to tissue edema. Also in the context of ischemia-reperfusion, an inflammatory response mediated by venular endothelium expressing specific adhesion molecules contributes to tissue injury. However, anti-inflammatory therapies failed in clinical studies and a multi-targeted approach for cardiac protection has been demanded.

CONCLUSION - Disturbances of the coronary microcirculation are involved in different pathophysiological aspects of reperfusion injury.

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
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