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Chronic Total Occlusion Percutaneous Coronary Intervention: Evidence and Controversies Cardiac Troponin Composition Characterization after Non ST-Elevation Myocardial Infarction: Relation with Culprit Artery, Ischemic Time Window, and Severity of Injury Myocardial Inflammation Predicts Remodeling and Neuroinflammation After Myocardial Infarction Uptake of Drug-Eluting Bioresorbable Vascular Scaffolds in Clinical Practice : An NCDR Registry to Practice Project Natural History of Spontaneous Coronary Artery Dissection With Spontaneous Angiographic Healing Contemporary Diagnosis and Management of Patients With Myocardial Infarction in the Absence of Obstructive Coronary Artery Disease: A Scientific Statement From the American Heart Association Patient Characteristics Associated With Antianginal Medication Escalation and De-Escalation Following Chronic Total Occlusion Percutaneous Coronary Intervention: Insights From the OPEN CTO Registry High-sensitivity troponin in the evaluation of patients with suspected acute coronary syndrome: a stepped-wedge, cluster-randomised controlled trial Impact of Oxidative Stress on the Heart and Vasculature: Part 2 of a 3-Part Series 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

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.

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